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Ahead of her 60th birthday on TuesdaySarah Fergusonhas opened up about her cosmetic treatments at the hands of her friendDr.GabrielaMercik- an aesthetician who has given her everything from laser facelifts to organic fillers.

In a candid interview with the Daily Mail, Ferguson and Mercik talked about thecosmetic procedures the Duchess of York has had done over the years,with Ferguson revealing she was Mercik'sguinea pig with new treatments.

The pair spoke to The Daily Mail about their close relationship, as well as Fergusons history with both invasive and non-invasive procedures including botox, mesotherapy and even stem cell therapy - specifically for Fergusons feet.

Sarah Ferguson in October 2019 (Getty Images for BFI)

Ferguson said she was comfortable talking about her treatments, sayingIm really happy to be open about what Ive had done.

Sarah Ferguson in 2010 (Getty Images)

Ferguson revealed in the interview that she used to get Botox, however as technology has advanced shes opted to move away from it. She explained, I had Botox a long time ago when there was nothing else available.

With her aesthetician calling it passe now, Ferguson added, I really dont like the frozen look. Im so animated and I like to be myself. I dont like the thought of needles and am very glad if I look well and happy.

Botox is a cosmetic procedure which is designed to help diminish wrinkles and fine lines, by injecting a chemical solution with a micro needle into specific target areas.

Sarah Ferguson in 2019 (PA)

It was revealed in the Daily Mail that Ferguson started getting mesotherapy in 2013, though she has since moved away from it in favour of other treatments.

Ferguson said that she had chosen mesotherapy to tackle sun damage, saying, I need to repair the damage that was done on the beach when I was a child. Its why I had the mesotherapy, the vitamin cocktail to hydrate and boost the skin.

According to HealthLine, mesotherapy involvesinjecting a mixture of vitamins, enzymes, hormones, and plant extracts. Designed to tighten skin and rejuvenate it, it also removes excess fat and is used by people to do everything from reduce cellulite, diminish wrinkles and tighten loose skin.

HealthLine continues, The technique uses very fine needles to deliver a series of injections into the middle layer (mesoderm) of skin. The idea behind mesotherapy is that it corrects underlying issues like poor circulation and inflammation that cause skin damage.

(Getty Images for GFI)

Following this, Ferguson chose to move onto organic fillers.

Face fillers are designed to both fade wrinkles as well as plump up parts of your face that you want to add volume to. In the case of Fergusons, hers were organic and were described as being non-invasive injectables.

Sarah Ferguson in 2017 (Getty Images)

One of Fergusons more unusual facial procedures involved something called a thread lift. She explained, Before I had it done I thought,Oh this is going to be painful, but it wasnt bad. My skin responded well. I think if you look at photos of me after I had it done, I look much better.

However, Mercik added that Ferguson had since swapped the threads for laser because its non-invasive.

Both Ferguson and Mercik explained what a thread lift involves. Patients have medical threads inserted into the skin to create a supportive mesh that pulls the face upwards - with the threads dissolving after 6-8 months and results lasting two years.

Ferguson explained, Its like garden trellising for sweet peas. You insert the threads under the skin with a fine needle and they hold everything up. They also encourage collagen production. It takes a couple of months, then the sweet peas bloom!

Mercik went into more technical details, explaining, We inserted nano peptides (synthetic growth factors) under the skin which, with the synthetic threads, stimulate collagen production.

Sarah Ferguson at Princess Eugenie's wedding (Getty Images)

Sarah Ferguson revealed that she personally swears by Merciks 6-Dimension Ultimate Laser Treatment facelift. Revealing to the Daily Mail that she much prefers it to Botox, Ferguson explained that she had actually had it done by Mercik prior to her daughter Princess Eugenies wedding.

She explained, Above all, it was being joyful for Eugenie that made me look good. But Id had some laser treatment on my face which helped, too.

She also added that she was undergoing it at the moment, ahead of her birthday on Tuesday. She said, Ive started the laser treatment, but its not finished yet. The collagen needs to rebuild. I hope it will all be done by my birthday.

Merciks laser facelift is non-invasive, pain-free, involves no recovery time and accomplished in no more than 90 minutes. It reportedly helps promote the skins natural production of youth-restoring collagen and is said to continue the work as the weeks pass.

Following a sunscreen-averse childhood (which involved Fergusons mother thinking Nivea moisturiser was sunscreen), Ferguson revealed that she was now very careful about preventing sun damage now - especially after her father and best friend died of skin cancer. She explained, It made me realise you have to look after your skin just as much as your other organs. It isnt just about aesthetics. We have to think about our skin health.

Thats why I dont go in the sun now, she continued. The tan I have is out of a bottle. Fake.

One of Fergusons more recent procedures includes a trip off to the Bahamas, which saw her undergo stem cell therapy to improve her feet. She explained, I think my toes were ruined by all the riding I did when I was young. They shaved the bone here and implanted stem cells 20 million of them taken from my midriff into my feet to make new cartilage.

Continued here:
Sarah Ferguson opens up about years of plastic surgery from Botox to fillers to stem cell therapy - Evening Standard

Skin Stem Cells Comments Off on Sarah Ferguson opens up about years of plastic surgery from Botox to fillers to stem cell therapy – Evening Standard | October 12th, 2019

Are there enough stem cells in your knees to heal the damage of osteoarthritis? If yes, why arent those stem cells fixing your knees now? Is it a lack of numbers?

Marc Darrow MD, JD. Thank you for reading my article. You can ask me your questions about bone marrow derived stem cells using the contact form below.

In 2011, doctors at the University of Aberdeen published research in the journal Arthritis and rheumatism that provided the first evidence that resident stem cells in the knee joint synovium underwent proliferation (multiplied) and chondrogenic differentiation (made themselves into cartilage cells) following injury.(1)

If the stem cells in your knee synovial lining are abundant and have the ability to rebuild cartilage after injury, why isnt your knee fixing itself?

One of those 40 studies was performed by researchers at theUniversity of Calgary in 2012. Among their questions, if the stem cells in the knee synovial lining are abundant and have the ability to rebuild cartilage after injury, why isnt the knee fixing itself? Here is what they published:

Since osteoarthritis leads to a progressive loss of cartilage and synovial progenitors (rebuilding) cells have the potential to contribute to articular cartilage repair, the inability of osteoarthritis synovial fluid Mesenchymal progenitor cells (stem cell growth factors) to spontaneously differentiate into chondrocytes suggests that cell-to-cell aggregation and/or communication may be impaired in osteoarthritis and somehow dampen the normal mechanism of chondrocyte replenishment from the synovium or synovial fluid. Should the cells of the synovium or synovial fluid be a reservoir of stem cells for normal articular cartilage maintenance and repair, these endogenous sources of chondro-biased cells would be a fundamental and new strategy for treating osteoarthritis and cartilage injury if this loss of aggregation & differentiation phenotype can be overcome.(2)

This research was supported in anew study from December 2017 In Nature reviews. The paper suggested that recognizing that joint-resident stem cells are comparatively abundant in the joint and occupy multiple niches (from the center of the joint to the out edges) will enable the optimization of single-stage therapeutic interventions for osteoarthritis.(3) The idea is to get these native stem cells to repair.

Now we know that there are many stem cells in the knee, when there is an injury there are more stem cells. If we can figure out how to get these stem cells turned on to the healing mode, the knee could heal itself of early stage osteoarthritis. So the problem is not the number of stem cells, BUT, communication.

This failure to communicate was also seen in other research. In 2016, another heavily cited paper, this time fromTehran University for Medical Sciences, noted that despite their larger numbers,the native stem cells act chaotically and are unable to regroup themselves into a healing mechanism and repair the bone, cartilage and other tissue. Introducing bone marrow stem cells into this environmentgets the native stem cells in line and redirects them to perform healing functions. The joint environmentis changed from chaotic to healing because of communication.(4) It should be pointed out that at the time of this article update (August 2018) 62 medical studies cited the research in this papers findings).

A recentpaper from a research team inAustralia confirms how this change of joint environment works. It starts with cell signalling a new communication network is built.

University of Iowa research published in theJournal of orthopaedic research

Serious meniscus injuries seldom heal and increase the risk for knee osteoarthritis; thus, there is a need to develop new reparative therapies. In that regard, stimulating tissue regeneration by autologous (from you, not donated) stem/progenitor cells has emerged as a promising new strategy.

(The research team) showed previously that migratory chondrogenic progenitor cells (mobile cartilage growth factors) were recruited to injured cartilage, where they showed a capability in situ (on the spot) tissue repair. Here, we tested the hypothesis that the meniscus contains a similar population of regenerative cells.

Explant studies revealed that migrating cells were mainly confined to the red zone (where the blood is and its growth factors) in normal menisci: However, these cells were capable of repopulating defects made in the white zone (the desert area where no blood flows. Migrating cell numbers increased dramatically in damaged meniscus. Relative to non-migrating meniscus cells, migrating cells were more clonogenic, overexpressed progenitor cell markers, and included a larger side population. (They were ready to heal) Gene expression profiling showed that the migrating population was more similar tochondrogenic progenitor cells (mobile cartilage growth factors) than other meniscus cells. Finally, migrating cells equaledchondrogenic progenitor cells in chondrogenic potential, indicating a capacity for repair of the cartilaginous white zone of the meniscus. These findings demonstrate that, much as in articular cartilage, injuries to the meniscus mobilize an intrinsic progenitor cell population with strong reparative potential.(6)

The intrinsic progenitor cell population with strong reparative potential are in your knee waiting to be mobilized.

So what are we to make of this research?There are a lot of stem cells in a knee waiting to repair. The problem is they are confused and not getting the correct instructions. Bone marrow stem cell therapy can fix the communication problem and begin the repair process anew.

A leading provider of bone marrow derived stem cell therapy, Platelet Rich Plasma and Prolotherapy11645 WILSHIRE BOULEVARD SUITE 120, LOS ANGELES, CA 90025

PHONE: (800) 300-9300

1 Kurth TB, Dellaccio F, Crouch V, Augello A, Sharpe PT, De Bari C. Functional mesenchymal stem cell niches in adult mouse knee joint synovium in vivo. Arthritis Rheum. 2011 May;63(5):1289-300. doi: 10.1002/art.30234.

2 Krawetz RJ, Wu YE, Martin L, Rattner JB, Matyas JR, Hart DA. Synovial Fluid Progenitors Expressing CD90+ from Normal but Not Osteoarthritic Joints Undergo Chondrogenic Differentiation without Micro-Mass Culture. Kerkis I, ed.PLoS ONE. 2012;7(8):e43616. doi:10.1371/journal.pone.0043616.

3 McGonagle D, Baboolal TG, Jones E. Native joint-resident mesenchymal stem cells for cartilage repair in osteoarthritis. Nature Reviews Rheumatology. 2017 Dec;13(12):719.

4Davatchi F, et al. Mesenchymal stem cell therapy for knee osteoarthritis: 5 years follow-up of three patients. Int J Rheum Dis. 2016 Mar;19(3):219-25.

5. Freitag J, Bates D, Boyd R, Shah K, Barnard A, Huguenin L, Tenen A.Mesenchymal stem cell therapy in the treatment of osteoarthritis: reparative pathways, safety and efficacy a review.BMC Musculoskelet Disord. 2016 May 26;17(1):230. doi: 10.1186/s12891-016-1085-9. Review.

6 Seol D, Zhou C, et al. Characteristics of meniscus progenitor cells migrated from injured meniscus. J Orthop Res. 2016 Nov 3. doi: 10.1002/jor.23472.

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Are there enough stem cells in your knees to heal the ...

Skin Stem Cells Comments Off on Are there enough stem cells in your knees to heal the … | September 24th, 2018

Embryonic stem cells (ES cells or ESCs) are pluripotent stem cells derived from the inner cell mass of a blastocyst, an early-stage pre-implantation embryo.[1][2] Human embryos reach the blastocyst stage 45 days post fertilization, at which time they consist of 50150 cells. Isolating the embryoblast, or inner cell mass (ICM) results in destruction of the blastocyst, a process which raises ethical issues, including whether or not embryos at the pre-implantation stage should have the same moral considerations as embryos in the post-implantation stage of development.[3][4] Researchers are currently focusing heavily on the therapeutic potential of embryonic stem cells, with clinical use being the goal for many labs. These cells are being studied to be used as clinical therapies, models of genetic disorders, and cellular/DNA repair. However, adverse effects in the research and clinical processes have also been reported.

Embryonic stem cells (ESCs), derived from the blastocyst stage of early mammalian embryos, are distinguished by their ability to differentiate into any cell type and by their ability to propagate. It is these traits that makes them valuable in the scientific/medical fields. ESC are also described as having a normal karyotype, maintaining high telomerase activity, and exhibiting remarkable long-term proliferative potential.[5]

Embryonic stem cells of the inner cell mass are pluripotent, meaning they are able to differentiate to generate primitive ectoderm, which ultimately differentiates during gastrulation 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 human body. Pluripotency distinguishes embryonic stem cells from adult stem cells, which are multipotent and can only produce a limited number of cell types.

Under defined conditions, embryonic stem cells are capable of propagating indefinitely in an undifferentiated state. Conditions must either prevent the cells from clumping, or maintain an environment that supports an unspecialized state.[2] While being able to remain undifferentiated, ESCs also have the capacity, when provided with the appropriate signals, to differentiate (presumably via the initial formation of precursor cells) into nearly all mature cell phenotypes.[6]

Due to their plasticity and potentially unlimited capacity for self-renewal, embryonic stem cell therapies have been proposed for regenerative medicine and tissue replacement after injury or disease. Pluripotent stem cells have shown potential in treating a number of varying conditions, including but not limited to: spinal cord injuries, age related macular degeneration, diabetes, neurodegenerative disorders (such as Parkinson's disease), AIDS, etc.[7] In addition to their potential in regenerative medicine, embryonic stem cells provide an alternative source of tissue/organs which serves as a possible solution to the donor shortage dilemma. Not only that, but tissue/organs derived from ESCs can be made immunocompatible with the recipient. Aside from these uses, embryonic stem cells can also serve as tools for the investigation of early human development, study of genetic disease and as in vitro systems for toxicology testing.[5]

According to a 2002 article in PNAS, "Human embryonic stem cells have the potential to differentiate into various cell types, and, thus, may be useful as a source of cells for transplantation or tissue engineering."[8]

However, embryonic stem cells are not limited to cell/tissue engineering.

