This report is 80% complete and can be delivered within three working days post order confirmation and will include the latest impact analysis of Covid-19 in 2020 and forecast. Global Regenerative Medicine Market By Therapy (Cell-Based Immunotherapy & Cell Therapy, Gene Therapy, Others), By Application (Musculoskeletal Disorders, Wound Care, Others), By Material (Synthetic Material, Biologically Derived Material, Others), By Cell (Autologous, Allogenic), By Product (Biologic, Cell -based Medical Devices, Others), By Technique (Microfracture, Mosaicplasty), By Distribution Channel (Hospitals, Clinics , Others), By Region, Forecast & Opportunities, 2025

New York, June 30, 2020 (GLOBE NEWSWIRE) -- Reportlinker.com announces the release of the report "Global Regenerative Medicine Market By Therapy, By Application, By Material, By Cell, By Product, By Technique, By Distribution Channel, By Region, Forecast & Opportunities, 2025" - https://www.reportlinker.com/p05916746/?utm_source=GNW

Global regenerative medicine market is expected to register a double digit CAGR through 2025 owing to their increasing use in repair, replacement or regeneration of cells, tissues and organs. Additionally, high prevalence of chronic & genetic dieses, emergence of stem cell technology and growing aging populations are some of the key factors driving the regenerative medicine market.

Regenerative medicines deal with process of replacing, engineering or regenerating human or animal cells, tissues or organs to restore or establish normal function.They are also being used to create solutions for organs that become permanently damaged.

These medicines are also used in treatment of some uncurable dieses like arthritis and diabetes. Increasing number of cancer patients, neurodegenerative, orthopedic, and other aging-associated disorders is creating a significant demand for regenerative medicine market globally. Various countries like United States, China and Japan are investing in stem cell research, which indicates a bright future for regenerative medicine manufacturers.

The global regenerative medicine market also faces some restraints like high treatment costs, stringent government regulations and operative inefficiency. High investment required for developing the medicine might also limit the market growth.

The market is segmented based on therapy, application, material, cell, product, technique, distribution channel and region.The application segment comprises of musculoskeletal disorders, wound care, oncology, neurology, ocular disorders, diabetes, cardiology and others.

Out of them, the musculoskeletal segment is expected to dominate the market during the forecast years owing to growing use of regenerative medicines for treating musculoskeletal disorders and increasing number of orthopedic diseases.Based on material, the regenerative medicine market is segmented into synthetic material, biologically derived material, genetically engineered material and pharmaceutical.

The biologically derived material dominated the regenerative medicine market in 2019 and is expected to further hold its position in the coming years due to its unique properties. This type of material promotes cellular interactions, increases proliferation and controls the manipulation of cellular behavior. Major players operating in the global regenerative medicine market include Novartis AG, Vericel, Integra Lifesciences, Mimedx Group, Stryker, Wright Medical, Roche, Bristol-Myers Squibb, Allergan, Corline Biomedical, Cook Biotech, Pfizer, Baxter, Boehringer Ingelheim, Caladrius Biosciences, Takara Bio, Medtronic, Osiris Therapeutics, Kite Pharma, Organogenesis and others. Due to growing demand from Asia-Pacific region, the manufacturers are focusing on countries like India and China where geriatric population is increasing rapidly.

Years considered for this report:

Historical Years: 2015-2018 Base Year: 2019 Estimated Year: 2020 Forecast Period: 20212025

Objective of the Study:

To analyze and forecast the market size of global regenerative medicine market. To classify and forecast global regenerative medicine market based on therapy, application, material, cell, product, technique, distribution channel and regional distribution. To identify drivers and challenges for global regenerative medicine market. To examine competitive developments such as expansions, new product launches, mergers & acquisitions, etc., in global regenerative medicine market. To conduct pricing analysis for global regenerative medicine market. To identify and analyze the profile of leading players operating in global regenerative medicine market. The analyst performed both primary as well as exhaustive secondary research for this study.Initially, the analyst sourced a list of manufacturers across the globe.

