An isolated cardiac muscle cell, beating

Cardiac muscle (heart muscle) is an involuntary, striated muscle that is found in the walls and histological foundation of the heart, specifically the myocardium. Cardiac muscle is one of three major types of muscle, the others being skeletal and smooth muscle. These three types of muscle all form in the process of myogenesis. The cells that constitute cardiac muscle, called cardiomyocytes or myocardiocytes, predominantly contain only one nucleus, although populations with two to four nuclei do exist.[1][2][pageneeded] The myocardium is the muscle tissue of the heart, and forms a thick middle layer between the outer epicardium layer and the inner endocardium layer.

Coordinated contractions of cardiac muscle cells in the heart pump blood out of the atria and ventricles to the blood vessels of the left/body/systemic and right/lungs/pulmonary circulatory systems. This complex mechanism illustrates systole of the heart.

Cardiac muscle cells, unlike most other tissues in the body, rely on an available blood and electrical supply to deliver oxygen and nutrients and remove waste products such as carbon dioxide. The coronary arteries help fulfill this function.

Cardiac muscle has cross striations formed by rotating segments of thick and thin protein filaments. Like skeletal muscle, the primary structural proteins of cardiac muscle are myosin and actin. The actin filaments are thin, causing the lighter appearance of the I bands in striated muscle, whereas the myosin filament is thicker, lending a darker appearance to the alternating A bands as observed with electron microscopy. However, in contrast to skeletal muscle, cardiac muscle cells are typically branch-like instead of linear.

Another histological difference between cardiac muscle and skeletal muscle is that the T-tubules in the cardiac muscle are bigger and wider and track laterally to the Z-discs. There are fewer T-tubules in comparison with skeletal muscle. The diad is a structure in the cardiac myocyte located at the sarcomere Z-line. It is composed of a single T-tubule paired with a terminal cisterna of the sarcoplasmic reticulum. The diad plays an important role in excitation-contraction coupling by juxtaposing an inlet for the action potential near a source of Ca2+ ions. This way, the wave of depolarization can be coupled to calcium-mediated cardiac muscle contraction via the sliding filament mechanism. Cardiac muscle forms these instead of the triads formed between the sarcoplasmic reticulum in skeletal muscle and T-tubules. T-tubules play critical role in excitation-contraction coupling (ECC). Recently, the action potentials of T-tubules were recorded optically by Guixue Bu et al.[3]

The cardiac syncytium is a network of cardiomyocytes connected to each other by intercalated discs that enable the rapid transmission of electrical impulses through the network, enabling the syncytium to act in a coordinated contraction of the myocardium. There is an atrial syncytium and a ventricular syncytium that are connected by cardiac connection fibres.[4] Electrical resistance through intercalated discs is very low, thus allowing free diffusion of ions. The ease of ion movement along cardiac muscle fibers axes is such that action potentials are able to travel from one cardiac muscle cell to the next, facing only slight resistance. Each syncytium obeys the all or none law.[5]

Intercalated discs are complex adhering structures that connect the single cardiomyocytes to an electrochemical syncytium (in contrast to the skeletal muscle, which becomes a multicellular syncytium during mammalian embryonic development). The discs are responsible mainly for force transmission during muscle contraction. Intercalated discs consist of three different types of cell-cell junctions: the actin filament anchoring adherens junctions, the intermediate filament anchoring desmosomes , and gap junctions. They allow action potentials to spread between cardiac cells by permitting the passage of ions between cells, producing depolarization of the heart muscle. However, novel molecular biological and comprehensive studies unequivocally showed that intercalated discs consist for the most part of mixed-type adhering junctions named area composita (pl. areae compositae) representing an amalgamation of typical desmosomal and fascia adhaerens proteins (in contrast to various epithelia).[6][7][8] The authors discuss the high importance of these findings for the understanding of inherited cardiomyopathies (such as arrhythmogenic right ventricular cardiomyopathy).

Under light microscopy, intercalated discs appear as thin, typically dark-staining lines dividing adjacent cardiac muscle cells. The intercalated discs run perpendicular to the direction of muscle fibers. Under electron microscopy, an intercalated disc's path appears more complex. At low magnification, this may appear as a convoluted electron dense structure overlying the location of the obscured Z-line. At high magnification, the intercalated disc's path appears even more convoluted, with both longitudinal and transverse areas appearing in longitudinal section.[9]

In contrast to skeletal muscle, cardiac muscle requires extracellular calcium ions for contraction to occur. Like skeletal muscle, the initiation and upshoot of the action potential in ventricular cardiomyocytes is derived from the entry of sodium ions across the sarcolemma in a regenerative process. However, an inward flux of extracellular calcium ions through L-type calcium channels sustains the depolarization of cardiac muscle cells for a longer duration. The reason for the calcium dependence is due to the mechanism of calcium-induced calcium release (CICR) from the sarcoplasmic reticulum that must occur during normal excitation-contraction (EC) coupling to cause contraction. Once the intracellular concentration of calcium increases, calcium ions bind to the protein troponin, which allows myosin to bind to actin and contraction to occur.

Until recently, it was commonly believed that cardiac muscle cells could not be regenerated. However, a study reported in the April 3, 2009 issue of Science contradicts that belief.[10] Olaf Bergmann and his colleagues at the Karolinska Institute in Stockholm tested samples of heart muscle from people born before 1955 who had very little cardiac muscle around their heart, many showing with disabilities from this abnormality. By using DNA samples from many hearts, the researchers estimated that a 4-year-old renews about 20% of heart muscle cells per year, and about 69 percent of the heart muscle cells of a 50-year-old were generated after he or she was born.

One way that cardiomyocyte regeneration occurs is through the division of pre-existing cardiomyocytes during the normal aging process.[11] The division process of pre-existing cardiomyocytes has also been shown to increase in areas adjacent to sites of myocardial injury. In addition, certain growth factors promote the self-renewal of endogenous cardiomyocytes and cardiac stem cells. For example, insulin-like growth factor 1, hepatocyte growth factor, and high-mobility group protein B1 increase cardiac stem cell migration to the affected area, as well as the proliferation and survival of these cells.[12] Some members of the fibroblast growth factor family also induce cell-cycle re-entry of small cardiomyocytes. Vascular endothelial growth factor also plays an important role in the recruitment of native cardiac cells to an infarct site in addition to its angiogenic effect.

Based on the natural role of stem cells in cardiomyocyte regeneration, researchers and clinicians are increasingly interested in using these cells to induce regeneration of damaged tissue. Various stem cell lineages have been shown to be able to differentiate into cardiomyocytes, including bone marrow stem cells. For example, in one study, researchers transplanted bone marrow cells, which included a population of stem cells, adjacent to an infarct site in a mouse model. Nine days after surgery, the researchers found a new band of regenerating myocardium.[13] However, this regeneration was not observed when the injected population of cells was devoid of stem cells, which strongly suggests that it was the stem cell population that contributed to the myocardium regeneration. Other clinical trials have shown that autologous bone marrow cell transplants delivered via the infarct-related artery decreases the infarct area compared to patients not given the cell therapy.[14]

Occlusion (blockage) of the coronary arteries by atherosclerosis and/or thrombosis can lead to myocardial infarction (heart attack), where part of the myocardium is injured due to ischemia (not receiving enough oxygen). This occurs because coronary arteries are functional end arteries - i.e. there is almost no overlap in the areas supplied by different arteries (anastomoses) so that if one fails, others cannot adequately perfuse the region, unlike in other tissues.

Certain viruses lead to myocarditis (inflammation of the myocardium). Cardiomyopathies are inherent diseases of the myocardium, many of which are caused by genetic mutations.

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Cardiac muscle - Wikipedia

Cardiac Stem Cells Comments Off on Cardiac muscle – Wikipedia | November 27th, 2016

SIGNIFICANCE:

Heart disease is the primary cause of death in the industrialized world. Cardiac failure is dictated by an uncompensated reduction in the number of viable and fully functional cardiomyocytes. While current pharmacological therapies alleviate the symptoms associated with cardiac deterioration, heart transplantation remains the only therapy for advanced heart failure. Therefore, there is a pressing need for novel therapeutic modalities. Cell-based therapies involving cardiac stem cells (CSCs) constitute a promising emerging approach for the replenishment of the lost tissue and the restoration of cardiac contractility.

CSCs reside in the adult heart and govern myocardial homeostasis and repair after injury by producing new cardiomyocytes and vascular structures. In the last decade, different classes of immature cells expressing distinct stem cell markers have been identified and characterized in terms of their growth properties, differentiation potential, and regenerative ability. Phase I clinical trials, employing autologous CSCs in patients with ischemic cardiomyopathy, are being completed with encouraging results.

Accumulating evidence concerning the role of CSCs in heart regeneration imposes a reconsideration of the mechanisms of cardiac aging and the etiology of heart failure. Deciphering the molecular pathways that prevent activation of CSCs in their environment and understanding the processes that affect CSC survival and regenerative function with cardiac pathologies, commonly accompanied by alterations in redox conditions, are of great clinical importance.

Further investigations of CSC biology may be translated into highly effective and novel therapeutic strategies aiming at the enhancement of the endogenous healing capacity of the diseased heart.

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Cardiac stem cells: biology and clinical applications.

Cardiac Stem Cells Comments Off on Cardiac stem cells: biology and clinical applications. | November 7th, 2016

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Article

The membrane scaffold SLP2 anchors a proteolytic hub in mitochondria containing PARL and the iAAA protease YME1L

These authors contributed equally to this work

The membrane scaffold SLP2 anchors a large protease complex containing the rhomboid protease PARL and the iAAA protease YME1L in the inner membrane of mitochondria, termed the SPY complex. Assembly into the SPY complex modulates PARL activity toward its substrate proteins PINK1 and PGAM5.

The membrane scaffold SLP2 anchors a large protease complex containing the rhomboid protease PARL and the iAAA protease YME1L in the inner membrane of mitochondria, termed the SPY complex. Assembly into the SPY complex modulates PARL activity toward its substrate proteins PINK1 and PGAM5.

SLP2 assembles with PARL and YME1L into the SPY complex in the mitochondrial inner membrane.

Assembly into SPY complexes modulates PARLmediated processing of PINK1 and PGAM5.

SLP2 restricts OMA1mediated processing of the OPA1.

Timothy Wai, Shotaro Saita, Hendrik Nolte, Sebastian Mller, Tim Knig, Ricarda RichterDennerlein, HansGeorg Sprenger, Joaquin Madrenas, Mareike Mhlmeister, Ulrich Brandt, Marcus Krger, Thomas Langer

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Avian influenza: zoonosis

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Supercourse: Epidemiology, the Internet, and Global Health

Cardiac Stem Cells Comments Off on Supercourse: Epidemiology, the Internet, and Global Health | October 16th, 2016

9thInternational Conference on Hematology

Date: November 02-04, 2017

Venue: Las Vegas, USA

Hematology 2016 has been designed with many interesting and informative scientific sessions; it includes all possible aspects of Hematology research.

Hematology

Erythrocytesare also known as red blood cells which carry oxygen to the body and collect carbon dioxide from the body by the use of hemoglobin and its life span of 120 days. along the side the leucocytes helps in protecting the healthy cells because the W.B.C (leucocytes) act as the defending cells in protecting the immune system from the foreign cells. Theseleucocytesare multipotent cells in bone marrow and there life span is of 3-4 days where the yellow blood cells are called as thrombocytes they are where small and irregular in shape they have life span of 5-9 days they are mostly seen in mammals they help in clotting of blood which are in fibrin form called as thrombosis these lead to heart stroke, blockage of blood in blood mostly in arms and legs. where C.B.C is known ascomplete blood countis done to know the number of cells in a body these are mainly done by lab technician presently they are been tested by automatic analyzer the high and low amount of cells will lead to many diseases. Decrease of R.B.C in the body these causes of anemia which leads to weakness, feeling of tired, shortness of breath and person will be noticeably pale. Formation of blood cellular components are called as Hematopoiesis and all the cellular blood components are derived from hematopoiesis stem cells in a healthy individual nearly 10111012new blood cells are produced these help in steady peripheral circulation. If there is a increases of R.B.C in the body these causes polycythemia these can be measured through hematocrit level.

Blood Disorders

Hemophilia Ais a genetic deficiency in clottingfactor VIII,which causes increased bleeding and usually affects males. About 70% of the time it is inherited as an X-linked recessive trait, but around 30% of cases arise from spontaneous mutations. Hemophilia B is ablood clottingdisorder caused by amutationof thefactor IXgene, leading to a deficiency of factor IX. It is the second-most common form ofhaemophilia, rarer thanhaemophilia A. It is sometimes calledChristmas disease, named afterStephen Christmas, the first patient described with this disease.In addition, the first report of its identification was published in the Christmas edition of theBritish Medical Journal.Hemophilia C is a mild form of haemophiliaaffecting both sexes. However, it predominantly occurs in Jews ofAshkenazidescent. It is the fourth most common coagulationdisorder aftervon Willebrand's diseaseandhaemophiliaAandB.In theUSAit is thought to affect 1 in 100,000 of the adult population, making it 10% as common as haemophilia A. Idiopathic thrombocytopenic purpura(ITP), also known asimmune thrombocytopenia,primary immune thrombocytopenia,primary immune thrombocytopenic purpuraorautoimmune thrombocytopenic purpura, is defined as isolated low platelet count (thrombocytopenia) with normalbone marrowand the absence of other causes of thrombocytopeniaVon Willebrand diseasesis the most common hereditarycoagulationabnormality described in humans. Platelets also called "thrombocytes" areblood cellswhose function (along with thecoagulation factors) is to stop bleeding by clumping and clogging blood vessel injuries.Platelets have nocell nucleus: Coagulation is highlyconservedthroughout biology; in allmammals, coagulation involves both a cellular (platelet) and aprotein(coagulation factor) component and these are occoured due togenetic blood disorders

Hematologic Malignancies

Lymphatic leukemiawhich effect the white blood cells(w.b.c) they are closely related to the lymphomas and some of them are unitary diseases which related to the adult T cells leukemia these come under the lymphoproliferative disorders. Mostly they involve in the B-cell sub type lymphocytes. The myeloid leukemia is preferred to the granulocyte precursor in the bone marrow and spinal cord and these arises the abnormal growth in the blood from tissues in the bone marrow. They are mainly related to the hematopoietic cells and these sub title into acute and chronic lymphoblastic leukemia. The acute leukemia is that rapidly producing immature blood cells as they are bulk number of cells healthy cells are not produced in bone marrow due this spill over the blood stream which spread to other body parts. Where as in chronic leukemia highly bulid of matured cells are formed but still abnormal white cells are formed these can not be treated immediately mostly seen in older people. The cancer which originate from white blood cells are called as lymphoma and this disorder is mainly seen inHodgkin lymphomathese diseases is treated by radiation and chemotherapy, orhematopoietic stem cell transplantation. The cancer which starts with in the cell are called as Non Hodgkin lymphocytes and these lymphocytes are of lymph nodes. The bone marrow which develops too many white blood cells leads tomultiple myleoma. The further details on malignance are been discussed inHematology oncology conference-2015.

Hematology and immunology

Blood groupsare of ABO type and but at present the Rh blood grouping of 50 well defined antigens in which 5 are more important they are D,C,c,E and e and Rh factors are of Rh positive and Rh negative which refers to the D-antigen. These D-antigen helps in prevention of erythroblast fetalis lacking of Rh antigen it defined as negative and presences of Rh antigen in blood leads to positive these leads to rh incompatibility. The prevention treatment of diseases related to the blood is called as the Hematology. The hematologists conduct works on cancer to. The disorder of immune system leading to hypersensitivity is called asClinical Immunologyand the abnormal growth of an infection are known as Inflammation and the arise of an abnormal immune response to the body or an immune suppression are known as Auto immune disorder. The stem cell therapy is used to treat or prevent a disease or a condition mostly Bone marrow stem cell therapy is seen and recently umbilical cord therapy Stem cell transplantation strategies remains a dangerous procedure with many possible complications; it is reserved for patients with life-threatening diseases.

Blood Transplantation

Theumbilical cordis a conduit between the developingembryoorfetusand theplacenta. The umbilical vein supplies the fetus with nutrient-richbloodfrom theplacenta The hematopoitic bone marrow transplant, the HSC are removed from a large bone of the donor, typically thepelvis, through a largeneedlethat reaches the center of the bone. Acute myeloid leukemia is a cancerof themyeloidline of blood cells, characterized by the rapid growth of abnormalwhite blood cellsthat accumulate in thebone marrowand interfere withthe production of normal blood cells and the Thrombosis is the formation of ablood clot inside ablood vessel, obstructing the flow ofbloodthrough thecirculatory system. TheHemostaticis a process which causes bleeding to stop, meaning to keep blood within a damaged blood vessel this is the first stage of wound healing. Metabolic syndromeis a disorder of energy utilization and storage, diagnosed by a co-occurrence of three out of five of the following medical conditions, obesity,elevated blood pressure,elevated fasting plasma glucose,high serum triglycerides, and lowhigh-density lipoprotein(HDL) levels. Metabolic syndrome increases the risk developingcardiovascular diseaseanddiabetes.