Current research focuses on differentiating ESCs into a variety of cell types for eventual use as cell replacement therapies (CRTs). Some of the cell types that have or are currently being developed include cardiomyocytes (CM), neurons, hepatocytes, bone marrow cells, islet cells and endothelial cells.[9] However, the derivation of such cell types from ESCs is not without obstacles, therefore current research is focused on overcoming these barriers. For example, studies are underway to differentiate ESCs in to tissue specific CMs and to eradicate their immature properties that distinguish them from adult CMs.[10]

Besides becoming an important alternative to organ transplants, ESCs are also being used in field of toxicology and as cellular screens to uncover new chemical entities (NCEs) that can be developed as small molecule drugs. Studies have shown that cardiomyocytes derived from ESCs are validated in vitro models to test drug responses and predict toxicity profiles.[9] ES derived cardiomyocytes have been shown to respond to pharmacological stimuli and hence can be used to assess cardiotoxicity like Torsades de Pointes.[17]

ESC-derived hepatocytes are also useful models that could be used in the preclinical stages of drug discovery. However, the development of hepatocytes from ESCs has proven to be challenging and this hinders the ability to test drug metabolism. Therefore, current research is focusing on establishing fully functional ESC-derived hepatocytes with stable phase I and II enzyme activity.[18]

Several new studies have started to address the concept of modeling genetic disorders with embryonic stem cells. Either by genetically manipulating the cells, or more recently, by deriving diseased cell lines identified by prenatal genetic diagnosis (PGD), modeling genetic disorders is something that has been accomplished with stem cells. This approach may very well prove invaluable at studying disorders such as Fragile-X syndrome, Cystic fibrosis, and other genetic maladies that have no reliable model system.

Yury Verlinsky, a Russian-American medical researcher who specialized in embryo and cellular genetics (genetic cytology), developed prenatal diagnosis testing methods to determine genetic and chromosomal disorders a month and a half earlier than standard amniocentesis. The techniques are now used by many pregnant women and prospective parents, especially couples who have a history of genetic abnormalities or where the woman is over the age of 35 (when the risk of genetically related disorders is higher). In addition, by allowing parents to select an embryo without genetic disorders, they have the potential of saving the lives of siblings that already had similar disorders and diseases using cells from the disease free offspring.[19]

Differentiated somatic cells and ES cells use different strategies for dealing with DNA damage. For instance, human foreskin fibroblasts, one type of somatic cell, use non-homologous end joining (NHEJ), an error prone DNA repair process, as the primary pathway for repairing double-strand breaks (DSBs) during all cell cycle stages.[20] Because of its error-prone nature, NHEJ tends to produce mutations in a cells clonal descendants.

ES cells use a different strategy to deal with DSBs.[21] Because ES cells give rise to all of the cell types of an organism including the cells of the germ line, mutations arising in ES cells due to faulty DNA repair are a more serious problem than in differentiated somatic cells. Consequently, robust mechanisms are needed in ES cells to repair DNA damages accurately, and if repair fails, to remove those cells with un-repaired DNA damages. Thus, mouse ES cells predominantly use high fidelity homologous recombinational repair (HRR) to repair DSBs.[21] This type of repair depends on the interaction of the two sister chromosomes formed during S phase and present together during the G2 phase of the cell cycle. HRR can accurately repair DSBs in one sister chromosome by using intact information from the other sister chromosome. Cells in the G1 phase of the cell cycle (i.e. after metaphase/cell division but prior the next round of replication) have only one copy of each chromosome (i.e. sister chromosomes arent present). Mouse ES cells lack a G1 checkpoint and do not undergo cell cycle arrest upon acquiring DNA damage.[22] Rather they undergo programmed cell death (apoptosis) in response to DNA damage.[23] Apoptosis can be used as a fail-safe strategy to remove cells with un-repaired DNA damages in order to avoid mutation and progression to cancer.[24] Consistent with this strategy, mouse ES stem cells have a mutation frequency about 100-fold lower than that of isogenic mouse somatic cells.[25]

On January 23, 2009, Phase I clinical trials for transplantation of oligodendrocytes (a cell type of the brain and spinal cord) derived from human ES cells into spinal cord-injured individuals received approval from the U.S. Food and Drug Administration (FDA), marking it the world's first human ES cell human trial.[26] The study leading to this scientific advancement was conducted by Hans Keirstead and colleagues at the University of California, Irvine and supported by Geron Corporation of Menlo Park, CA, founded by Michael D. West, PhD. A previous experiment had shown an improvement in locomotor recovery in spinal cord-injured rats after a 7-day delayed transplantation of human ES cells that had been pushed into an oligodendrocytic lineage.[27] The phase I clinical study was designed to enroll about eight to ten paraplegics who have had their injuries no longer than two weeks before the trial begins, since the cells must be injected before scar tissue is able to form. The researchers emphasized that the injections were not expected to fully cure the patients and restore all mobility. Based on the results of the rodent trials, researchers speculated that restoration of myelin sheathes and an increase in mobility might occur. This first trial was primarily designed to test the safety of these procedures and if everything went well, it was hoped that it would lead to future studies that involve people with more severe disabilities.[28] The trial was put on hold in August 2009 due to FDA concerns regarding a small number of microscopic cysts found in several treated rat models but the hold was lifted on July 30, 2010.[29]

In October 2010 researchers enrolled and administered ESTs to the first patient at Shepherd Center in Atlanta.[30] The makers of the stem cell therapy, Geron Corporation, estimated that it would take several months for the stem cells to replicate and for the GRNOPC1 therapy to be evaluated for success or failure.

In November 2011 Geron announced it was halting the trial and dropping out of stem cell research for financial reasons, but would continue to monitor existing patients, and was attempting to find a partner that could continue their research.[31] In 2013 BioTime (AMEX:BTX), led by CEO Dr. Michael D. West, acquired all of Geron's stem cell assets, with the stated intention of restarting Geron's embryonic stem cell-based clinical trial for spinal cord injury research.[32]

BioTime company Asterias Biotherapeutics (NYSE MKT: AST) was granted a $14.3 million Strategic Partnership Award by the California Institute for Regenerative Medicine (CIRM) to re-initiate the worlds first embryonic stem cell-based human clinical trial, for spinal cord injury. Supported by California public funds, CIRM is the largest funder of stem cell-related research and development in the world.[33]

The award provides funding for Asterias to reinitiate clinical development of AST-OPC1 in subjects with spinal cord injury and to expand clinical testing of escalating doses in the target population intended for future pivotal trials.[33]

AST-OPC1 is a population of cells derived from human embryonic stem cells (hESCs) that contains oligodendrocyte progenitor cells (OPCs). OPCs and their mature derivatives called oligodendrocytes provide critical functional support for nerve cells in the spinal cord and brain. Asterias recently presented the results from phase 1 clinical trial testing of a low dose of AST-OPC1 in patients with neurologically-complete thoracic spinal cord injury. The results showed that AST-OPC1 was successfully delivered to the injured spinal cord site. Patients followed 23 years after AST-OPC1 administration showed no evidence of serious adverse events associated with the cells in detailed follow-up assessments including frequent neurological exams and MRIs. Immune monitoring of subjects through one year post-transplantation showed no evidence of antibody-based or cellular immune responses to AST-OPC1. In four of the five subjects, serial MRI scans performed throughout the 23 year follow-up period indicate that reduced spinal cord cavitation may have occurred and that AST-OPC1 may have had some positive effects in reducing spinal cord tissue deterioration. There was no unexpected neurological degeneration or improvement in the five subjects in the trial as evaluated by the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) exam.[33]

The Strategic Partnership III grant from CIRM will provide funding to Asterias to support the next clinical trial of AST-OPC1 in subjects with spinal cord injury, and for Asterias product development efforts to refine and scale manufacturing methods to support later-stage trials and eventually commercialization. CIRM funding will be conditional on FDA approval for the trial, completion of a definitive agreement between Asterias and CIRM, and Asterias continued progress toward the achievement of certain pre-defined project milestones.[33]

The major concern with the possible transplantation of ESC into patients as therapies is their ability to form tumors including teratoma.[34] Safety issues prompted the FDA to place a hold on the first ESC clinical trial, however no tumors were observed.

The main strategy to enhance the safety of ESC for potential clinical use is to differentiate the ESC into specific cell types (e.g. neurons, muscle, liver cells) that have reduced or eliminated ability to cause tumors. Following differentiation, the cells are subjected to sorting by flow cytometry for further purification. ESC are predicted to be inherently safer than IPS cells created with genetically-integrating viral vectors because they are not genetically modified with genes such as c-Myc that are linked to cancer. Nonetheless, ESC express very high levels of the iPS inducing genes and these genes including Myc are essential for ESC self-renewal and pluripotency,[35] and potential strategies to improve safety by eliminating c-Myc expression are unlikely to preserve the cells' "stemness". However, N-myc and L-myc have been identified to induce iPS cells instead of c-myc with similar efficiency.[36]More recent protocols to induce pluripotency bypass these problems completely by using non-integrating RNA viral vectors such as sendai virus or mRNA transfection.

Due to the nature of embryonic stem cell research, there is a lot of controversial opinions on the topic. Since harvesting embryonic stem cells necessitates destroying the embryo from which those cells are obtained, the moral status of the embryo comes into question. Scientists argue that the 5-day old mass of cells is too young to achieve personhood or that the embryo, if donated from an IVF clinic (which is where labs typically acquire embryos from), would otherwise go to medical waste anyway. Opponents of ESC research counter that any embryo has the potential to become a human, therefore destroying it is murder and the embryo must be protected under the same ethical view as a developed human being.[37]

In vitro fertilization generates multiple embryos. The surplus of embryos is not clinically used or is unsuitable for implantation into the patient, and therefore may be donated by the donor with consent. Human embryonic stem cells can be derived from these donated embryos or additionally they can also be extracted from cloned embryos using a cell from a patient and a donated egg.[49] The inner cell mass (cells of interest), from the blastocyst stage of the embryo, is separated from the trophectoderm, the cells that would differentiate into extra-embryonic tissue. Immunosurgery, the process in which antibodies are bound to the trophectoderm and removed by another solution, and mechanical dissection are performed to achieve separation. The resulting inner cell mass cells are plated onto cells that will supply support. The inner cell mass cells attach and expand further to form a human embryonic cell line, which are undifferentiated. These cells are fed daily and are enzymatically or mechanically separated every four to seven days. For differentiation to occur, the human embryonic stem cell line is removed from the supporting cells to form embryoid bodies, is co-cultured with a serum containing necessary signals, or is grafted in a three-dimensional scaffold to result.[50]

Embryonic stem cells are derived from the inner cell mass of the early embryo, which are harvested from the donor mother animal. Martin Evans and Matthew Kaufman reported a technique that delays embryo implantation, allowing the inner cell mass to increase. This process includes removing the donor mother's ovaries and dosing her with progesterone, changing the hormone environment, which causes the embryos to remain free in the uterus. After 46 days of this intrauterine culture, the embryos are harvested and grown in in vitro culture until the inner cell mass forms egg cylinder-like structures, which are dissociated into single cells, and plated on fibroblasts treated with mitomycin-c (to prevent fibroblast mitosis). Clonal cell lines are created by growing up a single cell. Evans and Kaufman showed that the cells grown out from these cultures could form teratomas and embryoid bodies, and differentiate in vitro, all of which indicating that the cells are pluripotent.[41]

Gail Martin derived and cultured her ES cells differently. She removed the embryos from the donor mother at approximately 76 hours after copulation and cultured them overnight in a medium containing serum. The following day, she removed the inner cell mass from the late blastocyst using microsurgery. The extracted inner cell mass was cultured on fibroblasts treated with mitomycin-c in a medium containing serum and conditioned by ES cells. After approximately one week, colonies of cells grew out. These cells grew in culture and demonstrated pluripotent characteristics, as demonstrated by the ability to form teratomas, differentiate in vitro, and form embryoid bodies. Martin referred to these cells as ES cells.[42]

It is now known that the feeder cells provide leukemia inhibitory factor (LIF) and serum provides bone morphogenetic proteins (BMPs) that are necessary to prevent ES cells from differentiating.[51][52] These factors are extremely important for the efficiency of deriving ES cells. Furthermore, it has been demonstrated that different mouse strains have different efficiencies for isolating ES cells.[53] Current uses for mouse ES cells include the generation of transgenic mice, including knockout mice. For human treatment, there is a need for patient specific pluripotent cells. Generation of human ES cells is more difficult and faces ethical issues. So, in addition to human ES cell research, many groups are focused on the generation of induced pluripotent stem cells (iPS cells).[54]

On August 23, 2006, the online edition of Nature scientific journal published a letter by Dr. Robert Lanza (medical director of Advanced Cell Technology in Worcester, MA) stating that his team had found a way to extract embryonic stem cells without destroying the actual embryo.[55] This technical achievement would potentially enable scientists to work with new lines of embryonic stem cells derived using public funding in the USA, where federal funding was at the time limited to research using embryonic stem cell lines derived prior to August 2001. In March, 2009, the limitation was lifted.[56]

The iPSC technology was pioneered by Shinya Yamanakas lab in Kyoto, Japan, who showed in 2006 that the introduction of four specific genes encoding transcription factors could convert adult cells into pluripotent stem cells.[57] He was awarded the 2012 Nobel Prize along with Sir John Gurdon "for the discovery that mature cells can be reprogrammed to become pluripotent." [58]

In 2007 it was shown that pluripotent stem cells highly similar to embryonic stem cells can be generated by the delivery of three genes (Oct4, Sox2, and Klf4) to differentiated cells.[59] The delivery of these genes "reprograms" differentiated cells into pluripotent stem cells, allowing for the generation of pluripotent stem cells without the embryo. Because ethical concerns regarding embryonic stem cells typically are about their derivation from terminated embryos, it is believed that reprogramming to these "induced pluripotent stem cells" (iPS cells) may be less controversial. Both human and mouse cells can be reprogrammed by this methodology, generating both human pluripotent stem cells and mouse pluripotent stem cells without an embryo.[60]

This may enable the generation of patient specific ES cell lines that could potentially be used for cell replacement therapies. In addition, this will allow the generation of ES cell lines from patients with a variety of genetic diseases and will provide invaluable models to study those diseases.

However, as a first indication that the induced pluripotent stem cell (iPS) cell technology can in rapid succession lead to new cures, it was used by a research team headed by Rudolf Jaenisch of the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, to cure mice of sickle cell anemia, as reported by Science journal's online edition on December 6, 2007.[61][62]

On January 16, 2008, a California-based company, Stemagen, announced that they had created the first mature cloned human embryos from single skin cells taken from adults. These embryos can be harvested for patient matching embryonic stem cells.[63]

The online edition of Nature Medicine published a study on January 24, 2005, which stated that the human embryonic stem cells available for federally funded research are contaminated with non-human molecules from the culture medium used to grow the cells.[64] It is a common technique to use mouse cells and other animal cells to maintain the pluripotency of actively dividing stem cells. The problem was discovered when non-human sialic acid in the growth medium was found to compromise the potential uses of the embryonic stem cells in humans, according to scientists at the University of California, San Diego.[65]

However, a study published in the online edition of Lancet Medical Journal on March 8, 2005 detailed information about a new stem cell line that was derived from human embryos under completely cell- and serum-free conditions. After more than 6 months of undifferentiated proliferation, these cells demonstrated the potential to form derivatives of all three embryonic germ layers both in vitro and in teratomas. These properties were also successfully maintained (for more than 30 passages) with the established stem cell lines.[66]

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Embryonic stem cell - Wikipedia

Cardiac Stem Cells Comments Off on Embryonic stem cell – Wikipedia | September 23rd, 2018

Stem cell facts

What are stem cells?

Stem cells are cells that have the potential to develop into many different or specialized cell types. Stem cells can be thought of as primitive, "unspecialized" cells that are able to divide and become specialized cells of the body such as liver cells, muscle cells, blood cells, and other cells with specific functions. Stem cells are referred to as "undifferentiated" cells because they have not yet committed to a developmental path that will form a specific tissue or organ. The process of changing into a specific cell type is known as differentiation. In some areas of the body, stem cells divide regularly to renew and repair the existing tissue. The bone marrow and gastrointestinal tract are examples of areas in which stem cells function to renew and repair tissue.

