Monthly Archives: May 2020

Mike Tyson has attributed his incredible body transformation to stem cell therapy and a rigid vegan diet.

The youngest world heavyweight champion in history ballooned to more than 300lbs in weight at his heaviest almost a decade ago.

However, after drastically changing his diet and implementing revolutionary reparative medication, Iron Mike is looking more streamlined and more devastating than ever.

Tyson is reportedly considering making a return to the squared circle at the age of 53, with an announcement on his opponent expected this week.

Whilst training with UFC legends Vitor Belfort and Henry Cejudo, the former undisputed heavyweight champion displayed a significantly more shredded physique.

Prior to officially announcing his desire to return, Tyson was asked by rapper LL Cool J how he would get fighting fit in just six to eight weeks.

He told Rock the Bells Radio show on SiriusXM: Really I would just change my diet and just do cardio work. Cardio has to start, you have to have your endurance to go and do the process of training.

Mike Tyson

So something to do is get in cardio, I would try and get two hours of cardio a day, make sure you get that stuff in. Youre gonna make sure youre eating the right food.

For me its almost like slave food. Doing what you hate to do but doing it like its nothing. Getting up when you dont want to get up. Thats what it is. Its becoming a slave to life.

People think a slave to life is just enjoying drugs and living your life. Being a slave to life means being the best person you can be, being the best you can possibly be, and when you are at the best you can possibly be is when you no longer exist and nobody talks about you. Thats when youre at your best.

Tyson continued: My mind wouldnt belong to me. My mind would belong to somebody that disliked me enough to break my soul, and I would give them my mind for that period of time.

Six weeks of this and Id be in the best shape Ive ever dreamed of being in. As a matter of fact, Im going through that process right now. And you know what else I did, I did stem-cell research.

Stem-cell research (also known as regenerative medicine) promotes the repair response of diseased, dysfunctional or injured tissue using stem cells or their derivatives.

It is the latest advancement in organ transplantation and uses cells instead of donor organs, which are limited in supply.

After LL Cool J asked if that meant Tysons white blood cells had been spun and then put back in, Tyson continued: Yes. As they took the blood it was red and when it came back it was almost transfluid [sic], I could almost see through the blood, and then they injected it in me. And Ive been weird ever since, Ive got to get balanced now.

Getty Images - Getty

The necessity to repair the former heavyweight champion was caused by the excessive weight gain following his retirement in 2005 and his hedonistic lifestyle.

Excessive cocaine abuse left the heavyweight in a serious state of bother and led him to adopt a vegan lifestyle.

He told Totally Vegan Buzz: I was so congested from all the drugs and bad cocaine, I could hardly breathe. Tyson also revealed in the interview, I had high blood pressure, was almost dying, and had arthritis.

During aninterviewwith Oprah Winfrey in 2013, Tysoncredits his plant-based diet for saving his life.

Getty Images

He said: Well, my life is different today because I have stability in my life. Im not on drugs.

Im not out on the streets or in clubs and everything in my life that I do now is structured around the development of my life and my family. I lost weight.

I dropped over 100lbs and I just felt like changing my life, doing something different and I became a vegan.

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Vegan diet, intense cardio and stem cell therapy How Mike Tyson managed to get ripped at 53 as boxing c - talkSPORT.com

ORLANDO, Fla.--(BUSINESS WIRE)--Hesperos Inc., pioneers of the Human-on-a-Chip in vitro system, today announced a new peer-reviewed publication that describes how the companys functional Human-on-a-Chip system can be used as a drug discovery platform to identify therapeutic interventions targeting the preclinical stages of Alzheimers disease (AD) and mild cognitive impairment (MCI). The manuscript, titled A human induced pluripotent stem cell-derived cortical neuron human-on-a-chip system to study A42 and tau-induced pathophysiological effects on long-term potentiation, was published this week in Alzheimer's & Dementia: Translational Research & Clinical Interventions. The work was conducted in collaboration with the University of Central Florida and with David G. Morgan, Ph.D., Professor of Translational Neuroscience at Michigan State University, and expert in AD pathology.

