CAMBRIDGE, Mass., July 22, 2022 (GLOBE NEWSWIRE) -- Mersana Therapeutics, Inc. (NASDAQ: MRSN), a clinical-stage biopharmaceutical company focused on discovering and developing a pipeline of antibody-drug conjugates (ADCs) targeting cancers in areas of high unmet medical need, today announced that its Senior Vice President and Chief People Officer, Carla Poulson, has been named one of Savoy Magazine’s 2022 Most Influential Black Executives in Corporate America.

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Mersana Therapeutics Chief People Officer Carla Poulson Named One of Savoy Magazine’s 2022 Most Influential Black Executives in Corporate America

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NEW YORK, July 22, 2022 (GLOBE NEWSWIRE) -- Fairway Consulting Group (FCG), a leading recruiting firm focused on providing outstanding talent solutions for the pharmaceutical, biotechnology, diagnostic, and medical device industries, today announced the Company is expanding amid continued growth. In the past 8 years, FCG has nearly tripled its annual placements.

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Fairway Consulting Group Announces Expansion Amid Growth

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New York, NY, and Tel Aviv, ISRAEL, July 22, 2022 (GLOBE NEWSWIRE) -- via NewMediaWire -- Todos Medical, Ltd. (OTCQB: TOMDF), a comprehensive medical diagnostics and related solutions company, today announced that its majority-owned joint venture 3CL Pharma Ltd. reported the preprint in ResearchGate of case study #8 entitled “A Case Review: Effects of 3CL Protease Inhibitors Paxlovid® and Tollovid™ in a Patient with Chronic Long COVID” overseen by Dr. Lee Morgentaler in concert with Andrew A. Blumenthal, RN ADS of a patient who was experiencing symptoms of Post-Acute Sequelae of COVID (PASC, or “Long COVID”) for 27 months and experienced benefit with a 5-day course of Paxlovid® treatment followed by over 30 days of supplementation with 3CL protease inhibitor immune support dietary supplement Tollovid™. The pre-publication can be viewed at: https://www.researchgate.net/publication/362174359_3CL_Protease_Inhibitors_IN_Chronic_Long_Covid_A_Case_Review_Effects_of_3CL_Protease_Inhibitors_PaxlovidR_and_Tollovid_in_a_Patient_with_Chronic_Long_Covid.

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Todos Medical Announces Preprint of Chronic Long COVID Case Study #8 of Paxlovid® Treatment Followed by Tollovid™  Dietary Supplementation

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Conference Call to be held Wednesday July 27, at 9:00am Eastern Time Conference Call to be held Wednesday July 27, at 9:00am Eastern Time

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Alimera Sciences to Report Second Quarter 2022 Financial Results on Wednesday, July 27, 2022, and Provide Corporate Update

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Underwriters’ full exercise of option brings gross proceeds to $264.5 million Underwriters’ full exercise of option brings gross proceeds to $264.5 million

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Revolution Medicines Announces Closing of Upsized Public Offering of Common Stock and Full Exercise of Underwriters' Option to Purchase Additional...

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EDISON, N.J., July 22, 2022 (GLOBE NEWSWIRE) -- Hepion Pharmaceuticals, Inc. (NASDAQ:HEPA), a clinical mid-stage biopharmaceutical company focused on Artificial Intelligence (“AI”)-driven therapeutic drug development for the treatment of non-alcoholic steatohepatitis (“NASH”) and hepatocellular carcinoma (“HCC”), announced today that its 2022 annual meeting of stockholders (the “Annual Meeting”) has been further adjourned to Friday, August 5, 2022 at 9:00 a.m. Eastern Time with respect to Proposal 4 (Authorized Share Increase), as described in Hepion’s definitive proxy statement filed with the U.S. Securities and Exchange Commission (the “SEC”) on April 29, 2022 (the “Proxy Statement”).

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Hepion Pharmaceuticals Announces Further Adjournment of Annual Meeting of Stockholders

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ORLANDO, FL, July 22, 2022 (GLOBE NEWSWIRE) -- Immune Therapeutics, Inc. (OTC Pink: IMUN) (“Immune” or “IMUN”), a specialty pharmaceutical company involved in the acquisition, development and commercialization of pharmaceutical and biotechnology products that have a short and well-defined path to market, is pleased to announce the appointment of Dr. Stephen “Steve” Wilson as Immune’s Chief Executive Officer (CEO), President, and interim Chief Financial Officer (CFO) effective July 19, 2022; he will continue to serve as a member of the Company’s Board of Directors.

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Immune Therapeutics, Inc. Appoints Dr. Stephen Wilson as Chief Executive Officer

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SAN DIEGO, July 22, 2022 (GLOBE NEWSWIRE) -- Revelation Biosciences Inc. (NASDAQ: REVB) (the “Company” or “Revelation”), a clinical-stage life sciences company that is focused on the development of immunologic?based therapies for the prevention and treatment of disease, today announced topline data for its Phase 1b CLEAR clinical study to evaluate the effect of intranasal REVTx-99b on nasal challenge allergen in participants with allergic rhinitis to rye grass pollen.

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Revelation Biosciences Inc. Announces Topline Data for Phase 1b CLEAR Clinical Study of REVTx-99b for the Treatment of Allergic Rhinitis

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HAIFA, Israel, July 25, 2022 (GLOBE NEWSWIRE) -- Pluri Inc. (Nasdaq: PLUR) (TASE: PLUR) (“Pluri” or the “Company”), a leading biotechnology company, today announced its name change (from Pluristem Therapeutics Inc. Nasdaq: PSTI), reflecting a broader strategy of leveraging its 3D cell expansion technology to develop innovative cell-based products that can be harnessed for a range of fields beyond medicine, providing solutions for various areas of the life sciences. As of July 26, 2022, Pluri will begin trading on Nasdaq under the new ticker symbol “PLUR,” CUSIP number 72942G 104.

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Pluristem Therapeutics Inc. Changes its Name to “Pluri Inc.” Reflecting the Company’s Strategy to Leverage its Innovative 3D Cell-based...

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Basel, July 25, 2022 – Sandoz, a global leader in generic and biosimilar medicines, announced today that the US Food and Drug Administration (FDA) has accepted its biologics license application (BLA) for a proposed first-of-a-kind biosimilar natalizumab, developed by Polpharma Biologics.

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Applications for proposed first-of-a-kind multiple sclerosis biosimilar natalizumab accepted by US FDA and EMA

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COPENHAGEN, Denmark, July 25, 2022 – Bavarian Nordic A/S (OMX: BAVA) announced today that the European Commission (EC) has extended the marketing authorization for the Company’s smallpox vaccine, IMVANEX® to include protection from monkeypox and disease caused by vaccinia virus. The approval, which follows a positive opinion by the Committee for Medicinal Products for Human Use (CHMP) on July 22, 2022, is valid in all European Union Member States as well as in Iceland, Liechtenstein, and Norway.