The best and most readily understood example of a stem cell in humans is that of the fertilized egg, or zygote. A zygote is a single cell that is formed by the union of a sperm and ovum. The sperm and the ovum each carry half of the genetic material required to form a new individual. Once that single cell or zygote starts dividing, it is known as an embryo. One cell becomes two, two become four, four become eight, eight become sixteen, and so on, doubling rapidly until it ultimately grows into an entire sophisticated organism composed of many different kinds of specialized cells. That organism, a person, is an immensely complicated structure consisting of many, many, billions of cells with functions as diverse as those of your eyes, your heart, your immune system, the color of your skin, your brain, etc. All of the specialized cells that make up these body systems are descendants of the original zygote, a stem cell with the potential to ultimately develop into all kinds of body cells. The cells of a zygote are totipotent, meaning that they have the capacity to develop into any type of cell in the body.

The process by which stem cells commit to become differentiated, or specialized, cells is complex and involves the regulation of gene expression. Research is ongoing to further understand the molecular events and controls necessary for stem cells to become specialized cell types.

Stem Cells:One of the human body's master cells, with the ability to grow into any one of the body's more than 200 cell types.

All stem cells are unspecialized (undifferentiated) cells that are characteristically of the same family type (lineage). They retain the ability to divide throughout life and give rise to cells that can become highly specialized and take the place of cells that die or are lost.

Stem cells contribute to the body's ability to renew and repair its tissues. Unlike mature cells, which are permanently committed to their fate, stem cells can both renew themselves as well as create new cells of whatever tissue they belong to (and other tissues).

Why are stem cells important?

Stem cells represent an exciting area in medicine because of their potential to regenerate and repair damaged tissue. Some current therapies, such as bone marrow transplantation, already make use of stem cells and their potential for regeneration of damaged tissues. Other therapies that are under investigation involve transplanting stem cells into a damaged body part and directing them to grow and differentiate into healthy tissue.

Embryonic stem cells

During the early stages of embryonic development the cells remain relatively undifferentiated (immature) and appear to possess the ability to become, or differentiate, into almost any tissue within the body. For example, cells taken from one section of an embryo that might have become part of the eye can be transferred into another section of the embryo and could develop into blood, muscle, nerve, or liver cells.

Cells in the early embryonic stage are totipotent (see above) and can differentiate to become any type of body cell. After about seven days, the zygote forms a structure known as a blastocyst, which contains a mass of cells that eventually become the fetus, as well as trophoblastic tissue that eventually becomes the placenta. If cells are taken from the blastocyst at this stage, they are known as pluripotent, meaning that they have the capacity to become many different types of human cells. Cells at this stage are often referred to as blastocyst embryonic stem cells. When any type of embryonic stem cells is grown in culture in the laboratory, they can divide and grow indefinitely. These cells are then known as embryonic stem cell lines.

Fetal stem cells

The embryo is referred to as a fetus after the eighth week of development. The fetus contains stem cells that are pluripotent and eventually develop into the different body tissues in the fetus.

Adult stem cells

Adult stem cells are present in all humans in small numbers. The adult stem cell is one of the class of cells that we have been able to manipulate quite effectively in the bone marrow transplant arena over the past 30 years. These are stem cells that are largely tissue-specific in their location. Rather than typically giving rise to all of the cells of the body, these cells are capable of giving rise only to a few types of cells that develop into a specific tissue or organ. They are therefore known as multipotent stem cells. Adult stem cells are sometimes referred to as somatic stem cells.

The best characterized example of an adult stem cell is the blood stem cell (the hematopoietic stem cell). When we refer to a bone marrow transplant, a stem cell transplant, or a blood transplant, the cell being transplanted is the hematopoietic stem cell, or blood stem cell. This cell is a very rare cell that is found primarily within the bone marrow of the adult.

One of the exciting discoveries of the last years has been the overturning of a long-held scientific belief that an adult stem cell was a completely committed stem cell. It was previously believed that a hematopoietic, or blood-forming stem cell, could only create other blood cells and could never become another type of stem cell. There is now evidence that some of these apparently committed adult stem cells are able to change direction to become a stem cell in a different organ. For example, there are some models of bone marrow transplantation in rats with damaged livers in which the liver partially re-grows with cells that are derived from transplanted bone marrow. Similar studies can be done showing that many different cell types can be derived from each other. It appears that heart cells can be grown from bone marrow stem cells, that bone marrow cells can be grown from stem cells derived from muscle, and that brain stem cells can turn into many types of cells.

Peripheral blood stem cells

Most blood stem cells are present in the bone marrow, but a few are present in the bloodstream. This means that these so-called peripheral blood stem cells (PBSCs) can be isolated from a drawn blood sample. The blood stem cell is capable of giving rise to a very large number of very different cells that make up the blood and immune system, including red blood cells, platelets, granulocytes, and lymphocytes.

All of these very different cells with very different functions are derived from a common, ancestral, committed blood-forming (hematopoietic), stem cell.

Umbilical cord stem cells

Blood from the umbilical cord contains some stem cells that are genetically identical to the newborn. Like adult stem cells, these are multipotent stem cells that are able to differentiate into certain, but not all, cell types. For this reason, umbilical cord blood is often banked, or stored, for possible future use should the individual require stem cell therapy.

Induced pluripotent stem cells

Induced pluripotent stem cells (iPSCs) were first created from human cells in 2007. These are adult cells that have been genetically converted to an embryonic stem celllike state. In animal studies, iPSCs have been shown to possess characteristics of pluripotent stem cells. Human iPSCs can differentiate and become multiple different fetal cell types. iPSCs are valuable aids in the study of disease development and drug treatment, and they may have future uses in transplantation medicine. Further research is needed regarding the development and use of these cells.

Why is there controversy surrounding the use of stem cells?

Embryonic stem cells and embryonic stem cell lines have received much public attention concerning the ethics of their use or non-use. Clearly, there is hope that a large number of treatment advances could occur as a result of growing and differentiating these embryonic stem cells in the laboratory. It is equally clear that each embryonic stem cell line has been derived from a human embryo created through in-vitro fertilization (IVF) or through cloning technologies, with all the attendant ethical, religious, and philosophical problems, depending upon one's perspective.

What are some stem cell therapies that are currently available?

Routine use of stem cells in therapy has been limited to blood-forming stem cells (hematopoietic stem cells) derived from bone marrow, peripheral blood, or umbilical cord blood. Bone marrow transplantation is the most familiar form of stem cell therapy and the only instance of stem cell therapy in common use. It is used to treat cancers of the blood cells (leukemias) and other disorders of the blood and bone marrow.

In bone marrow transplantation, the patient's existing white blood cells and bone marrow are destroyed using chemotherapy and radiation therapy. Then, a sample of bone marrow (containing stem cells) from a healthy, immunologically matched donor is injected into the patient. The transplanted stem cells populate the recipient's bone marrow and begin producing new, healthy blood cells.

Umbilical cord blood stem cells and peripheral blood stem cells can also be used instead of bone marrow samples to repopulate the bone marrow in the process of bone marrow transplantation.

In 2009, the California-based company Geron received clearance from the U. S. Food and Drug Administration (FDA) to begin the first human clinical trial of cells derived from human embryonic stem cells in the treatment of patients with acute spinal cord injury.

What are experimental treatments using stem cells and possible future directions for stem cell therapy?

Stem cell therapy is an exciting and active field of biomedical research. Scientists and physicians are investigating the use of stem cells in therapies to treat a wide variety of diseases and injuries. For a stem cell therapy to be successful, a number of factors must be considered. The appropriate type of stem cell must be chosen, and the stem cells must be matched to the recipient so that they are not destroyed by the recipient's immune system. It is also critical to develop a system for effective delivery of the stem cells to the desired location in the body. Finally, devising methods to "switch on" and control the differentiation of stem cells and ensure that they develop into the desired tissue type is critical for the success of any stem cell therapy.

Researchers are currently examining the use of stem cells to regenerate damaged or diseased tissue in many conditions, including those listed below.

References

REFERENCE:

"Stem Cell Information." National Institutes of Health.

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SOURCE G-CON Manufacturing

iCON Cell Therapy Platform Launched with Shipment of the 1st BERcellFLEX PODs

COLLEGE STATION, Texas, Sept. 5, 2018 /PRNewswire-PRWeb/ --Following up on the launch of the iCON Turnkey Facility Platform for a mAb manufacturing facility late last year, IPS-Integrated Project Services, LLC and G-CON Manufacturing have successfully designed and delivered the first BERcellFLEX PODs for the manufacturing of autologous cell therapies. The iCON solution provides a pre-fabricated modular cleanroom infrastructure for the drug manufacturers' requirements for both clinical and commercial manufacture of critical therapies. Following the iCON model, IPS provided the engineering design while G-CON built, tested and delivered the BERcellFLEX CAR-T processing suites in both twelve (12) foot and twenty-four (24) foot wide POD configurations.

"This is an exciting time for our companies as the iCON platform is being adopted by clients who recognize that new innovative approaches are needed to meet the growing demand for cell and gene therapy manufacturing" said Dennis Powers, Vice President of Business Development and Sales Engineering at G-CON Manufacturing Inc. "We believe that the iCON platform approach with its faster and more predictable project schedules for new facility construction are essential for supplying life changing therapies to the patients that need them."

"The gene therapy industry needs standardized solutions to meet its speed to market requirements," said Tom J. Piombino, Vice President & Process Architect at IPS. "In addition to our larger 2K mAb facility platform that we rolled out earlier this year, the BERcellFLEX12 and 24 represent a line of gene/cell therapy products that operating companies can buy today, ready-to-order, in either an open or closed-processing format with little to no engineering time we start fabricating almost immediately after URS alignment. Multiple cellFLEX units can be installed to scale up/out from Phase 1 Clinical production to Commercial Manufacturing and serve the needs of thousands of CAR-T patients per year. Being able to meet this critical need is consistent with our vision; we're thrilled to be able to offer this modular solution to help our clients get therapies to their patients."

About iCON The iCON platform, the collaborative efforts of IPS and G-CON Manufacturing, Inc., is redefining facility project execution for the biopharma industry where there is a growing need for more rapidly deployable and flexible manufacturing capability. iCON has launched turnkey designs for monoclonal antibody facilities and autologous cell therapies, and is developing platforms for cell and gene therapies, vaccines, OSD, and aseptic filling. An iCON solution can be deployed for:

About G-CON G-CON Manufacturing designs, produces and installs prefabricated cleanroom PODs. G-CON's cleanroom POD portfolio encompasses a variety of different dimensions and purposes, from laboratory environments to personalized medicine and production process platforms. The POD cleanroom units are unique from traditional cleanroom structures due to the ease of scalability, mobility and the ability to repurpose the PODs once the production process reaches the end of its lifecycle. For more information, please visit the Company's website at http://www.gconbio.com.

About IPS IPS is a global leader in developing innovative facility and bioprocess solutions for the biotechnology and pharmaceutical industries. Through operational expertise and industry-leading knowledge, skill and passion, IPS provides consulting, architecture, engineering, construction management, and compliance services that allow clients to create and manufacture life-impacting products around the world. Headquartered in Blue Bell, PA-USA, IPS is one of the largest multi-national companies servicing the life sciences industry with over 1,100 professionals in the US, Canada, Brazil, UK, Ireland, Switzerland, Singapore, China, and India. Visit our website at http://www.ipsdb.com.

2017 PR Newswire. All Rights Reserved.

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There was a very sad example of this in the last decade.There's a wonderful drug, and a class of drugs actually,but the particular drug was Vioxx, andfor people who were suffering from severe arthritis pain,the drug was an absolute lifesaver,but unfortunately, for another subset of those people,they suffered pretty severe heart side effects,and for a subset of those people, the side effects wereso severe, the cardiac side effects, that they were fatal.But imagine a different scenario,where we could have had an array, a genetically diverse array,of cardiac cells, and we could have actually testedthat drug, Vioxx, in petri dishes, and figured out,well, okay, people with this genetic type are going to havecardiac side effects, people with these genetic subgroupsor genetic shoes sizes, about 25,000 of them,are not going to have any problems.The people for whom it was a lifesavercould have still taken their medicine.The people for whom it was a disaster, or fatal,would never have been given it, andyou can imagine a very different outcome for the company,who had to withdraw the drug.

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Consistency

Quality Control and Testing

Product Selection & Support

HiPSC Custom Services

Human Induced Pluripotent Stem Cells (HiPSC)Top:HiPSC express pluriotency markers OCT4, Nanog, LIN28 and SSEA-4.Bottom:HiPSC differentiate into cell derivatives from the 3 embryonic layers: Neuronal marker beta III tubulin (TUJ1), Smooth Muscle Actin (SMA) and Hepatocyte Nuclear Factor 3 Beta (HNF3b).

Cutting-edge development and manufacturing provides high quality, thoroughly-characterized HiPSC cells to researchers around the world. HiPSC are generated from somatic cells, eliminating ethical considerations associated with scientific work based on embryonic stem cells. Furthermore, being donor/patient-specific, they open possibilities for a wide variety of studies in biomedical research. Donor somatic cells carry the genetic makeup of the diseased patient, hence HiPSC can be used directly to model disease on a dish.

Thus, one of the main uses of HiPSC has been in genetic disease modeling in organs and tissues, such as the brain (Alzheimers, Autism Spectrum Disorders), heart (Familial Hypertrophic, Dilated, and Arrhythmogenic Right Ventricular Cardiomyopathies), and skeletal muscle (Amyotrophic Lateral Sclerosis, Spinal Muscle Atrophy). The combination of HiPSC technology and gene editing strategies such as the CRISPR/Cas9 system creates a powerful platform in which disease-causing mutations can be created on demand and sets of isogenic cell lines (with and without mutations) serve as convenient tools for disease modeling studies.

Other applications of HiPSC and iPSC-differentiated cells include drug screening, development, efficacy and toxicity assessment. As an example, through the FDA-backed CiPA (Comprehensive in vitro Pro-Arrhythmia Assessment) initiative, HiPSC-derived cardiac muscle cells (cardiomyocytes) are poised to constitute a new standard model for the evaluation of cardiotoxicity of new drugs, which is the main reason of drug withdrawal from the market. Finally, HiPSC-differentiated cells are being used in early stage technology development for applications in regenerative medicine. Bio-printing and tissue constructs have also been considered as attractive applications for HiPSC.

Human iPSC and Derived Cells are forResearch Use Only (RUO). Not for human clinical or therapeutic use.

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iPSCells Represent a Superior Approach

iPS cell-derived cardiomyocyte patch demonstrates spontaneous and synchronized contractions after 4 days in culture.

One of the greatest promises of human stem cells is to transform these early-stage cells into treatments for devastating diseases. Stem cells can potentially be used to repair damaged human tissues and to bioengineer transplantable human organs using various technologies, such as 3D printing. Using stem cells derived from another person (allogeneic transplantation) or from the patient (autologous transplantation), research efforts are underway to develop new therapies for historically difficult to treat conditions. In the past, adult stem and progenitor cells were used, but the differentiation of these cell types has proven to be difficult to control. Initial clinical trials using induced pluripotent stem (iPS) cells indicate that they are far superior for cellular therapy applications because they are better suited to scientific manipulation.