To date, more than 100 potential therapeutics in development for AD have been abandoned or failed during clinical trials. These therapeutics relied on research conducted in preclinical animal studies, which often are unable to accurately capture the full spectrum of the human disease phenotype, including differences in drug metabolism and excretion between humans and animals. Therefore, there is a need for human models, especially those that accurately recapitulate the functional impairments during the preclinical phases of AD and MCI.

Hesperos offers a breakthrough technology that provides a human cell-based assay based on cognitive function metrics to evaluate drugs designed to restore cognition at early stages of the Alzheimers continuum, said Dr. Morgan. This system can serve as a novel drug discovery platform to identify compounds that rescue or alleviate the initial neuronal deficits caused by A1-42 and/or tau oligomers, which is a main focus of clinical trials.

In 2018, Hesperos received a Phase I Small Business Innovation Research (SBIR) grant from the National Institute on Aging (NIA) division within the US National Institutes of Health (NIH) to help create a new multi-organ human-on-a-chip model for testing AD drugs. Research conducted under this grant included a study to assess therapeutic interventions based on functional changes in neurons, not neuronal death.

In the recent Alzheimer's & Dementia publication, Hesperos describes its in vitro human induced pluripotent stem cell (iPSC)-derived cortical neuron human-on-a-chip system for the evaluation of neuron morphology and function after exposure to toxic A and tau oligomers as well as brain extracts from AD transgenic mouse models.

Researchers are now focusing on biomarker development and therapeutic intervention before symptoms arise in AD and MCI, said James Hickman, Ph.D., Chief Scientist at Hesperos and Professor at the University of Central Florida. By studying functional disruption without extensive cell loss, we now have a screening methodology for drugs that could potentially evaluate therapeutic efficacy even before the neurodegeneration in MCI and AD occurs.

The researchers found that compared to controls, treatment with toxic A and tau oligomers or brain extracts on the iPSC cortical neurons significantly impaired information processing as demonstrated by reduction in high-frequency stimulation-induced long-term potentiation (LTP), a process that is thought to underlie memory formation and learning. Additionally, oligomer and brain extract exposure led to dysfunction in iPSC cortical neuron electrophysiological activity, including decreases in ion current and action potential firing.

While exposure to the toxic oligomers and brain extracts caused morphological defects in the iPSC cortical neurons, there was no significant loss in cell viability.

Clinical success for AD therapies has been challenging since preclinical animal studies often do not translate to humans, said Michael L. Shuler, Ph.D., Chief Executive Officer of Hesperos. With our recent study, we are now one step closer in developing an AD multi-organ model to better evaluate drug metabolism in the liver, penetration through the blood-brain barrier and the effects on neuronal cells.

About Alzheimers Disease/Preclinical Stage AD

AD is a progressive disease that is characterized by memory loss and deterioration of cognitive function. Preclinical AD is the first stage of the disease, and it begins long before any symptoms become apparent. It is thought that symptoms do not manifest until there is a significant death of neuronal cells, which is caused by the aggregation of toxic amyloid beta (A) and tau oligomers, typically during the earliest stages of the disease. Unfortunately, treatment after the diagnosis of MCI may be too late to reverse or modify disease progression.

To read the full manuscript, please visit https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/trc2.12029.

About Hesperos

Hesperos, Inc. is a leading provider of Human-on-a-Chip microfluidic systems to characterize an individuals biology. Founders Michael L. Shuler and James J. Hickman have been at the forefront of every major scientific discovery in this realm, from individual organ-on-a-chip constructs to fully functional, interconnected multi-organ systems. With a mission to revolutionize toxicology testing as well as efficacy evaluation for drug discovery, the company has created pumpless platforms with serum-free cellular mediums that allow multi-organ system communication and integrated computational PKPD modeling of live physiological responses utilizing functional readouts from neurons, cardiac, muscle, barrier tissues and neuromuscular junctions as well as responses from liver, pancreas and barrier tissues. Created from human stem cells, the fully human systems are the first in vitro solutions to accurately predict in vivo functions without the use of animal models. More information is available at http://www.hesperosinc.com.

Hesperos and Human-on-a-Chip are trademarks of Hesperos Inc. All other brands may be trademarks of their respective holders.