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Bavarian Nordic Receives European Approval of Extension of Vaccine Label to Include Monkeypox

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Global Stem Cell ManufacturingMarket Is Expected To Reach USD 21.71 Billion By 2029 At A CAGR Of 9.1 percent.

Maximize Market Research has published a report on theGlobal Stem Cell Manufacturing Marketthat provides a detailed analysis for the forecast period of 2022 to 2029.

Global Stem Cell ManufacturingMarket Scope:

The report provides comprehensive market insights for industry stakeholders, including an explanation of complicated market data in simple language, the industrys history and present situation, as well as expected market size and trends. The research investigates all industry categories, with an emphasis on key companies such as market leaders, followers, and new entrants. The paper includes a full PESTLE analysis for each country. A thorough picture of the competitive landscape of major competitors in theGlobal Stem Cell Manufacturingmarket by goods and services, revenue, financial situation, portfolio, growth plans, and geographical presence makes the study an investors guide.

Request Free Sample:@https://www.maximizemarketresearch.com/request-sample/73762

Global Stem Cell Manufacturing Market Overview:

Observing stem cells evolve into cells in bones, the circulatory system, nerve cells, and other organs of the body may help scientists understand how illnesses and disorders occur. Stem cells can be programmed to generate particular cells that can be utilized in humans to grow and mend tissues that have been damaged or harmed by sickness. Stem cell therapy may assist people with spinal cord injuries, metabolic disorders, Parkinsons disease, amyotrophic lateral sclerosis, Alzheimers disease, cardiovascular disorders, brain hemorrhage, burns, malignancy, and rheumatoid arthritis. Stem cells can be used to create new tissue for transplant and genetic engineering. Doctors are always learning more about stem cells and how they might be used in transplant and cellular therapies.

Global Stem Cell ManufacturingMarketDynamics:

Stem cells are crucial in illness treatment and specialized research initiatives such as customized therapy and genetic testing. As public and commercial stakeholders throughout the world become more aware of stem cells therapeutic potential and the scarcity of therapeutic approaches for rare illnesses, they are increasingly focusing on the development of stem cell-based technology.

Specialized procedures are required for stem cell separation, refinement, and storage (such as expansion, differentiation, cell culture media preparation, and cryopreservation). Additionally, the production scale-up of stem cell lines and associated items is frequently accompanied by major technological challenges that impede the whole production process and result in large operational expenses. As a result, stem cell products are frequently more expensive than pharmaceutical medications and biopharmaceuticals.

Additionally, the growing popularity of tailored medications is driving the market growth. Scientists are researching novel procurement strategies that can be used to manufacture tailored medications. For example, iPSC treatments are created by taking a little amount of a patients plasma or skin cells and reprogramming them to make new cells and tissue for transplant. As a result, future tailored treatments can be produced using these cells.

Global Stem Cell ManufacturingMarketRegional Insights:

North America (particularly the United States) held the largest market share in 2021, owing to factors such as the availability of significant contenders active in creating stem cell treatments, enhanced medical facilities, significant R&D financial backing available, and favorable initiatives from healthcare organizations, as well as robust reimbursement. Because of government initiatives and serious scientific activity in the country, the United States leads the continentsGlobal Stem Cell Manufacturingmarket.

Healthcare organizations are promoting cellular therapies for rising ailments. Due to higher advancement of stem cell-based treatments, federal actions for creating regenerative medications, the creation of multiple stem cell banks, and the continents increasing clinical studies for genetic manipulation and medical technology, the APACGlobal Stem Cell Manufacturingmarket is expected to grow at the fastest rate during the forecast period.

Global Stem Cell ManufacturingMarketSegmentation:

By Product:

By Application:

By Technology:

By Therapy:

Global Stem Cell ManufacturingMarket Key Competitors:

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Maximize Market Research is a multifaceted market research and consulting company with professionals from several industries. Some of the industries we cover include medical devices, pharmaceutical manufacturers, science and engineering, electronic components, industrial equipment, technology and communication, cars and automobiles, chemical products and substances, general merchandise, beverages, personal care, and automated systems. To mention a few, we provide market-verified industry estimations, technical trend analysis, crucial market research, strategic advice, competition analysis, production and demand analysis, and client impact studies.

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Global Stem Cell Manufacturing Market Value Projected To Reach USD 21.71 Billion By 2029, Registering A CAGR Of 9.1% - Digital Journal

Spinal Cord Stem Cells Comments Off on Global Stem Cell Manufacturing Market Value Projected To Reach USD 21.71 Billion By 2029, Registering A CAGR Of 9.1% – Digital Journal | July 16th, 2022

After a meeting like the 2022 ASCO Annual Meeting, one cannot help but be reinvigorated to continue advancing cancer care and feel optimistic about the future of oncology, says John M. Burke, MD.

After seeing all the amazing presentations at the American Society of Oncology (ASCO) Annual Meeting, I cannot help but reflect on how far our field has come over the course of my 20-year career.

In 2000, I moved from San Francisco, California, to New York, New York, to begin my fellowship at Memorial Sloan Kettering Cancer Center. My first rotation was on the inpatient myeloma, lymphoma, and autologous stem cell transplant service, where I encountered patients with myeloma and painful bone lesions causing fractures and spinal cord compressions. We treated patients with myeloma with chemotherapy and autologous stem cell transplant. Thalidomide (Thalomid) was starting to make a splash by showing strong efficacy in myeloma trials, and bortezomib (Velcade) emerged during those years, as well.

Nevertheless, the state of the art was exemplified by an article in the New England Journal of Medicine in 2003, describing the results of an Intergroupe Francophone du Mylome (IFM) trial. Myeloma patients were treated with vincristine, doxorubicin, and dexamethasone induction followed by single or double autologous stem cell transplant. The median event-free survival was 2 years and the median overall survival was 4 years, which seem grim by modern standards.

Fast forward about 20 years to the Plenary Session of the 2022 ASCO Annual Meeting, at which we saw the results of modern therapy in the DETERMINATION trial (NCT01208662). Patients treated with the modern standard regimen of lenalidomide (Revlimid), bortezomib, and dexamethasone followed by autologous stem cell transplant achieved a median progression-free survival of 5.5 years. In the IFM trial 20 years ago, approximately 50% of patients were alive at 4 years. In DETERMINATION, 85% of patients were alive at 4 years. Weve come a long way.