CDIs iPS cell-derived iCell and MyCell products are integral to the development of a range ofcell therapyapplications. A study using iCell Cardiomyocytesas part of a cardiac patch designed to treat heart failure is now underway. This tissue-engineered implantable patch mayemerge as apotential myocardial regeneration treatment.

Another study done with iPS cell-derived cells and kidney structures has marked an important first step towards regenerating, and eventually transplanting, a functioning human organ. In this work, iCell Endothelial Cellswere used to help to recapitulatethe blood supply of a laboratory-generated kidney scaffold. This type of outcome will be crucial for circulation and nutrient distribution in any rebuilt organ.

iCell Endothelial Cells revascularize kidney tissue. (Data courtesy of Dr. Jason Wertheim, Northwestern University)

CDI and its partners are leveraging iPS cell-derived human retinal pigment epithelial (RPE) cells to develop and manufacture autologous treatments for dry age-related macular degeneration (AMD). The mature RPE cells will be derivedfrom the patients own blood cells using CDIs MyCell process. Ifapproved by the FDA, this autologous cellular therapy wouldbe one of the first of its kind in the U.S.

Learn more about the technologybehind the development of these iPScell-derived cellular therapies.

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Stem cells have the incredible ability to develop into a variety of different cell types within the body. In addition, stem cells can play a crucial role in internally repairing many types of tissues. During this process, stem cells divide, replenishing other cells without limit.

While stem cells have been used by medical professionals for a wide variety of reasons in order to treat injuries, ailments, and diseases affecting every part of the body, the use of stem cells in the treatment of spinal damage may be the most exciting and potent use yet. Through the application of these spinal treatments, patients have the ability to recover not only more completely, but also in a more natural and therefore more complete manner than ever before. When paired with the insight of a skilled spinal surgeon, the results can be astonishing.

If you or a loved one is suffering from spine damage and are looking to learn more about how stem cell treatments can help you, get in touch with the expert back team at ProMed SPINE today by filling out ouronline contact form. Schedule a consultation with us and begin the path to recovery today!

Stem cells differ from other cell types because they are unspecialized and therefore capable of renewing themselves through cell division. Under certain physiologic or experimental conditions, they have the ability to become tissue or even organ-specific cells with special functions. Given these unique regenerative abilities, stem cells offer new potential in the enhancement of every surgery.

Rather then undergoing an invasive surgery that wont actually repair damage from degenerative disc disease, stem cell spinal treatments are short, minimally invasive and capable of healing the damage that has been done to the disc. Stem cell therapy produces new disc cells inside the disc itself, allowing it to rebuild to a like-new condition. When treating degenerative disc disease, bone marrow is extracted from the patients hipbone and stem cells are filtered out using a centrifuge. Then stem cells are injected into the disc with the help of an x-ray. After this step, the patient is free to go home and begin the recovery process. Over the next few months to a year, patients will experience a lessening of back pain as the disc begins to restore itself. It is quite common for patients who have undergone stem cell injections to experience complete relief from back pain and a vast improvement in their overall quality of life.

Stem cells can also be used to enhance the effects of a spinal fusion surgery. A lack of useful new bone growth after this type of surgery can be a significant problem. This new technology helps patients grow new bone and avoid harvesting a bone graft from the patients own hip or using bone from a deceased donor. By avoiding these steps, patients are able to recover faster and prevent painful procedures.

A major component of stem cells is their ability to reinforce stronger, healthier healing in patients. Oftentimes, the body is in a weakened state following a surgical procedure and therefore more susceptible to developing infection. Stem cells unique ability to replenish themselves offers the body fresh, healthy cells that are not nearly as vulnerable to incurring infection so that the body can heal more quickly and effectively.

After undergoing a surgery and the rehabilitation process that follows, many patients are left with unsightly scars. These scars are often painful reminders of a traumatic event and, in some cases, cause self-consciousness or outright embarrassment due to their appearance. Stem cells have become an increasingly useful aid in ridding patients of unattractive scars so that they can fully recover from their injuries. Stem cells are useful in the treatment of scarring in three major ways: they carry anti-inflammatory properties that prevent excessive scarring, are capable of replenishing normal cells in the tissue through differentiation, and finally, stem cells dissolve the excess collagen in scar tissue by emitting large amounts of enzymes whose specific function is to dissolve scar tissue.

Click here to learnmore about stem cell therapy from WebMD.com.

The potential medical benefits of stem cell research are unparalleled in the healing and rejuvenating processes following a spinal procedure. Whether you are facing a major surgery or are considering your options concerning continued pain and physical limitations, knowing what options may be best for you is vital in the search for skilled medical care. Schedule an appointment with a laser spine surgeonto find out how stem cell therapy can be used to help you find a healthier and happier life.

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Skin is the body's largest organ. Loss of the skin barrierresults in fluid and heat loss and the risk of infection. Thetraditional treatment for deep burns is to cover them with healthyskin harvested from another part of the body. But in cases ofextensive burns, there often isn't enough healthy skin toharvest.

During phase I of AFIRM, WFIRM scientists designed, built andtested a printer designed to print skin cells onto burn wounds. The"ink" is actually different kinds of skin cells. A scanner is usedto determine wound size and depth. Different kinds of skin cellsare found at different depths. This data guides the printer as itapplies layers of the correct type of cells to cover the wound. Youonly need a patch of skin one-tenth the size of the burn to growenough skin cells for skin printing.

During Phase II of AFIRM, the WFIRM team will explore whether atype of stem cell found in amniotic fluid and placenta (afterbirth)is effective at healing wounds. The goal of the project is to bringthe technology to soldiers who need it within the next 5 years.

This video -- with a mock hand and burn -- demonstrates the process.

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COPD

Over 32 million Americans suffer from chronic obstructive pulmonary disease (also known as COPD). COPD is a progressive lung disease, however regenerative medicine, such as lung regeneration therapies using stem cells are showing potential for COPD by encouraging tissue repair and reducing inflammation to the diseased lung tissue.

Following up with stem cell therapy and exome therapy immediately in the first 36 to 48 hours after stroke symptoms surface has proven to be crucial to long-term recovery and regaining mobility again. Cell therapy also calms post-stroke inflammation in the body, and reduces risk of serious infections.

Parkinsons is a neurodegenerative brain disorder caused by the gradual loss of dopamine-producing cells in the brain. It afflicts more than 1 million people in the U.S., and currently, there is no known cure. Stem cell therapies have been showing incredible progress. Using induced pluripotent stem (iPS) cells, a mature cell can be reprogrammed into an embryonic-like, healthy and highly-functioning state, which has the potential to become a dopamine-producing cell in the brain.

A thick, full head of hair is possible, naturally! Stem cell and exosome therapy promotes healing from within to naturally stimulate hair follicles, which encourages new hair growth. Using your own stem cells, Platelet Rich Plasma (PRP) and exosomes, you can regrow your own healthy, thick hair naturally and restore your confidence!

Erectile Dysfunction (ED) is the inability to achieve or maintain an erection sufficient for satisfactory sexual intercourse. Regenerative medicine offers a non-surgical option that commonly uses the patients own stem cells, exosomes, and other sources of growth factors to regenerate healthy tissue to improve performance and sensation.

If chronic joint pain is derailing your active lifestyle, then youre not alone. Regenerative medicine offers a non-surgical option that commonly uses the patients own stem cells, exosomes, and other sources of growth factors to reduce inflammation, promote natural healing and regenerate healthy tissue surrounding the joint for relief.

Multiple Sclerosis (MS) affects 400,000 people in the U.S., and occurs when the body has an abnormal immune system response and attacks the central nervous system. Regenerative medicine now offers treatment for MS with stem cell therapy, which is an exciting and rapidly developing field of therapy. Stem cells work to repair damaged cells these new cells can become replacement cells to restore normal functionality.

Spinal cord injuries are as complex as they are devastating. Today, cellular treatments, usually a combination of therapies, such as stem cell, Platelet Rich Plasma (PRP) and exosome therapy with growth factors are showing promise in contributing to spinal cord repair and reducing inflammation at the site of injury.

If you have chronic nerve injury pain that doesnt fade, your health care provider may recommend surgery to reverse the damage. However, regenerative medicine offers a non-surgical option to repair damaged tissue and reduce inflammation at the site of injury. Stem cell therapy commonly uses the patients own stem cells, exosomes, and other sources of growth factors to regenerate healthy tissue.

Neuropathy also called peripheral neuropathy occurs when nerves are damaged and cant send messages from the brain and spinal cord to the muscles, skin and other parts of the body. Simply put, the two areas stop communicating. Stem cell and exosome therapies treat damaged nerves affected by neuropathy, and they have the ability to replicate and create new, healthy cells, while repairing damaged tissue.

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Five million people in the U.S. suffer with heart failure, resulting in ~60,000 deaths/year at a cost of $30 billion/year. Heart failure occurs when the heart is damaged and becomes unable to meet the demands placed on it. Unlike other organs, the heart is unable to fully repair itself after injury. One of the common causes for the development of heart damage is a heart attack. After a myocardial infarction (heart attack), irreversible loss of contracting heart muscle cells occurs, resulting in scar formation and subsequently heart failure. Current therapies designed to treat heart attack patients in the acute setting include medical therapies and catheter-based technologies that aim to open the blocked coronary arteries with the hope of salvaging as much of the jeopardized heart muscle cells as possible. Unfortunately, despite advances over the past 2 decades, it is rarely possible to rescue the at-risk heart muscle cells from some degree of irreversible injury and death.

Attention has turned to new methods of treating heart attack and heart failure patients in both the acute and chronic settings after their event. Heart transplantation remains the ultimate approach to treating end-stage heart failure patients but this therapy is invasive, costly, some patients are not candidates for transplantation given their other co-morbidities, and most importantly, there are not enough organs for transplanting the increasing number of patients who need this therapy. As such, newer therapies are needed to treat the millions of patients with debilitating heart conditions. Recently, it has been discovered that stem cells may hold therapeutic potential for these patients. Experimental studies in animals have revealed encouraging results when pluripotent stem cells are introduced into the heart around areas of myocardial infarction. These therapies appear to result in improvement in the contractile function of the heart.

However, numerous questions remain unanswered concerning the use of pluripotent stem cells as therapy for patients with heart attack and heart failure. Human embryonic stem (ES) cells and induced pluripotent stem (iPS) cells grow and divide indefinitely while maintaining the potential to develop into many tissues of the body, including heart muscle. They provide an unprecedented opportunity to both study human heart muscle in culture in the laboratory, and advance the possibility of their use in therapy for damaged heart muscle. We have developed methods for identifying and isolating specific types of human ES and iPS cells, stimulating them to become human heart muscle cells, and delivering these into the hearts of rodents that have had a heart attack. This research will refine and advance such approaches in small and large animals, develop clinical grade cells for use, and ultimately initiate clinical trials for patients suffering from heart disease.

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A new therapy could restore healthy and protective skin to patients with a rare genetic disease.

iStock.com/Andrey Prokhorov

By Kelly ServickNov. 8, 2017 , 1:00 PM

A 7-year-old who lost most of his skin to a rare genetic disease has made a dramatic recovery after receiving an experimental gene therapy, researchers announced today. The treatmenta whole-body graft of genetically modified stem cellsis the most ambitious attempt yet to treat a severe form of epidermolysis bullosa (EB), an often-fatal group of conditions that cause skin to blister and tear off at the slightest touch.

The new approach can address only a subset of the genetic mutations that cause EB. But the boys impressive recoveryhes now back inschool and is even playing soccercould yield insights that help researchers use stem cells to treat other genetic skin conditions.

It is very unusual that we would see a publication with a single case study anymore, but this one is a little different, says Jakub Tolar, a bone marrow transplant physician at the Masonic Cancer Center, University of Minnesotain Minneapolis who is developing therapies for EB. This is one of these [studies] that can determine where the future of the field is going to go.

EB results from mutations to any of several genes that encode proteins crucial for anchoring the outer layer of skin, the epidermis, to the tissue below. The missing or defective protein can cause skin to slough off from minor damage, creating chronic injuries prone to infection. Some forms of EB can be lethal in infancy, and some predispose patients to an aggressive and deadly skin cancer. The only treatment involves painfully dressing and redressing wounds daily. Bandage costs can approach $100,000 a year, says Peter Marinkovich, a dermatologist at Stanford University in Palo Alto, California, who treats EB patients. Theyre like walking burn victims, he says.

In fact, the new approach is similar to an established treatment for severe burns, in which sheets of healthy skin are grown from a patients own cells and grafted over wounds. But stem cell biologist and physician Michele De Luca of the University of Modena and Reggio Emilia in Italy and his colleagues have been developing a way to counteract an EB-causing mutation by inserting a new gene into the cells used for grafts. His group has already treated two EB patients with this approach. They publishedencouraging resultsfrom their first attemptwith small patches of gene-corrected skin on a patients legsin 2006.

In 2015, De Lucas team got a desperate request from doctors in Germany. Their young patient had a severe form of the disease known as junctional EB, caused by a mutation in a gene encoding part of the protein laminin 332, which makes up a thin membrane just below the epidermis. It was the same gene De Lucas team was targeting in an ongoing clinical trial, but this case was especially dire: Lacking most of his skin, the boy had contracted multiple infections and was in a life-threatening septic state. The emergency treatment would be the first test of their gene therapy approach over such a large and severely damaged area.

De Lucas team used a patch of skin a little bigger than a U.S. postage stamp from an unblistered part of the boys groin to culture epidermal cells, which include stem cells that periodically regenerate the skin. They infected those cells with a retrovirus bearing healthy copies of the needed gene,LAMB3, and grew them into sheets ranging from 50 to 150 square centimeters. In two surgeries, a team at Ruhr University in Bochum, Germany, covered the boys arms, legs, back, and some of his chest in the new skin.

After a month,most of the new skin had begun to regenerate, covering 80% of the boys body in strong and elastic epidermis, the researchers report online today inNature. Whats more, hes developed no blisters in the grafted areas in the 2 years since the surgery.

Other researchers have long been concerned that using a retrovirus to insert genes at random points in cells genomes might cause cancer. (In the early 2000s, five children who participated in a retrovirus-based gene therapy trial for severe combined immunodeficiencydeveloped leukemia.) But the current study found no evidence that the insertion affected cancer genes.

De Luca and colleagues were also able to track which grafted cells regenerated the skin over time by using the different locations of the genetic insert as markers for individual cells and their progeny. They found that most cells from the graft disappeared after a few months, but a small population of long-lived cells called holoclones formed colonies that renewed the epidermis.

Epidermal stem cells known as holoclones (shown in pink) were responsible for regenerating the young epidermolysis bullosapatients skin, whileother cell types disappeared over time.

News & Views/Nature; adapted by E. Petersen/Science

Thats an important lesson, Tolar says; it suggests that future attempts to correct genetic skin diseases should focus on culture conditions that nourish these stem cells, and potentially even target them for modification. If you have a gene correction strategy, he says, youd better have these primitive epidermal stem cells in mind.