Subsequently, the analyst conducted primary research surveys with the identified companies.While interviewing, the respondents were also enquired about their competitors.

Through this technique, the analyst could include the manufacturers which could not be identified due to the limitations of secondary research. The analyst examined the manufacturers, distribution channels and presence of all major players across the globe. The analyst calculated the market size of global regenerative medicine market using a bottom-up approach, wherein data for various end-user segments was recorded and forecast for the future years. The analyst sourced these values from the industry experts and company representatives and externally validated through analyzing historical data of these product types and applications for getting an appropriate, overall market size.

Various secondary sources such as company websites, news articles, press releases, company annual reports, investor presentations and financial reports were also studied by the analyst.

Key Target Audience:

Regenerative medicine manufacturers, suppliers, distributors and other stakeholders Government bodies such as regulating authorities and policy makers Organizations, forums and alliances related to regenerative medicines Market research and consulting firms The study is useful in providing answers to several critical questions that are important for the industry stakeholders such as manufacturers, suppliers, partners, end users, etc., besides allowing them in strategizing investments and capitalizing on market opportunities.

Report Scope:

In this report, global regenerative medicine market has been segmented into following categories, in addition to the industry trends which have also been detailed below: Market, By Therapy: o Cell-Based Immunotherapy & Cell Therapy o Gene Therapy o Tissue-Engineering o Immunomodulation Therapy o Blood Transfusion o Bone Marrow Transplantation o Plasma Rich Plasma Therapy o Prolotherapy o Others Market, By Application: o Musculoskeletal Disorders o Wound Care o Oncology o Neurology o Ocular Disorders o Diabetes o Cardiology o Others Market, By Material: o Synthetic Material - Biodegradable Synthetic Polymers - Scaffold - Artificial Vascular Graft Materials - Hydrogel Materials o Biologically Derived Material - Collagen - Xenogeneic Material o Genetically Engineered Material - Genetically Manipulated Cells - 3D Polymer Technology - Transgenic - Fibroblast - Neural Stem Cells - Gene-activated Matrices o Pharmaceutical - Small Molecules - Biologics Market, By Cell: o Autologous o Allogenic Market, By Product: o Biologic o Cell -based Medical Devices o Biopharmaceutical o Biomaterial Market, By Technique: o Microfracture o Mosaicplasty Market, By Distribution Channel: o Hospitals o Clinics o Online o Others Market, By Region: o North America - United States - Canada - Mexico o Europe - Germany - France - United Kingdom - Italy - Spain o Asia-Pacific - China - Japan - India - South Korea - Australia o Middle East & Africa - South Africa - Saudi Arabia - UAE o South America - Brazil - Argentina - Colombia

Competitive Landscape

Company Profiles: Detailed analysis of the major companies present in global regenerative medicine market.

Available Customizations:

With the given market data, we offers customizations according to a companys specific needs. The following customization options are available for the report:

Company Information

Detailed analysis and profiling of additional market players (up to five).

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Global Regenerative Medicine Market By Therapy, By Application, By Material, By Cell, By Product, By Technique, By Distribution Channel, By Region,...

SAN CARLOS, Calif., July 01, 2020 (GLOBE NEWSWIRE) -- BioCardia, Inc. [NASDAQ:BCDA], a leader in the development of comprehensive solutions for cardiovascular regenerative therapies, today announced activation of a pivotal trial studying the Companys investigational CardiAMP cell therapy in the treatment of chronic myocardial ischemia (CMI), as well as completion of the first site initiation visit in the trial.