Diagnosis and Treatment

Palliative careis amultidisciplinary approachto specialisedmedical carefor people with seriousillnesses The spleen, similar in structure to a largelymph node, acts as a blood filter. Anticoagulants(antithrombics) are a class of drugs that work to prevent thecoagulation(clotting) of blood. Some anticoagulants are used in medical equipment, such astest tubes ,blood transfusionbags, andrenal dialysisequipment. Anvena cava filteris a type of vascular filter, amedicaldevice that is implanted byinterventional radiologistsor vascular surgeons into theinferior vena cavato presumably prevent life-threateningpulmonary emboliistherapyusingionizing radiation, generally as part of cancer treatmentto control or killmalignantcells. Radiation therapy may be curative in a number of types of cancer if they are localized to one area of the body. The subspecialty ofoncologythat focuses on radiotherapy is calledradiation oncology. Translational research is another term fortranslated researchandtranslational science, Applying knowledge from basic science is a major stumbling block in science, partially due to the compartmentalization within science. Targeted drug delivery is a method of deliveringmedicationto a patient in a manner that increases theconcentrationof the medication in some parts of the body relative to others.

New Drug Development in Haematology

The development of antibiotic resistance in particular stems from the drugs targeting only specific bacterial molecules. Because the drugisso specific, any mutation in these molecules will interfere with or negate its destructive effect, resulting in antibiotic resistance. Known asDrug deliveryConditions treated with combination therapy includetuberculosis,leprosy,cancer,malaria, andHIV/AIDS. One major benefit of combination therapies is that they reduce development ofdrug resistance, since a pathogen or tumor is less likely to have resistance to multiple drugs simultaneously.Artemisinin-based monotherapies for malaria are explicitly discouraged to avoid the problem of developing resistance to the newer treatment. Drug Induced Blood Disorders causes of sickle cell anemia,pale skin non steroids antiinflammatory drugswhich causes ulcers Using drug repositioning, pharmaceutical companies have achieved a number successes, for examplePfizer'sViagrainerectile dysfunctionandCelgene'sthalidomidein severe erythema nodosum leprosum. Smaller companies, including Ore Pharmaceuticals,Biovista, Numedicus,Melior Discoveryand SOM Biotech are also performing drug repositioning on a systematic basis. These companies use a combination of approaches including in silico biology and in vivo/in vitro experimentation to assess a compound and develop and confirm hypotheses concerning its usage for new indications.

Hematology Research

Lymphatic diseasesthis is a type of cancer of the lymphatic system. It can start almost any where in the body. It's believed to be caused by HIV, Epstein-Barr Syndrome, age and family history. Symptoms include weight loss, fever, swollen lymph nodes, night sweats, itchy skin, fatigue, chest pain, coughing and/or trouble swallowing. Thelymphatic systemis part of thecirculatory system, comprising a network oflymphatic vesselsthat carry a clear fluid called lymph directionally towards the heart. The lymphatic system was first described in the seventeenth century independently byOlaus RudbeckandThomas Bartholin. Unlike thecardiovascular systemthe lymphatic system is not a closed system. The human circulatory system processes an average of 20 litres ofbloodper day throughcapillary filtrationwhich removesplasmawhile leaving theblood cells. Roughly 17 litres of the filtered plasma get reabsorbed directly into the blood vessels, while the remaining 3 litres are left behind in theinterstitial fluid. One of the main functions of the lymph system is to provide an accessory return route to the blood for the surplus 3 litres. Lymphatic diseases are ofNon-Hodgkin's Lymphoma, Hodgkins. Thethymusis a specialized primarylymphoidorgan of theimmune system. Within the thymus,T cellsor Tlymphocytesmature. T cells are critical to theadaptive immune system, where the body adapts specifically to foreign invaders.One of the example of lymph node development. Formation oflymph nodeinto the tumor which lead to cancer called oncology.

Various Aspects of Haematology

Pediatric Haematology and Oncologyis an internationalpeer-reviewedmedical journalthat covers all aspects ofpediatrichematologyandoncology. The journal covers immunology, pathology, and pharmacology in relation to blood diseases and cancer in children and shows how basic experimental research can contribute to the understanding of clinical problems. Physicians specialized in hematology are known ashematologistsorhaematologists. Their routine work mainly includes the care and treatment of patients with hematological diseases, although some may also work at the hematology laboratory viewingblood filmsandbone marrowslides under themicroscope, interpreting various hematological test results andblood clotting testresults. In some institutions, hematologists also manage the hematology laboratory. Physicians who work in hematology laboratories, and most commonly manage them, are pathologists specialized in the diagnosis of hematological diseases, referred to as hematopathologistsorhaematopathologists.Experimental Hematologyis apeer-reviewedmedical journalofhematology, which publishesoriginal researcharticles and reviews, as well as the abstracts of the annual proceedings of theSociety for Hematology and Stem Cells and they should be done under theHematology guidlines.

Blood Based Products

Ablood substituteis a substance used to mimic and fulfill some functions ofbiologicalblood. It aims to provide an alternative toblood transfusion, which is transferring blood orblood-based productsfrom one person into another. Thus far, there are no well-acceptedoxygen-carryingblood substitutes, which is the typical objective of ared blood celltransfusion; however, there are widely available non-bloodvolume expandersfor cases where only volume restoration is required. These are helping doctors and surgeons avoid the risks of disease transmission and immune suppression, address the chronic blood donor shortage, and address the concerns of Jehovah's Witnesses and others who have religious objections to receiving transfused blood.Pathogen reductionusing riboflavin and UV lightis a method by which infectiouspathogensinblood for transfusionare inactivated by addingriboflavinand irradiating withUV light. This method reduces the infectious levels of disease-causing agents that may be found in donated blood components, while still maintaining good quality blood components for transfusion. This type of approach to increase blood safety is also known as pathogen inactivation in the industry. Anartificial cellorminimal cellis an engineered particle that mimics one or many functions of abiological cell. The term does not refer to a specific physical entity, but rather to the idea that certain functions or structures of biological cells can be replaced or supplemented with a synthetic entity. Often, artificial cells are biological or polymeric membranes which enclose biologically active materials. As such,nanoparticles,liposomes,polymersomes, microcapsules and a number of other particles have qualified as artificial cells.Manufacturing of semi synthetic products of drugs are known as therapeutic biological products.Anticoagulants(antithrombics) are a class of drugs that work to prevent thecoagulation(clotting) of blood. Such substances occur naturally in leeches and blood-sucking insects.

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Hematology Conferences | Blood Disorder Conferences | USA ...

Cardiac Stem Cells Comments Off on Hematology Conferences | Blood Disorder Conferences | USA … | October 9th, 2016

The 5th International Conference on Tissue Engineering & Regenerative Medicine which is going to be held during September 12-14, 2016 at Berlin, Germany will bring together world-class personalities working on stem cells, tissue engineering and regenerative medicine to discuss materials-related strategies for disease remediation and tissue repair.

Tissue Regeneration

In the field of biology, regeneration is the progression of renewal, regeneration and growth that makes it possible for genomes, cells, organ regeneration to natural changes or events that cause damage or disturbance.This study is carried out as craniofacial tissue engineering, in-situtissue regeneration, adipose-derived stem cells for regenerative medicine which is also a breakthrough in cell culture technology. The study is not stopped with the regeneration of tissue where it is further carried out in relation with cell signaling, morphogenetic proteins. Most of the neurological disorders occurred accidental having a scope of recovery by replacement or repair of intervertebral discs repair, spinal fusion and many more advancements. The global market for tissue engineering and regeneration products such as scaffolds, tissueimplants, biomimetic materials reached $55.9 billion in 2010 and it is expected to reach $89.7 billion by 2016 at a compounded annual growth rate (CAGR) of 8.4%. It grows to $135 billion by 2024.

Related Conferences

5th InternationalConference on Tissue Engineering and Regenerative Medicine September 12-14, 2016 Berlin, Germany; 5th International Conference onCell and Gene Therapy May 19-21, 2016 San Antonio, USA; InternationalConference on Cancer Immunologyand ImmunotherapyJuly 28-30, 2016 Melbourne, Australia; InternationalConference on Molecular BiologyOctober 13-15, 2016 Dubai, UAE; Tissue Niches and Resident Stem Cells in Adult Epithelia Gordon Research Conference, Regulation of Tissue Homeostasis by Signalling in the Stem Cell Niche August 7-12, Hong Kong, China; 10 Years of IPSCs, Cell Symposia, September 25-27, 2016 Berkeley, CA, USA; World Stem Cells and Regenerative Medicine Congress May 18-20, 2016 London, UK; Notch Signaling in Development, Regeneration and Disease Gordon Research Conference, July 31-August 5, 2016 Lewiston, ME, USA

Designs for Tissue Engineering

The developing field of tissue engineering aims to regenerate damaged tissues by combining cells from the body withbioresorbablematerials, biodegradable hydrogel, biomimetic materials, nanostructures andnanomaterials, biomaterials and tissue implants which act as templates for tissue regeneration, to guide the growth of new tissue by using with the technologies. The global market for biomaterials, nanostructures and bioresorbable materials are estimated to reach $88.4 billion by 2017 from $44.0 billion in 2012 growing at a CAGR of 15%. Further the biomaterials market estimated to be worth more than 300 billion US Dollars and to be increasing 20% per year.

Related Conferences

5th International ConferenceonCell and Gene Therapy May 19-21, 2016 San Antonio, USA; International Conference on Restorative Medicine October 24-26, 2016 Chicago, USA; InternationalConference on Molecular Biology October 13-15, 2016 Dubai, UAE; 2nd International Conference on Bio-banking August 18-19, 2016 Portland, USA; ISSCR Annual Meeting 22-25 June, 2016 San Francisco, California, USA; Keystone Cardiac Development, Regeneration and Repair (Z2) April 3 7, 2016 Snowbird, Utah, USA;EMBL Hematopoietic Stem Cells: From the Embryo to the Aging Organism, June 3-5, 2016 Heidelberg, Germany; ISSCR Pluripotency: From basic science to therapeutic applications March 22-24, 2016 Kyoto, Japan

Organ Engineering

This interdisciplinary engineering has attracted much attention as a new therapeutic means that may overcome the drawbacks involved in the current artificial organs and organtransplantationthat have been also aiming at replacing lost or severely damaged tissues or organs. Tissue engineering and regenerative medicine is an exciting research area that aims at regenerative alternatives to harvested tissues for organ transplantation with soft tissues. Although significant progress has been made in thetissue engineeringfield, many challenges remain and further development in this area will require ongoing interactions and collaborations among the scientists from multiple disciplines, and in partnership with the regulatory and the funding agencies. As a result of the medical and market potential, there is significant academic and corporate interest in this technology.

Related Conferences

International Conference on Restorative Medicine October 24-26, 2016 Chicago, USA; 5th InternationalConference on Cell and Gene Therapy May 19-21, 2016 San Antonio, USA; 5th International Conference on Regenerative Medicine September 12-14, 2016 Berlin, Germany; 2nd International Conference on Tissue preservation August 18-19, 2016 Portland, USA;Cell and Gene TherapyJanuary 25-27, 2016 Washington D.C., USA; ISSCR Stem Cell Models of Neural Degeneration and Disease February 1-3, 2016 Dresden, Germany; Craniofacial Morphogenesis and Tissue Regeneration March 12-18, 2016 California, USA; Keystone Stem Cells and Cancer (C1) March 6-10, Colorado, USA; Keystone Stem Cells and Regeneration in the Digestive Organs (X6) March 13 17 Colorado, USA

Cancer Stem Cells

The characterization of cancer stem cell is done by identifying the cell within a tumor that possesses the capacity to self-renew and to cause theheterogeneous lineagesof cancer cells that comprise the tumor. This stem cell which acts as precursor for the cancer acts as a tool against it indulging the reconstruction of cancer stem cells, implies as the therapeutic implications and challenging the gaps globally. The global stem cell market will grow from about $5.6 billion in 2013 to nearly $10.6 billion in 2018, registering a compound annual growth rate (CAGR) of 3.6% from 2013 through 2018. The Americas is the largest region of globalstem cellmarket, with a market share of about $2.0 billion in 2013. The region is projected to increase to nearly $3.9 billion by 2018, with a CAGR of 13.9% for the period of 2013 to 2018. Europe is the second largest segment of the global stem cell market and is expected to grow at a CAGR of 13.4% reaching about $2.4 billion by 2018 from nearly $1.4 billion in 2013.

Related Conferences

5th InternationalConference Cell and Gene Therapy May 19-21, 2016 San Antonio, USA; International Conference on Molecular Biology October 13-15, 2016 Dubai, UAE; 5th International Conference on Tissue EngineeringSeptember 12-14, 2016 Berlin, Germany; 2nd International Conference on Tissue preservationAugust 18-19, 2016 Portland, USA; Molecular and Cellular Basis of Growth and Regeneration (A3) January 10 14, 2016 Colorado, USA; Cell and Gene TherapyJanuary 25-27, 2016 Washington D.C., USA; ISSCR Stem Cell Models of Neural Degeneration and Disease March 13 17, 2016 Dresden, Germany; Craniofacial Morphogenesis and Tissue Regeneration March 12-18, 2016 California, USA; World Stem Cells Congress May 18-20, 2016 London, UK

Bone Tissue Engineering

Tissue engineering ofmusculoskeletal tissues, particularly bone and cartilage, is a rapidly advancing field. In bone, technology has centered on bone graft substitute materials and the development of biodegradable scaffolds. Recently, tissue engineering strategies have included cell and gene therapy. The availability of growth factors and the expanding knowledge base concerning the bone regeneration with modern techniques like recombinant signaling molecules, solid free form fabrication of scaffolds, synthetic cartilage, Electrochemical deposition,spinal fusionand ossification are new generated techniques for tissue-engineering applications. The worldwide market for bone and cartilage repairs strategies is estimated about $300 million. During the last 10/15 years, the scientific community witnessed and reported the appearance of several sources of stem cells with both osteo and chondrogenic potential.

Related Conferences

5th International Conference on Tissue Engineering and Regenerative Medicine September 12-14, 2016 Berlin, Germany; 3rd 2nd International Conference on Tissue preservation and Bio-banking August 18-19, 2016 Portland, USA; 5th International Conference on Cell and Gene Therapy May 19-21, 2016 San Antonio, USA; International Conference on Restorative Medicine October 24-26, 2016 Chicago, USA; 10th World Biomaterials Congress May 17-22, 2016 Quebec, Canada; 2016 TERMIS-EU Conference June 28- July1, 2016 Uppsala, Sweden; 2016 TERMIS-AP Conference Tamsui Town of New Taipei City May 23-28, 2016; 2016 TERMIS-AM Conference September 3-6, 2016, San Diego, USA; Pluripotency: From basic science to therapeutic applications 22-24 March 2016 Kyoto, Japan

Scaffolds

Scaffolds are one of the three most important elements constituting the basic concept of regenerative medicine, and are included in the core technology of regenerative medicine. Every day thousands of surgical procedures are performed to replace or repair tissue that has been damaged through disease or trauma. The developing field of tissue engineering (TE) aims to regeneratedamaged tissuesby combining cells from the body with highly porous scaffold biomaterials, which act as templates for tissue regeneration, to guide the growth of new tissue. Scaffolds has a prominent role in tissue regeneration the designs, fabrication, 3D models, surface ligands and molecular architecture, nanoparticle-cell interactions and porous of thescaffoldsare been used in the field in attempts to regenerate different tissues and organs in the body. The world stem cell market was approximately 2.715 billion dollars in 2010, and with a growth rate of 16.8% annually, a market of 6.877 billion dollars will be formed in 2016. From 2017, the expected annual growth rate is 10.6%, which would expand the market to 11.38 billion dollars by 2021.

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InternationalConference on Restorative MedicineOctober 24-26, 2016 Chicago, USA; 5th InternationalConference onCell and Gene TherapyMay 19-21, 2016 San Antonio, USA; 5th InternationalConference on Regenerative MedicineSeptember 12-14, 2016 Berlin, Germany; 2ndInternational Conference on Tissue preservationAugust 18-19, 2016 Portland, USA;Cell and Gene TherapyJanuary 25-27, 2016 Washington D.C., USA; ISSCRStem Cell Modelsof Neural Degeneration and Disease February 1-3, 2016 Dresden, Germany; Craniofacial Morphogenesis andTissue RegenerationMarch 12-18, 2016 California, USA; KeystoneStem Cells and Cancer(C1) March 6-10, Colorado, USA; KeystoneStem Cells and Regenerationin the Digestive Organs (X6) March 13 17 Colorado, USA

Tissue Regeneration Technologies

Guided tissue regeneration is defined as procedures attempting to regenerate lost periodontal structures through differential tissue responses. Guidedbone regenerationtypically refers to ridge augmentation or bone regenerative procedures it typically refers to regeneration of periodontal therapy. The recent advancements and innovations in biomedical and regenerative tissue engineering techniques include the novel approach of guided tissue regeneration and combination ofnanotechnologyand regenerative medicine.