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Hesperos Human-on-a-Chip System Used to Model Preclinical Stages of Alzheimer's Disease and Mild Cognitive Impairment - Business Wire

Acute lung injury (ALI) is a devastating disease process involving pulmonary edema and atelectasis caused by capillary membrane injury [1]. The main clinical manifestation is the acute onset of hypoxic respiratory failure, which can subsequently trigger a cascade of serious complications and even death [2]. Thus, ALI causes a considerable financial burden for health care systems throughout the world. ALI can result from various causes, including multiple traumas, large-volume blood transfusions, and bacterial and viral infections [2, 3]. A variety of viruses, including influenza virus, coronavirus (CoV), adenovirus, cytomegalovirus (CMV), and respiratory syncytial virus (RSV), are associated with ALI [4]. Importantly, most viruses, whose hosts are various animal species, can cause severe and rapidly spreading human infections. In the early 2000s, several outbreaks of influenza virus and CoV emerged, causing human respiratory and intestinal diseases worldwide, including the more recent SARS-CoV-2 infection [5,6,7]. To date, SARS-CoV-2 has affected more than 80,000 people, causing nearly 3300 deaths in China and more than 1,800,000 people, causing nearly 110,000 deaths all over the world (http://2019ncov.chinacdc.cn/2019-nCoV/).

Infectious respiratory diseases caused by different viruses are associated with similar respiratory symptoms ranging from the common cold to severe acute respiratory syndrome [8]. This makes the clinical distinction between different agents involved in infection very difficult [8, 9]. Currently, the clinical experience mainly includes antibacterial and antiviral drug treatment derived from handling several outbreaks of influenza virus and human CoVs. Numerous agents have been identified to inhibit the entry and/or replication of these viruses in cell culture or animal models [10]. Although these antiviral drugs can effectively prevent and eliminate the virus, the full recovery from pneumonia and ALI depends on the resistance of the patient. Recently, stem cell-based therapy has become a potential approved tool for the treatment of virus-induced lung injury [11,12,13]. Here, we will give a brief overview of influenza virus and CoVs and then present the cell-based therapeutic options for lung injury caused by different kinds of viruses.

Influenza virus and human CoV are the two most threatening viruses for infectious lung injury [14]. These pathogens can be transmitted through direct or indirect physical contact, droplets, or aerosols, with increasing evidence suggesting that airborne transmission, including via droplets or aerosols, enhances the efficiency of viral transmission among humans and causes uncontrolled infectious disease [15]. Throughout human history, outbreaks and occasional pandemics caused by influenza virus and CoV have led to approximately hundreds of millions of deaths worldwide [16].

Influenza virus is a well-known human pathogen that has a negative-sense RNA genome [17]. According to its distinct antigenic properties, the influenza virus can be divided into 4 subtypes, types A, B, C, and D. Influenza A virus (IAV) lineages in animal populations cause economically important respiratory disease. Little is known about the other human influenza virus types B, C, and D [18]. Further subtypes are characterized by the genetic and antigenic properties of the hemagglutinin (HA) and neuraminidase (NA) glycoproteins [19]. Sporadic and seasonal infections in swine with avian influenza viruses of various subtypes have been reported. The most recent human pandemic virusesH1N1 from swine and H5N1 from aviancause severe respiratory tract disease and lung injury in humans [20, 21].

CoVs, a large family of single-stranded RNA viruses, typically affect the respiratory tract of mammals, including humans. CoVs are further divided into four genera: alpha-, beta-, gamma-, and delta-CoVs. Alpha- and beta-CoVs can infect mammals, and gamma- and delta-CoVs tend to infect birds, but some of these viruses can also be transmitted to mammals [22]. Human CoVs were considered relatively harmless respiratory pathogens in the past. Infections with the human CoV strains 229E, OC43, NL63, and HKU1 usually result in mild respiratory illness, such as the common cold [23]. In contrast, the CoV responsible for the 2002 severe acute respiratory syndrome (SARS-CoV), the 2012 Middle East respiratory syndrome CoV (MERS-CoV), and, more recently, the SARS-CoV-2 have received global attention owing to their genetic variation and rapid spread in human populations [5,6,7].