The CardiAMP CMI Trial is studyingCardiAMP cell therapy, an autologous cell therapy formulation designed to stimulate the bodys natural healing response for the treatment of refractory angina, estimated to impact between 600,000 and 1,800,000 patients in the United States.1 It has been reported that these patients suffer from poor perceived health status and psychological distress, have significant impairments in quality of life, and represent a burden to the health care system due to significant resource use.2

The study has been approved by the FDA to enroll up to 343 patients at up to 40 centers. The purpose of the study is to determine the safety and efficacy of CardiAMP cell therapy in the treatment of patients with refractory angina pectoris and CMI. The FDA has said that the trial qualifies as a pivotal trial to produce the primary data to support market registration for the CardiAMP cell therapy for this significant unmet clinical need.

The Center for Medicare and Medicaid Services (CMS) will reimburse investigational sites for patient screening, patient treatment, the investigational cell therapy product, and standard of care follow-up visits at a level similar to that being provided for the ongoing pivotal CardiAMP Heart Failure Trial.

The first site initiation visit took place last week at the University of Florida at Gainesville, under the leadership of R. David Anderson, MD. Patient recruitment is expected to begin shortly.

We are pleased to be activating a second pivotal trial for the CardiAMP cell therapy and expanding our relationship with the clinical research team at the University of Florida under the guidance of Dr. Anderson, who is also the site principal investigator of the ongoing CardiAMP Heart Failure Trial and a world class interventional cardiologist, said BioCardia Chief Executive Officer Peter Altman, Ph.D. We are also delighted to announce the experienced and distinguished executive steering committee for the trial, which includes Dr. Timothy Henry of The Christ Hospital, Dr. Carl Pepine of the University of Florida, Dr. Amish Raval of the University of Wisconsin, and Dr. Bernard Gersh of the Mayo Graduate School of Medicine.

Based on our experience with 75 patients randomized in the CardiAMP Heart Failure trial, the effective CD34+ cell dosage in the CardiAMP Chronic Myocardial Ischemia trial is likely to be greater than the effective CD34+ dosage advanced in previously published trials for selected CD34+ cells which demonstrated compelling clinical results, said BioCardia Chief Medical Officer Eric Duckers, M.D. 3 This is possible with patient selection, efficient delivery, and point of care cell processing, which are the pillars of the CardiAMP therapy.

For additional information, please visit http://www.clinicaltrials.gov.

About BioCardia:BioCardia, Inc., headquartered in San Carlos, CA, is developing regenerative biologic therapies to treat cardiovascular disease. CardiAMP autologous and NK1R+ allogenic cell therapies are the Companys biotherapeutic platforms in clinical development. The Company's products include theHelix biotherapeutic delivery system and its steerable guide and sheath catheter portfolio.BioCardia also partners with other biotherapeutic companies to provide its Helix system and clinical support to their programs studying therapies for the treatment of heart failure, chronic myocardial ischemia and acute myocardial infarction. For more information, visit http://www.BioCardia.com.

Forward Looking Statements:This press release contains forward-looking statements that are subject to many risks and uncertainties. Forward-looking statements include references to future enrollment and cell dosage in this second pivotal clinical trial and statements regarding our intentions, beliefs, projections, outlook, analyses or current expectations. Such factors include, among others, the inherent uncertainties associated with developing new products or technologies and obtaining regulatory approvals. These forward-looking statements are made as of the date of this press release, and BioCardia assumes no obligation to update the forward-looking statements.

INVESTOR CONTACT:David McClung, Chief Financial Officerinvestors@BioCardia.com, (650) 226-0120

MEDIA CONTACT:Michelle McAdam, Chronic Communications, Inc.michelle@chronic-comm.com, (310) 902-1274

Original post:
BioCardia Announces Activation of Pivotal Trial Studying CardiAMP Cell Therapy Trial to Treat Chronic Myocardial Ischemia - GlobeNewswire

Batten disease is a family of 13 rare, genetically distinct conditions. Collectively, they are the most prevalent cause of neurodegenerative disease in children, affecting 1 in 12,500 live births in the U.S. One of the Batten disease genes is CLN6. How mutations in this gene lead to the disease has been a mystery, but a study led by researchers at Baylor College of Medicine and published in the Journal of Clinical Investigation reveals how defective CLN6 can result in Batten disease.