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5th InternationalConferenceCell and Gene TherapyMay 19-21, 2016 San Antonio, USA; InternationalConference on Restorative MedicineOctober 24-26, 2016 Chicago, USA; InternationalConference on Molecular BiologyOctober 13-15, 2016 Dubai, UAE; 2nd InternationalConference on Bio-bankingAugust 18-19, 2016 Portland, USA;ISSCR Annual Meeting22-25 June, 2016 San Francisco, California, USA; KeystoneCardiac Development, Regeneration and Repair (Z2) April 3 7, 2016 Snowbird, Utah, USA;EMBLHematopoietic Stem Cells: From the Embryo to the Aging Organism, June 3-5, 2016 Heidelberg, Germany; ISSCRPluripotency: From basic science to therapeutic applications March 22-24, 2016 Kyoto, Japan

Regeneration and Therapeutics

Regenerative medicinecan be defined as a therapeutic intervention which replaces or regenerates human cells, tissues or organs, to restore or establish normal function and deploys small molecule drugs, biologics, medical devices and cell-based therapies. It deals with the different therapeutic uses like stem cells for tissue repair, tissue injury and healing process, cardiacstem cell therapyfor regeneration, functional regenerative recovery, effects of aging on tissuerepair/regeneration, corneal regeneration & degeneration. The global market is expected to reach $25.5 billion by 2011 and will further grow to $36.1 billion by 2016 at a CAGR of 7.2%. It is expected to reach $65 billion mark by 2024.

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Regenerative medicine

Regenerative medicine is a branch oftranslational researchin tissue engineering and molecular biology which deals with the process of replacing, engineering or regenerating human cells, tissues or organs to restore or establish normal function. The latest developments involve advances in cell and gene therapy and stem cell research, molecular therapy, dental and craniofacial regeneration.Regenerative medicineshave the unique ability to repair, replace and regenerate tissues and organs, affected due to some injury, disease or due to natural aging process. These medicines are capable of restoring the functionality of cells and tissues. The global regenerative medicine market will reach $ 67.6 billion by 2020 from $16.4 billion in 2013, registering a CAGR of 23.2% during forecast period (2014 - 2020). Small molecules and biologics segment holds prominent market share in the overall regenerative medicine technology market and is anticipated to grow at a CAGR of 18.9% during the forecast period.

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Applications of Tissue Engineering

The applications of tissue engineering and regenerative medicine are innumerable as they mark the replacement of medication andorgan replacement. The applications involve cell tracking andtissue imaging, cell therapy and regenerative medicine, organ harvesting, transport and transplant, the application of nanotechnology in tissue engineering and regenerative medicine and bio banking. Globally the research statistics are increasing at a vast scale and many universities and companies are conducting events on the subject regenerative medicine conference like tissue implants workshops, endodontics meetings, tissue biomarkers events, tissue repair meetings, regenerative medicine conferences, tissue engineering conference, regenerative medicine workshop, veterinary regenerative medicine, regenerative medicine symposiums, tissue regeneration conferences, regenerative medicine congress.

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Regenerative Medicine Market

There are strong pricing pressures from public healthcare payers globally as Governments try to reduce budget deficits. Regenerative medicine could potentially save public health bodies money by reducing the need for long-term care and reducing associated disorders, with potential benefits for the world economy as a whole.The global market fortissue engineeringand regeneration products reached $55.9 billion in 2010, is expected to reach $59.8 billion by 2011, and will further grow to $89.7 billion by 2016 at a compounded annual growth rate (CAGR) of 8.4%. It grows to $135 billion to 2024. The contribution of the European region was 43.3% of the market in 2010, a value of $24.2 billion. Themarketis expected to reach $25.5 billion by 2011 and will further grow to $36.1 billion by 2016 at a CAGR of 7.2%. It grows to $65 billion to 2024.

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Regenerative Medicine Europe

Leading EU nations with strong biotech sectors such as the UK and Germany are investing heavily in regenerative medicine, seeking competitive advantage in this emerging sector. The commercial regenerative medicine sector faces governance challenges that include a lack of proven business models, an immature science base and ethical controversy surrounding hESC research. The recent global downturn has exacerbated these difficulties: private finance has all but disappeared; leading companies are close to bankruptcy, and start-ups are struggling to raise funds. In the UK the government has responded by announcing 21.5M funding for the regenerative medicine industry and partners. But the present crisis extends considerably beyond regenerative medicine alone, affecting much of the European biotech sector. A 2009 European Commission (EC) report showed the extent to which the global recession has impacted on access to VC finance in Europe: 75% of biopharma companies in Europe need capital within the next two years if they are to continue their current range of activities.

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InternationalConference on Restorative MedicineOctober 24-26, 2016 Chicago, USA; 5th InternationalConference onCell and Gene TherapyMay 19-21, 2016 San Antonio, USA; 5th InternationalConference on Regenerative MedicineSeptember 12-14, 2016 Berlin, Germany; 2ndInternational Conference on Tissue preservationAugust 18-19, 2016 Portland, USA;Cell and Gene TherapyJanuary 25-27, 2016 Washington D.C., USA; ISSCRStem Cell Modelsof Neural Degeneration and Disease February 1-3, 2016 Dresden, Germany; Craniofacial Morphogenesis andTissue RegenerationMarch 12-18, 2016 California, USA; KeystoneStem Cells and Cancer(C1) March 6-10, Colorado, USA; KeystoneStem Cells and Regenerationin the Digestive Organs (X6) March 13 17 Colorado, USA

Embryonic Stem Cell

Embryonic stem cells are pluripotent, meaning they are able to grow (i.e. differentiate) into all derivatives of the three primary germ layers: ectoderm, endoderm and mesoderm. In other words, they can develop into each of the more than 200 cell types of the adult body as long as they are specified to do so. Embryonic stem cells are distinguished by two distinctive properties: their pluripotency, and their ability to replicate indefinitely. ES cells are pluripotent, that is, they are able to differentiate into all derivatives of the three primary germ layers: ectoderm, endoderm, and mesoderm. These include each of the more than 220 cell types in the adult body. Pluripotency distinguishes embryonic stem cells from adult stem cells found in adults; while embryonic stem cells can generate all cell types in the body, adult stem cells are multipotent and can produce only a limited number of cell types. Additionally, under defined conditions, embryonic stem cells are capable of propagating themselves indefinitely. This allows embryonic stem cells to be employed as useful tools for both research and regenerative medicine, because they can produce limitless numbers of themselves for continued research or clinical use.

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5th InternationalConference on Tissue Engineering and Regenerative MedicineSeptember 12-14, 2016 Berlin, Germany; 5th InternationalConference onCell and Gene TherapyMay 19-21, 2016 San Antonio, USA; InternationalConference on Cancer Immunologyand ImmunotherapyJuly 28-30, 2016 Melbourne, Australia; InternationalConference on Molecular BiologyOctober 13-15, 2016 Dubai, UAE; Tissue Niches andResident Stem Cells in Adult EpitheliaGordon Research Conference,Regulation of Tissue Homeostasisby Signalling in the Stem Cell Niche August 7-12, Hong Kong, China;10 Years of IPSCs, Cell Symposia, September 25-27, 2016 Berkeley, CA, USA; WorldStem Cells and Regenerative Medicine CongressMay 18-20, 2016 London, UK; Notch Signaling in Development,Regenerationand Disease Gordon Research Conference, July 31-August 5, 2016 Lewiston, ME, USA

Stem Cell Transplant

Stem cell transplantation is a procedure that is most often recommended as a treatment option for people with leukemia, multiple myeloma, and some types of lymphoma. It may also be used to treat some genetic diseases that involve the blood. During a stem cell transplant diseased bone marrow (the spongy, fatty tissue found inside larger bones) is destroyed with chemotherapy and/or radiation therapy and then replaced with highly specialized stem cells that develop into healthy bone marrow. Although this procedure used to be referred to as a bone marrow transplant, today it is more commonly called a stem cell transplant because it is stem cells in the blood that are typically being transplanted, not the actual bone marrow tissue.

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5th InternationalConference Cell and Gene TherapyMay 19-21, 2016 San Antonio, USA; InternationalConference on Molecular BiologyOctober 13-15, 2016 Dubai, UAE; 5th InternationalConference on Tissue EngineeringSeptember 12-14, 2016 Berlin, Germany; 2nd InternationalConference on Tissue preservationAugust 18-19, 2016 Portland, USA; Molecular and Cellular Basis ofGrowth and Regeneration(A3) January 10 14, 2016 Colorado, USA;Cell and Gene TherapyJanuary 25-27, 2016 Washington D.C., USA; ISSCRStem Cell Modelsof Neural Degeneration and Disease March 13 17, 2016 Dresden, Germany; Craniofacial Morphogenesis andTissue RegenerationMarch 12-18, 2016 California, USA;World Stem Cells CongressMay 18-20, 2016 London, UK

Market Analysis Report:

Tissue engineering is an interdisciplinary field that applies the principles of engineering and life sciences toward the development of biological substitutes that restore, maintain, or improve tissue function or a whole organ. Regenerative medicine is not one discipline. It can be defined as a therapeutic intervention which replaces or regenerates human cells, tissues or organs, to restore or establish normal function and deploys small molecule drugs, biologics, medical devices and cell-based therapies

Currently it has emerged as a rapidly diversifying field with the potential to address the worldwide organ shortage issue and comprises of tissue regeneration and organ replacement. Regenerative medicine could potentially save public health bodies money by reducing the need for long-term care and reducing associated disorders, with potential benefits for the world economy as a whole.The global tissue engineering and regeneration market reached $17 billion in 2013. This market is expected to grow to nearly $20.8 billion in 2014 and $56.9 billion in 2019, a compound annual growth rate (CAGR) of 22.3%. On the basis of geography, Europe holds the second place in the global market in the field of regenerative medicine & tissue engineering. In Europe countries like UK, France and Germany are possessing good market shares in the field of regenerative medicine and tissue engineering. Spain and Italy are the emerging market trends for tissue engineering in Europe.

Tissue engineering is "an interdisciplinary field that applies the principles of engineering and life sciences toward the development of biological substitutes that restore, maintain, or improve tissue function or a whole organ. Currently it has emerged as a rapidly diversifying field with the potential to address the worldwide organ shortage issue and comprises of tissue regeneration and organ replacement. A novel set of tissue replacement parts and implementation strategies had shown a great revolution in this field. Cells placed on or within the tissue constructs is the most common methodology in tissue engineering.

Regenerative medicine is not one discipline. It can be defined as a therapeutic intervention which replaces or regenerates human cells, tissues or organs, to restore or establish normal function and deploys small molecule drugs, biologics, medical devices and cell-based therapies

This field continues to evolve. In addition to medical applications, non-therapeutic applications include using tissues as biosensors to detect biological or chemical threat agents, and tissue chips that can be used to test the toxicity of an experimental medication. Tissue Engineering and Regenerative Medicine is the major field in Medicine, which is still under research and the advancements are maximizing day to day.

Regenerative Medicine-2015 is an engrossed a vicinity of cognizant discussions on novel subjects like Tissue Regeneration, Materials & Designs for Tissue Engineering, Stem CellTools to Battle Cancer, Bioreactors in Tissue Engineering, Regeneration & Therapeutics, Cord Blood & Regenerative Medicine and Clinical Medicine, to mention a few. The three days event implants a firm relation of upcoming strategies in the field of Tissue Science & Regenerative Medicine with the scientific community. The conceptual and applicable knowledge shared, will also foster organizational collaborations to nurture scientific accelerations.We bring together business, creative, and technology leaders from the tissue engineering, marketing, and research industry for the most current and relevant.

Berlin is one of the largest and most diverse science regions in Europe. Roughly 200,000 people from around the world teach, research, work and study here. Approximately 17 percent of all students come from abroad, most of them from China, Russia and the USA. Many cooperative programs link Berlins institutes of higher education with partner institutes around the world. Berlin is a city of science at the heart of Europe a city whose history of scientific excellence stems from its many important research institutions and its long track record of scientific breakthroughs. Berlin has numerous modern Technology Centers. Their science-oriented infrastructure makes them attractive locations for young, technology-oriented companies.

Germany places great emphasis on globally networked research cooperation. Many organizations support international researchers and academics: Today more than 32,000 are being supported with scholarships. Besides this, research funding in Germany has the goal of financing the development of new ideas and technologies. The range covers everything from basic research in natural sciences, new technologies to structural research funding at institutions of higher education. On the basis of geography, the regenerative medicine bone and joint market Europe hold the second place in the global market in the field of regenerative medicine & tissue engineering. The market growth is expected to reach $65 billion by 2024 in Europe. In Europe countries like UK, France, and Germany are possessing good market share in the field of regenerative medicine and tissue engineering. Spain and Italy are the emerging market trends for tissue engineering in Europe. As per the scope and emerging market for tissue engineering and regenerative medicine Berlin has been selected as Venue for the 5th International Conference on Tissue Science and Regenerative Medicine.

Meet Your Target MarketWith members from around the world focused on learning about Advertising and marketing, this is the single best opportunity to reach the largest assemblage of participants from the tissue engineering and regenerative medicine community. The meeting engrossed a vicinity of cognizant discussions on novel subjects like Tissue Regeneration, Materials & Designs for Tissue Engineering, Stem CellTools to Battle Cancer, Bioreactors in Tissue Engineering, Regeneration & Therapeutics, Cord Blood & Regenerative Medicine and Clinical Medicine, to mention a few. The three days event implants a firm relation of upcoming strategies in the field of Tissue Engineering & Regenerative Medicine with the scientific community. The conceptual and applicable knowledge shared, will also foster organizational collaborations to nurture scientific accelerations.Conduct demonstrations, distribute information, meet with current and potential customers, make a splash with a new product line, and receive name recognition.

International Stem Cell Forum (ISCF)

International Society for Stem Cell Research (ISSCR)

UK Medical Research Council (MRC)

Australian Stem Cell Center

Canadian Institutes of Health Research (CIHR)

Euro Stem Cell (ACR)

Center for Stem Cell Biology

Stem Cell Research Singapore

UK National Stem Cell Network

Spain Mobile Marketing Association

European Marketing Confederation (EMC)

European Letterbox Marketing Association(ELMA)

European Sales & Marketing Association (ESMA)

The Incentive Marketing Association (IMA Europe)

European Marketing Academy

Figure 1: Statistical Analysis of Societies and Associations

Source: Reference7

Presidents or Vice Presidents/ Directors of Associations and Societies, CEOs of the companies associated with regenerative medicine and tissue engineering Consumer Products. Retailers, Marketing, Advertising and Promotion Agency Executives, Solution Providers (digital and mobile technology, P-O-P design, retail design, and retail execution), Professors and Students from Academia in the study of Marketing and Advertising filed.

Industry 40%

Academia 50%

Others 10%

See the rest here:
Regenerative Medicine Conferences | Tissue Engineering ...

Cardiac Stem Cells Comments Off on Regenerative Medicine Conferences | Tissue Engineering … | October 3rd, 2016

Track-1 Cell Therapy:

Cell therapyas performed by alternativemedicinepractitioners is very different from the controlled research done by conventionalstem cellmedical researchers. Alternative practitioners refer to their form of cell therapy by several other different names includingxenotransplanttherapy,glandular therapy, and fresh cell therapy. Proponents ofcell therapyclaim that it has been used successfully to rebuild damaged cartilage in joints, repair spinal cord injuries,strengthen a weakenedimmune system, treat autoimmune diseases such as AIDS, and help patients withneurological disorderssuch as Alzheimers disease,Parkinson's diseaseand epilepsy.

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Track-2 Gene therapy:

Gene therapyand cell therapy are overlapping fields of biomedical research with the goals of repairing the direct cause of genetic diseases in the DNA orcellularpopulation, respectively. The development of suitablegene therapytreatments for manygenetic diseasesand some acquired diseases has encountered many challenges and uncovered new insights into gene interactions and regulation. Further development often involves uncovering basic scientific knowledge of the affected tissues, cells, and genes, as well as redesigning vectors, formulations, and regulatory cassettes for the genes.Cell therapyis expanding its repertoire of cell types for administration.Cell therapytreatment strategies include isolation and transfer of specific stem cell populations, administration of effector cells, and induction of mature cells to becomepluripotent cells, and reprogramming of mature cells.

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Track-3 Cell and gene therapy products:

Articles containing or consisting ofhuman cellsor tissues that are intended for implantation,transplantation, infusion, or transfer to a human recipient.Gene therapiesare novel and complex products that can offer unique challenges in product development. Hence, ongoing communication between the FDA and stakeholders is essential to meet these challenges.Gene therapy productsare being developed around the world, the FDA is engaged in a number of international harmonization activities in this area.

Examples:Musculoskeletal tissue, skin, ocular tissue, human heart valves;vascular graft, dura mater, reproductive tissue/cells, Stem/progenitor cells,somatic cells, Cells transduced withgene therapyvectors , Combination products (e.g., cells or tissue + device)

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Track-4 Cellular therapy:

Cellular therapy, also calledlive cell therapy, cellular suspensions, glandular therapy, fresh cell therapy, sick cell therapy,embryonic cell therapy, andorgan therapy- refers to various procedures in which processed tissue from animal embryos, foetuses or organs, is injected or taken orally. Products are obtained from specific organs or tissues said to correspond with the unhealthy organs or tissues of the recipient. Proponents claim that the recipient's body automatically transports the injected cells to thetarget organs, where they supposedly strengthen them and regenerate their structure. The organs and glands used in cell treatment include brain, pituitary,thyroid, adrenals, thymus, liver,kidney, pancreas, spleen, heart,ovary, testis, and parotid. Several different types of cell or cell extract can be given simultaneously - some practitioners routinely give up to 20 or more at once.