DETERMINATION represents only an infinitesimal fraction of the degree of innovation demonstrated at the ASCO meeting: an antibody-drug conjugate besting conventional chemotherapy in patients with low expression of the HER2 target in breast cancer; a KRAS inhibitor demonstrating marked activity in KRAS-mutated nonsmall cell lung cancer; a bispecific antibody redirecting T cells to suppress diffuse large B-cell lymphoma; an antibody-drug conjugate added to chemotherapy, extending survival in Hodgkin lymphoma compared with the decades-old standard-of-care regimen; and a checkpoint inhibitor rendering mismatch repairdeficient rectal cancer completely helpless.

After a meeting like this, one cannot help but be reinvigorated to continue advancing cancer care and feel optimistic about the future of oncology. We have a lot of progress to celebrateand a lot more to accomplish.

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Innovative Therapies, Care Equity Highlight 2022 ASCO Annual Meeting - Targeted Oncology

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The Seoul National University Hospital (SNUH) said its research team has opened a way to raise bone marrow's success rate drastically.

The team has discovered a special macrophage that allows mass-producing top hematopoietic stem cells (HSCs) for the first time globally. By making the most of this special macrophage, we expect to mass-produce the youngest HSCs that are also most capable of differentiating, it said.

Bone marrow (HSC) transplantation is an important treatment that provides blood cancer patients with a chance to be cured. Medical professionals can also expand the techniques indications to treat blood diseases, such as dysplastic anemia, bone marrow dysplasia syndrome, lymphoma, multiple myeloma, complex immunodeficiency, and autoimmune diseases.

A technique is needed to amplify top HSCs to improve bone marrow transplantations efficiency, but it remains in its infancy. In addition, cells that maintain homeostasis by controlling the dormancy and proliferation of HSCs are also difficult to prove.

A joint research team of Ludwig-Maximilian University in Germany, Queen Mary University in the U.K., and Harvard University in the U.S. has claimed that red blood cells expressing large amounts of the DARC (ACKR1) protein were crucial in maintaining the homeostasis of HSCs, which, however, has failed to be proven objectively.

The SNUH team, led by Professors Kim Hyo-soo and Kwon Yoo-wook, researched key cells and the mechanisms responsible for controlling HSC homeostasis and found a few macrophages expressing triple protein markers (SMA, COX2, DARC) can maintain homeostasis of top HSCs.

When the DARC-Kai1 protein bond is dissolved, hematopoietic stem cells begin to increase, resulting in mass production of blood cells and vice versa when the macrophages DARC protein and the HSCs Kai1 protein combine. Subsequently, if this bonding is controlled, the researchers expect a culture method that mass-produces top HSCs with excellent hematopoietic function can be developed.

This mechanism can also be used to develop treatments for bone marrow dysfunction, such as leukemia and malignant anemia, and increase the success rate of bone marrow transplants.

"If a method is commercialized to mass-produce and store top HSCs while maintaining their youthfulness, it will be possible to develop a customized treatment that can quickly help patients needing a bone marrow transplant," Professor Kim said.

This study was published in the Cell Stem Cell journal.

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SNUH team finds a key cell that keeps top hematopoietic stem cells young - KBR

Bone Marrow Stem Cells Comments Off on SNUH team finds a key cell that keeps top hematopoietic stem cells young – KBR | July 16th, 2022

Introduction

Traumatic brain injury is one of the main causes of deaths, disabilities, and hospitalization in the world. In the USA, around 30% of all injury-related deaths are due to traumatic brain injury.1 Globally, traumatic brain injury affects the lives of about 10 million people each year.2 It happened as the brain tissue is damaged by an external force, the result of direct impact, rapid acceleration or deceleration, a piercing object, and blast waves from an explosion.3 Visual impairment, cognitive dysfunction, hearing loss, and mental health disorders are among the most common complications affecting traumatic brain injury patients and their families. The pathophysiology of traumatic brain injury is not clear since the structure of the brain is complex with many cell types such as neurons, astrocytes, oligodendrocytes, microglia, and multiple subtypes of these cells. Traumatic brain injury occurs in two phases. These are primary (acute) and secondary (late) brain injuries. The primary injury is the initial blow to the head; in this phase, brain tissue and cells such as neurons, glial cells, endothelial cells, and the bloodbrain barrier are damaged by mechanical injury. The secondary injury occurs after primary injury and in these late phases, several toxins are released from the injured cells leading to the formation of cytotoxic cascades, which increase the initial brain damage.4 The primary brain injury causes the dysfunction of the bloodbrain barrier and initiates local inflammation and secondary neuronal injury. In addition, severe and long-term inflammation causes severe neurodegenerative and inflammatory diseases. Repairing of tissue damage needs the inhibition of secondary injury and rapid regeneration of injured tissue.5 Depending on the nature of the injury, neurons and neuroglial cells may be damaged; excessive bleeding may happen, axons may be destroyed and a contusion may occur.6 Moreover, the pathogenesis of traumatic brain injury involves bloodbrain barrier damage, neural inflammation, and diffuse neuronal degeneration.7 Unlike other organs, it has long been thought that mature brain tissue cannot be able to repair itself after injury.8 However, the current research indicated that multipotent neural stem/progenitor cells are residing in some areas of the brain throughout the lifespan of an animal, implying the mature brains ability to produce new neurons and neuroglial cells.9 In the previous decades, several studies have shown that the mature neurons in the hippocampal dentate gyrus of the brain play significant roles in hippocampal-induced learning and memory activities,9 while new olfactory interneurons produced from the subventricular zone are essential for the appropriate functioning of the olfactory bulb network and some specific olfactory behaviors.10 After traumatic brain injuries, clinical evidence indicated that endogenous neural progenitor cells might play an important role in regenerative medicine to treat brain injury because an increased neurogenic regeneration ability has been reported in different types of brain injury models of animal and human studies.11 Nowadays, there is a new therapeutic approach for traumatic brain injury that involves the use of stem cells for neural regeneration and restoration. Exogenous stem cell transplantation has been found to accelerate immature neuronal development and increase endogenous cellular proliferation in the damaged brain region.12 A better understanding of the endogenous neural stem cells regenerative ability as well as the effect of exogenous neural stem cells on proliferation and differentiation may help researchers better understand how to increase functional recovery and brain tissue repair following injury. Therefore, in this study, we discussed the therapeutic effects of stem cells in the repair of traumatic brain injury.

Traumatic brain injury causes severe stress on the brain, making it extremely hard to keep appropriate cognitive abilities. Even though many organs in the body, for example, the skin, can regenerate following injury, the brain tissue may not easily repair. In the adult brain, endogenous neural stem cells are primarily localized to the subventricular zone of the lateral ventricles and the subgranular zone of the hippocampal dentate gyrus.13 In the subventricular zone, neural stem/progenitor cells generate neuronal and oligodendroglial progenies.14 Most of the new neurons produced from the subventricular zone migrate via the rostral migratory stream, eventually becoming olfactory interneurons in the olfactory bulb.15 A few subventricular zone-derived new neurons travel into cortical areas for an unknown cause but may be related to tissue repair or renewal mechanisms.16 Similarly, newly produced dentate gyrus cells travel laterally into the dentate granule cell layer and become fully mature in a few weeks through a process known as adult hippocampus neurogenesis.17 However, it is still unknown whether these neural stem cells in the subventricular zone and dentate gyrus regions can replace the lost neurons following injury.