The current results could benefit several thousand EB patients across the world, Marinkovich says, but it wont work for all of them. More than half have a form of the disease called EB simplex, which is causednot by a missing protein, but by mutations that produce an active but dysfunctional protein. For these errors, correction with a gene-editing tool like CRISPR makes more sense, De Luca says.

The grafts also cant repair damage to internal surfaces such as the esophagus, Tolar notes, which occurs in some EB cases. Fortunately, that wasnt an issue for the boy in this study. The treatment is a good step in the right direction, he says, but its not curative.

Both De Luca and Marinkovichs teams are exploring a similar gene therapy for another major form of the disease, called dystrophic EB, caused by a different genetic error affecting a larger protein. Biotech companies are working with each group to test the approach in larger clinical trials.

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A stem cell or bone marrow transplant replaces damaged blood cells with healthy ones. It can be used to treat conditions affecting the blood cells, such as leukaemia and lymphoma.

Stem cells arespecial cells produced bybone marrow (aspongytissue found in the centre of some bones) that can turn into different types of blood cells.

The three maintypes of blood cellthey can become are:

A stem cell transplant involves destroying any unhealthy blood cells and replacing them with stem cells removed from the blood or bone marrow.

Stem cell transplants are used to treat conditions in which the bone marrow is damaged and is no longer able to produce healthy blood cells.

Transplants can also be carried out to replace blood cells that are damaged or destroyed as a result of intensive cancer treatment.

Conditions that stem cell transplants can be used to treat include:

A stem cell transplant will usually only be carried out if other treatments haven't helped, the potential benefits of a transplant outweigh the risks and you're in relatively good health, despite your underlying condition.

A stem cell transplant can involve taking healthy stem cells from the blood or bone marrow of one person ideally a close family member with the same or similar tissue type (see below) and transferring them to another person. This is called an allogeneic transplant.

It's also possible to remove stem cells from your own body and transplant them later, after any damaged or diseased cells have been removed. This is called an autologous transplant.

Astem celltransplant has five main stages. These are:

Having a stem cell transplant can be an intensive and challenging experience. You'll usually need to stay in hospital fora month or more until the transplant starts to take effect and itcan takea year or two to fully recover.

Read more about what happens during a stem cell transplant.

Stem celltransplants arecomplicated procedures with significant risks. It's important that you're aware of both the risks and possible benefits before treatment begins.

Possible problems that can occur during or after the transplant process include:

Read more about the risks of having a stem cell transplant.

Ifit isn't possible to use your own stem cells for the transplant (see above), stem cells will need to come from a donor.

To improve the chances ofthetransplant being successful, donated stem cells need tocarry a special genetic marker known as a human leukocyte antigen (HLA) that'sidentical or very similar to that of the person receiving the transplant.

The best chance of getting a match is from a brother or sister, or sometimes another close family member. If there are no matches in your close family,a search of theBritish Bone Marrow Registry will be carried out.

Most peoplewill eventually find a donor in the registry,although a small number of people may find it very hard or impossibleto find a suitable match.

The NHS Blood and Transplant website has more information about stem cell and bone marrow donation.

Page last reviewed: 08/10/2015

Next review due: 01/10/2018

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Spinal cord injury is the injury to the spinal cord, a very serious form of trauma with enduring effects on the patients daily life. The spinal cord is approximately 18 inches long and extends from brain base at the neck and ending just above the buttocks. It has numerous nerves known as upper motor neurons (UMNs) and is responsible for transmitting signals back and forth from the brain to different parts on the body.Human beings are in a position to feel pain and move their limbs because messages are sent via the spinal cord, therefore if the spinal cord is damaged some or all of these impulses may not be sent.

Usually, a spinal cord injury happens as a result of an impulsive accident or event, we list here some of the most common causes of spinal cord injury:

An aggressive attack like being stabbed or shot Diving into very shallow water and hitting the bottom Trauma to the face, head, back or the neck region during a motor accident Falling from a very high height Electrical accident Injuries while engaging in sports Severe twist of the torso middle portion

1) Incomplete spinal cord injuries; the spinal cord is partially affected and in this case, the patient retains some functions depending on the degree of the injury. Some of the common types of partial spinal cord include anterior cord syndrome, central cord syndrome and brown-sequard syndrome.

2) Complete spinal cord injuries; this type occurs when the spinal cord is fully damaged and there is no function below the level of injury. However, with proper treatment and physical therapy, it is possible for a patient to regain some functions.

Challenges walking Loss of control of bladder or bowels Difficulties moving arms and legs Headaches Unconsciousness Pain, pressure, and stiffness in the neck/or back region Spreading numbness feelings Unnatural head positioning Signs of shock Loss of libido Loss of fertility Bedsores How are spinal cord injuries diagnosed?

Usually, physicians examine patients for spinal cord injuries based on factors like the location, type and the symptoms of the injury. However, no single test can assess 100% these injuries; instead, doctors depend on a number of protocols such as:

Clinical evaluation; the doctor will keenly observe your symptoms, carry out blood tests, ask detailed questions about your condition and follow your eye movement Imaging tests; the doctor may request a magnetic reasoning imaging or radiological imaging to view the spinal column, spinal cord, and brain

Stem cells are found in all multi-cellular organisms and are well known for their remarkable ability to differentiate into almost any other type of cell. Therefore depending on the disease, stem cells can be transplanted into the patient to assist renewal and regeneration of the previously dying cells.This principle is now being used for a spinal cord injury using stem cells; it assists patients with the recovery process and restores their physiological and sensory ability.Currently, no stem cell therapy has been approved as a complete cure for spinal injuries. Stem cell therapy is used to improve conditions and symptoms whilst allowing the patient to enjoy a better quality of life after injury.

Exogenous and endogenous repair.While in exogenous repair the stem cells are first grown in the lab and then injected into the patient, in endogenous repair stem cells are injected into the injured site and the results depend on the bodys ability to change stem cells into the needed cells.

Adult neural stem cells can differentiate into different cell types. Consequently, researchers are taking advantage of this regenerative ability and are trying to come up with ways to reintroduce the bodys own stem cells into the damaged spinal cord. Research in rats shows that transplanting oligodendrocyte (support cells that make myelin) and astrocyte (boost nerve function) precursors from the neural stem cells can protect axons and reduce motor neuron damage.

Embryonic stem cells are the best type of stem cells and researchers are developing ways to turn embryonic stem cells into oligodendrocyte which have successfully repaired neural functions in animal models. However, using the same approach in a clinical trial is very challenging; it is close to impossible to make oligodendrocyte without also making other unasked for cells.

Induced Pluripotent Stem cells (IPs) are just like embryonic stem cells and can be made from the skin or any other tissue cell. They are easily reachable and offer a great source of cells that match the patients profile, hence theres no chance of rejection.

By combining the Anti CD2 human clonal antibodies and Anti-cytokines monoclonal antibodies, we create injections. This helps to reduce the inflammation, axonal degeneration and to prevent demyelination. Lysis functions of leukocyte cells get enhanced as well.

Spinal laser therapyIV laser therapyIV OxygenShock Wave TherapyPeptides injectionsPhysiotherapyEnzymes & Nutrition

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I can see him in his glass-fronted Cambridge office from the foosball table in the light-filled central atrium. Hes standing there talking to a visitor and seems to be finishing up. This entire side of the third floor in MITs new Media Lab building is partitioned with glass, and professor Hugh Herr and his colleagues and whatever madness theyre up to in their offices and the open, gadget-filled, lower-floor lab are on display. Several people, myself included, are peering down, hoping to see a bit of magic.

Months ago, when I e-mailed Herr to propose writing an article about him, I told him about my rare bone cancer and resulting partial paralysis below the waist as a way to explain my interest in his work. Though I didnt tell him this, I also harbored a secret wish that he could help me. People write to Herr, a 52-year-old engineer and biophysicist, daily about his inspiring example. Theyve heard him promise an end to disability. They have conditions that medicine cant fix and futures they cant stand to consider. Theyre wishing for his intervention, wanting of hope. Crossing his threshold, Im the lucky one. Im here.

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Herr welcomes me into his office, a clean, well-ordered space. Theres a round glass table with a laptop on it, a handful of hard office chairs, and a pair of prosthetic legs Herr designed that are arranged like statuary behind us, one in either corner. Above us on a wall looms a large mounted photograph of another pair of prosthetics. These are hand-carved from solid ash, with vines and flowers and six-inch heels. The real-life legs were famously worn by a friend of Herrs, the amputee track-and-field athlete and actress Aimee Mullins.

I have hobbled into Herrs office with a dented $20 stock metal cane on one side and a foot-lifting Blue Rocker brace on the other. (The dent is from my recently firing the cane at the wall.) I had imagined Herr noticing the cane and asking more about my story to see how he could fix me, like he has fixed so many others. The moment I realize that the meeting Id imagined isnt the meeting were going to haveIm here as a reporter, not a friend or patient, after allI start to stammer. Herr deftly resets the conversation by suggesting we look at his computer.

On it are the PowerPoint slides of his next big project, a breathtaking $100 million, five-year proposal focused on paralysis, depression, amputation, epilepsy, and Parkinsons disease. The work will be funneled through Herrs new brainchild, MITs Center for Extreme Bionics, a team of faculty and researchers assembled in 2014 that he codirects. After exploring various interventions for each condition, Herr and his colleagues will apply to the FDA to conduct human trials. One to-be-explored intervention in the brain might, with the right molecular knobs turned, augment empathy. If we increase human empathy by 30 percent, would we still have war? Herr asks. We may not.

As he continues with the presentation hes been giving to technologists, engineers, health researchers, and potential donorslast December alone, he keynoted in Dubai, Istanbul, and Las Vegaseach revolutionary intervention he mentions yields a boyish grin and a look that affirms: Yes, you heard that right. In a talk I hear him give a few weeks later, hell dare to characterize incurable paralysis as low-hanging fruit. In his outspoken willingness to fix everything, even things that some argue should be left alone, he knows how he sounds. If half the audience is frightened and the other half is intrigued, I know Ive done a good job, he says.

Herr on a 5.12 route on Arizonas Mount Lemmon in 1986. (Beth Wald/Aurora)

Herr calmly ticks off one condition after another. He shows me an animation of an innovative surgery that will restore an amputees lost proprioception, giving a person the ability to feel and control a prosthetic as if it were their own limb. In another slide, of a paralyzed man in a bulky walk-assisting exoskeleton suit, he asks me to imagine a futuristic treatment that uses light to control cells in muscle tissue. Then he presents a video clip of a rat with a severed spinal cord dragging around its paralyzed hind legs.

Having dragged my mostly unresponsive left leg around for two years, I think I know something about the rodents life. In the next clip, however, that rat, just 90 days later, is walking on all fours. A team at the MIT center led by Herrs colleague Robert Langer successfully regrew the rats spinal cord by implanting a dissolvable scaffold seeded with neural stem cells. In Herrs world, the limbless can be whole again, the paralyzed can walk. Making the extraordinary seem ordinary is maybe the whole point.

Herr himself is proof positive. Trim, fit, and handsome, he is the showpiece for the Center for Extreme Bionics. Im kind of what theyre selling, he says. The fuss over Herr has been building for decades but reached new levels in 2014, courtesy of his TED Talk, which has now been viewed in excess of 7.3 million times. In it, Herr describes the horrific 1982 winter climbing accident in New Hampshires White Mountains during which he suffered severe frostbite, leading to the amputation of both legs below the knee. Then 17, Herr was told hed never climb again. Instead, he rebuilt himself almost immediately, willfully reshaping his artificial legs and realizing that he wasnt handicapped, the technology was.

By hacking his prosthetic devices for his vertical world, he was able to quickly return to climbing, becoming the first athletedecades before Oscar Pistoriusto blur the line between para and not. His accomplishments landed him on the cover of Outside a year after his accident, something that sticks with him not because of the many accolades other climbers bestowed on him, or even the controversy it reignited around the tragic death of one of his rescuers, but because of the questions the article raised about how far Herr would be able to go. I was a sad case. I was going to end up in this machine shop, disabled, Herr recalls of the piece, pausing to let the perceived insult ripen in his mind. Yeah, its a real sad story.

The triumphant, fully realized man in the TED Talk is a marvel. His outrage at the unnecessary suffering from disability is fiercely personal. What first-time viewers like me invariably fixate on is the way Herr gracefully owns the stage. Hes wearing pants that end above the knee, revealing shimmering high-tech silver and black prosthetics. Herr is focused on what hes saying, not what his artificial legs are doing. The crime of physical impairment is that it often steals from a persons sense of self. If you didnt look below his knees, youd never guess that Herr is missing half of each leg. He walks through the world the way we all would hope to.

He has effectively ended his disability, or at least the perception of it, just as he said he would. Inspired by his accident, he earned a masters degree in mechanical engineering at MIT in 1993, followed by a Ph.D. at Harvard in biophysics. Ever since, Herr has produced a string of breakthrough products, starting with a computer-controlled artificial knee in 2003. In 2004, he created the biomechatronics group at MIT, a now 40-person R&D lab drawing on the fields of biology, mechanics, and electronics to restore function to those whove lost it. Three years later, the team produced a powered ankle-foot prosthesis that allows an amputee to walk with speed and effort comparable to those with biological legs. Called the emPower, the apparatus weighs a few pounds and houses 12 sensors, three computers, tensioning springs, and muscle-tendon actuators. The ankle system is manufactured by a private company Herr started called BionX.

Last year, Herr advanced another of his labs goals, to improve human performance beyond what nature intends by creating a brace-like exoskeleton device that reduces the metabolic cost of walking. The implications for people who want to get places fasteror perhaps a soldier trying to conserve energy on a long marchare vast.

In the near future, Herr and his colleagues at the MIT center are committed to, among other things, reversing paralysis. Herrs goal is to develop a synthetic spinal cord thataids the damaged original. A prosthesis, in other words.

In his office, Herr draws up his pant leg and rolls down a silicone sleeve to show me a newly developed fabric that lines the socket of his prosthetic and cushions the problematic intersection between the biological stump and the man-made limb. The exquisitely comfortable fitdigitally derived, he explains, but highly personalis something he delights over with a savoring gush.

With our first meeting nearing its end, I grow distracted thinking about the wounded few Herr has smiled upon. In 2014, he worked on a bionic prosthetic for the dancer Adrianne Haslet-Davis, who lost her left leg in the Boston Marathon bombing. Currently, hes working with Hari Budha Magar, a double-amputee former Gurkha soldier who plans to climb Mount Everest in 2018, and also Jim Ewing, an old New Hampshire climbing buddy. Ewing was climbing a wall on vacation in the Cayman Islands in 2014 when he fell with his teen daughter on belay. She couldnt brake the rope, and he plummeted some 60 feet, shattering his pelvis and left foot on impact.

The dancer, the Gurkha, the climber, and Herr himself are examples of what he often describes as the millions of humans who might appear broken but are not. Haslet-Davis, on a bionic limb embedded with dance intelligence, brilliantly performed the rumba again, and Ewing underwent a pioneering amputation procedure developed by Herrs biomechatronics team in partnership with MIT colleague and surgeon Matthew Carty, who performed the operation at Brigham and Womens Faulkner Hospital, to prepare Ewing for an advanced prosthesis. Magar will be outfitted with short prosthetics to reduce leg drag and sophisticated crutches for speed as he attempts Everest history.