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Track-5 Cancer gene therapy:

Cancer therapiesare drugs or other substances that block the growth and spread ofcancerby interfering with specific molecules ("molecular targets") that are involved in the growth, progression, and spread ofcancer. Many cancer therapies have been approved by the Food and Drug Administration (FDA) to treat specific types of cancer. The development of targetedtherapiesrequires the identification of good targets that is, targets that play a key role in cancer cell growth and survival. One approach to identify potential targets is to compare the amounts of individualproteinsin cancer cells with those in normal cells.Proteinsthat are present in cancer cells but not normal cells or that are more abundant incancercells would be potential targets, especially if they are known to be involved incell growthor survival.

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Track-6 Nano therapy:

Nano Therapymay be defined as the monitoring, repair, construction and control of human biological systems at themolecular level, using engineerednanodevicesand nanostructures. Basic nanostructured materials, engineeredenzymes, and the many products of biotechnology will be enormously useful in near-term medical applications. However, the full promise ofnanomedicineis unlikely to arrive until after the development of precisely controlled or programmable medical Nano machines andnanorobots.

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Track-7 Skin cell therapy:

Stem cellshave newly become a huge catchphrase in theskincarebiosphere. Skincare specialists are not usingembryonic stem cells; it is impossible to integrate live materials into a skincare product. Instead, scientists are creating products with specialized peptides andenzymesor plantstem cellswhich, when applied topically on the surface, help to protect the human skinstem cellsfrom damage and deterioration or stimulate the skins own stem cells. Currently, the technique is mainly used to save the lives of patients who have third degree burns over very large areas of their bodies.

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Track-8 HIV gene therapy:

Highly activeantiretroviral therapydramatically improves survival inHIV-infected patients. However, persistence of HIV in reservoirs has necessitated lifelong treatment that can be complicated bycumulative toxicities, incomplete immune restoration, and the emergence of drug-resistant escapemutants. Cell and gene therapies offer the promise of preventing progressiveHIV infectionby interfering with HIV replication in the absence of chronicantiviral therapy.

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Track-9 Diabetes for gene therapy:

Cell therapyapproaches for this disease are focused on developing the most efficient methods for the isolation ofpancreasbeta cells or appropriatestem cells, appropriate location forcell transplant, and improvement of their survival upon infusion. Alternatively, gene andcell therapyscientists are developing methods to reprogram some of the other cells of the pancreas to secreteinsulin. Currently ongoingclinical trialsusing these gene andcell therapystrategies hold promise for improved treatments of type I diabetes in the future. The firstgene therapyapproach to diabetes was put forward shortly after the cloning of theinsulingene. It was proposed that non-insulin producing cells could be made into insulin-producingcells using a suitable promoter and insulin gene construct, and that these substitute cells could restore insulin production in type 1 and some type 2 diabetics.

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Track-10 Viral gene therapy:

Converting avirusinto a vector Theviral life cyclecan be divided into two temporally distinct phases: infection and replication. Forgene therapyto be successful, an appropriate amount of a therapeutic gene must be delivered into the target tissue without substantial toxicity. Eachviral vectorsystem is characterized by an inherent set of properties that affect its suitability for specific gene therapy applications. For some disorders, long-term expression from a relatively small proportion of cells would be sufficient (for example, genetic disorders), whereas otherpathologiesmight require high, but transient,gene expression. For example, gene therapies designed to interfere with a viral infectious process or inhibit the growth ofcancer cellsby reconstitution of inactivated tumour suppressor genes may require gene transfer into a large fraction of theabnormal cells.

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Track-11 Stem cell therapies:

Stem cells have tremendous promise to help us understand and treat a range of diseases, injuries and other health-related conditions. Their potential is evident in the use ofblood stem cellsto treat diseases of the blood, a therapy that has saved the lives of thousands of children withleukaemia; and can be seen in the use ofstem cellsfor tissue grafts to treat diseases or injury to the bone, skin and surface of the eye. Some bone, skin andcorneal(eye) injuries and diseases can be treated bygraftingor implanting tissues, and the healing process relies on stem cells within thisimplanted tissue.

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Track-12 Stem cell preservation:

The ability to preserve the cells is critical to theirclinicalapplication. It improves patient access to therapies by increasing the genetic diversity of cells available. In addition, the ability to preserve cells improves the "manufacturability" of acell therapyproduct by permitting the cells to be stored until the patient is ready for administration of the therapy, permitting inventory control of products, and improving management of staffing atcell therapyfacilities. Finally, the ability to preservecell therapiesimproves the safety of cell therapy products by extending the shelf life of a product and permitting completion of safety and quality control testing before release of the product for use. preservation permits coordination between the manufacture of the therapy and patient care regimes.

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Track-13 Stem cell products:

The globalstemcell,Stem cell productsmarket will grow from about $5.6 billion in 2013 to nearly $10.6 billion in 2018, registering a compound annual growth rate (CAGR) of 13.6% from 2013 through 2018.This trackdiscusses the implications ofstemcellresearchand commercial trends in the context of the current size and growth of thepharmaceutical market, both in global terms and analysed by the most important national markets.

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Track-14 Genetically inherited diseases:

Agenetic diseaseis any disease that is caused by an abnormality in an individual'sgenome, the person's entiregeneticmakeup. The abnormality can range from minuscule to major -- from a discrete mutation in a single base in the DNA of a single gene to a grosschromosome abnormalityinvolving the addition or subtraction of an entirechromosomeor set of chromosomes.Most genetic diseases are the direct result of a mutation in one gene. However, one of the most difficult problems ahead is to find out how genes contribute to diseases that have a complex pattern ofinheritance, such as in the cases of diabetes,asthma,cancerandmental illness. In all these cases, no one gene has the yes/no power to say whether a person has a disease or not. It is likely that more than one mutation is required before the disease is manifest, and a number of genes may each make a subtle contribution to a person's susceptibility to a disease; genes may also affect how a person reacts toenvironmental factors.

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Track-15 Plant stem cells:

Plantshave emerged as powerful production platforms for the expression of fully functional recombinantmammalian proteins. These expression systems have demonstrated the ability to produce complexglycoproteinsin a cost-efficient manner at large scale. The full realization of thetherapeuticpotential of stem cells has only recently come into the forefront ofregenerative medicine. Stem cells are unprogrammed cells that can differentiate into cells with specific functions.Regenerative therapiesare used to stimulate healing and might be used in the future to treat various kinds of diseases.Regenerative medicinewill result in an extended healthy life span. A fresh apple is a symbol for beautiful skin. Hair greying for example could be shown to result from the fact that themelanocyte stem cellsin the hair follicle have died off.

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Track-16 Plant stem cell rejuvenation:

Asplantscannot escape from danger by running or taking flight, they need a special mechanism to withstandenvironmental stress. What empowers them to withstand harsh attacks and preserve life is the stem cell. According to Wikipedia, plantstem cellsnever undergo theagingprocess but constantly create new specialized and unspecialized cells, and they have the potential to grow into any organ, tissue, or cell in the body. The everlasting life is due to the hormones auxin andgibberellin. British scientists found that plant stem cells were much more sensitive toDNAdamage than other cells. And once they sense damage, they trigger death of these cells.

Rejuvenate with Plant Stem Cells

Detoxifyand release toxins on a cellular level. Nourishyour body with vital nutrients. Regenerateyour cells and diminish the effects of aging.

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Track-17 Clinical trials in cell and gene therapy:

Aclinical trialis a research study that seeks to determine if a treatment is safe and effective. Advancing new cell andgene therapies(CGTs) from the laboratory into early-phaseclinical trialshas proven to be a complex task even for experienced investigators. Due to the wide variety ofCGTproducts and their potential applications, a case-by-case assessment is warranted for the design of each clinical trial.

Objectives:Determine thepharmacokineticsof this regimen by the persistence of modified T cells in the blood of these patients, Evaluate theimmunogenicityof murine sequences in chimeric anti-CEA Ig TCR, Assess immunologic parameters which correlate with the efficacy of this regimen in these patients, Evaluate, in a preliminary manner, the efficacy of this regimen in patients with CEA bearingtumours.

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Track-18 Molecular epigenetics:

Epigeneticsis the study of heritable changes in thephenotypeof a cell or organism that are not caused by its genotype. The molecular basis of anepigeneticprofile arises from covalent modifications of protein andDNAcomponents ofchromatin. The epigenetic profile of a cell often dictates cell fate, as well as mammalian development,agingand disease. Epigenetics has evolved to become the science that explains how the differences in the patterns ofgene expressionin diverse cells or tissues are executed and inherited.

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Track-19 Bioengineering therapeutics:

The goals ofbioengineeringstrategies for targetedcancertherapies are (1) to deliver a high dose of an anticancer drug directly to a cancer tumour, (2) to enhance drug uptake by malignant cells, and (3) to minimize drug uptake by non-malignant cells. In ESRD micro electro mechanical systems andnanotechnologyto create components such as robust silicon Nano pore filters that mimic natural kidney structure for high-efficiency toxin clearance. It also usestissue engineeringto build a miniature bioreactor in which immune-isolated human-derived renal cells perform key functions, such as reabsorption of water and salts.In drug delivery for a leading cause ofblindness, photo-etching fabrication techniques from themicrochipindustry to create thin-film and planar micro devices (dimensions in millionths of meters) with protectivemedicationreservoirs andnanopores(measured in billionths of meters) for insertion in the back of the eye to deliver sustained doses of drug across protective retinalepithelial tissuesover the course of several months.

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Track-20 Advanced gene therapy:

Advanced therapiesare different fromconventional medicines, which are made from chemicals or proteins.Gene-therapymedicines:these contain genes that lead to atherapeuticeffect. They work by inserting 'recombinant' genes into cells, usually to treat a variety of diseases, including genetic disorders, cancer or long-term diseases.Somatic-cell therapymedicines:these contain cells or tissues that have been manipulated to change their biological characteristics.Advanced Cell &Gene Therapyprovides guidanceinprocess development, GMP/GTP manufacturing,regulatory affairs, due diligence and strategy, specializing in cell therapy,gene therapy, and tissue-engineeredregenerative medicineproducts.

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Cell Therapy Conferences | Spain | Worldwide Events ...

Cardiac Stem Cells Comments Off on Cell Therapy Conferences | Spain | Worldwide Events … | September 23rd, 2016

Muscle is a soft tissue found in most animals. Muscle cells contain protein filaments of actin and myosin that slide past one another, producing a contraction that changes both the length and the shape of the cell. Muscles function to produce force and motion. They are primarily responsible for maintaining and changing posture, locomotion, as well as movement of internal organs, such as the contraction of the heart and the movement of food through the digestive system via peristalsis.

Muscle tissues are derived from the mesodermal layer of embryonic germ cells in a process known as myogenesis. There are three types of muscle, skeletal or striated, cardiac, and smooth. Muscle action can be classified as being either voluntary or involuntary. Cardiac and smooth muscles contract without conscious thought and are termed involuntary, whereas the skeletal muscles contract upon command.[1] Skeletal muscles in turn can be divided into fast and slow twitch fibers.

Muscles are predominantly powered by the oxidation of fats and carbohydrates, but anaerobic chemical reactions are also used, particularly by fast twitch fibers. These chemical reactions produce adenosine triphosphate (ATP) molecules that are used to power the movement of the myosin heads.[2]

The term muscle is derived from the Latin musculus meaning "little mouse" perhaps because of the shape of certain muscles or because contracting muscles look like mice moving under the skin.[3][4]

The anatomy of muscles includes gross anatomy, which comprises all the muscles of an organism, and microanatomy, which comprises the structures of a single muscle.

Muscle tissue is a soft tissue, and is one of the four fundamental types of tissue present in animals. There are three types of muscle tissue recognized in vertebrates:

Cardiac and skeletal muscles are "striated" in that they contain sarcomeres that are packed into highly regular arrangements of bundles; the myofibrils of smooth muscle cells are not arranged in sarcomeres and so are not striated. While the sarcomeres in skeletal muscles are arranged in regular, parallel bundles, cardiac muscle sarcomeres connect at branching, irregular angles (called intercalated discs). Striated muscle contracts and relaxes in short, intense bursts, whereas smooth muscle sustains longer or even near-permanent contractions.

Skeletal (voluntary) muscle is further divided into two broad types: slow twitch and fast twitch:

The density of mammalian skeletal muscle tissue is about 1.06kg/liter.[8] This can be contrasted with the density of adipose tissue (fat), which is 0.9196kg/liter.[9] This makes muscle tissue approximately 15% denser than fat tissue.

All muscles are derived from paraxial mesoderm. The paraxial mesoderm is divided along the embryo's length into somites, corresponding to the segmentation of the body (most obviously seen in the vertebral column.[10] Each somite has 3 divisions, sclerotome (which forms vertebrae), dermatome (which forms skin), and myotome (which forms muscle). The myotome is divided into two sections, the epimere and hypomere, which form epaxial and hypaxial muscles, respectively. The only epaxial muscles in humans are the erector spinae and small intervertebral muscles, and are innervated by the dorsal rami of the spinal nerves. All other muscles, including those of the limbs are hypaxial, and inervated by the ventral rami of the spinal nerves.[10]

During development, myoblasts (muscle progenitor cells) either remain in the somite to form muscles associated with the vertebral column or migrate out into the body to form all other muscles. Myoblast migration is preceded by the formation of connective tissue frameworks, usually formed from the somatic lateral plate mesoderm. Myoblasts follow chemical signals to the appropriate locations, where they fuse into elongate skeletal muscle cells.[10]

Skeletal muscles are sheathed by a tough layer of connective tissue called the epimysium. The epimysium anchors muscle tissue to tendons at each end, where the epimysium becomes thicker and collagenous. It also protects muscles from friction against other muscles and bones. Within the epimysium are multiple bundles called fascicles, each of which contains 10 to 100 or more muscle fibers collectively sheathed by a perimysium. Besides surrounding each fascicle, the perimysium is a pathway for nerves and the flow of blood within the muscle. The threadlike muscle fibers are the individual muscle cells (myocytes), and each cell is encased within its own endomysium of collagen fibers. Thus, the overall muscle consists of fibers (cells) that are bundled into fascicles, which are themselves grouped together to form muscles. At each level of bundling, a collagenous membrane surrounds the bundle, and these membranes support muscle function both by resisting passive stretching of the tissue and by distributing forces applied to the muscle.[11] Scattered throughout the muscles are muscle spindles that provide sensory feedback information to the central nervous system. (This grouping structure is analogous to the organization of nerves which uses epineurium, perineurium, and endoneurium).

This same bundles-within-bundles structure is replicated within the muscle cells. Within the cells of the muscle are myofibrils, which themselves are bundles of protein filaments. The term "myofibril" should not be confused with "myofiber", which is a simply another name for a muscle cell. Myofibrils are complex strands of several kinds of protein filaments organized together into repeating units called sarcomeres. The striated appearance of both skeletal and cardiac muscle results from the regular pattern of sarcomeres within their cells. Although both of these types of muscle contain sarcomeres, the fibers in cardiac muscle are typically branched to form a network. Cardiac muscle fibers are interconnected by intercalated discs,[12] giving that tissue the appearance of a syncytium.

The filaments in a sarcomere are composed of actin and myosin.

The gross anatomy of a muscle is the most important indicator of its role in the body. There is an important distinction seen between pennate muscles and other muscles. In most muscles, all the fibers are oriented in the same direction, running in a line from the origin to the insertion. However, In pennate muscles, the individual fibers are oriented at an angle relative to the line of action, attaching to the origin and insertion tendons at each end. Because the contracting fibers are pulling at an angle to the overall action of the muscle, the change in length is smaller, but this same orientation allows for more fibers (thus more force) in a muscle of a given size. Pennate muscles are usually found where their length change is less important than maximum force, such as the rectus femoris.

Skeletal muscle is arranged in discrete muscles, an example of which is the biceps brachii (biceps). The tough, fibrous epimysium of skeletal muscle is both connected to and continuous with the tendons. In turn, the tendons connect to the periosteum layer surrounding the bones, permitting the transfer of force from the muscles to the skeleton. Together, these fibrous layers, along with tendons and ligaments, constitute the deep fascia of the body.

The muscular system consists of all the muscles present in a single body. There are approximately 650 skeletal muscles in the human body,[13] but an exact number is difficult to define. The difficulty lies partly in the fact that different sources group the muscles differently and partly in that some muscles, such as palmaris longus, are not always present.

A muscular slip is a narrow length of muscle that acts to augment a larger muscle or muscles.

The muscular system is one component of the musculoskeletal system, which includes not only the muscles but also the bones, joints, tendons, and other structures that permit movement.

The three types of muscle (skeletal, cardiac and smooth) have significant differences. However, all three use the movement of actin against myosin to create contraction. In skeletal muscle, contraction is stimulated by electrical impulses transmitted by the nerves, the motoneurons (motor nerves) in particular. Cardiac and smooth muscle contractions are stimulated by internal pacemaker cells which regularly contract, and propagate contractions to other muscle cells they are in contact with. All skeletal muscle and many smooth muscle contractions are facilitated by the neurotransmitter acetylcholine.

The action a muscle generates is determined by the origin and insertion locations. The cross-sectional area of a muscle (rather than volume or length) determines the amount of force it can generate by defining the number of sarcomeres which can operate in parallel.[citation needed] The amount of force applied to the external environment is determined by lever mechanics, specifically the ratio of in-lever to out-lever. For example, moving the insertion point of the biceps more distally on the radius (farther from the joint of rotation) would increase the force generated during flexion (and, as a result, the maximum weight lifted in this movement), but decrease the maximum speed of flexion. Moving the insertion point proximally (closer to the joint of rotation) would result in decreased force but increased velocity. This can be most easily seen by comparing the limb of a mole to a horse - in the former, the insertion point is positioned to maximize force (for digging), while in the latter, the insertion point is positioned to maximize speed (for running).