People with Batten disease have problems with their cells ability to clear cellular waste, which then accumulates to toxic levels, said first author Dr. Lakshya Bajaj, who was working on this project while a doctorate student in the laboratory of Dr. Marco Sardiello at Baylor. Bajaj is currently a post-doctoral associate at Harvard Medical School.

In cells, lysosomes process cellular waste. They are sacs containing enzymes, a type of proteins that break down waste products into its constituent components that the cell can recycle or discard. In Batten disease caused by mutations in CLN6, the lysosomes do not process waste effectively for unknown reasons. This results in waste accumulation. Batten disease is a type of lysosomal storage disorder. Although all types of cells can be affected by defects in lysosomal waste management, brain cells, neurons, are particularly susceptible.

Waste accumulation in neurons perturbs many cellular processes and eventually results in cell death. This leads to the progressive degeneration of motor, physical and intellectual abilities observed in Batten disease patients, Bajaj said.

CLN6: another piece of the Batten disease puzzle

The connection of CLN6 with Batten disease was a bit of a mystery. This protein is not found in lysosomes, but in the endoplasmic reticulum, a structure inside cells where proteins, including lysosomal enzymes, are made. The endoplasmic reticulum is separate from the lysosomes. So, how do defects in a protein located outside of the lysosomes interfere with lysosomal function?

The Sardiello lab had previously solved a similar mystery involving CLN8, another protein located in the endoplasmic reticulum and whose mutations also cause a type of Batten disease.

We showed that CNL8 assists on the exit of lysosomal enzymes from the endoplasmic reticulum en route to the lysosomes. When CLN8 is defective, the transport of enzymes from their place of synthesis to the final destination is deficient and the lysosomes end up having fewer enzymes to work with, said Sardiello, associate professor of molecular and human genetics at Baylor and corresponding author of this work.

CLN6 and CLN8 work together

The clinical manifestations of Batten disease caused by CLN8 mutations and those of Batten disease due to defective CLN6 are remarkably similar. This and other evidence led the researchers to suspect that CLN6 and CLN8 might be working together.

Their investigations revealed that CLN6 and CLN8 do interact with each other forming a molecular complex that collects lysosomal enzymes at the endoplasmic reticulum and mediates their trafficking towards the lysosomes.

We propose that CLN8 and CLN6 together herd the enzymes into a hub, a sort of bus stop. Then, CLN8 escorts the enzymes on the bus en route to the lysosomes, while CLN6 remains at the bus stop. CLN8 returns to the bus stop after delivering the enzymes, and they repeat the process, Bajaj said. When CLN6 is defective, the enzymes are not effectively herded into the bus stop and fewer are transported to the lysosomes.

The researchers are interested in finding whether other factors are involved in transporting enzymes to the lysosomes. For instance, whether there are other bus conductors or herders of lysosomal enzymes involved that, if defective, may also contribute to Batten disease.

Other contributors to this work include Jaiprakash Sharma, Alberto di Ronza, Pengcheng Zhang, Aiden Eblimit, Rituraj Pal, Dany Roman, John R. Collette, Clarissa Booth, Kevin T. Chang, Richard N. Sifers, Sung Y. Jung, Jill M. Weimer, Rui Chen and Randy W. Schekman. The authors are affiliated with one or more of the following institutions: Baylor College of Medicine; Texas Childrens Hospital; University of California, Berkeley; Sanford Research, Sioux Falls, South Dakota; and Sanford School of Medicine at the University of South Dakota.