So far, several studies have assessed the degree of neurogenesis in these two areas and have demonstrated that significant numbers of new cells are continuously generated.9,18 For example, the rat dentate gyrus generates about 9000 new cells each day or 270,000 cells every month.18 A current clinical finding indicated that the whole granular cell population in the deep layer and half of the superficial layer of the olfactory bulb were replaced by newly produced mature neurons for a year.19 A similar study also revealed that adult-produced neurons account for around 10% of the overall number of dentate granule cells in the hippocampus and they are uniformly distributed along the anterior-posterior axis of the dentate gyrus.19 After the finding of continuous adult neurogenesis during the lifetime in the adult animal brain, the functional roles and the significance of this adult neurogenesis, mainly hippocampal neurogenesis concerning learning and memory processes, have been widely explored. Previous studies showed factors that increase hippocampal neurogenesis such as exposure to enriched environments, physical activity, or growth factor therapy may improve cognitive abilities.2022

The newly formed granular cells in the mature dentate gyrus can become functional neurons in the normal hippocampus by demonstrating passive membrane characteristics, generating action potentials, and receiving functional synaptic inputs, as seen in the adult dentate gyrus neurons.23 For instance, mouse strains hereditarily having poor levels of neurogenesis carry out low learning activities than those with a higher level of baseline neurogenesis.2325 A variety of physical and chemical signals influence the proliferation and maturational destiny of cells in the subventricular zone and dentate gyrus. For instance, biochemical variables including serotonin, glucocorticoids, ovarian hormones, and growth factors strongly regulate the proliferative response, implying that cell proliferation in these areas has a significant physiological role.26,27 Besides, physical factors such as exercise and stress produce changes in cell proliferation implying a significant role in network adaptation.28,29 For example, physical exercise might cognitively and physically enhance the production of cells and neurogenesis within the subventricular zone and dentate gyrus, but stress inhibits this type of cellular activity. Furthermore, the physiologic role of these new cells depends on the number of cells being produced, survival rate, differentiation ability, and integration of cells into existing neuronal circuity.24,30

The subventricular zone and hippocampus contain neural stem cells that respond to a variety of stimuli. Different kinds of experimental traumatic brain injury models such as fluid percussive injury,31,32 controlled cortical impact injury,33,34 closed-head weight drop injury,35 and acceleration-impact injury36 have shown increased neural stem cells activation. All of these experimental studies have shown the most prevalent and notable endogenous cell response after traumatic brain injury is an elevated cell proliferation within neurogenic areas of the dentate gyrus and subventricular zone. It is well accepted that enhanced production of new neurons following the traumatic brain injury was detected predominantly in the hippocampus in the more seriously injured animals in many experimental studies.37 More studies have discovered that injury-enhanced new granule neurons send out axonal projections into the targeted CA3 region implying their integration into the existing hippocampal circuitry,37,38 and this injury-induced endogenous neurogenic stem cells response is directly associated with the inherent cognitive functional recovery after traumatic brain injury of rodents.39,40

In the human brain, the extent and physiology of the adult neural generation are not well understood. A study on human brain samples taken from the autopsy revealed neural stem cells with proliferative ability have been observed within the subventricular zone and the hippocampus.41,42 Conversely, a more recent study has shown that neurogenesis in the subventricular zone and movement of new neurons from the subventricular zone to the olfactory bulbs and neocortex are restricted and only seen in the early childhood period.43,44 Therefore, credible evidence of traumatic brain injury-initiated neurogenesis in the human brain is inadequate because of the difficulties of collecting human brain samples and technical challenges to birth-dating neural stem cells.

After traumatic brain injury, injury-initiated neural cell loss is permanent. Given the restricted amount of endogenous neurogenic stem cells, neural transplantation supplementing exogenous stem cells to the damaged brain tissue is a potential treatment for post-traumatic brain injury regeneration.45 Especially, the transplanted cells will not only be able to replace the damaged neural cells but also give neurotrophic support in hopes of reestablishing and stabilizing the damaged brain tissue.45 Clinical evidence revealed intervention with stem cell secretome may significantly improve neural inflammation after traumatic brain injury and other neurological deficits in humans.46 Besides, the combined effects of bioscaffold and exosomes can aid in the transportation of stem cells to damaged areas as well as enhance their survival and facilitate successful treatment.47 Despite the rapid progression of brain infarction, the decreased proliferation of neural stem cells, and the delayed initiation of neurological recovery were observed in the aged rat model compared with a young rat after stroke, the restorative capability of the brain by stem cell therapy is still present in the aged rat.48 Compared to stem cell monotherapies which are still uniformly failed in clinical practice, combination therapy with hypothermia has potential therapeutic effects on the physiology of the aged brain and may be required for effective protection of the brain following stroke.49 After several years of biomaterials study for regeneration of peripheral nerve, a new 3D printing strategy is developing as a good substitution for nerve autograft over large gap injuries. The applications of 3D printing technologies can help in improving long-distance peripheral nerve regeneration since it is a leading device to give one path for better nerve guidance.50 Up to now, various categories of stem cell therapy have been tested for post-traumatic brain injury. These include embryonic stem cells, adult-derived neural stem cells, mesenchymal stem cells, and induced pluripotent stem cells.

Embryonic stem cells obtained from fetal or embryonic brain tissues are highly considered for neural transplantation because of their ability of plasticity and have the capacity to self-repair and differentiation into all germinal layers. They can differentiate, migrate, and innervate as transplanted into a receiver brain tissue.51 In previous clinical brain injury studies, neural stem cells derived from the embryonic human brain could survive for a long time, migrating to the contralateral cortex and differentiating into mature neural cells and microglia following transplantation into the damaged brain tissue.52 Implanted neurogenic stem cells obtained from human fetal stem cells may differentiate into adult neurons and release growth factors increasing the cognitive functional recovery of the damaged brain.53 Interestingly, the long-term survival rate of transplanted neural stem cells obtained from mice embryonic brains was seen for up to 1 year with a high degree of migration in the damaged brain and maturation into neurons or neuroglial cells along with enhanced motor and spatial learning functions of the brain tissue.5456 In addition, embryonic stem cells expressing growth factors or early differentiated into neurotransmitter expressing adult neurons after in vitro manipulation have revealed improved transplant survival and neuronal differentiation following grafted into the damaged brain, and the receivers have better recovery in motor and cognitive activities.5759 Even though embryonic stem cells have a high rate of survival and plasticity in neuronal transplantation, the ethical concerns, risk of transplant rejection, and the likelihood of teratoma development restrict their therapeutic use for traumatic brain injury.45