Muscular activity accounts for much of the body's energy consumption. All muscle cells produce adenosine triphosphate (ATP) molecules which are used to power the movement of the myosin heads. Muscles have a short-term store of energy in the form of creatine phosphate which is generated from ATP and can regenerate ATP when needed with creatine kinase. Muscles also keep a storage form of glucose in the form of glycogen. Glycogen can be rapidly converted to glucose when energy is required for sustained, powerful contractions. Within the voluntary skeletal muscles, the glucose molecule can be metabolized anaerobically in a process called glycolysis which produces two ATP and two lactic acid molecules in the process (note that in aerobic conditions, lactate is not formed; instead pyruvate is formed and transmitted through the citric acid cycle). Muscle cells also contain globules of fat, which are used for energy during aerobic exercise. The aerobic energy systems take longer to produce the ATP and reach peak efficiency, and requires many more biochemical steps, but produces significantly more ATP than anaerobic glycolysis. Cardiac muscle on the other hand, can readily consume any of the three macronutrients (protein, glucose and fat) aerobically without a 'warm up' period and always extracts the maximum ATP yield from any molecule involved. The heart, liver and red blood cells will also consume lactic acid produced and excreted by skeletal muscles during exercise.

At rest, skeletal muscle consumes 54.4 kJ/kg(13.0kcal/kg) per day. This is larger than adipose tissue (fat) at 18.8kJ/kg (4.5kcal/kg), and bone at 9.6kJ/kg (2.3kcal/kg).[14]

The efferent leg of the peripheral nervous system is responsible for conveying commands to the muscles and glands, and is ultimately responsible for voluntary movement. Nerves move muscles in response to voluntary and autonomic (involuntary) signals from the brain. Deep muscles, superficial muscles, muscles of the face and internal muscles all correspond with dedicated regions in the primary motor cortex of the brain, directly anterior to the central sulcus that divides the frontal and parietal lobes.

In addition, muscles react to reflexive nerve stimuli that do not always send signals all the way to the brain. In this case, the signal from the afferent fiber does not reach the brain, but produces the reflexive movement by direct connections with the efferent nerves in the spine. However, the majority of muscle activity is volitional, and the result of complex interactions between various areas of the brain.

Nerves that control skeletal muscles in mammals correspond with neuron groups along the primary motor cortex of the brain's cerebral cortex. Commands are routed though the basal ganglia and are modified by input from the cerebellum before being relayed through the pyramidal tract to the spinal cord and from there to the motor end plate at the muscles. Along the way, feedback, such as that of the extrapyramidal system contribute signals to influence muscle tone and response.

Deeper muscles such as those involved in posture often are controlled from nuclei in the brain stem and basal ganglia.

The afferent leg of the peripheral nervous system is responsible for conveying sensory information to the brain, primarily from the sense organs like the skin. In the muscles, the muscle spindles convey information about the degree of muscle length and stretch to the central nervous system to assist in maintaining posture and joint position. The sense of where our bodies are in space is called proprioception, the perception of body awareness. More easily demonstrated than explained, proprioception is the "unconscious" awareness of where the various regions of the body are located at any one time. This can be demonstrated by anyone closing their eyes and waving their hand around. Assuming proper proprioceptive function, at no time will the person lose awareness of where the hand actually is, even though it is not being detected by any of the other senses.

Several areas in the brain coordinate movement and position with the feedback information gained from proprioception. The cerebellum and red nucleus in particular continuously sample position against movement and make minor corrections to assure smooth motion.

The efficiency of human muscle has been measured (in the context of rowing and cycling) at 18% to 26%. The efficiency is defined as the ratio of mechanical work output to the total metabolic cost, as can be calculated from oxygen consumption. This low efficiency is the result of about 40% efficiency of generating ATP from food energy, losses in converting energy from ATP into mechanical work inside the muscle, and mechanical losses inside the body. The latter two losses are dependent on the type of exercise and the type of muscle fibers being used (fast-twitch or slow-twitch). For an overall efficiency of 20 percent, one watt of mechanical power is equivalent to 4.3 kcal per hour. For example, one manufacturer of rowing equipment calibrates its rowing ergometer to count burned calories as equal to four times the actual mechanical work, plus 300 kcal per hour,[15] this amounts to about 20 percent efficiency at 250 watts of mechanical output. The mechanical energy output of a cyclic contraction can depend upon many factors, including activation timing, muscle strain trajectory, and rates of force rise & decay. These can be synthesized experimentally using work loop analysis.

A display of "strength" (e.g. lifting a weight) is a result of three factors that overlap: physiological strength (muscle size, cross sectional area, available crossbridging, responses to training), neurological strength (how strong or weak is the signal that tells the muscle to contract), and mechanical strength (muscle's force angle on the lever, moment arm length, joint capabilities).

Vertebrate muscle typically produces approximately 2533N (5.67.4lbf) of force per square centimeter of muscle cross-sectional area when isometric and at optimal length.[16] Some invertebrate muscles, such as in crab claws, have much longer sarcomeres than vertebrates, resulting in many more sites for actin and myosin to bind and thus much greater force per square centimeter at the cost of much slower speed. The force generated by a contraction can be measured non-invasively using either mechanomyography or phonomyography, be measured in vivo using tendon strain (if a prominent tendon is present), or be measured directly using more invasive methods.

The strength of any given muscle, in terms of force exerted on the skeleton, depends upon length, shortening speed, cross sectional area, pennation, sarcomere length, myosin isoforms, and neural activation of motor units. Significant reductions in muscle strength can indicate underlying pathology, with the chart at right used as a guide.

Since three factors affect muscular strength simultaneously and muscles never work individually, it is misleading to compare strength in individual muscles, and state that one is the "strongest". But below are several muscles whose strength is noteworthy for different reasons.

Humans are genetically predisposed with a larger percentage of one type of muscle group over another. An individual born with a greater percentage of Type I muscle fibers would theoretically be more suited to endurance events, such as triathlons, distance running, and long cycling events, whereas a human born with a greater percentage of Type II muscle fibers would be more likely to excel at sprinting events such as 100 meter dash.[citation needed]

Exercise is often recommended as a means of improving motor skills, fitness, muscle and bone strength, and joint function. Exercise has several effects upon muscles, connective tissue, bone, and the nerves that stimulate the muscles. One such effect is muscle hypertrophy, an increase in size. This is used in bodybuilding.

Various exercises require a predominance of certain muscle fiber utilization over another. Aerobic exercise involves long, low levels of exertion in which the muscles are used at well below their maximal contraction strength for long periods of time (the most classic example being the marathon). Aerobic events, which rely primarily on the aerobic (with oxygen) system, use a higher percentage of Type I (or slow-twitch) muscle fibers, consume a mixture of fat, protein and carbohydrates for energy, consume large amounts of oxygen and produce little lactic acid. Anaerobic exercise involves short bursts of higher intensity contractions at a much greater percentage of their maximum contraction strength. Examples of anaerobic exercise include sprinting and weight lifting. The anaerobic energy delivery system uses predominantly Type II or fast-twitch muscle fibers, relies mainly on ATP or glucose for fuel, consumes relatively little oxygen, protein and fat, produces large amounts of lactic acid and can not be sustained for as long a period as aerobic exercise. Many exercises are partially aerobic and partially anaerobic; for example, soccer and rock climbing involve a combination of both.

The presence of lactic acid has an inhibitory effect on ATP generation within the muscle; though not producing fatigue, it can inhibit or even stop performance if the intracellular concentration becomes too high. However, long-term training causes neovascularization within the muscle, increasing the ability to move waste products out of the muscles and maintain contraction. Once moved out of muscles with high concentrations within the sarcomere, lactic acid can be used by other muscles or body tissues as a source of energy, or transported to the liver where it is converted back to pyruvate. In addition to increasing the level of lactic acid, strenuous exercise causes the loss of potassium ions in muscle and causing an increase in potassium ion concentrations close to the muscle fibres, in the interstitium. Acidification by lactic acid may allow recovery of force so that acidosis may protect against fatigue rather than being a cause of fatigue.[18]

Delayed onset muscle soreness is pain or discomfort that may be felt one to three days after exercising and generally subsides two to three days later. Once thought to be caused by lactic acid build-up, a more recent theory is that it is caused by tiny tears in the muscle fibers caused by eccentric contraction, or unaccustomed training levels. Since lactic acid disperses fairly rapidly, it could not explain pain experienced days after exercise.[19]

Independent of strength and performance measures, muscles can be induced to grow larger by a number of factors, including hormone signaling, developmental factors, strength training, and disease. Contrary to popular belief, the number of muscle fibres cannot be increased through exercise. Instead, muscles grow larger through a combination of muscle cell growth as new protein filaments are added along with additional mass provided by undifferentiated satellite cells alongside the existing muscle cells.[13]

Biological factors such as age and hormone levels can affect muscle hypertrophy. During puberty in males, hypertrophy occurs at an accelerated rate as the levels of growth-stimulating hormones produced by the body increase. Natural hypertrophy normally stops at full growth in the late teens. As testosterone is one of the body's major growth hormones, on average, men find hypertrophy much easier to achieve than women. Taking additional testosterone or other anabolic steroids will increase muscular hypertrophy.

Muscular, spinal and neural factors all affect muscle building. Sometimes a person may notice an increase in strength in a given muscle even though only its opposite has been subject to exercise, such as when a bodybuilder finds her left biceps stronger after completing a regimen focusing only on the right biceps. This phenomenon is called cross education.[citation needed]

Inactivity and starvation in mammals lead to atrophy of skeletal muscle, a decrease in muscle mass that may be accompanied by a smaller number and size of the muscle cells as well as lower protein content.[20] Muscle atrophy may also result from the natural aging process or from disease.

In humans, prolonged periods of immobilization, as in the cases of bed rest or astronauts flying in space, are known to result in muscle weakening and atrophy. Atrophy is of particular interest to the manned spaceflight community, because the weightlessness experienced in spaceflight results is a loss of as much as 30% of mass in some muscles.[21][22] Such consequences are also noted in small hibernating mammals like the golden-mantled ground squirrels and brown bats.[23]

During aging, there is a gradual decrease in the ability to maintain skeletal muscle function and mass, known as sarcopenia. The exact cause of sarcopenia is unknown, but it may be due to a combination of the gradual failure in the "satellite cells" that help to regenerate skeletal muscle fibers, and a decrease in sensitivity to or the availability of critical secreted growth factors that are necessary to maintain muscle mass and satellite cell survival. Sarcopenia is a normal aspect of aging, and is not actually a disease state yet can be linked to many injuries in the elderly population as well as decreasing quality of life.[24]

There are also many diseases and conditions that cause muscle atrophy. Examples include cancer and AIDS, which induce a body wasting syndrome called cachexia. Other syndromes or conditions that can induce skeletal muscle atrophy are congestive heart disease and some diseases of the liver.

Neuromuscular diseases are those that affect the muscles and/or their nervous control. In general, problems with nervous control can cause spasticity or paralysis, depending on the location and nature of the problem. A large proportion of neurological disorders, ranging from cerebrovascular accident (stroke) and Parkinson's disease to CreutzfeldtJakob disease, can lead to problems with movement or motor coordination.

Symptoms of muscle diseases may include weakness, spasticity, myoclonus and myalgia. Diagnostic procedures that may reveal muscular disorders include testing creatine kinase levels in the blood and electromyography (measuring electrical activity in muscles). In some cases, muscle biopsy may be done to identify a myopathy, as well as genetic testing to identify DNA abnormalities associated with specific myopathies and dystrophies.

A non-invasive elastography technique that measures muscle noise is undergoing experimentation to provide a way of monitoring neuromuscular disease. The sound produced by a muscle comes from the shortening of actomyosin filaments along the axis of the muscle. During contraction, the muscle shortens along its longitudinal axis and expands across the transverse axis, producing vibrations at the surface.[25]

The evolutionary origin of muscle cells in metazoans is a highly debated topic. In one line of thought scientists have believed that muscle cells evolved once and thus all animals with muscles cells have a single common ancestor. In the other line of thought, scientists believe muscles cells evolved more than once and any morphological or structural similarities are due to convergent evolution and genes that predate the evolution of muscle and even the mesoderm - the germ layer from which many scientists believe true muscle cells derive.

Schmid and Seipel argue that the origin of muscle cells is a monophyletic trait that occurred concurrently with the development of the digestive and nervous systems of all animals and that this origin can be traced to a single metazoan ancestor in which muscle cells are present. They argue that molecular and morphological similarities between the muscles cells in cnidaria and ctenophora are similar enough to those of bilaterians that there would be one ancestor in metazoans from which muscle cells derive. In this case, Schmid and Seipel argue that the last common ancestor of bilateria, ctenophora, and cnidaria was a triploblast or an organism with three germ layers and that diploblasty, meaning an organism with two germ layers, evolved secondarily due to their observation of the lack of mesoderm or muscle found in most cnidarians and ctenophores. By comparing the morphology of cnidarians and ctenophores to bilaterians, Schmid and Seipel were able to conclude that there were myoblast-like structures in the tentacles and gut of some species of cnidarians and in the tentacles of ctenophores. Since this is a structure unique to muscle cells, these scientists determined based on the data collected by their peers that this is a marker for striated muscles similar to that observed in bilaterians. The authors also remark that the muscle cells found in cnidarians and ctenophores are often contests due to the origin of these muscle cells being the ectoderm rather than the mesoderm or mesendoderm. The origin of true muscles cells is argued by others to be the endoderm portion of the mesoderm and the endoderm. However, Schmid and Seipel counter this skepticism about whether or not the muscle cells found in ctenophores and cnidarians are true muscle cells by considering that cnidarians develop through a medusa stage and polyp stage. They observe that in the hydrozoan medusa stage there is a layer of cells that separate from the distal side of the ectoderm to form the striated muscle cells in a way that seems similar to that of the mesoderm and call this third separated layer of cells the ectocodon. They also argue that not all muscle cells are derived from the mesendoderm in bilaterians with key examples being that in both the eye muscles of vertebrates and the muscles of spiralians these cells derive from the ectodermal mesoderm rather than the endodermal mesoderm. Furthermore, Schmid and Seipel argue that since myogenesis does occur in cnidarians with the help of molecular regulatory elements found in the specification of muscles cells in bilaterians that there is evidence for a single origin for striated muscle.[26]

In contrast to this argument for a single origin of muscle cells, Steinmetz et al. argue that molecular markers such as the myosin II protein used to determine this single origin of striated muscle actually predate the formation of muscle cells. This author uses an example of the contractile elements present in the porifera or sponges that do truly lack this striated muscle containing this protein. Furthermore, Steinmetz et al. present evidence for a polyphyletic origin of striated muscle cell development through their analysis of morphological and molecular markers that are present in bilaterians and absent in cnidarians, ctenophores, and bilaterians. Steimetz et al. showed that the traditional morphological and regulatory markers such as actin, the ability to couple myosin side chains phosphorylation to higher concentrations of the positive concentrations of calcium, and other MyHC elements are present in all metazoans not just the organisms that have been shown to have muscle cells. Thus, the usage of any of these structural or regulatory elements in determining whether or not the muscle cells of the cnidarians and ctenophores are similar enough to the muscle cells of the bilaterians to confirm a single lineage is questionable according to Steinmetz et al. Furthermore, Steinmetz et al. explain that the orthologues of the MyHc genes that have been used to hypothesize the origin of striated muscle occurred through a gene duplication event that predates the first true muscle cells (meaning striated muscle), and they show that the MyHc genes are present in the sponges that have contractile elements but no true muscle cells. Furthermore, Steinmetz et all showed that the localization of this duplicated set of genes that serve both the function of facilitating the formation of striated muscle genes and cell regulation and movement genes were already separated into striated myhc and non-muscle myhc. This separation of the duplicated set of genes is shown through the localization of the striated myhc to the contractile vacuole in sponges while the non-muscle myhc was more diffusely expressed during developmental cell shape and change. Steinmetz et al. found a similar pattern of localization in cnidarians with except with the cnidarian N. vectensis having this striated muscle marker present in the smooth muscle of the digestive track. Thus, Steinmetz et al. argue that the pleisiomorphic trait of the separated orthologues of myhc cannot be used to determine the monophylogeny of muscle, and additionally argue that the presence of a striated muscle marker in the smooth muscle of this cnidarian shows a fundamentally different mechanism of muscle cell development and structure in cnidarians.[27]

Steinmetz et al. continue to argue for multiple origins of striated muscle in the metazoans by explaining that a key set of genes used to form the troponin complex for muscle regulation and formation in bilaterians is missing from the cnidarians and ctenophores, and of 47 structural and regulatory proteins observed, Steinmetz et al. were not able to find even on unique striated muscle cell protein that was expressed in both cnidarians and bilaterians. Furthermore, the Z-disc seemed to have evolved differently even within bilaterians and there is a great deal diversity of proteins developed even between this clade, showing a large degree of radiation for muscle cells. Through this divergence of the Z-disc, Steimetz et al. argue that there are only four common protein components that were present in all bilaterians muscle ancestors and that of these for necessary Z-disc components only an actin protein that they have already argued is an uninformative marker through its pleisiomorphic state is present in cnidarians. Through further molecular marker testing, Steinmetz et al. observe that non-bilaterians lack many regulatory and structural components necessary for bilaterians muscle formation and do not find any unique set of proteins to both bilaterians and cnidarians and ctenophores that are not present in earlier, more primitive animals such as the sponges and amoebozoans. Through this analysis the authors conclude that due to the lack of elements that bilaterians muscles are dependent on for structure and usage, nonbilaterian muscles must be of a different origin with a different set regulatory and structural proteins.[27]