Usually, the influenza virus can enter the columnar epithelial cells of the respiratory tract, such as the trachea, bronchi, and bronchioles. Subsequently, the influenza virus begins to replicate for an asymptomatic period of time and then migrate to the lung tissue to cause acute lung and respiratory injury [24]. Similar to those with influenza virus infection, patients with SARS, MERS, or SARS-CoV-2 present with various clinical features, ranging from asymptomatic or mild respiratory illness to severe ALI, even with multiple organ failure [5,6,7]. The pathogenesis of ALI caused by influenza virus and human CoV is often associated with rapid viral replication, marked inflammatory cell infiltration, and elevated proinflammatory cytokine/chemokine responses [25]. Interestingly, in IAV- and human CoV-infected individuals, the pulmonary pathology always involves diffuse alveolar damage, but viral RNA is present in only a subset of patients [26]. Some studies suggest that an overly exaggerated immune response, rather than uncontrolled viral spread, is the primary cause in fatal cases caused by virus infection [27]. Several immune cell types have been found to contribute to damaging host responses, providing novel approaches for therapeutic intervention [28].

IAV infection, the most common cause of viral pneumonia, causes substantial seasonal and pandemic morbidity and mortality [29]. Currently, antiviral drugs are the primary treatment strategy for influenza-induced pneumonia. However, antiviral drugs cannot repair damaged lung cells. Here, we summarize the present studies of stem cell therapy for influenza virus-induced lung injury.

Mesenchymal stem/stromal cells (MSCs) constitute a heterogeneous subset of stromal regenerative cells that can be harvested from several adult tissue types, including bone marrow, umbilical cord, adipose, and endometrium [30]. They retain the expression of the markers CD29, CD73, CD90, and CD105 and have a rapid proliferation rate, low immunogenicity, and low tumorigenicity [30]. MSCs also have self-renewal and multidifferentiation capabilities and exert immunomodulatory and tissue repair effects by secreting trophic factors, cytokines, and chemokines [31]. Due to these beneficial biological properties, MSCs and their derivatives are attractive as cellular therapies for various inflammatory diseases, including virus-induced lung injury.

Several studies on IAV-infected animal models have shown the beneficial effects of the administration of different tissue-derived MSCs [32,33,34,35]. H5N1 virus infection reduces alveolar fluid clearance (AFC) and enhances alveolar protein permeability (APP) in human alveolar epithelial cells, which can be inhibited by coculture with human bone marrow-derived MSCs (BMSCs) [32]. Mechanistically, this process can be mediated by human BMSC secreted angiopoietin-1 (Ang1) and keratinocyte growth factor (KGF) [32]. Moreover, in vivo experiments have shown that human BMSCs have a significant anti-inflammatory effect by increasing the number of M2 macrophages and releasing various cytokines and chemokines, such as interleukin (IL)-1, IL-4, IL-6, IL-8, and IL-17 [32]. Similar anti-inflammatory effects have been achieved in another virus-induced lung injury model. The intravenous injection of mouse BMSCs into H9N2 virus-infected mice significantly attenuates H9N2 virus-induced pulmonary inflammation by reducing chemokine (GM-CSF, MCP-1, KC, MIP-1, and MIG) and proinflammatory cytokine (IL-1, IL-6, TNF-, and IFN-) levels, as well as reducing inflammatory cell recruitment into the lungs [33]. Another study on human BMSCs cocultured with CD8+ T cells showed that MSCs inhibit the proliferation of virus-specific CD8+ T cells and the release of IFN- by specific CD8+ T cells [36].

In addition, human umbilical cord-derived MSCs (UC-MSCs) were found to have a similar effect as BMSCs on AFC, APP, and inflammation by secreting growth factors, including Ang1 and hepatocyte growth factor (HGF), in an in vitro lung injury model induced by H5N1 virus [34]. UC-MSCs also promote lung injury mouse survival, increase the body weight, and decreased the APP levels and inflammation in vivo [34]. Unlike Ang1, KGF, and HGF mentioned above, basic fibroblast growth factor 2 (FGF2) plays an important role in lung injury therapy via immunoregulation. The administration of the recombinant FGF2 protein improves H1N1-induced mouse lung injury and promotes the survival of infected mice by recruiting and activating neutrophils via the FGFR2-PI3K-AKT-NFB signaling pathway [37]. FGF2-overexpressing MSCs have an enhanced therapeutic effect on lipopolysaccharide-induced ALI, as assessed by the proinflammatory factor level, neutrophil quantity, and histopathological index of the lung [38].