Neural stem cells are multipotent cells that can differentiate into neural cells but have a limited ability to differentiate into other tissue types.60 Neurogenic stem cells are located in the subventricular zones of the lateral ventricle, the hippocampal dentate gyrus, and other areas of the brain like the cerebral cortex, amygdala, hypothalamus, and substantia nigra. They could be isolated, developed in culture media, and produce many neural lineages that can be used in the treatment of neurological disorders as an important element of cellular-replacement therapy.61 Adult neural stem cells were transplanted into damaged parts of the brain in a traumatic brain injury rat model. These cells survived the transplantation process and moved to a damaged site when expressing markers for adult microglia and oligodendrocytes.62 Interestingly, one most recent study indicated that Korean red ginseng extract-mediated astrocytic heme oxygenase-1 induction contributes to the proliferation and differentiation of adult neural stem cells by upregulating astrocyteneuronal system cooperation.63 Another study revealed that following neural stem cell transplantation to the hippocampal region, injured rats had developed better cognitive function.64 The administration of combined therapies such as human neural stem/progenitor cells and curcumin-loaded noisome nanoparticles significantly improve brain edema, gliosis, and inflammatory responses in the traumatic brain injury rat model.65 Furthermore, in traumatic brain injury rat models, as neural stem cells were injected intravenously, they resulted in a decreased neurologic impairment and less edema because of the anti-inflammatory and anti-apoptotic features of neural stem cells.60,66 The ideal transplantation timeframe is 714 days,60 beyond which the glial scar forms, restricting perfusion and graft survival.67 The ability to transport cells to the desired location is a key obstacle with neural stem cell transplantation. Neural stem cells can be administered intrathecally, intravenously, and intra-arterial infusion. Conversely, a nanofiber scaffold implantation was proposed by Walker et al as a new strategy to be implemented to give the support essential for cell proliferation, which provides direction to future research.68

Mesenchymal stem cells are multipotent stromal that can differentiate into mesenchymal and non-mesenchymal tissue, such as neural tissue.69 They are obtained from different types of tissues.70 The accessibility, availability, and differentiation ability of these cells have drawn the attention of researchers performing studies in regenerative medicine. A previous study revealed the differentiation capacity of mesenchymal stem cells into neuronal cells. This study found that when rat and human mesenchymal stem cells are exposed to various experimental culture conditions, they can differentiate into neural and neuroglial cells.69 Besides, mesenchymal stem cells have also been demonstrated to enhance the proliferation and differentiation of native neural stem cells; the mechanism of which may be directly associated with chemokines produced by mesenchymal stem cells or indirectly through stimulation of adjacent astrocytes.70 In addition to their capacity to differentiate, mesenchymal stem cells selectively move to damaged tissues in traumatic brain injury rat models, where they develop into neurons and astrocytes and enhance motor function.71 The possible mechanism of action through which this occurs is linked to chemokines, growth factors,72 and adhesion factors, like the vascular cell adhesion molecule (VCAM-1), which permits mesenchymal stem cells to adhere to the endothelium of damaged organ.73 Mesenchymal stem cell transplantation has become a potential and safe treatment of choice for traumatic brain injuries because of its anti-inflammatory capability by regulating leukocyte and inflammatory factors such as IL-6, CRP, and TNF-a.74,75 Treatment with mesenchymal stem cell-derived extracellular vesicles greatly increased neurogenesis and neuroplasticity in a pig model of hemorrhagic stroke and traumatic brain damage.76 Currently, stem cell therapy using mesenchymal stromal cells has been widely investigated in preclinical models and clinical trials for the treatment of several neurological illnesses, including traumatic brain injury. Mesenchymal stem cells investigated for the treatment of traumatic brain injury in these clinical trials include bone marrow-derived stem cells, amnion-derived multipotent progenitor cells, adipose-derived stem cells, umbilical cord-derived stem cells, and peripheral blood-derived stem cells.7779 Those undifferentiated mesenchymal-derived cells have a heterogeneous cell population that includes stem and progenitor cells. They can be stimulated to differentiate into a neuronal cell phenotype in vitro. In the damaged brain tissue, these cells can generate a large number of growth factors, cytokines, and extracellular matrix substances that have neurotrophic or neuroprotective effects.80,81

From all mesenchymal stem cells, the effect of bone marrow-derived mesenchymal stem cells on traumatic brain injury has been fully investigated. According to previous studies, mesenchymal stem cells injected directly into the injured brain, or through intravenous or intra-arterial injections during the acute, sub-acute, or chronic phase following traumatic brain injury, have been shown to significantly reduce neurological abnormalities in motor and cognitive abilities.7779,82 The therapeutic effect of mesenchymal stem cells is mostly because of the bioactive molecules they produced to facilitate the endogenous plasticity and remodeling of the recipient brain tissue instead of direct neural repair as direct neuronal differentiation and long-term viability were rarely seen.80 A more recent study found that the injection of cell-free exosomes obtained from human bone marrow-derived mesenchymal stromal cells can increase the functional recovery of damaged animals after traumatic brain injury.83 Another study used a traumatic rodent model to evaluate the anti-inflammatory and immunoregulatory properties of mesenchymal stem cells. When compared to the control group, neurological function was improved in the treatment groups from 3 to 28 days. Mesenchymal stem cell therapy significantly decreased the amount of microglia or macrophages, neutrophils, CD3 lymphocytes, apoptotic cells in the damaged cortex, and proinflammatory cytokines.81 The main challenge of using mesenchymal stem cells for traumatic brain injury treatment is the long-term possibility of brain malignancy development because of the mesenchymal stromal cells ability to antitumor response suppression.84

In a recent study, seven traumatic brain injury patients were given a mesenchymal stem cells transplant during a cranial operation and then administered a second dose intravenously. At the end of the 6-month follow-up period, patients exhibited better neurological function with no signs of toxicity.85

Recent studies revealed that the administration of exosomes-derived human umbilical cord mesenchymal stem improves sensorimotor function and spatial learning activities in rat models following brain injuries. Furthermore, the applications of these cells extensively decreased proinflammatory cytokine expression via inhibiting the NF-B signaling pathway, reduced neuronal apoptosis, reduced inflammation, and increased neural regeneration ability in the injured cortex of rats following the injuries.86 Human umbilical cord-derived mesenchymal stem cells have better anti-inflammatory activity that may prevent and decrease secondary brain injury caused by the immediate discharge of inflammatory factors following traumatic brain injury.87 In traumatic brain injury rat models, the transplantation of umbilical cord-derived mesenchymal stem cells triggers the trans-differentiation of T-helper 17 into T regulatory, which in turn repairs neurological deficits and improves learning and memory function.88