In another take on the argument, Andrikou and Arnone use the newly available data on gene regulatory networks to look at how the hierarchy of genes and morphogens and other mechanism of tissue specification diverge and are similar among early deuterostomes and protostomes. By understanding not only what genes are present in all bilaterians but also the time and place of deployment of these genes, Andrikou and Arnone discuss a deeper understanding of the evolution of myogenesis.[28]

In their paper Andrikou and Arnone argue that to truly understand the evolution of muscle cells the function of transcriptional regulators must be understood in the context of other external and internal interactions. Through their analysis, Andrikou and Arnone found that there were conserved orthologues of the gene regulatory network in both invertebrate bilaterians and in cnidarians. They argue that having this common, general regulatory circuit allowed for a high degree of divergence from a single well functioning network. Andrikou and Arnone found that the orthologues of genes found in vertebrates had been changed through different types of structural mutations in the invertebrate deuterostomes and protostomes, and they argue that these structural changes in the genes allowed for a large divergence of muscle function and muscle formation in these species. Andrikou and Arnone were able to recognize not only any difference due to mutation in the genes found in vertebrates and invertebrates but also the integration of species specific genes that could also cause divergence from the original gene regulatory network function. Thus, although a common muscle patterning system has been determined, they argue that this could be due to a more ancestral gene regulatory network being coopted several times across lineages with additional genes and mutations causing very divergent development of muscles. Thus it seems that myogenic patterning framework may be an ancestral trait. However, Andrikou and Arnone explain that the basic muscle patterning structure must also be considered in combination with the cis regulatory elements present at different times during development. In contrast with the high level of gene family apparatuses structure, Andrikou and Arnone found that the cis regulatory elements were not well conserved both in time and place in the network which could show a large degree of divergence in the formation of muscle cells. Through this analysis, it seems that the myogenic GRN is an ancestral GRN with actual changes in myogenic function and structure possibly being linked to later coopts of genes at different times and places.[28]

Evolutionarily, specialized forms of skeletal and cardiac muscles predated the divergence of the vertebrate/arthropod evolutionary line.[29][dead link] This indicates that these types of muscle developed in a common ancestor sometime before 700 million years ago (mya). Vertebrate smooth muscle was found to have evolved independently from the skeletal and cardiac muscle types.

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Muscle - Wikipedia, the free encyclopedia

Cardiac Stem Cells Comments Off on Muscle – Wikipedia, the free encyclopedia | September 22nd, 2016

For years, pediatric cardiologists have been trying to understand the origin of a puzzling structural defect of the heart muscle wall, a congenital problem called left ventricular non-compaction(LVNC). In people with this defect, the muscle of the hearts biggest pumping chamber looks spongy rather than smooth and solid.

For such congenital cardiomyopathies, currently there is no effective therapy, and the only cure is heart transplantation, said StanfordsJoseph Wu, MD, PhD, a cardiologist who led a new study of the condition that published online this week inNature Cell Biology.

His team was looking for a new way to address a very old research problem: They didnt know how much they could trust studies done on animal models of the disease. Mouse and rat models of LVNC also have spongy heart muscle, but its not clear if their defect starts the same way as in humans, nor whether findings from rodent studies could help treat humans.

So Wus team used innovative stem cell techniques instead. They took skin and blood cells donated by four members of a family affected by LVNC and converted them into induced pluripotent stem cells, which are stem cells made in a lab from adult cells. Using these stem cells, the researchers then made human heart muscle cells that they could study in a dish. That gave them a way to study what was happening in patients hearts without taking heart muscle biopsies.

Before starting their work, the researchers already knew that LVNC begins long before birth, when the heart muscle fails to make an important developmental shift. In the earliest stages of cardiac development, its normal for the muscle to be spongy. At about 8 weeks of gestation, the human heart muscle is supposed to compress into a thick, compact mass, but that shift doesnt happen correctly in LVNC patients. Earlier studies gave conflicting information about why: maybe the heart muscle cells were proliferating too little, or maybe too much.

Another mystery about the disease is its range of severity, which varies from no symptoms at all to complete heart failure. As the new paper describes, the family who agreed to have their cells studied is a good example. Of three siblings who donated cells for research, one had already had a heart transplant, while the other two had hearts that pumped normally in spite of deeper trabeculations (the scientific word for the spongy formations). Meanwhile, their father had an enlarged heart, but no sponginess in his heart muscle and no other symptoms.

Using the heart muscle cells derived from all four people, the researchers identified the gene defect that causes LVNC in this family; it codes for a cardiac transcription factor or a protein that controls the expression of other genes called TBX20. The scientists conducted several experiments to figure out how the TBX20 abnormality changes heart muscle cell proliferation with the abnormality, the cells dont proliferate enough, it turns out. They also explored the exact signaling pathways that cause the problem, showing that the magnitude of signaling abnormalities could explain differences in symptom severity between family members. They created a mouse model with the familys gene defect for further characterization, and also showed that blocking the faulty signal from the altered TBX20 could restore the mutated cells ability to proliferate. Its possible that some day, they might be able to turn these findings into a drug that could correct heart muscle formation in affected fetuses before birth.

The new findings still leave unanswered questions about the origins of LVNC. Cardiologists suspect the problem can arise in several ways, and theyll need to study many more families to find out if TBX20 mutations are a common or rare cause. But the paper does demonstrate how induced pluripotent stem cells can overcome a research hurdle, and suggests that the same methods could help scientists tackling other hard-to-study conditions.

This study shows the feasibility of modeling such developmental defects using human tissue-specific cells, rather than relying on animal cells or animal models, Wu said. It opens up an exciting new avenue for research into congenital heart disease that could help literally the youngest in utero patients.

Previously: One of the most promising minds of his generation: Joseph Wu takes stem cells to heart, Stem cells create faithful replicas of native tissue, according to Stanford study and A cheaper, faster way to find genetic defects in heart patients Photo by amanda tipton

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How Does A Heart Defect Start? Stanford Scientists Use ...

Cardiac Stem Cells Comments Off on How Does A Heart Defect Start? Stanford Scientists Use … | September 21st, 2016

14th International Conference on Clinical & Experimental Cardiology is among the Worlds leading Scientific Conference. The three day event on Cardiology practices will host 60+ Scientific and technical sessions and sub-sessions on cutting edge research and latest research innovations in the field of cardiology and cardiac surgeries across the globe. This year annual Cardiology conference will comprises of 14 major sessions designed to offer comprehensive sessions that address current issues in various field of Cardiology. The attendees can find some- Exclusive Sessions and Panel discussions on latest innovations in Cardiac Surgeries and Heart Failure. This is the excellent platform to showcase the latest products and formulations in the field of Cardiology.

Theme:The Science of Heart Discovery

Scientific sessions:

Track: Clinical Cardiology

Cardiology is a branch of medicine dealing with disorders of the heart be it human or animal. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians who specialize in this field of medicine are called cardiologists, a specialty of internal medicine. Pediatric cardiologists are pediatricians who specialize in cardiology. Physicians who specialize in cardiac surgery are called cardiothoracic surgeons or cardiac surgeons, a specialty of general surgery. Clinical Cardiology is an American journal about Cardiology founded in 1978. It provides a forum for the coordination of clinical research in diagnostics, cardiovascular medicine and cardiovascular surgery.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Heart Failure

Heart failure is a condition caused by the heart failing to pump enough blood around the body at the right pressure. It usually occurs because the heart muscle has become too weak or stiff to work properly. If you have heart failure, it does not mean your heart is about to stop working. It means the heart needs some support to do its job, usually in the form of medicines. Breathlessness, feeling very tired and ankle swelling is the main symptoms of heart failure. But all of these symptoms can have other causes, only some of which are serious. The symptoms of heart failure can develop quickly (acute heart failure). If this happens, you will need to be treated in hospital. But they can also develop gradually (chronic heart failure). The most common causes are heart attack, high blood pressure, cardiomyopathy (diseases of the heart muscle. Sometimes these are inherited from your family and sometimes they are caused by other things, such as viral infections).

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Heart Diseases

Heart disease include heart diseases that is any type of disorder that affects the heart. Heart disease meetings comes under cardiology conferences that comprises the heart diseases tracks that means the same as cardiac disease but not the cardiovascular diseases. This condition results from a buildup of plaque on the inside of the arteries, which reduces blood flow to the heart and increases the risk of a heart attack and other heart complications. In this sub topic Heart disease we have different types of heart diseases i.e. Coronary heart diseases, Pediatric heart diseases, Congenital Heart Diseases, myocardial infarction etc.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Obesity and Heart

People with a body mass index (BMI) of 30 or higher are considered obese. The term obesity is used to describe the health condition of anyone significantly above his or her ideal healthy weight. Obesity increases the risk for heart disease and stroke. But it harms more than just the heart and blood vessel system. It's also a major cause of gallstones, osteoarthritis and respiratory problems. Obesity is intimately intertwined with multiple health conditions that underlie cardiovascular disease including high blood pressure, diabetes, and abnormal blood cholesterol. In addition, weight gain is a frequent consequence of heart-damaging lifestyle choices such as lack of exercise and a fat-laden diet. Obesity also can lead to heart failure. This is a serious condition in which your heart can't pump enough blood to meet your body's needs.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Cardiac Drugs

Cardiac Drugs are the drugs which are used in any way to treat conditions of the heart or the circulatory or vascular system. Many classes of cardiovascular agents are available to treat the various cardiovascular conditions. They are a complicated group of drugs with many being used for multiple heart conditions. Prescription drugs and medicines for diseases relating to the structure and function of the heart and blood vessels. In this sub topic we have Sodium, potassium, calcium channel blockers, ACE-inhibitors and Cardiac biomarkers. There are 6 associations and societies and the main association for Cardiac Therapeutic Agents in USA. 50 universities are working on Cardiac Therapeutic Agents. There are 120 Companies in USA that are making Cardiac Therapeutic Agents in Cardiology. 3new drugs were introduced in 2015. There are many types of cardiovascular drugs in the market that include Cardiac glycosides, antiarrhythmic agents, antianginal agents and antihypertensive agents.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Cardiac Imaging and technology

Advances in imaging technology have sparked fundamental changes in the approach to cardiac care. One of the most accurate diagnostic techniques cardiac imaging employs new, non-invasive and minimally invasive radiology technology to produce three-dimensional images of the heart. The imaging tools help to discover medical problems that several years ago were undetectable using conventional methods of diagnosis. Cardiac imaging techniques include coronary catheterization, echocardiogram, and intravascular ultrasound.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Women & CVD

Cardiovascular disease (CVD) heart disease and stroke is the biggest killer of women globally, killing more women than all cancers, tuberculosis, HIV/AIDS and malaria combined. Heart disease is the leading cause of death for women in the United States, killing 292,188 women in 2009 thats 1 in every 4 female deaths. While some women have no symptoms, others experience angina (dull, heavy to sharp chest pain or discomfort), pain in the neck/jaw/throat or pain in the upper abdomen or back. These may occur during rest, begin during physical activity, or be triggered by mental stress. Sometimes heart disease may be silent and not diagnosed until a woman experiences signs or symptoms of a heart attack, heart failure, an arrhythmia or stroke. Women with diabetes have higher CVD mortality rates than men with diabetes. Women who engage in physical activity for less than an hour per week have 1.48 times the risk of developing coronary heart disease, compared to women who do more than three hours of physical activity per week. Go Red for Women is a major international awareness campaign dedicated to the prevention, diagnosis and control of heart disease and stroke in women.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Pediatric Cardiology

Pediatric Cardiology is responsible for the diagnosis of congenital heart defects, performing diagnostic procedures such as echocardiograms, cardiac catheterizations, and for the ongoing management of the sequel of heart disease in infants, children and adolescents. The division is actively involved in research aimed at preventing both congenital and acquired heart disease in children. Finally, the division is committed to educating the next generation of physicians, and offers advanced training in pediatric cardiology.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Cardiac Nursing

Cardiac nursing is a nursing specialty that works with patients who suffer from various conditions of the cardiovascular system. Cardiac nurses help treat conditions such as unstable angina, cardiomyopathy, coronary artery disease, congestive heart failure, myocardial infarction and cardiac dysrhythmia under the direction of a cardiologist. Cardiac nurses perform postoperative care on a surgical unit, stress test evaluations, cardiac monitoring, vascular monitoring, and health assessments. Cardiac nurses work in many different environments, including coronary care units (CCU), cardiac catheterization, intensive care units (ICU), operating theatres, cardiac rehabilitation centers, clinical research, cardiac surgery wards, cardiovascular intensive care units (CVICU), and cardiac medical wards.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Diabetic Cardiovascular Diseases

The term diabetic heart disease (DHD) refers to heart disease that develops in people who have diabetes. Diabetes is a disease in which the body's blood glucose (sugar) level is too high. Normally, the body breaks down food into glucose and carries it to cells throughout the body. The cells use a hormone called insulin to turn the glucose into energy. There is a clear-cut relationship between diabetes and cardiovascular disease. Coronary heart disease is recognized to be the cause of death for 80% of people with diabetes; however, the NHS states that heart attacks are largely preventable. Cardiovascular disease is the leading cause of mortality for people with diabetes. Hypertension, abnormal blood lipids and obesity, all risk factors in their own right for cardiovascular disease, occur more frequently in people with diabetes. Several advances in treating heart disease over the past two decades have improved the chances of surviving a heart attack or stroke. However, as the incidence of diabetes steadily increases, so does the number of new cases of heart disease and cardiovascular complications.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Cardiac Surgery

Cardiovascular surgery is surgery on the heart or great vessels performed by cardiac surgeons. Frequently, it is done to treat complications of ischemic heart disease (for example, coronary artery bypass grafting), correct congenital heart disease, or treat valvular heart disease from various causes including endocarditis, rheumatic heart disease and atherosclerosis. It also includes heart transplantation. The development of cardiac surgery and cardiopulmonary bypass techniques has reduced the mortality rates of these surgeries to relatively low ranks. Coronary artery bypass grafting (CABG) is the most common type of heart surgery. CABG improves blood flow to the heart. Surgeons use CABG to treat people who have severe coronary heart disease (CHD).

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Current Research in Cardiology

Advances in medicine means that if CHD is detected at an early stage it can be treated successfully to extend the survival rate. Successful treatment is more likely if the disease is detected at its earliest stages. Our current research focuses on the early detection of CHD in order to halt or reverse the progress of the disease. The ongoing research includes pioneering the use of heart scanning in the early diagnosis of heart disease in diabetics, Development of Nuclear Cardiology techniques for the detection of heart disease, Drug development and evaluation of treatments used in heart disease, Identification of novel biological markers to predict the presence of heart disease, analysis of ethnic and socio-economic differences in heart disease risk.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Cardiologists Training & Education

Cardiologists provide health care to prevent, diagnose and treat diseases and conditions of the heart and cardiovascular system, including the arteries. Because the field of cardiology encompasses so many different types of diseases and procedures, there are many different types of cardiology one may choose to practice depending on his or her interests and skill sets, and the type of work theyd like to do. Cardiologists receive extensive education, including four years of medical school and three years of training in general internal medicine. After this, a cardiologist spends three or more years in specialized training. Many cardiologists are specially trained in this technique, but others specialize in office diagnosis, the performance and interpretation of echocardiograms, ECGs, and exercise tests. Still others have special skill in cholesterol management or cardiac rehabilitation and fitness. All cardiologists know how and when these tests are needed and how to manage cardiac emergencies.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

Track:Advances in Cardiologists Education

Advances in Cardiology Education presents the current thinking of international experts regarding the underlying mechanisms of cardiovascular risk and the pathogenesis and pathophysiology of heart and its related disorders. This session gives new insights into the relationship between arterial stiffness, cardiovascular diagnosis, vascular study and atherosclerosis, but also establishes the possible interactions with age and other cardiovascular factors such as high blood pressure, diabetes and hyperlipidemia.

RelevantConferences:9thArrhythmiasConference July 14-15, 2016 Brisbane, Australia;CardioVascular MedicineConference August 01-02, 2016 Manchester, UK;EchocardiographyConference July 18-19, 2016 Berlin, Germany; 8th Global Cardiologists Annual Meeting July 18-20, 2016 Berlin, Germany; Atherosclerosis and Clinical Cardiology Conference July 11-12, 2016 Philadelphia, Pennsylvania, USA; Ischemic Heart Diseases Conference October 20-21, 2016 Chicago, Illinois, USA; Hypertension & Health Care Conference August 11-12, 2016 Toronto, Canada; 11thCardiac Conference September 12-13, 2016 Philadelphia, Pennsylvania, USA; 13thEuropean Cardiology Congress October 17-19, 2016 Rome, Italy; 19th Annual Update on Pediatric and Congenital Cardiovascular Disease February 24- 28, 2016, Orlando, USA; American Cardiology Congress 2016; ACC Annual Meeting 2016; American Cardiology Congress 2016; European Cardiology Congress August 27 - 31, 2016 Rome, Italy; International Conference and Expo on Cardiology and Cardiac surgery April 04-06, 2016, Dubai, UAE; 21st World Congress on Heart Disease, July 30-August 1, 2016, Boston, MA, USA.