MSCs secrete various soluble factors and extracellular vesicles (EVs), which carry lipids, proteins, DNA, mRNA, microRNAs, small RNAs, and organelles. These biologically active components can be transferred to recipient cells to exert anti-inflammatory, antiapoptotic, and tissue regeneration functions [39]. EVs isolated from conditioned medium of pig BMSCs have been demonstrated to have anti-apoptosis, anti-inflammation, and antiviral replication functions in H1N1-affected lung epithelial cells and alleviate H1N1-induced lung injury in pigs [35]. Moreover, the preincubation of EVs with RNase abrogates their anti-influenza activity, suggesting that the anti-influenza activity of EVs is due to the transfer of RNAs from EVs to epithelial cells [35]. Exosomes are a subset of EVs that are 50200nm in diameter and positive for CD63 and CD81 [40]. Exosomes isolated from the conditioned medium of UC-MSCs restore the impaired AFC and decreased APP in alveolar epithelial cells affected by H5N1 virus [34]. In addition, the ability of UC-MSCs to increase AFC is superior to that of exosomes, which indicates that other components secreted by UC-MSCs have synergistic effects with exosomes [34].

Despite accumulating evidence demonstrating the therapeutic effects of MSC administration in various preclinical models of lung injury, some studies have shown contrasting results. Darwish and colleagues proved that neither the prophylactic nor therapeutic administration of murine or human BMSCs could decrease pulmonary inflammation or prevent the progression of ALI in H1N1 virus-infected mice [41]. In addition, combining MSC administration with the antiviral agent oseltamivir was also found to be ineffective [41]. Similar negative results were obtained in another preclinical study. Murine or human BMSCs were administered intravenously to H1N1-induced ARDS mice [42]. Although murine BMSCs prevented influenza-induced thrombocytosis and caused a modest reduction in lung viral load, murine or human BMSCs failed to improve influenza-mediated lung injury as assessed by weight loss, the lung water content, and bronchoalveolar lavage inflammation and histology, which is consistent with Darwishs findings [42]. However, the mild reduction in viral load observed in response to murine BMSC treatment suggests that, on balance, MSCs are mildly immunostimulatory in this model [42]. Although there are some controversial incidents in preclinical research, the transplant of menstrual-blood-derived MSCs into patients with H7N9-induced ARDS was conducted at a single center through an open-label clinical trial (http://www.chictr.org.cn/). MSC transplantation significantly lowered the mortality and did not result in harmful effects in the bodies of the patients [43]. This clinic study suggests that MSCs significantly improve the survival rate of influenza virus-induced lung injury.

The effects of exogenous MSCs are exerted through their isolation and injection into test animals. There are also some stem/progenitor cells that can be activated to proliferate when various tissues are injured. Basal cells (BCs), distributed throughout the pseudostratified epithelium from the trachea to the bronchioles, are a class of multipotent tissue-specific stem cells from various organs, including the skin, esophagus, and olfactory and airway epithelia [44, 45]. Previously, TPR63+/KRT5+ BCs were shown to self-renew and divide into club cells and ciliated cells to maintain the pseudostratified epithelium of proximal airways [46]. Several studies have shown that TPR63+/KRT5+ BCs play a key role in lung repair and regeneration after influenza virus infection. When animals typically recover from H1N1 influenza infection, TPR63+/KRT5+ BCs accumulate robustly in the lung parenchyma and initiate an injury repair process to maintain normal lung function by differentiating into mature epithelium [47]. Lineage-negative epithelial stem/progenitor (LNEP) cells, present in the normal distal lung, can activate a TPR63+/KRT5+ remodeling program through Notch signaling after H1N1 influenza infection [48]. Moreover, a population of SOX2+/SCGB1A/KRT5 progenitor cells can generate nascent KRT5+ cells as an early response to airway injury upon H1N1 influenza virus infection [49]. In addition, a rare p63+Krt5 progenitor cell population also responds to H1N1 virus-induced severe injury [50]. This evidence suggests that these endogenous lung stem/progenitor cells (LSCs) play a critical role in the repopulation of damaged lung tissue following severe influenza virus infection (Table2).