This work was supported by NIH grants NS079618 and GM127492 and grants from the Gwenyth Gray Foundation, Beyond Batten Disease Foundation and NCL-Stiftung. This project was supported in part by IDDRC grant number 1U54 HD083092 from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the Integrated Microscopy Core and the Proteomics Core at Baylor College of Medicine with funding from NIH (DK56338, and CA125123), CPRIT (RP150578, RP170719), the Dan L Duncan Comprehensive Cancer Center and the John S. Dunn Gulf Coast Consortium for Chemical Genomics.

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Solving the CNL6 mystery in Batten disease - Milwaukee Community Journal

Global Stem Cell Banking Market: Overview

The demand within the global stem cell banking market is growing on account of advancements in the field of regenerative medicine. The medical fraternity has become extremely focused towards the development of artificial tissues that can infuse with the human body. Furthermore, medical analysis and testing has gathered momentum across biological laboratories and research institutes. Henceforth, it is integral to develop stem cell samples and repositories that hold relevance in modern-day research. The need for regenerative medicine emerges from the growing incidence of internal tissue rupture. Certain types of tissues do not recover for several years, and may even be damaged permanently. Therefore, the need for stem cell banking is expected to grow at a significant pace.

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In a custom report, TMR Research digs into the factors that have aided the growth of the global stem cell banking market. The global stem cell banking market can be segmented on the basis of bank size, application, and region. The commendable developments that have incepted across the US healthcare industry has given a thrust to the growth of the North America stem cell banking market.

Global Stem Cell Banking Market: Notable Developments

The need for improved regenerative medication and anatomy has played an integral role in driving fresh developments within the stem cell banking market.

Gallant has emerged as a notable market entity that has remained as the torchbearer of innovation within the global stem cell banking market. The company has recently launched stem cell banking for dogs, and has attracted the attention of the masses. As people become increasingly concerned about their pets, the new move by Gallant shall help the company in earning the trust of the consumers. Moreover, it can move several notches higher on the innovation index.

Cells4Life has also remained at the forefront of developments within the global stem cell banking market. After suffering backlash for its error in cord blood stem cell promotion, the company is expected to use effective public relation strategies to regain its value in the market.

Global Stem Cell Banking Market: Growth Drivers

Development of improved facilities for storage of stem cells has played an integral role in driving market demand. Furthermore, the unprecedented demand for improved analysis of regenerative medications has also created new opportunities within the global stem cell banking market. Medical research has attracted investments from global investors and stakeholders. The tremendous level of resilience shown by biological researchers to develop stem cell samples has aided market growth. Henceforth, the total volume of revenues within the global stem cell banking market is slated to multiply.

Commercialization of stem cell banks has emerged as matter of concern for the healthcare industry. However, this trend has also helped in easy storage and procurement of cells stored during the yester years of children. Presence of sound procedures to register at stem cell banks, and the safety offered by these entities, has generated fresh demand within the global market. New regional territories are opening to the idea of stem cell banking. Several factors are responsible for the growth of this trend. Primarily, improvements in stem cell banking can have favourable impact on the growth of the healthcare industry. Moreover, the opportunities for revenue generation associated with the development of functional stem cell banks has aided regional market growth.

The global stem cell banking market is segmented on the basis of:

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Stem Cell Banking Market Global Industry Analysis and Opportunity and Forecast 2018 to 2028 - Cole of Duty

The reports seemed to take doctors by surprise: The respiratory virus that causes Covid-19 made some patients nauseous. It left others unable to smell. In some, it caused acute kidney injury.

As the pandemic grew from an outbreak affecting thousands in Wuhan, China, to some 10 million cases and 500,000 deaths globally as of late June, the list of symptoms has also exploded. The Centers for Disease Control and Prevention constantly scrambled to update its list in an effort to help clinicians identify likely cases, a crucial diagnostic aid at a time when swab tests were in short supply and typically took (and still take) days to return results. The loss of a sense of smell made the list only in late April.

For many diseases, it can take years before we fully characterize the different ways that it affects people, said nephrologist Dan Negoianu of Penn Medicine. Even now, we are still very early in the process of understanding this disease.