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Cardiac Stem Cells Comments Off on Cardiology Conferences | Events | Meetings | Florida | USA … | September 8th, 2016

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Challenges in identifying the best source of stem cells ...

Cardiac Stem Cells Comments Off on Challenges in identifying the best source of stem cells … | October 26th, 2015

Endogenous cardiac stem cells (eCSCs) are tissue-specific stem progenitor cells harboured within the adult mammalian heart.

They were first discovered in 2003 by Bernardo Nadal-Ginard, Piero Anversa and colleagues [1][2] in the adult rat heart and since then have been identified and isolated from mouse, dog, porcine and human hearts.[3][4]

The adult heart was previously thought to be a post mitotic organ without any regenerative capability. The identification of eCSCs has provided an explanation for the hitherto unexplained existence of a subpopulation of immature cycling myocytes in the adult myocardium. Indeed, recent evidence from a genetic fate-mapping study established that stem cells replenish adult mammalian cardiomyocytes lost by cardiac wear and tear and injury throughout the adult life.[5] Moreover, it is now accepted that myocyte death and myocyte renewal are the two sides of the proverbial coin of cardiac homeostasis in which the eCSCs play a central role.[6] These findings produced a paradigm shift in cardiac biology and opened new opportunities and approaches for future treatment of cardiac diseases by placing the heart squarely amongst other organs with regenerative potential such as the liver, skin, muscle, CNS. However, they have not changed the well-established fact that the working myocardium is mainly constituted of terminally differentiated contractile myocytes. This fact does not exclude, but is it fully compatible with the heart being endowed with a robust intrinsic regenerative capacity which resides in the presence of the eCSCs throughout the individual lifespan.

Briefly, eCSCs have been first identified through the expression of c-kit, the receptor of the stem cell factor and the absence of common hematopoietic markers, like CD45. Afterwards, different membrane markers (Sca-1, Abcg-2, Flk-1) and transcription factors (Isl-1, Nkx2.5, GATA4) have been employed to identify and characterize these cells in the embryonic and adult life.[7] eCSCs are clonogenic, self renewing and multipotent in vitro and in vivo,[8] capable of generating the 3 major cell types of the myocardium: myocytes, smooth muscle and endothelial vascular cells.[9] They express several markers of stemness (i.e. Oct3/4, Bmi-1, Nanog) and have significant regenerative potential in vivo.[10] When cloned in suspension they form cardiospheres,[11] which when cultured in a myogenic differentiation medium, attach and differentiate into beating cardiomyocytes.

In 2012, it was proposed that Isl-1 is not a marker for endogenous cardiac stem cells.[12] That same year, a different group demonstrated that Isl-1 is not restricted to second heart field progenitors in the developing heart, but also labels cardiac neural crest.[13] It has also been reported that Flk-1 is not a specific marker for endogenous and mouse ESC-derived Isl1+ CPCs. While some eCSC discoveries have been brought into question, there has been success with other membrane markers. For instance, it was demonstrated that the combination of Flt1+/Flt4+ membrane markers identifies an Isl1+/Nkx2.5+ cell population in the developing heart. It was also shown that endogenous Flt1+/Flt4+ cells could be expanded in vitro and displayed trilineage differentiation potential. Flt1+/Flt4+ CPCs derived from iPSCs were shown to engraft into the adult myocardium and robustly differentiate into cardiomyocytes with phenotypic and electrophysiologic characteristics of adult cardiomyocytes.[14]

With the myocardium now recognized as a tissue with limited regenerating potential,[15] harbouring eCSCs that can be isolated and amplified in vitro [16] for regenerative protocols of cell transplantation or stimulated to replicate and differentiate in situ in response to growth factors,[17] it has become reasonable to exploit this endogenous regenerative potential to replace lost/damaged cardiac muscle with autologous functional myocardium.

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Endogenous cardiac stem cell - Wikipedia, the free ...

Cardiac Stem Cells Comments Off on Endogenous cardiac stem cell – Wikipedia, the free … | October 23rd, 2015

An isolated cardiac muscle cell, beating

Cardiac muscle (heart muscle) is involuntary striated muscle that is found in the walls and histological foundation of the heart, specifically the myocardium. Cardiac muscle is one of three major types of muscle, the others being skeletal and smooth muscle. These three types of muscle all form in the process of myogenesis. The cells that constitute cardiac muscle, called cardiomyocytes or myocardiocytes, contain only three nuclei.[1][2][pageneeded] The myocardium is the muscle tissue of the heart, and forms a thick middle layer between the outer epicardium layer and the inner endocardium layer.

Coordinated contractions of cardiac muscle cells in the heart propel blood out of the atria and ventricles to the blood vessels of the left/body/systemic and right/lungs/pulmonary circulatory systems. This complex mechanism illustrates systole of the heart.

Cardiac muscle cells, unlike most other tissues in the body, rely on an available blood and electrical supply to deliver oxygen and nutrients and remove waste products such as carbon dioxide. The coronary arteries help fulfill this function.

Cardiac muscle has cross striations formed by rotating segments of thick and thin protein filaments. Like skeletal muscle, the primary structural proteins of cardiac muscle are myosin and actin. The actin filaments are thin, causing the lighter appearance of the I bands in striated muscle, whereas the myosin filament is thicker, lending a darker appearance to the alternating A bands as observed with electron microscopy. However, in contrast to skeletal muscle, cardiac muscle cells are typically branch-like instead of linear.

Another histological difference between cardiac muscle and skeletal muscle is that the T-tubules in the cardiac muscle are bigger and wider and track laterally to the Z-discs. There are fewer T-tubules in comparison with skeletal muscle. The diad is a structure in the cardiac myocyte located at the sarcomere Z-line. It is composed of a single T-tubule paired with a terminal cisterna of the sarcoplasmic reticulum. The diad plays an important role in excitation-contraction coupling by juxtaposing an inlet for the action potential near a source of Ca2+ ions. This way, the wave of depolarization can be coupled to calcium-mediated cardiac muscle contraction via the sliding filament mechanism. Cardiac muscle forms these instead of the triads formed between the sarcoplasmic reticulum in skeletal muscle and T-tubules. T-tubules play critical role in excitation-contraction coupling (ECC). Recently, the action potentials of T-tubules were recorded optically by Guixue Bu et al.[3]

The cardiac syncytium is a network of cardiomyocytes connected to each other by intercalated discs that enable the rapid transmission of electrical impulses through the network, enabling the syncytium to act in a coordinated contraction of the myocardium. There is an atrial syncytium and a ventricular syncytium that are connected by cardiac connection fibres.[4] Electrical resistance through intercalated discs is very low, thus allowing free diffusion of ions. The ease of ion movement along cardiac muscle fibers axes is such that action potentials are able to travel from one cardiac muscle cell to the next, facing only slight resistance. Each syncyntium obeys the all or none law.[5]

Intercalated discs are complex adhering structures that connect the single cardiomyocytes to an electrochemical syncytium (in contrast to the skeletal muscle, which becomes a multicellular syncytium during mammalian embryonic development). The discs are responsible mainly for force transmission during muscle contraction. Intercalated discs are described to consist of three different types of cell-cell junctions: the actin filament anchoring adherens junctions, the intermediate filament anchoring desmosomes , and gap junctions. They allow action potentials to spread between cardiac cells by permitting the passage of ions between cells, producing depolarization of the heart muscle. However, novel molecular biological and comprehensive studies unequivocally showed that intercalated discs consist for the most part of mixed-type adhering junctions named area composita (pl. areae compositae) representing an amalgamation of typical desmosomal and fascia adhaerens proteins (in contrast to various epithelia).[6][7][8] The authors discuss the high importance of these findings for the understanding of inherited cardiomyopathies (such as arrhythmogenic right ventricular cardiomyopathy).

Under light microscopy, intercalated discs appear as thin, typically dark-staining lines dividing adjacent cardiac muscle cells. The intercalated discs run perpendicular to the direction of muscle fibers. Under electron microscopy, an intercalated disc's path appears more complex. At low magnification, this may appear as a convoluted electron dense structure overlying the location of the obscured Z-line. At high magnification, the intercalated disc's path appears even more convoluted, with both longitudinal and transverse areas appearing in longitudinal section.[9]

In contrast to skeletal muscle, cardiac muscle requires extracellular calcium ions for contraction to occur. Like skeletal muscle, the initiation and upshoot of the action potential in ventricular cardiomyocytes is derived from the entry of sodium ions across the sarcolemma in a regenerative process. However, an inward flux of extracellular calcium ions through L-type calcium channels sustains the depolarization of cardiac muscle cells for a longer duration. The reason for the calcium dependence is due to the mechanism of calcium-induced calcium release (CICR) from the sarcoplasmic reticulum that must occur during normal excitation-contraction (EC) coupling to cause contraction. Once the intracellular concentration of calcium increases, calcium ions bind to the protein troponin, which allows myosin to bind to actin and contraction to occur.

Until recently, it was commonly believed that cardiac muscle cells could not be regenerated. However, a study reported in the April 3, 2009 issue of Science contradicts that belief.[10] Olaf Bergmann and his colleagues at the Karolinska Institute in Stockholm tested samples of heart muscle from people born before 1955 who had very little cardiac muscle around their heart, many showing with disabilities from this abnormality. By using DNA samples from many hearts, the researchers estimated that a 20-year-old renews about 1% of heart muscle cells per year, and about 45 percent of the heart muscle cells of a 50-year-old were generated after he or she was born.

One way that cardiomyocyte regeneration occurs is through the division of pre-existing cardiomyocytes during the normal aging process.[11] The division process of pre-existing cardiomyocytes has also been shown to increase in areas adjacent to sites of myocardial injury. In addition, certain growth factors promote the self-renewal of endogenous cardiomyocytes and cardiac stem cells. For example, insulin-like growth factor 1, hepatocyte growth factor, and high-mobility group protein B1 increase cardiac stem cell migration to the affected area, as well as the proliferation and survival of these cells.[12] Some members of the fibroblast growth factor family also induce cell-cycle re-entry of small cardiomyocytes. Vascular endothelial growth factor also plays an important role in the recruitment of native cardiac cells to an infarct site in addition to its angiogenic effect.

Based on the natural role of stem cells in cardiomyocyte regeneration, researchers and clinicians are increasingly interested in using these cells to induce regeneration of damaged tissue. Various stem cell lineages have been shown to be able to differentiate into cardiomyocytes, including bone marrow stem cells. For example, in one study, researchers transplanted bone marrow cells, which included a population of stem cells, adjacent to an infarct site in a mouse model. Nine days after surgery, the researchers found a new band of regenerating myocardium.[13] However, this regeneration was not observed when the injected population of cells was devoid of stem cells, which strongly suggests that it was the stem cell population that contributed to the myocardium regeneration. Other clinical trials have shown that autologous bone marrow cell transplants delivered via the infarct-related artery decreases the infarct area compared to patients not given the cell therapy.[14]

Occlusion (blockage) of the coronary arteries by atherosclerosis and/or thrombosis can lead to myocardial infarction (heart attack), where part of the myocardium is injured due to ischemia (not receiving enough oxygen). This occurs because coronary arteries are functional end arteries - i.e. there is almost no overlap in the areas supplied by different arteries (anastomoses) so that if one fails, others cannot adequately perfuse the region, unlike in other tissues.

Certain viruses lead to myocarditis (inflammation of the myocardium). Cardiomyopathies are inherent diseases of the myocardium, many of which are caused by genetic mutations.

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Cardiac muscle - Wikipedia, the free encyclopedia

Cardiac Stem Cells Comments Off on Cardiac muscle – Wikipedia, the free encyclopedia | September 25th, 2015

George Reed's heart wasn't doing so well: He's 71, and after suffering a heart attack years earlier, Reed had undergone open heart surgery and was put on multiple medications. But nothing seemed to help the dizziness and chest pain he experienced daily.

"I'd get dizzy and just fall over -- sometimes twice a day. I would run my head into the concrete. I was a bloody mess," the Perry, Ohio, native says. Despite his doctor's best efforts, Reed continued to experience angina, a type of chest pain that occurs when the heart doesn't get enough oxygen-rich blood; it can be accompanied by dizziness. So when he was recommended for an experimental study that would inject his own stem cells into his damaged heart, Perry signed on. "I needed something to change," he says.

Researchers gave Reed a drug commonly used in bone marrow transplants that stimulates the marrow to make more stem cells. Then they removed some of Reed's blood, isolated the stem cells and injected them into and around the damaged areas of his heart.

"The goal was to grow new blood vessels with stem cells from the patient's own body," says Dr. Tim Henry, a co-author of the study and director of research at the Minneapolis Heart Institute Foundation.

Within a few months, Reed, along with many of the other 100 or so patients at 26 hospital centers who'd received this stem cell treatment, reported feeling better than he had in years.

"When it started kicking in, I felt like a kid. I felt good," Reed says. He wasn't passing out and falling down anymore.

For Jay Homstad, 49, who was part of the Minnesota branch of the study, he felt the changes most in his ability to walk and be active.

"My activity level increased tenfold. Before, I struggled with chest pain every day. My activity level was about as close to zero as you could get. Now I can participate ... just in life. It may sound silly, but the best part is that in the wintertime I could go out and walk with my dog along the Red River. When you're walking through snow that is waist deep, you can tell there's a difference," Homstad says.

Homstad had had about a dozen surgeries and nine stents put in before he enrolled in the study, but he still struggled with angina daily. Within a few months of the stem cell shots, he could walk farther, and his chest pain subsided and was kept at bay for nearly four years.

"These are people for whom other treatment hasn't worked. They're debilitated by their chest pain, but their other options are really limited, that's why we picked them," says Henry. If the positive results seen in this study hold up in the next phase of the study, which is set to begin enrollment in the fall, this type of cardiac stem cell injection could be added to the arsenal of weapons against angina. The upcoming phase three trial has already been approved by the Food and Drug Administration.

Shot to the Heart, Before It's too Late

While several smaller studies have suggested that injecting stem cells into damaged heart tissue might be effective, this study, in its scope and rigor, was the first of its kind. A total of 167 patients were recruited and randomly assigned to receive a lower dose of stem cells, a higher dose or a placebo. The patients didn't know who got what treatment, and neither did the doctors treating them.

When tracked for a year after the injection, patients who received the lower dose of stem cells could last longer during a treadmill exercise than those who had received the placebo, and they averaged seven fewer episodes of chest pain in a week. To put this in perspective, a popular drug to treat angina, Ranolazine, reduced chest pain by fewer than two episodes a week in clinical trials.

Although the goal of the stem cell shots was to grow new blood vessels, it's impossible to tell if these stem cells were actually growing into blood vessels or if they were just triggering some other kind of healing process in the body, Henry says. Tests in animal models, however, do suggest that new blood vessels are forming, says Dr. Marco Costa, a co-author of the study and George Reed's doctor at UH Case Medical Center in Cleveland.

For now, the only gauge of the injections is improvement in symptoms.

Despite the positive results of the study, cardiologists remain "cautiously optimistic" about stem cells as a treatment for angina.

"The number of patients is relatively small, so this trial would probably not carry much scientific weight," says Dr. Jeff Brinker, a professor of cardiology at Johns Hopkins University. The results did justify the next, larger trial, he says, which would offer more answers as to whether this treatment is actually working the way researchers suspect.

The fact that lower doses of stem cells were puzzlingly more effective than larger ones is cause for caution, says Dr. Steve Nissen, chairman of the department of cardiovascular medicine at the Cleveland Clinic.

"The jury is still out for stem cell therapies to treat heart disease," says Dr. Cam Paterson, a cardiologist at the University of North Carolina at Chapel Hill.

But the results so far provide cautious hope for heart patients like George Reed and Jay Homstad.

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Injecting the Heart With Stem Cells Helps Chest Pain - ABC ...

Cardiac Stem Cells Comments Off on Injecting the Heart With Stem Cells Helps Chest Pain – ABC … | September 13th, 2015

Stem Cell Therapy: Helping the Body Heal Itself

Stem cells are natures own transformers. When the body is injured, stem cells travel the scene of the accident. Some come from the bone marrow, a modest number of others, from the heart itself. Additionally, theyre not all the same. There, they may help heal damaged tissue. They do this by secreting local hormones to rescue damaged heart cells and occasionally turning into heart muscle cells themselves. Stem cells do a fairly good job. But they could do better for some reason, the heart stops signaling for heart cells after only a week or so after the damage has occurred, leaving the repair job mostly undone. The partially repaired tissue becomes a burden to the heart, forcing it to work harder and less efficiently, leading to heart failure.

Initial research used a patients own stem cells, derived from the bone marrow, mainly because they were readily available and had worked in animal studies. Careful study revealed only a very modest benefit, so researchers have moved on to evaluate more promising approaches, including:

No matter what you may read, stem cell therapy for damaged hearts has yet to be proven fully safe and beneficial. It is important to know that many patients are not receiving the most current and optimal therapies available for their heart failure. If you have heart failure, and wondering about treatment options, an evaluation or a second opinion at a Center of Excellence can be worthwhile.

Randomized clinical trials evaluating these different approaches typically allow enrollment of only a few patients from each hospital, and hence what may be available at the Cleveland Clinic varies from time to time. To inquire about current trials, please call 866-289-6911 and speak to our Resource Nurses.