Taken together, the present in vitro (Table1) and in vivo (Table2) results show that MSCs and LSCs are potential cell sources to treat influenza virus-induced lung injury.

Lung injury caused by SARS, MERS, or SARS-CoV-2 poses major clinical management challenges because there is no specific treatment that has been proven to be effective for each infection. Currently, virus- and host-based therapies are the main methods of treatment for spreading CoV infections. Virus- and host-based therapies include monoclonal antibodies and antiviral drugs that target the key proteins and pathways that mediate viral entry and replication [51].The major challenges in the clinical development of novel drugs include a limited number of suitable animal models for SARS-CoV, MERS-CoV, and SARS-CoV-2 infections and the current absence of new SARS and MERS cases [51]. Although the number of cases of SARS-CoV-2-induced pneumonia patients is continuously increasing, antibiotic and antiviral drugs are the primary methods to treat SARS-CoV-2-infected patients. Similar to that of IAV, human CoV-mediated damage to the respiratory epithelium results from both intrinsic viral pathogenicity and a robust host immune response. The excessive immune response contributes to viral clearance and can also worsen the severity of lung injury, including the demise of lung cells [52]. However, the present treatment approaches have a limited effect on lung inflammation and regeneration.

Stem cell therapy for influenza virus-induced lung injury shows promise in preclinical models. Although it is difficult to establish preclinical models of CoV-induced lung injury, we consider stem cell therapies to be effective approaches to improve human CoV-induced lung injury. Acute inflammatory responses are one of the major underlying mechanisms for virus-induced lung injury. Innate immune cells, including neutrophils and inflammatory monocytes-macrophages (IMMs), are major innate leukocyte subsets that protect against viral lung infections [53]. Both neutrophils and IMMs are rapidly recruited to the site of infection and play crucial roles in the host defense against viruses. Neutrophils and IMMs can activate Toll-like receptors (TLRs) and produce interferons (IFNs) and other cytokines/chemokines [54]. There are two functional effects produced by the recruitment of neutrophils and IMMs: the orchestration of effective adaptive T cell responses and the secretion of inflammatory cytokines/chemokines [55]. However, excessive inflammatory cytokine and chemokine secretion impairs antiviral T cell responses, leading to ineffective viral clearance and reduced survival [56].

MSCs are known to suppress both innate and adaptive immune responses. MSCs have been suggested to inhibit many kinds of immune cells, including T cells, B cells, dendritic cells (DCs), and natural killer (NK) cells in vitro and in vivo [57] (Fig.1). Several molecules, including IL-1, TNF-, and INF-, most of which are produced by inflammatory cells, are reported to be involved in MSC-mediated immunosuppression [58]. Furthermore, MSCs can produce numerous immunosuppressive molecules, such as IL-6, PGE2, IDO, and IL-10, in response to inflammatory stimuli. PGE2 has been reported to mediate the MSC-mediated suppression of T cells, NK cells, and macrophages. Moreover, PGE2 has been found to act with IDO to alter the proliferation of T cells and NK cells [59]. In contrast, MSCs have come to be recognized as one type of adult stem cell actively participating in tissue repair by closely interacting with inflammatory cells and various other cell types [60]. Numerous reports have demonstrated that MSCs can release an array of growth and inhibitory factors, such as EGF, FGF, PDGF, and VEGF, and express several leukocyte chemokines, such as CXCL9, CCL2, CXCL10, and CXCL11. These factors provide an important microenvironment to activate adaptive immunity for lung repair [61]. Thus, the dual functions of MSCs may improve lung recovery after human CoV-induced ALI. Recently, MSCs was transplanted intravenously to enrolled patients with COVID-19 pneumonia. After treatment, the pulmonary function and symptoms of these patients were significantly improved. Meanwhile, the peripheral lymphocytes were increased, the C-reactive protein decreased, the level of TNF- was significantly decreased, and the overactivated cytokine-secreting immune cells disappeared. In addition, a group of regulatory DC cell population dramatically increased. Thus, the intravenous transplantation of MSCs was effective for treatment in patients with COVID-19 pneumonia [62, 63].