The stories Herr tells, the future he sees, the beautifully functioning artificial limb before meits all I can do not to show him my atrophied left leg and ask for his godlike intervention to fix what I know is broken. But I dont, not yet.

When I wrote Herr to tell him about my interest in his work, I summarized my case history. I explained how in the summer of 2014, I found myself with increasingly debilitating nerve and lower-back pain. When I finally got an MRI, I learned that I had an extremely rare bone cancer called chordoma that had spread from my lower lumbar vertebrae into my right hip flexor. Radiation and a difficult multi-stage surgery successfully removed the softball-size tumor, but months later, possibly due to a loss of blood to the spinal cord, Id yet to regain sensation or strength in my hips and legs. The doctors didnt know if it was permanent, but the prognosis didnt look good.

Jim Ewing and his robotic prosthetic. (Boston Globe/Getty)Aimee Mullins. (Lynn Johnson/Getty)Mountaineer Hari Budha Magar. (Himalayan Ski Trek)

Id expected a rapid, maybe even exceptional recovery. I am an athlete and adventurer who has had the good fortune to do a lot of cool stuff over the years. Id become a whitewater guide, climbed Grand Teton, raced the hill climb at Mount Washington on foot and by bike, and mountain-biked half the 3,000-mile-plus Great Divide route. I expected to complete the other half someday.

Id progressed from a walker to a cane, from a recumbent tricycle to a pedal-assist e-bike. Then my nerve regeneration halted. In May 2015, after the surgery, Id contacted Boston neurologist Bill David for muscle and nerve testing. An avid cyclist and kindredspirit, hed hopefully stuck needles into my skin every six months to chart my recovery. Late last year, he confirmed what I had already sensed. Short of a miracle, Id gone about as far as I could. I really wish that we had met on a mountain or river as opposed to a medical clinic, David said.

Id negotiated several stages of recovery, but the one I feared most was right nowat the end, my future fixed. Ive been coming to grips with who I am as an incomplete paraplegic and figuring out how to make the best version of this new person, I wroteto Herr.

Id imagined a stirring epilogue to our encounters, a moment perhaps when a radical trial arose and a crazy volunteer was needed. To be closer to the person I once was, I would try anythinginjected viruses, exoskeletal suits, implants. When I got together with a close friend for lunch, I told her how the story with Herr was progressing, and how the limbs he created were so advanced that Id read about people wanting them even though their leg complications didnt medically require amputation. She listened carefully. Let me ask you something, she said. Would you, um, get your legs cut off?

Exactly when in his childhood Hugh Herr decided to become the worlds best climber is impossible to pinpoint, but the goal was nurtured during family road trips across the West. He and his older brothers climbed, fished, and hiked in the American and Canadian Rockies, whetting the youthful Herrs appetite for adventure. The Shawangunk Mountains in New York were a four-and-a-half-hour drive from the Herrs home in Lancaster, Pennsylvania. The Gunks were an emerging mecca in the seventies, and Herr quickly established himself as a prodigy, climbing this stuff when I was 11 that only adults had done, and at 15 that no one else had done, he says.

When he and Jeff Batzer, a friend from Lancaster, drove to New Hampshires Mount Washington in January 1982 for a weekend ice-climbing outing, it wasnt to do anything audacious. Theyd attempt a classic route in Huntingtons Ravine, and maybe, depending on the weather and avalanche conditions, summit Mount Washington before racing down for the 12-hour drive home. Herr was a 17-year-old junior in high school, his friend Batzer, 20.

The decision to tack on the summit of Washington turned out to be a tragic mistake. They left a sleeping bag and bivy sack behind to reduce weight but encountered howling winds and blizzard conditions near the top, and they ended up losing their way, mistakenly descending into a different valley from where theyd come.

After four days trekking through a storm in deep snow and below-freezing temperatures to find their way out, Herr was no longer able to walk. Early on in the odyssey, he had punched through a frozen streambed into shin-deep water, soaking his boots and pants, and was suffering from severe frostbite. In Second Ascent, a biography by Alison Osius, Herr said that he had reconciled himself to death when a backcountry snowshoer saw some of Batzers tracks and followed them to a makeshift shelter the two were bivouacked in. The climbers were evacuated to a nearby hospital in Littleton, where doctors treated both for hypothermia and frostbite. Herrs legs were in terrible shape. At the hospital, he learned that doctors might not be able to save them and that a member of his search party, a 28-year-old climbing-school instructor named Albert Dow, had been killed in an avalanche. Two months later, doctors amputated Herrs legs four inches below the knee. Batzers fingers on his right hand were amputated, along with his left foot and the toes on his right foot.

I asked my doctor after the amputation what Id be able to do with my new body, Herr recalls. The doctor said, What do you want to do? I said I wanted to drive a car, ride my bike, and climb. The doctor said youll be able to drive a car, but with hand controls. He said I would not be able to ride a bike or return to climbing.

Herr did all of the above within a year. He worked closely with his prosthetist on one pair of artificial legs after another and tinkered on his own in the machine shop of a vocational school hed begun attending in 1981. He soon figured out that he could hack his artificial limbs to suit the requirements of particular climbing routes. He built limbs that extended or shortened his stature; he carved out feet with wedge ends to slice into crevices. He began to knock off routes that he hadnt been able to do previously, including leading an ascent of Vandals at Skytop, the first 5.13 on the East Coast. It ignited a new controversy: that his adaptations were a form of cheating. Herr likes to tell audiences that he invited his affronted rivals to chop off their own legs.

Some people were bitter and angry about the accident, says Jim Ewing, a summer roommate of Herrs in the 1980s, and with Hugh coming back and climbing so well, they started making up excuses, saying things like, He can stand on a dime, his feet dont get sore, he doesnt have calf fatigue. Id just look at these people and think, By God, you havent seen this guy crawl to the toilet in the middle of the night because he doesnt have his legs on. He is handicapped; it is a handicap. People had no idea.

The 1982 rescue. (Jim Cole/AP)Herr in the hospital. (Jim Cole/AP)Herr in 1984. (Peter Lewis)

While there was a lot of media attention about Herrs accident, he kept private the struggles and self-doubt he faced after he lost his legs. When he returned to New Hampshire to climb again 18 months later, the unease from locals over Dows death and Herrs resurgence was palpable.

The harsh early views of Herr didnt soon go away. When I asked him what he thought when the American Alpine Club last year honored him at a celebratory awards evening in Denver, he said he was stunned. They had named him a new inductee of the Hall of Mountaineering Excellence for lasting contributions on and off the mountain. It shocked me, he said. The initial story line of the accident was that these young, irresponsible, incompetent climbers caused the death of an experienced, beloved local climber. That narrative went on for a very long time. So for two decades at least, I wouldnt even expect the American Alpine Club to invite me to be in the audience.

When Herr talks about Albert Dow, who he never met, its with the fondness of a friend. That was Albert! he recounts about Dows insistence that he go looking for Herr and Batzer because hed want someone to do the same for him. Last year, Herr told a Reddit audience that he strives to honor Dow. I hate the idea that his death somehow enabled me to live so I could do good work, he says. What I like is that his kindness and who he wasand his sacrificeinspired me to work really hard.

In 1985, Herr free-climbed New Hampshires exceptionally steep and unprotected Stage Fright, with his friend Jim Surette on belay. It was a significant and life-threatening milestone, and afterward Herr had a dream that set his new path. He describes a nightmare in which Surette, bunking on a neighboring couch, throws off his covers to reveal mangled, bloody, amputated legs. We both go Aaah! in the dream, says Herr, but then I turn to Jimmy and say, Dont worry, Jimmy, its just a dream. Im the one without legs. Prior to that, in all my dreams I would be running and jumping, and I would have my biological legs. It was the first time my brain recognized my new state.

Some mightve interpreted the nightmare with melancholy, an attempt to come to terms with a sorrowful lifelong condition. Herr saw it as a beautiful vision.

The auditorium is full at the Princeton, New Jersey, headquarters of the Robert Wood Johnson Foundation, all 150 in attendance looking stage left as Herr introduces an image of himself in a New Hampshire hospital room decades earlier. What do you see? he asks.

It is Herr in the moments after his legs have been amputated. The 17-year-old is gazing down at a white sheet and the outline of his stumps. The audience is riveted.

What do you see? he asks again. I see a new beginning, he declares. I see beauty.

Herr, who prefers to use the term unusual instead of handicapped or disabled, often says that he wouldnt want his biological legs back. He loves the legs he started building after the accident and has steadily improved upon for the past several decades.

His meteoric rise in academia is almost as improbable as his comeback to elite climbing. I actually graduated from high school not being able to take 10 percent of 100, he says. I had no idea what a percent was. His older brothers were all in construction. He understood that the family trade was unavailable to him, so he shut himself away and applied the same obsessive focus to science that hed once reserved for climbing. He read everything he could find and enrolled at the local college, Millersville University.

Wed watch all these films of animals locomoting to try to learn about motion, says Don Eidam, his first adviser at Millersville and an unapologetic superfan who writes a newsletter about Herr. Hed put all these ideas on my blackboard, and the chalk would literally be disintegrating. Hed call me at midnight with an idea. Ive never met anyone so committed or intense.

In 1991, Herr became the first student from Millersville to be accepted at MIT. The academic degrees, innovations, and honors have since overflowed. He is the holder or coholder of over 100 patents. The powered prosthesis he developed for ankle-foot amputees was the product of a special mind with a special motivation. By copying the behavior of a biologically intact leg, Herr and his biomechatronics lab were able to create a breakthrough replacement. In 2011, Time crowned him the leader of the bionic age. Last year he won Europes top prize for inventors, the prestigious Princess of Asturias Award.

In Hughs mind, he has not successfully innovated until people are able to benefit from his innovation, says Tyler Clites, a Harvard-MIT student who has worked in Herrs lab for six years. He has said to me, Look, Tyler, Ive invented hundreds of times, but Ive only ever innovated twice. The two items, his prosthetic knee and the ankle-foot, are the only ones commercially available to others.

The idea of an endlessly upgradable human is something Herr feels in his bones. I believe in the near future, in a decade or two, when you walk down the streets of Boston, youll routinely see people wearing bionic systems, Herr told ABC News in a 2016 interview. In 100 years, he thinks the human form will be unrecognizable. The inference is that the abnormal will be normal, beauty rethought and reborn. Unusual people like Herr will have come home.

At a small luncheon after his talk in New Jersey, the organizers ask me to say a few words about my condition. I give a five-minute recap of my struggles with cancer, the spinal-cord complication, and my up-and-down recovery. It is my first time speaking publicly about my situation. As I do, I sneak a glance or two at Herr. I wonder what he thinks hearing me tell my story. He is sitting immediately to my right, raking through a towering salad.

There is no clear signal from him, but I leave feeling that Ive pulled ever so slightly into his orbit. I am also beginning to understand the weight he bears of being a savior. A friend who saw his impassioned SXSW talk in 2015 told me how she raced up to thank him afterward, only to encounter a different guy. He was polite but aloof. She was put off, but I think I understand. The man has to set boundaries. He cant save everybody.

You might say that Herrs the sort of disrupter the research world needs, or you might say hes overpromising. One spinal-cord-injury scientist I spoke with wasnt so sure that a bold tech solution is the answer in a field long focused on the biology of nerve regeneration.

Nicholas Negroponte, the cofounder and former director of the MIT Media Lab, says Herrs sense of humor helps him handle any negative commentary. Its particularlyimportant when you do and say risky things, some of which invite harsh criticism, he says. You smile and keep going, because you know youre right.

A week after his talk in New Jersey, Herr and I meet up at a seafood restaurant near his MIT office. I arrive 30 minutes early, wanting to get situated. Having lived with my disability for some time now, I understand that I cant just sweep in like I used to. Herr, to my surprise, given his packed schedule, arrives ten minutes early.

Bomb survivor Adrianne Haslet-Davis. (Michael Dwyer/AP)

Herr told me earlier that he rarely pushes himself on climbs anymore. He proudly mentioned his two preteen, homeschooled daughters, who are avid hikers and spend almost every weekend with Herrs former wife, Patricia Ellis Herr, in the White Mountains happily exhausting themselves. They long ago summited Mount Washington and have high-pointed in 46 of the 50 states.

Herr and I talk at length about some of the people he has worked with and why. The Haslet-Davis project took a group from his biomechatronics lab 200 days to create the prosthetic, counting down to the 2014 TED Talk. She said she wanted to dance again. I really related, he says. He told himself, Im an MIT professor, I have resources. The timeline was tight enough that there was a TED Talk plan A (with her) and plan B (without). As everyone knows who has watched the video, Herrs team hit its deadline. Haslet-Davis unforgettably danced again, and there wasnt a dry eye because of it.

But as incredible as the moment was, its a source of frustration that the prosthetic cant be permanently handed over to Haslet-Davis. While Herr would love to give it to her, its a prototype that would cost millions to reproduce. As for Herrs climbing buddy Jim Ewing, thats a similarly uncertain situation. Months after Ewing had his foot amputated, he was fitted with a newly designed ankle-foot prosthetic that responds to his brain waves and allows him to feel his appendage. It is also a prototype that Ewing will eventually have to return.

Haslet-Davis and Ewing understood that they were part of a research project and wouldnt be able to keep the prototypes. Meanwhile, Herrs knee and ankle prosthetics, which cost tens of thousands of dollars, arent yet widely covered by insurance and remain too expensive for most who have a need for them. Herr has been in discussions with insurers to try and change that. According to Amputee Coalition of America estimates, there are 185,000 new lowerextremity amputations annually in the U.S. By contrast, there are only 1,700 emPower ankles in circulation right now. About half of them are worn by vets, paid for through reimbursements covered by the Department of Veterans Affairs.

Herrs work is important and coming from a good place, says Alisha Sarang-Sieminski, an associate professor of bioengineering at the Massachusetts-based Franklin W. Olin College of Engineering, a school involved in numerous projects related to lower-cost accessibility design. But people have different needs for different contexts. Also, so much of the high tech is really not accessible to very many people financially. Should people keep building them? Definitely. Should we also explore basic solutions? Yes.

Still, Ewings pioneering amputation is a huge success for Herrs group, the Brigham and Womens surgical team, and, most notably, Ewing. When I visited him at a climbing gym near Portland, Maine, he was planning a trip back to the Cayman Islands. For Ewing, the amputation has reduced the acute pain he used to feel in his biological foot and dramatically changed his outlook. He says that after his accident, he contemplated suicide. Being alive isnt enough, he says. Breathing isnt enough. I had to do something. Hugh understood my motivation probably better than I did.

Herr hadnt seen Ewing for years when he got an e-mail from him asking for advice about his foot. He was in a bad place, says Herr. Also, I really felt for his daughter. I know guilt so well, that poor girl.

Ewing says that the way hed set up the ropes is to blame for his daughters inability to brake the fall. Though she has returned to climbing at the gym and bouldering, she wasnt interested in rope climbing in the accidents aftermath, and Ewing worried that hed ruined the sporta passion theyd shared for yearsfor her.