To see the therapeutic effects of transplanted induced pluripotent stem cells compared to that of embryonic stem cells, Wang et al demonstrated animal models of ischemia and three different treatment options, which consist of pluripotent stem cells, embryonic stem cells, and phosphate-buffered saline for the control. The rodents were given an injection into the left lateral ventricle of the brain. Embryonic stem cell treatment group rodents showed a significant improvement in glucose metabolism within two-week period. However, 1 month following treatment, neuroimaging tests were done and it was revealed that both pluripotent stem cell and embryonic stem cell treatment groups had improved neurologic scores as compared to the control group, suggesting that the treatment groups showed better recovery of their cognitive function. Further investigation indicated that the implanted cells survived and traveled to the area of injury. Finally, the investigator of this study concluded that induced pluripotent stem cells may be a better option than embryonic stem cells.57 Different studies showed that induced pluripotent stem cells improved motor and cognitive function in the host mouse brain tissue, and these cells migrate the injured brain areas from the injection site.89,90 Until now, there are limited studies on induced pluripotent stem cell therapy for brain injuries. This is because of the difficulty of obtaining induced pluripotent stem cells, high therapy costs, and technique limitations.

In preclinical and clinical trials, advanced progress has been made in stem cell-based therapy for traumatic brain injury patients. Various studies reported the therapeutic effect of stem cells for regenerating damaged brain tissue. However, because of the complexity and variability of brain injuries, post-traumatic brain injury neuronal regeneration and repair remain a long-term goal. There are numerous unresolved challenges for successful stem cell treatment. For endogenous restoration via mature neural regeneration, methods guiding the movement of new neuronal cells to the area of damaged tissue and maintaining long-term survival are very important. In stem cell therapy, the inherent features of transplanted cells and the local host micro-environment influences the fate of grafted cells, an appropriate cell source, and a host environment, which are required for effective transplantation. Therefore, these problems should be solved in preclinical traumatic brain injury trials before stem cell-based treatments could be used in the clinic. The therapeutic application of neural stem cell treatment, whether via manipulation of endogenous or implantation of exogenous neural stem cells, is a method that has been shown in multiple studies to have substantial potential to increase brain function recovery in persons suffering from traumatic brain injury-related disability. However, further studies need to be done on the therapeutic application of stem cells for traumatic brain injury due to our poor understanding of possible consequences, unknown ethical issues, routes of administration, and the use of mixed treatment.

All authors declared no conflicts of interest for this study.

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Fibrosis is the thickening of various tissues caused by the deposition of fibrillar extracellular matrix (ECM) in tissues and organs as part of the bodys wound healing response to various forms of damage. When accompanied by chronic inflammation, fibrosis can go into overdrive and produce excess scar tissue that can no longer be degraded. This process causes many diseases in multiple organs, including lung fibrosis induced by smoking or asbestos, liver fibrosis induced by alcohol abuse, and heart fibrosis often following heart attacks. Fibrosis can also occur in the bone marrow, the spongy tissue inside some bones that houses blood-producing hematopoietic stem cells (HSCs) and can lead to scarring and the disruption of normal functions.

Chronic blood cancers known as myeloproliferative neoplasms (MPNs) are one example, in which patients can develop fibrotic bone marrow, or myelofibrosis, that disrupts the normal production of blood cells. Monocytes, a type of white blood cell belonging to the group of myeloid cells, are overproduced from HSCs in neoplasms and contribute to the inflammation in the bone marrow environment, or niche. However, how the fibrotic bone marrow niche itself impacts the function of monocytes and inflammation in the bone marrow was unknown.

Now, a collaborative team from Penn, Harvard, the Dana-Farber Cancer Institute (DFCI), and Brigham and Womens Hospital has created a programmable hydrogel-based in vitro model mimicking healthy and fibrotic human bone marrow. Combining this system with mouse in vivo models of myelofibrosis, the researchers demonstrated that monocytes decide whether to enter a pro-inflammatory state and go on to differentiate into inflammatory dendritic cells based on specific mechanical properties of the bone marrow niche with its densely packed ECM molecules. Importantly, the team found a drug that could tone down these pathological mechanical effects on monocytes, reducing their numbers as well as the numbers of inflammatory myeloid cells in mice with myelofibrosis. The findings are published in Nature Materials.

We found that stiff and more elastic slow-relaxing artificial ECMs induced immature monocytes to differentiate into monocytes with a pro-inflammatory program strongly resembling that of monocytes in myelofibrosis patients, and the monocytes to differentiate further into inflammatory dendritic cells, says co-first author Kyle Vining, who recently joined Penn.More viscous fast-relaxing artificial ECMs suppressed this myelofibrosis-like effect on monocytes. This opened up the possibility of a mechanical checkpoint that could be disrupted in myelofibrotic bone marrow and also may be at play in other fibrotic diseases. Vining will be appointedassistant professor of preventive and restorative sciences in theSchool of Dental Medicine and the Department of Materials Sciences in theSchool of Engineering and Applied Science, pending approval by Penn Dental Medicines personnel committees and the Provosts office.

Vining worked on the study as a postdoctoral fellow at Harvard in the lab of David Mooney. Our study shows that the differentiation state of monocytes, which are key players in the immune system, is highly regulated by mechanical changes in the ECM they encounter, says Mooney, who co-led the study with DFCI researcher Kai Wucherpfennig. Specifically, the ECMs viscoelasticity has been a historically under-appreciated aspect of its mechanical properties that we find correlates strongly between our in vitro and the in vivo models and human disease. It turns out that myelofibrosis is a mechano-related disease that could be treated by interfering with the mechanical signaling in bone marrow cells.

Mooney is also the Robert P. Pinkas Family Professor of Bioengineering at Harvard and leads the Wyss Institutes Immuno-Materials Platform. Wucherpfennig is director of DFCIs Center for Cancer Immunotherapy Research, professor of neurobiology at Brigham and Harvard Medical School, and an associate member of the Broad Institute of MIT and Harvard. Mooney, together with co-senior author F. Stephen Hodi, also heads the Immuno-engineering to Improve Immunotherapy (i3) Center, which aims to create new biomaterials-based approaches to enhance immune responses against tumors. The new study follows the Centers road map. Hodi is director of the Melanoma Center and The Center for Immuno-Oncology at DFCI and professor of medicine at Harvard Medical School.

The mechanical properties of most biological materials are determined by their viscoelastic characteristics. Unlike purely elastic substances like a vibrating quartz, which store elastic energy when mechanically stressed and quickly recover to their original state once the stress is removed, slow-relaxing viscoelastic substances also have a viscous component. Like the viscosity of honey, this allows them to dissipate stress under mechanical strain by rapid stress relaxation. Viscous materials are thus fast-relaxing materials in contrast to slow-relaxing purely elastic materials.