Stem cell therapies for treatment of influenza virus and coronavirus-induced lung injury. CoVs, coronavirus; MSCs, mesenchymal stem/stromal cells; LSCs, lung stem/progenitor cells; NK cells, natural killer cells; DC cells, dendritic cells

In addition, endogenous LSCs also play an important role in lung cell reconstitution after virus-induced ALI. In particular, TPR63+/KRT5+ airway BCs comprise approximately equal numbers of stem cells and committed precursors and give rise to differentiated luminal cells during steady state and epithelial repair after lung injury [44, 64]. Research has shown that KRT5+ cells repopulate damaged alveolar parenchyma following influenza virus infection [47]. However, there is still little evidence for the role of altered TPR63+/KRT5+ stem cells during lung injury repair caused by human CoVs.

In summary, exogenous MSCs may modulate human CoV-induced lung injury repair and regeneration through their immunoregulatory properties. These cells are capable of interacting with various types of immune cell, including neutrophils, macrophages, T cells, B cells, NK cells, and DCs. Furthermore, viral infections can activate endogenous LSCs to produce new lung cells and maintain lung function (Fig.1). Thus, we propose that MSCs and LSCs are two potential cell sources for treating human CoV-induced lung injury.

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Stem cell therapy: a potential approach for treatment of influenza virus and coronavirus-induced acute lung injury - BMC Blogs Network

Stem Cell Source Market Latest Research Report 2020:

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Scope of Stem Cell Source Market:Products in the Stem Cell Source classification furnish clients with assets to get ready for tests, tests, and evaluations.

Major Company Profiles Covered in This Report

BD Bioscience, Beckman Coulter, Ge Healthcare, Merck Millipore, Miltenyi Biotec, Pluriselect Life Science, Sigma-Aldrich Corporation, Stemcell Technologies, Terumo BCT, Thermo Fisher ScientificCompany 13,

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Stem Cell Source Market Report Covers the Following Segments:

Market segment by Type, the product can be split into

Reagent, Instrument, Others,

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Hospital, Biotechnology Research Center, Others,

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United States

Europe

China

Japan

Southeast Asia

India

Central & South America

North America

Europe

Asia-Pacific

South America

Center East and Africa

United States, Canada and Mexico

Germany, France, UK, Russia and Italy

China, Japan, Korea, India and Southeast Asia

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Stem Cell Source Market Size Analysis and Growth (2020-2025) - 3rd Watch News

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Market split the breakdown knowledge by company, products, end-user, and prime countries, Stem Cell Cartilage Regeneration Market history knowledge from 2015 to 2019 and forecast to 2026.

Analysis of Stem Cell Cartilage Regeneration Market regarding individual growth trends, future prospects, and their contribution to the overall Stem Cell Cartilage Regeneration Market.

Global Stem Cell Cartilage Regeneration Market 2020 report analyzes competitive expansions like agreements, new product launches, and Stem Cell Cartilage Regeneration Market acquisition.

Research report target the key international Stem Cell Cartilage Regeneration players to characterize sales volume, Stem Cell Cartilage Regeneration revenue, growth potential, drivers, SWOT analysis, and Stem Cell Cartilage Regeneration development plans in coming years.

**Note:Access insightful study with over 150+ pages, list of tables & figures, profiling 20+ companies.

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Highlights of the Global Stem Cell Cartilage Regeneration report:

The report has been collated on the basis of synthesis, analysis, and interpretation of data accumulated with regards to the parent market from various resources. Additionally, study has been made of the economic conditions and other economic indicators and factors to evaluate their respective impact on the Stem Cell Cartilage Regeneration Market, along with the present impact, so as to make strategic and informed forecasts about the scenarios in the market. This is primarily because of the untapped potentials present in the developing nations, in terms of product pricing and revenue generation.

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Stem Cell Cartilage Regeneration Market: Analysis of Prevailing Trends In The Parent Market 2026 - Cole of Duty

This report studies the Stem Cell Cartilage Regenerationmarket status and outlook of global and United States, from angles of players, regions, product types and end industries; this report analyzes the top players in global and United States market, and splits the Stem Cell Cartilage Regenerationmarket by product type and applications/end industries.

Among the several objectives of the research study, it provides a detailed description of recent trends, technological advancements, and various platforms, which further are beneficial to improve the performance of the companies.