Meanwhile, the gift Herr has given Ewing is exceptional. It might be the first time Herr is not the most technologically advanced lower-limb amputee. Herr often describes himself and others facing disabilities as astronauts testing new life-enabling technologies. As for his own legs, Herr wants to go even further but would need to leave the U.S. to undergo the operation he has in mind. Id love to do it, he says, without revealing any details about the procedure. Im just weighing the risk. I definitely dont want to go backwards.

In the short term, hes using a newly designed set of titanium legs and pushing forward on his work, noting hoped-for funding this year from the military to show we can synthetically take over a paralyzed limb. Herr then asks about my rehabilitation experience. This is finally my chance, I think, to ask if theres anything he can do for me.

I tell him that I identify with amputees and often wonder how some people without legs are more adept than some of us with them. Every time I watch a person with artificial legs walking, I selfishly wonder, Why not me? Why not us? Herr says they have some good ideas but acknowledges that the field has been way more successful in the amputation arena than with spinal-cord injuries. Its hard, he says.

While Herr has complete autonomy selecting projects in his lab, his interventions are rare, and they dont happen unless the time and circumstances are right. Often, people ask for help and I dont have the resources or the solution, he says. Exceptions like Haslet-Davis and Ewing come from feeling deeply about it and being in the position to make it happen.

I realize talking to Herr that its not my story thats weak, its the technology. Id incorrectly understood his comment about an imminent cure. Paralysis is lowhanging fruit in that its a condition they can impact in ten to twenty years instead of fifty. There are no toys to play with in Herrs lab closet. Not yet.

Before Herr and I wrap up our last visit, I ask what hed do if he were at an impasse. Its clear, at least to me, that Im talking about myself. Being a scientist, he focuses on process. He says he throws everything and anything at a problem. He visualizes each idea as a rock and starts turning them over. He mentions an acquaintance who came to see him earlier in the day who was struggling with depression. Herr started in, imagining at hyperspeed all the places the person might go and hadnt yet. Acupuncture? No? Meditation? No? Are you running? No? What medications have you tried? One? One! Theres like 20 antidepressants! Go, go, go! he says he wanted to plead. He chuckles at his overexuberance, but his belief is real. This can be solved!

When I say goodbye to Herr and watch him bound down from the upper level of the restaurant to the rain-drenched sidewalk, Im struck by a malaise. Maybe its the rain. Maybe its the opportunity lost. Maybe its the way he flipped a switch on his emPower ankle and raced effortlessly into the street. But then I think about Herr turning over one rock at a time and the span of possibilities he presented to help with depression. Im not out of options. There are hundreds of researchers working on a paralysis cure, and I immediately think of a world map I saw recently on a website with dozens of bright red circles representing centers of innovation. I can hear the words of my neurologist, who on my last visit leaned in with something else when he said goodbye. Keep moving, he urged. Theres even a clinic in New Hampshire I heard about where theyve produced exceptional walking recoveries using a robotic gait trainer available nowhere else in the U.S.

I begin to wonder, was Herrs story about his depressed acquaintance allegorical? An on-the-spot intervention? Had I just been, ever so lightly, smiled upon, too?

Longtime Outside contributor Todd Balf is the author of The Last River. Guido Vitti is anOutsidecontributing photographer.

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Press Release

Researchers at Ohio State University Wexner Medical Center uncovered a novel pathway for hair follicular regeneration. Palm tocotrienol complex (EVNol SupraBio) is shown to induce hair follicle growth via protein expression of epidermal E-cadherin dependent beta-catenin - the key signaling molecule for inducing pluripotent stem cells in the adult skin.

In this study (1), male mice with mutated leptin receptor were applied with either 5mg/cm2 palm tocotrienol rich fraction (TRF) (ie. EVNol SupraBio - bioenhanced palm tocotrienol complex, supplied by ExcelVite) or placebo on shaved dorsal skin thrice per week for 21 days and the evaluation of hair growth was recorded by the color of dorsal skin. The mechanism of palm TRF-induced hair growth, the dependency on the loss of E-cadherin and the activation of beta-catenin for hair follicle formation were examined by quantification of gene expressions, immunoprecipitation and immunoblots.

When compared to placebo, palm TRF treated group showed significantly increased number of anagen (ie. cycle of growth) hair follicles, increased fetal characteristics of hair follicular development in the adult skin, increased epidermal keratinocyte proliferation, significant decreased E-cadherin expression that was associated with high translocation of beta-catenin-Tf3, leading to upregulation of gene expressions of Oct4, Sox9, Klf4, c-Myc and Nanog skin-specific pluripotent factors that support hair follicular regeneration. These factors are also known as the Yamanaka Transcription Factors discovered by Dr. Shinya Yamanaka, joint-recipient of the 2012 Nobel Prize in Physiology or Medicine. Prof. Yamanaka discovered that mature cells can be reprogrammed to become pluripotent.

The researchers concluded that palm TRF suppression of epidermal E-cadherin induced beta-catenin and nuclear translocation is the novel pathway that leads to expressions of pluripotent factors and subsequently promotes anagen hair cycling in adult skin.

What we have shown is that Palm TRF can induce hair folliculogenesis, which means that it can enrich the skin stem cell reserves. This novel epidermal pathway of hair follicular regeneration can have widespread impact on skin function including skin aging and repair, says Prof. Chandan Sen, the lead researcher at Ohio State University Wexner Medical Center.

Prior to the above discovery, researchers from University Science Malaysia had reported and patented the unique benefits of tocotrienols (EVNol SupraBio) in supporting hair growth in subjects with on-going hair loss (2).

We are thrilled with this new discovery, especially this novel pathway that affirmed our previous clinical findings for EVNol SupraBio in hair growth, (US Patent No: 7,211,274; Trop. Life Sci. Res. 2010). Taken together this latest study and previous published papers explain the mechanism as to how EVNol SupraBio may help in promoting hair growth in subjects experiencing hair loss, says Bryan See, Business Development Manager, ExcelVite.

Source:

About ExcelVite

ExcelVite Sdn. Bhd., incorporated in Malaysia in 2013, is the leading and largest producer of natural full spectrum tocotrienol / tocopherol complex (EVNol, and EVNol SupraBio), natural mixed-carotene complex (EVTene), phytosterol complex (EVRol), and red palm oil concentrate (EVSpectra) in the world via a patented technology.

ExcelVite is the only tocotrienol producer that operates in accordance to GMP (PIC/S) Guide to Good Manufacturing Practice for Medicinal Products. Its laboratory is accredited with ISO/IEC 17025 accreditation.

EVNol SupraBio is a patented (US Patent No. 6,596,306) self-emulsifying palm tocotrienol complex that ensures optimal tocotrienols oral absorption.

ExcelVite manufactures and markets its products under the tradenames: EVNol, EVNol SupraBio, EVTene, EVRol, and EVSpectra. These branded ingredients are Non-GMO, Kosher and Halal certified. ExcelVite supports the production of certified sustainable palm oil (CSPO) through RSPO Credits.

Websites:www.excelvite.com andwww.tocotrienol.org

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Latest Research Unveiled Novel Pathway For T3 In Hair Follicle Regeneration - Natural Products INSIDER

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by David M. Panchision*

Diseases of the nervous system, including congenital disorders, cancers, and degenerative diseases, affect millions of people of all ages. Congenital disorders occur when the brain or spinal cord does not form correctly during development. Cancers of the nervous system result from the uncontrolled spread of aberrant cells. Degenerative diseases occur when the nervous system loses functioning of nerve cells. Most of the advances in stem cell research have been directed at treating degenerative diseases. While many treatments aim to limit the damage of these diseases, in some cases scientists believe that damage can be reversed by replacing lost cells with new ones derived from cells that can mature into nerve cells, called neural stem cells. Research that uses stem cells to treat nervous system disorders remains an area of great promise and challenge to demonstrate that cell-replacement therapy can restore lost function.

The nervous system is a complex organ made up of nerve cells (also called neurons) and glial cells, which surround and support neurons (see Figure 3.1). Neurons send signals that affect numerous functions including thought processes and movement. One type of glial cell, the oligodendrocyte, acts to speed up the signals of neurons that extend over long distances, such as in the spinal cord. The loss of any of these cell types may have catastrophic results on brain function.

Although reports dating back as early as the 1960s pointed towards the possibility that new nerve cells are formed in adult mammalian brains, this knowledge was not applied in the context of curing devastating brain diseases until the 1990s. While earlier medical research focused on limiting damage once it had occurred, in recent years researchers have been working hard to find out if the cells that can give rise to new neurons can be coaxed to restore brain function. New neurons in the adult brain arise from slowly-dividing cells that appear to be the remnants of stem cells that existed during fetal brain development. Since some of these adult cells still retain the ability to generate both neurons and glia, they are referred to as adult neural stem cells.

These findings are exciting because they suggest that the brain may contain a built-in mechanism to repair itself. Unfortunately, these new neurons are only generated in a few sites in the brain and turn into only a few specialized types of nerve cells. Although there are many different neuronal cell types in the brain, we now know that these new neurons can quot;plug inquot; correctly to assist brain function.1 The discovery of these cells has spurred further research into the characteristics of neural stem cells from the fetus and the adult, mostly using rodents and primates as model species. The hope is that these cells may be able to replenish those that are functionally lost in human degenerative diseases such as Parkinson's Disease, Huntington's Disease, and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease), as well as from brain and spinal cord injuries that result from stroke or trauma.

Scientists are applying these new stem cell discoveries in two ways in their experiments. First, they are using current knowledge of normal brain development to modulate stem cells that are harvested and grown in culture. Researchers can then transplant these cultured cells into the brain of an animal model and allow the brain's own signals to differentiate the stem cells into neurons or glia. Alternatively, the stem cells can be induced to differentiate into neurons and glia while in the culture dish, before being transplanted into the brain. Much progress has been made the last several years with human embryonic stem (ES) cells that can differentiate into all cell types in the body. While ES cells can be maintained in culture for relatively long periods of time without differentiating, they usually must be coaxed through many more steps of differentiation to produce the desired cell types. Recent studies, however, suggest that ES cells may differentiate into neurons in a more straightforward manner than may other cell types.

Figure 3.1. The NeuronWhen sufficient neurotransmitters cross synapses and bind receptors on the neuronal cell body and dendrites, the neuron sends an electrical signal down its axon to synaptic terminals, which in turn release neurotransmitters into the synapse that affects the following neuron. The brain neurons that die in Parkinson's Disease release the transmitter dopamine. Oligodendrocytes supply the axon with an insulating myelin sheath.

2001 Terese Winslow

Second, scientists are identifying growth (trophic) factors that are normally produced and used by the developing and adult brain. They are using these factors to minimize damage to the brain and to activate the patient's own stem cells to repair damage that has occurred. Each of these strategies is being aggressively pursued to identify the most effective treatments for degenerative diseases. Most of these studies have been carried out initially with animal stem cells and recipients to determine their likelihood of success. Still, much more research is necessary to develop stem cell therapies that will be useful for treating brain and spinal cord disease in the same way that hematopoietic stem cell therapies are routinely used for immune system replacement (see Chapter 2).

The majority of stem cell studies of neurological disease have used rats and mice, since these models are convenient to use and are well-characterized biologically. If preliminary studies with rodent stem cells are successful, scientists will attempt to transplant human stem cells into rodents. Studies may then be carried out in primates (e.g., monkeys) to offer insight into how humans might respond to neurological treatment. Human studies are rarely undertaken until these other experiments have shown promising results. While human transplant studies have been carried out for decades in the case of Parkinson's disease, animal research continues to provide improved strategies to generate an abundant supply of transplantable cells.

The intensive research aiming at curing Parkinson's disease with stem cells is a good example for the various strategies, successful results, and remaining challenges of stem cell-based brain repair. Parkinson's disease is a progressive disorder of motor control that affects roughly 2% of persons 65 years and older. Triggered by the death of neurons in a brain region called the substantia nigra, Parkinson's disease begins with minor tremors that progress to limb and bodily rigidity and difficulty initiating movement. These neurons connect via long axons to another region called the striatum, composed of subregions called the caudate nucleus and the putamen. These neurons that reach from the substantia nigra to the striatum release the chemical transmitter dopamine onto their target neurons in the striatum. One of dopamine's major roles is to regulate the nerves that control body movement. As these cells die, less dopamine is produced, leading to the movement difficulties characteristic of Parkinson's disease. Currently, the causes of death of these neurons are not well understood.

For many years, doctors have treated Parkinson's disease patients with the drug levodopa (L-dopa), which the brain converts into dopamine. Although the drug works well initially, levodopa eventually loses its effectiveness, and side-effects increase. Ultimately, many doctors and patients find themselves fighting a losing battle. For this reason, a huge effort is underway to develop new treatments, including growth factors that help the remaining dopamine neurons survive and transplantation procedures to replace those that have died.

The strategy to use new cells to replace lost ones is not new. Surgeons first attempted to transplant dopamine-releasing cells from a patient's own adrenal glands in the 1980s.2,3 Although one of these studies reported a dramatic improvement in the patients' conditions, U.S. surgeons were only able to achieve modest and temporary improvement, insufficient to outweigh the risks of such a procedure. As a result, these human studies were not pursued further.

Another strategy was attempted in the 1970s, in which cells derived from fetal tissue from the mouse substantia nigra was transplanted into the adult rat eye and found to develop into mature dopamine neurons.4 In the 1980s, several groups showed that transplantation of this type of tissue could reverse Parkinson's-like symptoms in rats and monkeys when placed in the damaged areas.The success of the animal studies led to several human trials beginning in the mid-1980s.5,6 In some cases, patients showed a lessening of their symptoms. Also, researchers could measure an increase in dopamine neuron function in the striatum of these patients by using a brain-imaging method called positron emission tomography (PET) (see Figure 3.2).7

The NIH has funded two large and well-controlled clinical trials in the past 15 years in which researchers transplanted tissue from aborted fetuses into the striatum of patients with Parkinson's disease.7,8 These studies, performed in Colorado and New York, included controls where patients received quot;shamquot; surgery (no tissue was implanted), and neither the patients nor the scientists who evaluated their progress knew which patients received the implants. The patients' progress was followed for up to eight years. Unfortunately, both studies showed that the transplants offered little benefit to the patients as a group. While some patients showed improvement, others began to suffer from dyskinesias, jerky involuntary movements that are often side effects of long-term L-dopa treatment. This effect occurred in 15% of the patients in the Colorado study.7 and more than half of the patients in the New York study.8 Additionally, the New York study showed evidence that some patients' immune systems were attacking the grafts.

However, promising findings emerged from these studies as well. Younger and milder Parkinson's patients responded relatively well to the grafts, and PET scans of patients showed that some of the transplanted dopamine neurons survived and matured. Additionally, autopsies on three patients who died of unrelated causes, years after the surgeries, indicated the presence of dopamine neurons from the graft. These cells appeared to have matured in the same way as normal dopamine neurons, which suggested that they were acting normally in the brain.

Figure 3.2. Positron Emission Tomography (PET) images from a Parkinson's patient before and after fetal tissue transplantation. The image taken before surgery (left) shows uptake of a radioactive form of dopamine (red) only in the caudate nucleus, indicating that dopamine neurons have degenerated. Twelve months after surgery, an image from the same patient (right) reveals increased dopamine function, especially in the putamen. (Reprinted with permission from N Eng J Med 2001;344(10) p. 710.)