The team developed an alginate-based hydrogel system that mimics the viscoelasticity of natural ECM and allowed them to tune the elasticity independent from other physical and biochemical properties. By tweaking the balance between elastic and viscous properties in these artificial ECMs, they could recapitulate the viscoelasticity of healthy and scarred fibrotic bone marrow, whose elasticity is increased by excess ECM fibers. Human monocytes placed into these artificial ECMs constantly push and pull at them and in turn respond to the materials mechanical characteristics.

Next, the team investigated how the mechanical characteristics of stiff and elastic hydrogels compared to those in actual bone marrow affected by myelofibrosis. They took advantage of a mouse model in which an activating mutation in a gene known as Jak2 causes MPN, pro-inflammatory signaling in the bone marrow, and development of myelofibrosis, similar to the disease process in human patients with MPN. When they investigated the mechanical properties of bone marrow in the animals femur bones, using a nanoindentation probe, the researchers measured a higher stiffness than in non-fibrotic bone marrow. Importantly, we found that the pathologic grading of myelofibrosis in the animal model was significantly correlated with changes in viscoelasticity, said co-first author Anna Marneth, who spearheaded the experiments in the mouse model as a postdoctoral fellow working with Ann Mullally, a principal investigator at Brigham and DFCI, and another senior author on the study.

An important question was whether monocytes response to the mechanical impact of the fibrotic bone marrow niche could be therapeutically targeted. The researchers focused on an isoform of the phosphoinositide 3-kinase (PI3K)-gamma protein, which is specifically expressed in monocytes and closely related immune cells. PI3K-gamma is known for regulating the assembly of a cell-stiffening filamentous cytoskeleton below the cell surface that expands in response to mechanical stress, which the team also observed in monocytes encountering a fibrotic ECM. When they added a drug that inhibits PI3K-gamma to stiff elastic artificial ECMs, it toned down their pro-inflammatory response and, when given as an oral treatment to myelofibrosis mice, significantly lowered the number of monocytes and dendritic cells in their bone marrow.

This research opens new avenues for modifying immune cell function in fibrotic diseases that are currently difficult to treat. The results are also highly relevant to human cancers with a highly fibrotic microenvironment, such as pancreatic cancer, says Wucherpfennig.

Adapted from a press release written by Benjamin Boettner of the Wyss Institute for Biologically Inspired Engineering at Harvard University.

Other authors on the study are Harvards Kwasi Adu-Berchie, Joshua M. Grolman, Christina M. Tringides, Yutong Liu, Waihay J. Wong, Olga Pozdnyakova, Mariano Severgnini, Alexander Stafford, and Georg N. Duda.

The study was funded by the National Cancer Institute of the National Institutes of Health (Grant CA214369), National Institute of Dental & Craniofacial Research of the National Institutes of Health (grants DE025292 and DE030084), Food and Drug Administration (Grant FD006589), and Harvard University Materials Research Science and Engineering Center (Grant DMR 1420570).

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Deconstructing the mechanics of bone marrow disease | Penn Today - Penn Today

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Krabbe disease is one of many hundreds of inherited metabolic disorders. Named after the Danish neurologist Knud Krabbe, the disease causes progressive damage to the nervous system, eventually resulting in the death of the individual. The disease is common in newborns before they reach six months of age and treatment must start at the earliest. Most newborns affected by Krabbe disease do not reach the age of two.

Krabbe disease is caused due to genetic mutation on the 14th chromosome in an infant. A child needs to inherit two copies of the abnormal genome from both its parents, after which it has a 25 percent chance of inheriting both the recessive genes and developing the disease.

On inheriting the defective genome, the body doesnt produce enough of the enzyme galactosylceramidase (GALC). Galactosylceramidase is essential for breaking down unmetabolised lipids like glycosphingolipid and psychosine in the brain. These unmetabolised lipids are toxic to some of the non-neuron cells present in the brain.

Late-onset Krabbe disease, however, can be caused by a different genetic mutation which leads to a lack of a different enzyme, known as active saposin A.

Symptoms between early-onset and late-onset Krabbe disease differ slightly. Infants suffering from early-onset Krabbe disease suffer from symptoms like excessive irritability, difficulty swallowing, vomiting, unexplained fevers, and partial unconsciousness. Other common neuropathic symptoms include hypersensitivity to sound, muscle weakness, slowing of mental and motor development, spasticity, deafness, optic atrophy, optic nerve enlargement, blindness, and paralysis.

Late-onset Krabbe disease emerges with symptoms like the development of cross-eyes, slurred speech, slow development, and loss of motor functions.

The disease is diagnosed after a physician conducts a primary physical exam. A blood or skin tissue biopsy can test for GALC levels in the body and low levels can indicate the presence of Krabbe disease. Further testing through imaging scans (MRI), nerve conduction studies, eye examination, genetic testing and amniocentesis can also help diagnose the disease.

There is no cure for Krabbe disease. Treatment is mostly palliative in nature with a focus towards dealing with symptoms and providing supportive care. Experimental trials using hematopoietic stem cell transplant (HSCT), bone marrow transplantation, stem cell therapy, and gene therapy have seen some results in the small number of patients that they have been used on.

(Edited by : Shoma Bhattacharjee)

First Published:Jul 15, 2022, 06:32 AM IST

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Krabbe disease, which mostly affects newborns causes, symptoms, and treatment - CNBCTV18

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Under embargo until Thursday 14 July 2022 at 16:00 (London time), 14 July 2022 at 11:00 (US Eastern Time).

Newswise The discovery of 14 inherited genetic changes which significantly increase the risk of a person developing a symptomless blood disorder associated with the onset of some types of cancer and heart disease is published today in Nature Genetics. The finding, made in one of the largest studies of its kind through genetic data analysis on 421,738 people, could pave the way for potential new approaches for the prevention and early detection of cancers including leukaemia.

Led by scientists from the Universities of Bristol and Cambridge, the Wellcome Sanger Institute, the Health Research Institute of Asturias in Spain, and AstraZeneca, the study reveals that specific inherited genetic changes affect the likelihood of developing clonal haematopoiesis, a common condition characterised by the development of expanding clones of multiplying blood cells in the body, driven by mutations in their DNA.

Although symptomless, the disorder becomes ubiquitous with age and is a risk factor for developing blood cancer and other age-related diseases. Its onset is a result of genetic changes in our blood-making cells.

All human cells acquire genetic changes in their DNA throughout life, known as somatic mutations, with a specific subset of somatic mutations driving cells to multiply. This is particularly common in professional blood-making cells, known as blood stem cells, and results in the growth of populations of cells with identical mutations known as clones.