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Key players in global Stem Cell Cartilage Regeneration market include: Anika Therapeutics, Biomet, BioTissue Technologies, DePuy (Johnson & Johnson), Genzyme, CellGenix, EMD Serono, Sanofi Aventis, Smith & Nephew, Zimmer

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This report provides pin-point analysis for changing competitive dynamics

It provides a forward looking perspective on different factors driving or restraining market growth

It provides a six-year forecast assessed on the basis of how the market is predicted to grow

It helps in understanding the key product segments and their future

It provides pin point analysis of changing competition dynamics and keeps you ahead of competitors

It helps in making informed business decisions by having complete insights of market and by making in-depth analysis of market segments

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Stem Cell Cartilage Regeneration Market 2020 by Manufacturers, Regions, Product Types, Application, Sales, Revenue and Forecast to 2027 | Anika...

Allogeneic Stem Cell Therapy Market 2018: Global Industry Insights by Global Players, Regional Segmentation, Growth, Applications, Major Drivers, Value and Foreseen till 2024

The report provides both quantitative and qualitative information of global Allogeneic Stem Cell Therapy market for period of 2018 to 2025. As per the analysis provided in the report, the global market of Allogeneic Stem Cell Therapy is estimated to growth at a CAGR of _% during the forecast period 2018 to 2025 and is expected to rise to USD _ million/billion by the end of year 2025. In the year 2016, the global Allogeneic Stem Cell Therapy market was valued at USD _ million/billion.

This research report based on Allogeneic Stem Cell Therapy market and available with Market Study Report includes latest and upcoming industry trends in addition to the global spectrum of the Allogeneic Stem Cell Therapy market that includes numerous regions. Likewise, the report also expands on intricate details pertaining to contributions by key players, demand and supply analysis as well as market share growth of the Allogeneic Stem Cell Therapy industry.

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Allogeneic Stem Cell Therapy Market Overview:

The Research projects that the Allogeneic Stem Cell Therapy market size will grow from in 2018 to by 2024, at an estimated CAGR of XX%. The base year considered for the study is 2018, and the market size is projected from 2018 to 2024.

The report on the Allogeneic Stem Cell Therapy market provides a birds eye view of the current proceeding within the Allogeneic Stem Cell Therapy market. Further, the report also takes into account the impact of the novel COVID-19 pandemic on the Allogeneic Stem Cell Therapy market and offers a clear assessment of the projected market fluctuations during the forecast period. The different factors that are likely to impact the overall dynamics of the Allogeneic Stem Cell Therapy market over the forecast period (2019-2029) including the current trends, growth opportunities, restraining factors, and more are discussed in detail in the market study.

Leading manufacturers of Allogeneic Stem Cell Therapy Market:

The key players covered in this studyEscape Therapeutics, Inc.Lonza Group Ltd.Osiris Therapeutics (Smith & Nephew)NuVasiveChiesi PharmaceuticalsJCR PharmaceuticalPharmicellAnterogenMolMed S.p.A.Takeda (TiGenix)

Market segment by Type, the product can be split intoAdult Stem Cell TherapyHuman Embryonic Stem Cell TherapyInduced Pluripotent Stem Cell TherapyOthersMarket segment by Application, split intoMusculoskeletal DisorderWounds & InjuriesCardiovascular DiseasesOthers

Market segment by Regions/Countries, this report coversNorth AmericaEuropeChinaJapanSouth Korea

The study objectives of this report are:To analyze global Allogeneic Stem Cell Therapy status, future forecast, growth opportunity, key market and key players.To present the Allogeneic Stem Cell Therapy development in North America, Europe, China, Japan and South Korea.To strategically profile the key players and comprehensively analyze their development plan and strategies.To define, describe and forecast the market by type, market and key regions.

In this study, the years considered to estimate the market size of Allogeneic Stem Cell Therapy are as follows:History Year: 2015-2019Base Year: 2019Estimated Year: 2020Forecast Year 2020 to 2026For the data information by region, company, type and application, 2019 is considered as the base year. Whenever data information was unavailable for the base year, the prior year has been considered.

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Some important highlights from the report include:

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The Questions Answered by Allogeneic Stem Cell Therapy Market Report:

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COVID-19: Responding to the business impacts of Allogeneic Stem Cell Therapy Revenue, Opportunity, Forecast and Value Chain 2019-2020 - Cole of Duty