Researchers in Sweden followed the severity of dyskinesia in patients for eleven years after neural transplantation and found that the severity was typically mild or moderate. These results suggested that dyskinesias were due to effects that were distinct from the beneficial effects of the grafts.9 Dyskinesias may therefore be related to the ways that transplantation disturbs other cells in the brain and so may be minimized by future improvements in therapy. Another study that involved the grafting of cells both into the striatum (the target of dopamine neurons) and the substantia nigra (where dopamine neurons normally reside) of three patients showed no adverse effects and some modest improvement in patient movement.10 To determine the full extent of therapeutic benefits from such a procedure and confirm the reliability of these results, this study will need to be repeated with a larger patient population that includes the appropriate controls.

The limited success of these studies may reflect variations in the fetal tissue used for transplantation, which is of limited quantity and can not be standardized or well-characterized. The full complement of cells in these fetal tissue samples is not known at present. As a result, the tissue remains the greatest source of uncertainty in patient outcome following transplantation.

The major goal for Parkinson's investigators is to generate a source of cells that can be grown in large supply, maintained indefinitely in the laboratory, and differentiated efficiently into dopamine neurons that work when transplanted into the brain of a Parkinson's patient. Scientists have investigated the behavior of stem cells in culture and the mechanisms that govern dopamine neuron production during development in their attempts to identify optimal culture conditions that allow stem cells to turn into dopamine-producing neurons.

Preliminary studies have been carried out using immature stem cell-like precursors from the rodent ventral midbrain, the region that normally gives rise to these dopamine neurons. In one study these precursors were turned into functional dopamine neurons, which were then grafted into rats previously treated with 6-hydroxy-dopamine (6-OHDA) to kill the dopamine neurons in their substantia nigra and induce Parkinson's-like symptoms. Even though the percentage of surviving dopamine neurons was low following transplantation, it was sufficient to relieve the Parkinson's-like symptoms.11 Unfortunately, these fetal cells cannot be maintained in culture for very long before they lose the ability to differentiate into dopamine neurons.

Cells with features of neural stem cells have been derived from ES-cells, fetal brain tissue, brain tissue from neurosurgery, and brain tissue that was obtained after a person's death. There is controversy about whether other organ stem cell populations, such as hematopoietic stem cells, either contain or give rise to neural stem cells

Many researchers believe that the more primitive ES cells may be an excellent source of dopamine neurons because ES-cells can be grown indefinitely in a laboratory dish and can differentiate into any cell type, even after long periods in culture. Mouse ES cells injected directly into 6-OHDA-treated rat brains led to relief of Parkinson-like symptoms. Further investigation showed that these ES cells had differentiated into both dopamine and serotonin neurons.12 This latter type of neuron is generated in an adjacent region of the brain and may complicate the response to transplantation. Since ES cells can generate all cell types in the body, unwanted cell types such as muscle or bone could theoretically also be introduced into the brain. As a result, a great deal of effort is being currently put into finding the right quot;recipequot; for turning ES cells into dopamine neuronsand only this cell typeto treat Parkinson's disease. Researchers strive to learn more about normal brain development to help emulate the natural progression of ES cells toward dopamine neurons in the culture dish.

The recent availability of human ES cells has led to further studies to examine their potential for differentiation into dopamine neurons. Recently, dopamine neurons from human embryonic stem cells have been generated.13 One research group used a special type of companion cell, along with specific growth factors, to promote the differentiation of the ES cells through several stages into dopamine neurons. These neurons showed many of the characteristic properties of normal dopamine neurons.13 Furthermore, recent evidence of more direct neuronal differentiation methods from mouse ES cells fuels hope that scientists can refine and streamline the production of transplantable human dopamine neurons.

One method with great therapeutic potential is nuclear transfer. This method fuses the genetic material from one individual donor with a recipient egg cell that has had its nucleus removed. The early embryo that develops from this fusion is a genetic match for the donor. This process is sometimes called quot;therapeutic cloningquot; and is regarded by some to be ethically questionable. However, mouse ES cells have been differentiated successfully in this way into dopamine neurons that corrected Parkinsonian symptoms when transplanted into 6-OHDA-treated rats.14 Similar results have been obtained using parthenogenetic primate stem cells, which are cells that are genetic matches from a female donor with no contribution from a male donor.15 These approaches may offer the possibility of treating patients with genetically-matched cells, thereby eliminating the possibility of graft rejection.

Scientists are also studying the possibility that the brain may be able to repair itself with therapeutic support. This avenue of study is in its early stages but may involve administering drugs that stimulate the birth of new neurons from the brain's own stem cells. The concept is based on research showing that new nerve cells are born in the adult brains of humans. The phenomenon occurs in a brain region called the dentate gyrus of the hippocampus. While it is not yet clear how these new neurons contribute to normal brain function, their presence suggests that stem cells in the adult brain may have the potential to re-wire dysfunctional neuronal circuitry.

The adult brain's capacity for self-repair has been studied by investigating how the adult rat brain responds to transforming growth factor alpha (TGF), a protein important for early brain development that is expressed in limited quantities in adults.16 Injection of TGF into a healthy rat brain causes stem cells to divide for several days before ceasing division. In 6-OHDAtreated (Parkinsonian) rats, however, the cells proliferated and migrated to the damaged areas. Surprisingly, the TGF-treated rats showed few of the behavioral problems associated with untreated Parkinsonian rats.16 Additionally, in 2002 and 2003, two research groups isolated small numbers of dividing cells in the substantia nigra of adult rodents.17,18

These findings suggest that the brain can repair itself, as long as the repair process is triggered sufficiently. It is not clear, though, whether stem cells are responsible for this repair or if the TGF activates a different repair mechanism.

Many other diseases that affect the nervous system hold the potential for being treated with stem cells. Experimental therapies for chronic diseases of the nervous system, such as Alzheimer's disease, Lou Gehrig's disease, or Huntington's disease, and for acute injuries, such as spinal cord and brain trauma or stoke, are being currently developed and tested. These diverse disorders must be investigated within the contexts of their unique disease processes and treated accordingly with highly adapted cell-based approaches.

Although severe spinal cord injury is an area of intense research, the therapeutic targets are not as clear-cut as in Parkinson's disease. Spinal cord trauma destroys numerous cell types, including the neurons that carry messages between the brain and the rest of the body. In many spinal injuries, the cord is not actually severed, and at least some of the signal-carrying neuronal axons remain intact. However, the surviving axons no longer carry messages because oligodendrocytes, which make the axons' insulating myelin sheath, are lost. Researchers have recently made progress to replenish these lost myelin-producing cells. In one study, scientists cultured human ES cells through several steps to make mixed cultures that contained oligodendrocytes. When they injected these cells into the spinal cords of chemically-demyelinated rats, the treated rats regained limited use of their hind limbs compared with un-grafted rats.19 Researchers are not certain, however, whether the limited increase in function observed in rats is actually due to the remyelination or to an unidentified trophic effect of the treatment.

Getting neurons to grow new axons through the injury site to reconnect with their targets is even more challenging. While myelin promotes normal neuronal function, it also inhibits the growth of new axons following spinal injury. In a recent study to attempt post-trauma axonal growth, Harper and colleagues treated ES cells with a combination of factors that are known to promote motor neuron differentiation.20 The researchers then transplanted these cells into adult rats that had received spinal cord injuries. While many of these cells survived and differentiated into neurons, they did not send out axons unless the researchers also added drugs that interfered with the inhibitory effects of myelin. The growth effect was modest, and the researchers have not yet seen evidence of functional neuron connections. However, their results raise the possibility that signals can be turned on and off in the correct order to allow neurons to reconnect and function properly. Spinal injury researchers emphasize that additional basic and preclinical research must be completed before attempting human trials using stem cell therapies to repair the trauma-damaged nervous system.

Since myelin loss is at the heart of many other degenerative diseases, oligodendrocytes made from ES cells may be useful to treat these conditions as well. For example, scientists recently cultured human ES cells with a combination of growth factors to generate a highly enriched population of myelinating oligodendrocyte precursors.21,22 The researchers then tested these cells in a genetically-mutated mouse that does not produce myelin properly. When the growth factor-cultured ES cells were transplanted into affected mice, the cells migrated and differentiated into mature oligodendrocytes that made myelin sheaths around neighboring axons. These researchers subsequently showed that these cells matured and improved movement when grafted in rats with spinal cord injury.23 Improved movement only occurred when grafting was completed soon after injury, suggesting that some post-injury responses may interfere with the grafted cells. However, these results are sufficiently encouraging to plan clinical trials to test whether replacement of myelinating glia can treat spinal cord injury.

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is characterized by a progressive destruction of motor neurons in the spinal cord. Patients with ALS develop increasing muscle weakness over time, which ultimately leads to paralysis and death. The cause of ALS is largely unknown, and there are no effective treatments. Researchers recently have used different sources of stem cells to test in rat models of ALS to test for possible nerve cell-restoring properties. In one study, researchers injected cell clusters made from embryonic germ (EG) cells into the spinal cord fluid of the partially-paralyzed rats.24 Three months after the injections, many of the treated rats were able to move their hind limbs and walk with difficulty, while the rats that did not receive cell injections remained paralyzed. Moreover, the transplanted cells had migrated throughout the spinal fluid and developed into cells that displayed molecular characteristics of mature motor neurons. However, too few cells matured in this way to account for the recovery, and there was no evidence that the transplanted cells formed functional connections with muscles. The researchers suggest that the transplanted cells may be promoting recovery in some other way, such as by producing trophic factors.

This possibility was addressed in a second study in which scientists grew human fetal CNS stem cells in culture and genetically modified them to produce a trophic factor that promotes the survival of cells that are lost in ALS. When grafted into the spinal cords of the ALS-like rats, these cells secreted the desired growth factor and promoted the survival of the neurons that are normally lost in the ALS-like rats.25 While promising, these results highlight the need for additional basic research into functional recovery in ALS disease models.

Stroke affects about 750,000 patients per year in the

U.S. and is the most common cause of disability in adults. A stroke occurs when blood flow to the brain is disrupted. As a consequence, cells in affected brain regions die from insufficient amounts of oxygen. The treatment of stroke with anti-clotting drugs has dramatically improved the odds of patient recovery. However, in many patients the damage cannot be prevented, and the patient may permanently lose the functions of affected areas of the brain. For these patients, researchers are now considering stem cells as a way to repair the damaged brain regions. This problem is made more challenging because the damage in stroke may be widespread and may affect many cell types and connections.

However, researchers from Sweden recently observed that strokes in rats cause the brain's own stem cells to divide and give rise to new neurons.26 However, these neurons, which survived only a couple of weeks, are few in number compared to the extent of damage caused. A group from the University of Tokyo added a growth factor, bFGF, into the brains of rats after stroke and showed that the hippocampus was able to generate large numbers of new neurons.27 The researchers found evidence that these new neurons were actually making connections with other neurons. These and other results suggest that future stroke treatments may be able to coax the brain's own stem cells to make replacement neurons.

Taking an alternative approach, another group attempted transplantation as a means to treat the loss of brain mass after a severe stroke. By adding stem cells onto a polymer scaffold that they implanted into the stroke-damaged brains of mice, the researchers demonstrated that the seeded stem cells differentiated into neurons and that the polymer scaffold reduced scarring.28 Two groups transplanted human fetal stem cells in independent studies into the brains of stroke-affected rodents; these stem cells not only survived but migrated to the damaged areas of the brain.29,30 These studies increase our knowledge of how stem cells are attracted to diseased areas of the brain.

There is also increasing evidence from numerous animal disease models that stem cells are actively drawn to brain damage. Once they reach these damaged areas, they have been shown to exert beneficial effects such as reducing brain inflammation or supporting nerve cells. It is hoped that, once these mechanisms are better understood, this stem cell recruitment can potentially be exploited to mobilize a patient's own stem cells.

Similar lines of research are being considered with other disorders such as Huntington's Disease and certain congenital defects. While much attention has been called to the treatment of Alzheimer's Disease, it is still not clear if stem cells hold the key to its treatment. But despite the fact that much basic work remains and many fundamental questions are yet to be answered, researchers are hopeful that repair for once-incurable nervous system disorders may be amenable to stem cell based therapies.

Considerable progress has been made the last few years in our understanding of stem cell biology and devising sources of cells for transplantation. New methods are also being developed for cell delivery and targeting to affected areas of the body. These advances have fueled optimism that new treatments will come for millions of persons who suffer from neurological disorders. But it is the current task of scientists to bring these methods from the laboratory bench to the clinic in a scientifically sound and ethically acceptable fashion.

Notes:

* Chief, Developmental Neurobiology Program, Molecular, Cellular & Genomic Neuroscience Research Branch, Division of Neuroscience and Basic Behavioral Science, National Institute of Mental Health, National Institutes of Health, Email: panchisiond@mail.nih.gov

Chapter 2|Table of Contents|Chapter 4

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Repairing the Nervous System with Stem Cells | stemcells ...

Spinal Cord Stem Cells Comments Off on Repairing the Nervous System with Stem Cells | stemcells … | September 5th, 2017

iPSCells Represent a Superior Approach

iPS cell-derived cardiomyocyte patch demonstrates spontaneous and synchronized contractions after 4 days in culture.

One of the greatest promises of human stem cells is to transform these early-stage cells into treatments for devastating diseases. Stem cells can potentially be used to repair damaged human tissues and to bioengineer transplantable human organs using various technologies, such as 3D printing. Using stem cells derived from another person (allogeneic transplantation) or from the patient (autologous transplantation), research efforts are underway to develop new therapies for historically difficult to treat conditions. In the past, adult stem and progenitor cells were used, but the differentiation of these cell types has proven to be difficult to control. Initial clinical trials using induced pluripotent stem (iPS) cells indicate that they are far superior for cellular therapy applications because they are better suited to scientific manipulation.

CDIs iPS cell-derived iCell and MyCell products are integral to the development of a range ofcell therapyapplications. A study using iCell Cardiomyocytesas part of a cardiac patch designed to treat heart failure is now underway. This tissue-engineered implantable patch mayemerge as apotential myocardial regeneration treatment.

Another study done with iPS cell-derived cells and kidney structures has marked an important first step towards regenerating, and eventually transplanting, a functioning human organ. In this work, iCell Endothelial Cellswere used to help to recapitulatethe blood supply of a laboratory-generated kidney scaffold. This type of outcome will be crucial for circulation and nutrient distribution in any rebuilt organ.

iCell Endothelial Cells revascularize kidney tissue. (Data courtesy of Dr. Jason Wertheim, Northwestern University)

CDI and its partners are leveraging iPS cell-derived human retinal pigment epithelial (RPE) cells to develop and manufacture autologous treatments for dry age-related macular degeneration (AMD). The mature RPE cells will be derivedfrom the patients own blood cells using CDIs MyCell process. Ifapproved by the FDA, this autologous cellular therapy wouldbe one of the first of its kind in the U.S.

Learn more about the technologybehind the development of these iPScell-derived cellular therapies.

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Cellular Therapy - The World Leader in Stem Cell Technology

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