Using data from the UK Biobank, a large-scale biomedical database and research resource containing genetic and health information from half a million UK participants, the team were able to show how these genetic changes relate not only to blood cancers but also to tumours that develop elsewhere in the body such as lung, prostate and ovarian cancer.

The team found that clonal haematopoiesis accelerated the process of biological ageing itself and influenced the risk of developing atrial fibrillation, a condition marked by irregular heartbeats.

The findings also clearly established that smoking is one of the strongest modifiable risk factors for developing the disorder, emphasising the importance of reducing tobacco use to prevent the conditions onset and its harmful consequences.

Dr Siddhartha Kar, UKRI Future Leaders Fellow at the University of Bristol and one of the studys lead authors from Bristols MRC Integrative Epidemiology Unit(IEU), said: Our findings implicate genes and the mechanisms involved in the expansion of aberrant blood cell clones and can help guide treatment advances to avert or delay the health consequences of clonal haematopoiesis such as progression to cancer and the development of other diseases of ageing.

Professor George Vassiliou, Professor of Haematological Medicine at the University of Cambridge and one of the studys lead authors, added: Our study reveals that the cellular mechanisms driving clonal haematopoiesis can differ depending on the mutated gene responsible. This is a challenge as we have many leads to follow, but also an opportunity as we may be able to develop treatments specific to each of the main subtypes of this common phenomenon.

Dr Pedro M. Quiros, formerly researcher at the Wellcome Sanger Institute and the University of Cambridge, and now Group Leader at the Health Research Institute of Asturias (Spain) and another of the studys lead authors says: We were particularly pleased to see that some of the genetic pathways driving clonal haematopoiesis appear to be susceptible to pharmacological manipulation and represent prioritised targets for the development of new treatments.

The study was funded by UK Research and Innovation (UKRI), Cancer Research UK (CRUK), Wellcome, the Royal Society, the Carlos III Health Institute, the Leukaemia and Lymphoma Society, and the Rising Tide Foundation for Clinical Cancer Research.

Paper

Genome-wide analyses of 200,453 individuals yield new insights into the causes and consequences of clonal hematopoiesis by Kar SP, et al. in Nature Genetics.

Ends

Further information:

Clonal haematopoiesis is the development of mutations in genes involved in blood cell production. It is diagnosedwhen a test on a person's blood or bone marrow sample shows that blood cells are carrying one of the genetic mutations associated with the condition. Clonal haematopoiesis becomes increasingly common with age, affecting more than one in every ten individuals older than 60 years.

Notes to editors

Paper: an embargoed copy of the paper is available to download here.

Issued by the University of Bristol Media Team.

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In this free webinar, learn how live cell metabolic analysis paves the way not only for metabolic research, but also the manufacturing of significant cell and gene therapy (CGT) products. Attendees will learn how glycolysis metabolic process can be measured directly through the continuous measuring of glucose and lactate amounts in the culture media using electrochemical sensors which provides new scientific insights. The featured speakers will discuss how continuous monitoring is effectively utilized for the process development stage of CGT products and quality control during the manufacturing stage of CGT products. The speakers will also discuss how glucose and lactate can be monitored in the traditional lab environment using conventional 24-well plate and CO2 incubators without any sampling.

TORONTO (PRWEB) July 12, 2022

Among the various biological functions cells carry out to maintain life, metabolism is the key activity used to process nutrient molecules. It is also closely associated with cell proliferation and differentiation. Cell metabolic analysis would be very helpful to monitor these activities.

In the field of cancer immunotherapy such as CAR T and TCR-T therapy, stem cell research including embryonic stem (ES) and induced pluripotent stem (iPS) cells and commercial cell and gene therapy (CGT) manufacturing process development investigating and understanding the metabolic activities of cells are critical. To meet this need in the field, PHC Corporation will launch a continuous metabolic analyzer which leads to real-time visualization of the metabolic condition of living cells. This development will encourage new discoveries that have not been seen in previous studies.

Register for this webinar to learn how live cell metabolic analysis paves the way not only for metabolic research, but also the manufacturing of significant CGT products.

Join experts from PHC Corporation of North America, Ryosuke Takahashi, PhD VP, Cell and Gene Therapy Business; and Kenan Moss, Application Specialist, for the live webinar on Tuesday, July 26, 2022, at 11am EDT (4pm BST).

For more information, or to register for this event, visit Live Cell Metabolic Analysis Paving the Way for Metabolic Research and Cell & Gene Therapy.

ABOUT XTALKS

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To learn more about Xtalks visit http://xtalks.comFor information about hosting a webinar visit http://xtalks.com/why-host-a-webinar/

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Live Cell Metabolic Analysis Paving the Way for Metabolic Research and Cell & Gene Therapy, Upcoming Webinar Hosted by Xtalks - Benzinga

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By Nathan Sager

Published July 14, 2022 at 5:16 pm

A renowned burns specialist and his entire lab are continuing their work to develop 3-D printed skin at McMaster University in Hamilton.

Earlier this month, Dr. Marc Jeschke began a dual role at McMaster and Hamilton Health Sciences (HHS). Jeschke, who previously worked at the University of Toronto and Sunnybrook hospital, is now a professor of surgery at Mac and vice-president, research at HHS as well as medical director of its burns unit.

As part of the move, Jeschke is bringing his nearly 20-scientist burn research lab to Hamilton. The lab is supported by a gift from Charles and Margaret Juravinski through the Juravinski Research Institute. In a release from the university, Jeschke said McMaster is uniquely positioned for work across verious medical disciplines, since there are many partnerships with HHS and St. Josephs Healthcare Hmailton.

(McMaster) offers a more intimate environment than other institutions of its calibre and the quality of collaboration here is outstanding, said Jeschke.

People who suffer extensive and serious burns often end up with scarring for life. The Jeschke-headed lab has been developing a skin derivative that uses a patients own stem cells. It might one day greatly reduce scarring for people with extensive burns.

In 2020, researchers and developers from U of T and Sunnybrook became the first Canadian team to be honoured with a top prize from the 3D Pioneers Challenge for building and refining of the ReverTome handheld 3D skin printer. The printer can make new skin grown from stem cells in order to improve healing. Jeschke and his team contributed stem cell research to help inform development of the device.

The 3D Pioneers Challenge honours innovations in digital printing. The U of T-Sunnybrook team won from among a field of 52 finalists from 28 nations.

Jeschke said in the release that the therapy his lab is testing proved effective in porcine models. The clinical trial stage would be next.

The human body is so complex, but this stem-cell based therapy, if successful, will certainly change the way we care for burns and other injuries, he said.

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McMaster in Hamilton founds burn injury research program that is working on 3-D skin | inTheHammer - insauga.com

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