Cleveland Clinic is a large referral center for advanced heart disease and heart failure we offer a wide range of therapies including medications, devices and surgery. Patients will be evaluated for the treatments that best address their condition. Whether patients meet the criteria for stem cell therapy or not, they will be offered the most advanced array of treatment options.

Allogenic: from one person to another (for example: organ transplant)

Autogenic: use of one's own tissue

Myoblasts: immature muscle cells, may be able to change into functioning heart muscle cells

Stem Cells: cells that have the ability to reproduce, generate new cells, and send signals to promote healing

Transgenic: Use of tissue from another species. (for example: some heart valves from porcine or bovine tissue)

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Stem Cell Therapy for Heart Disease - Cleveland Clinic

Cardiac Stem Cells Comments Off on Stem Cell Therapy for Heart Disease – Cleveland Clinic | August 31st, 2015

A new method for delivering stem cells to damaged heart muscle has shown early promise in treating severe heart failure, researchers report.

In a preliminary study, they found the tactic was safe and feasible for the 48 heart failure patients they treated. And after a year, the patients showed a modest improvement in the heart's pumping ability, on average.

It's not clear yet whether those improvements could be meaningful, said lead researcher Dr. Amit Patel, director of cardiovascular regenerative medicine at the University of Utah.

He said larger clinical trials are underway to see whether the approach could be an option for advanced heart failure.

Other experts stressed the bigger picture: Researchers have long studied stem cells as a potential therapy for heart failure -- with limited success so far.

"There's been a lot of promise, but not much of a clinical benefit yet," said Dr. Lee Goldberg, who specializes in treating heart failure at the University of Pennsylvania.

Researchers are still sorting through complicated questions, including how to best get stem cells to damaged heart muscle, said Goldberg, who was not involved in the new study.

What's "novel" in this research, he said, is the technique Patel's team used to deliver stem cells to the heart. They took stem cells from patients' bone marrow and infused them into the heart through a large vein called the coronary sinus.

Patel agreed that the technique is the advance.

"Most other techniques have infused stem cells through the arteries," Patel explained. One obstacle, he said, is that people with heart failure generally have hardened, narrowed coronary arteries, and the infused stem cells "don't always go to where they should."

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Stem Cells Show Promise in Heart Failure Treatment

Cardiac Stem Cells Comments Off on Stem Cells Show Promise in Heart Failure Treatment | August 1st, 2015

Clara's Story

Clara had a severe heart attack in 2004. Before contacting us she had received adult stem cells from a company in Thailand - a process requiring at least a one week stay.

When she contacted Stemaid, she had just had an echocardiogram showing that her overall left ventricular ejection fraction was estimated to be 30 to 35%. She opted to receive one injection of 5 million Embryonic Stem Cells by Stemaid in November 2010. She arrived at 1pm and was done by 3pm the same day.

We received the following email from her in April 2011: I had an EKO last week and rate is 44%, up from the 33/35% it was before I received Stemaid's stem cells! . Are the stem cells still available and still as good?

The heart contains a small amount of stem cells, the cardiac stem cells, that are produced when there is a need for production of more heart cells or for an active replacement of damaged ones. These cardiac cells are produced in high quantity for about one week following an infarction, actively repairing the damaged areas of the heart.

However this high production stops after a week and the repair stops as well.

Initial studies showed that by introducing embryonic stem cells, the heart starts to repair again within minutes of their injection. More recent studies showed that the injection of embryonic stem cells actually triggers the production of cardiac stem cells for one week. Another week of active repair is offered each time that one receives embryonic stem cells.

If you have suffered from an infarction, we suggest a minimum of 3 injections of esc over the course of 3 weeks to get significant repair.

Some of the patients who have received Stemaid Embryonic Stem-Cells have agreed to be mentioned on our website so that we may illustrate the benefits of them.

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Heart Disease - Stemaid : Embryonic Stem-cells

Cardiac Stem Cells Comments Off on Heart Disease – Stemaid : Embryonic Stem-cells | August 1st, 2015

Stem Cell Clinical Research & Deployment Cardiovascular & Pulmonary Conditions

The Manhattan Regenerative Medicine Medical Group is proud to be part of the only Institutional Review Board (IRB)-based stem cell treatment network in the United States that utilizes fat-transfer surgical technology. The Manhattan Regenerative Medicine Medical Group offers IRB approved protocols and investigational use ofAdult Autologous Adipose-derived Stem Cells (ADSCs) for clinical research and deployment for numerous Cardiovascular and Pulmonary disorders, inclusive of:

Cardiovascular conditions include medical problems involving the heart and vascular system (the arterial and venous blood vessels). The most common cardiovascular condition is atherosclerotic coronary artery disease (ASCVD), which especially affects the coronary arteries and is the leading cause of heart attacks and death worldwide; and Congestive Heart Failure (CHF).

Other common cardiovascular conditions involve the cardiac muscle (CHF), cardiac valves, and heart rhythm. Many patients are typically treated with a multitude of medications; many patients require surgical interventions such as coronary angioplasty, coronary artery bypass, or other surgeries. Often patients, despite maximum therapy with medications and surgery, continue to suffer pain, discomfort, disability and have marked restrictions in their normal daily living activities.

The Manhattan Regenerative Medicine Medical Group is proud to be part of the only Institutional Review Board (IRB)-based stem cell treatment network in the United States that utilizes fat-transfer surgical technology. We have an array of ongoing IRB-approved protocols, andwe provide care for patients with a wide variety of disorders that may be treated with adult stem cell-based regenerative therapy.

The Manhattan Regenerative Medicine Medical Group offers IRB approved protocols and investigational use of Autologous Adult Adipose Derived Stem Cells (ADSCs) for clinical research and deployment for numerous cardiovascular conditions. These ADSCs cells are derived from fat an exceptionally abundant source of stem cells that has been removed during our mini-liposuction office procedure. The source of the regenerative stem cells actually comes from stromal vascular fraction (SVF) a protein rich segment from processed adipose tissue. SVF contains a mononuclear cell line (predominantly autologous mesenchymal stem cells), macrophage cells, endothelial cells, red blood cells, and important growth factors that facilitate the stem cell process and promote their activity. Our technology allows us to isolate high numbers of viable cells that we can deploy during the same surgical setting.

The SVF and stem cells are then deployed back into the patients body via injection or IV infusion on an outpatient basis; the total procedure takes less than two hours; and only local anesthesia is used. Not all cardiovascular problems respond to stem cell therapy, and each patient must be assessed individually to determine the potential for optimal results from this regenerative medicine process.

The Manhattan Regenerative Medicine Medical Group is committed not only to providing a high degree of quality care for our patients with cardiovascular problems but we are also highly committed to clinical stem cell research and the advancement of regenerative medicine. At the Miami Stem Cell Treatment Center we exploit anti-inflammatory, immuno-modulatory and regenerative properties of adult stem cells to mitigate cardiovascular conditions which are otherwise lethal to our bodies.

Myocardial infarction (heart attack) is responsible for significant cardiac muscle destruction and impairment due to ischemia (lack of blood flow). This can lead to further or recurrent restriction of blood flow thereby causing re-current infarct and pain on exertion (or even rest) known as chronic angina. Chronic angina causes restriction of daily activities of everyday living and is plagued with chest pain, chest pressure, and depression. This problem is caused most commonly by coronary artery disease which is very common in the United States and associated with significant morbidity and mortality.

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Cardiovascular Stem Cell Therapy

Cardiac Stem Cells Comments Off on Cardiovascular Stem Cell Therapy | July 2nd, 2015

Abstract

Myocardial infarctioninduced heart failure is a prevailing cause of death in the United States and most developed countries. The cardiac tissue has extremely limited regenerative potential, and heart transplantation for reconstituting the function of damaged heart is severely hindered mainly due to the scarcity of donor organs. To that end, stem cells with their extensive proliferative capacity and their ability to differentiate toward functional cardiomyocytes may serve as a renewable cellular source for repairing the damaged myocardium. Here, we review recent studies regarding the cardiogenic potential of adult progenitor cells and embryonic stem cells. Although large strides have been made toward the engineering of cardiac tissues using stem cells, important issues remain to be addressed to enable the translation of such technologies to the clinical setting.

Heart disease is a significant cause of morbidity and mortality worldwide. In the United States, heart failure is ranked number one as a cause of death, affecting over 5 million people and with more than 500,000 new cases diagnosed each year.1 The health care expenditures associated with heart failure were $26.7 billion in 2004 and are estimated to $33.2 billion in 2007. Although significant progress has been made in mechanical devices and pharmacological interventions, more than half of the patients with heart failure die within 5 years of initial diagnosis. Wide application of heart transplantation is severely hindered by the limited availability of donor organs. To this end, cardiac cell therapy may be an appealing alternative to current treatments for heart failure.

Recent investigations focusing on engineering cells and tissues to repair or regenerate damaged hearts in animal models and in clinical trials have yielded promising results. Considering the limited regenerative capacity of the heart muscle, renewable sources of cardiomyocytes are highly sought. Cells suitable for myocardial engineering should be nonimmunogenic, should be easy to expand to large quantities, and should differentiate into mature, fully functional cardiomyocytes capable of integrating to the host tissue. Adult progenitor cells (APCs) and embryonic stem cells (ESCs) have extensive proliferative potential and can adopt different cell fates, including that of heart cells. The recent advances in the fields of stem cell biology and heart tissue engineering have intensified efforts toward the development of regenerative cardiac therapies. In this article, we review findings pertaining to the cardiogenic potential of major APC populations and of ESCs (). We also discuss significant challenges in the way of realizing stem cellbased therapies aiming to reconstitute the normal function of heart.

Potential sources of stem/progenitor cells for cardiac repair. ESCs derived from the inner cell mass of a blastocyst can be manipulated ex vivo to differentiate toward heart cells. APCs residing in various tissues such as the BM and skeletal muscle may ...

Bone marrow (BM) is a heterogeneous tissue comprising of multiple cell types, including minute fractions of mesenchymal stem cells (MSCs; 0.0010.01% of total cells2) and hematopoietic stem cells (HSCs; 0.71.5cells/108 nucleated marrow cells3). The heterogeneity of BM makes challenging the identification of a subpopulation of cells capable of cardiogenesis, and studies of BM celltocardiac cell transdifferentiation should be examined through this prism.

The notion that BM-derived cells may contribute to the regeneration of the heart was first illustrated when dystrophic (mdx) female mice received BM cells from male wild-type mice.4 More than 2 months after the transplantation, tissues of the recipient mice were histologically examined for the presence of Y-chromosome+ donor cells. Besides the skeletal muscle, donor cells were identified in the cardiac region, suggesting that circulating BM cells contribute to the regeneration of cardiomyocytes.

Further supporting evidence was provided by Jackson et al.5 in studies using a side population (SP) of cells characterized by their intrinsic capacity to efflux Hoechst 33342 dye through the ATP-binding Bcrp1/ABCG2 transporter. The cells were isolated from the BM fraction of HSCs of Rosa26 mice constitutively expressing the -galactosidase reporter gene (LacZ). After SP cells were injected into mice with coronary occlusioninduced ischemia, cells coexpressing LacZ and cardiac -actinin were identified around the infarct region with a frequency of 0.02%. Endothelial engraftment was more prevalent (3.3%). The observed improvement in myocardial function may thus be attributed to the potential of BM cells to give rise to a rather endothelial progeny. This may be a parallel to cardiovascular progenitors from differentiating ESCs giving rise to cardiomyocytes, and endothelial and vascular smooth muscle lineages.6,7

Orlic et al.8 also reported the regeneration of infarcted myocardium after transplantation of lineage-negative (LIN)/C-KIT+ BM cells from transgenic mice constitutively expressing enhanced green fluorescent protein (eGFP). Cells were injected in the contracting wall close to the infarct area. Nine days after transplantation, an impressive 68% of the infarct was occupied by newly formed myocardium with eGFP+ cells displaying cardiomyocyte markers such as troponin, MEF2, NKX2.5, cardiac myosin, GATA-4, and -sarcomeric actin. Similar outcomes were reported by the same group9 when mouse C-KIT+ (but not screened for LIN) BM cells were transplanted.

Although these findings led to the conclusion that BM cells can repopulate a damaged heart, work by other investigators has casted doubt on this assertion. Balsam et al.10 noted that mice with infarcts receiving BM LIN/C-KIT+, C-KIT-enriched or THY1.1low/LIN/stem cell antigen-1 (SCA-1+) cells exhibited improved ventricular function. However, donor cells expressed granulocyte but not heart cell markers 1 month after injection. In another study,11 HSCs carrying a nuclear-localized LacZ gene flanked by the cardiac -myosin heavy chain promoter were delivered into the periinfarct zone of mice 5h after coronary artery occlusion. One to 4 weeks later, LacZ+ cells were absent in heart tissue sections from 117 mice that received HSCs. Similarly, no eGFP+ cells were detected in the infarcted hearts of mice infused with BM cells constitutively expressing eGFP. Finally, Nygren et al.12 in similar transplantation experiments observed only blood cells (mainly leukocytes) originating from BM HSCs in the infarcted myocardium without evidence of transdifferentiation of donor cells to cardiomyocytes.

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Stem Cells for Heart Cell Therapies - National Center for ...

Cardiac Stem Cells Comments Off on Stem Cells for Heart Cell Therapies – National Center for … | July 1st, 2015

Cardiac stem cells, which have the ability to differentiate (specialize) into mature heart cells and therefore could be used to repair damaged or diseased heart tissue, have garnered significant interest in the development of treatments for heart disease and cardiac defects. Cardiac stem cells can be derived from mature cardiomyocytes through the process of dedifferentiation, in which mature heart cells are stimulated to revert to a stem cell state. The stem cells can then be stimulated to redifferentiate into myocytes or endothelial cells. This approach enables millions of cardiac stem cells to be produced in the laboratory.

In 2009 a team of doctors at Cedars-Sinai Heart Institute in Los Angeles, California, reported the first attempted use of cardiac stem cell transplantation to repair damaged heart tissue. The team removed a small section of tissue from the heart of a patient who had suffered a heart attack, and the tissue was cultured in a laboratory. Cells that had been stimulated to dedifferentiate were then used to produce millions of cardiac stem cells, which were later reinfused directly into the heart of the patient through a catheter in a coronary artery. A similar approach was used in a subsequent clinical trial reported in 2011; this trial involved 14 patients suffering from heart failure who were scheduled to undergo cardiac bypass surgery. More than three months after treatment, there was slight but detectable improvement over cardiac bypass surgery alone in left ventricle ejection fraction (the percentage of the left ventricular volume of blood that is ejected from the heart with each ventricular contraction).

Stem cells derived from bone marrow, the collection of which is considerably less invasive than heart surgery, are also of interest in the development of regenerative heart therapies. The collection and reinfusion into the heart of bone marrow-derived stem cells within hours of a heart attack may limit the amount of damage incurred by the muscle.

There are many types of arterial diseases. Some are generalized and affect arteries throughout the body, though often there is variation in the degree they are affected. Others are localized. These diseases are frequently divided into those that result in arterial occlusion (blockage) and those that are nonocclusive in their manifestations.

Atherosclerosis, the most common form of arteriosclerosis, is a disease found in large and medium-sized arteries. It is characterized by the deposition of fatty substances, such as cholesterol, in the innermost layer of the artery (the intima). As the fat deposits become larger, inflammatory white blood cells called macrophages try to remove the lipid deposition from the wall of the artery. However, lipid-filled macrophages, called foam cells, grow increasingly inefficient at lipid removal and undergo cell death, accumulating at the site of lipid deposition. As these focal lipid deposits grow larger, they become known as atherosclerotic plaques and may be of variable distribution and thickness. Under most conditions the incorporation of cholesterol-rich lipoproteins is the predominant factor in determining whether or not plaques progressively develop. The endothelial injury that results (or that may occur independently) leads to the involvement of two cell types that circulate in the bloodplatelets and monocytes (a type of white blood cell). Platelets adhere to areas of endothelial injury and to themselves. They trap fibrinogen, a plasma protein, leading to the development of platelet-fibrinogen thrombi. Platelets deposit pro-inflammatory factors, called chemokines, on the vessel walls. Observations of infants and young children suggest that atherosclerosis can begin at an early age as streaks of fat deposition (fatty streaks).

Atherosclerotic lesions are frequently found in the aorta and in large aortic branches. They are also prevalent in the coronary arteries, where they cause coronary artery disease. The distribution of lesions is concentrated in points where arterial flow gives rise to abnormal shear stress or turbulence, such as at branch points in vessels. In general the distribution in most arteries tends to be closer to the origin of the vessel, with lesions found less frequently in more distal sites. Hemodynamic forces are particularly important in the system of coronary arteries, where there are unique pressure relationships. The flow of blood through the coronary system into the heart muscle takes place during the phase of ventricular relaxation (diastole) and virtually not at all during the phase of ventricular contraction (systole). During systole the external pressure on coronary arterioles is such that blood cannot flow forward. The external pressure exerted by the contracting myocardium on coronary arteries also influences the distribution of atheromatous obstructive lesions.

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cardiovascular disease :: Cardiac stem cells | Britannica.com

Cardiac Stem Cells Comments Off on cardiovascular disease :: Cardiac stem cells | Britannica.com | June 19th, 2015