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What they are understanding is that this coronavirus has such a diversity of effects on so many different organs, it keeps us up at night, said Thomas McGinn, deputy physician in chief at Northwell Health and director of the Feinstein Institutes for Medical Research. Its amazing how many different ways it affects the body.

One early hint that that would be the case came in late January, when scientists in China identified one of the two receptors by which the coronavirus, SARS-CoV-2, enters cells. It was the same gateway, called the ACE2 receptor, that the original SARS virus used. Studies going back some two decades had mapped the bodys ACE2 receptors, showing that theyre in cells that line the insides of blood vessels in what are called vascular endothelial cells in cells of the kidneys tubules, in the gastrointestinal tract, and even in the testes.

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Given that, its not clear why the new coronavirus ability to wreak havoc from head to toe came as a surprise to clinicians. Since ACE2 is also the receptor for SARS, its expression in other organs and cell types has been well-known, said Anirban Maitra of MD Anderson Cancer Center, who led a study mapping the receptor in cells of the GI tract. (Maitra is an expert in pancreatic cancer and, like many scientists this year, added Covid-19 to his research.)

Infecting cells is only the first way SARS-CoV-2 wreaks havoc. Patients with severe Covid-19 also suffer a runaway inflammatory response and, often, clot formation, said infectious disease physician Rochelle Walensky of Massachusetts General Hospital. That can cause symptoms as different as a lack of blood flow to the intestines and the red, inflamed Covid toe.

Weve had five cases of patients whove had to have their gut removed, Walensky said. You see these cases and you say, wait a minute; the virus is doing this, too? It has definitely been keeping us on our toes.

Venky Soundararajan had a hunch that the extent of ACE2 distribution throughout the body was lying in plain sight. The co-founder and chief scientific officer of nference, which uses artificial intelligence to mine existing knowledge, he and his colleagues turned their system into a hunt for ACE2 knowledge. Combing 100 million biomedical documents from published papers to genomic and other -omics databases, they uncovered multiple tissues and cell types with ACE2 receptors, they reported last month in the journal eLife.

They also calculated what percent of each cell type expresses reasonable amounts of ACE2, Soundararajan said. On average, about 40% of kidney tubule cells do, and in a surprise for a respiratory virus, cells in the GI tract were the strongest expressors of ACE2 receptors, he said.

The data mining found that ACE2 is also expressed in the noses olfactory cells. Thats not a new finding per se the nference system found it in existing databases, after all but it hadnt been appreciated by scientists or clinicians. It explains the loss or altered sense of smell that Covid-19 patients experience. Its importance became clear earlier this month, when scientists at the Mayo Clinic and nference reported that loss of a sense of smell is the earliest signature of Covid-19, appearing days before a positive swab test.

That study, using health records of 77,167 people tested for Covid-19, showed how the assumption that infection would first and foremost cause respiratory symptoms was misplaced. In the week before they were diagnosed, Covid-19 patients were 27 times more likely than people who tested negative for the virus to have lost their sense of smell. They were only 2.6 times more likely to have fever or chills, 2.2 times more likely to have trouble breathing or to be coughing, and twice as likely to have muscle aches. For months, government guidelines kept people not experiencing such typical signs of a respiratory infection from getting tested.

Faced with a disease the world had never seen before, physicians are learning as they go. By following the trail of ACE2 receptors, they are more and more prepared to look for, and treat, consequences of SARS-CoV-2 infection well beyond the obvious:

Gut: The coronavirus infects cells that line the inside of the large and small intestine, called gut enterocytes. That likely accounts for the diarrhea, nausea, and abdominal pain that about one-third of Covid-19 patients experience, said MD Andersons Maitra: The GI symptoms reflect physiological [dysfunction] of cells of the lower GI tract.

Why dont all patients have GI symptoms or indeed, the whole panoply of symptoms suggested by the near ubiquity of ACE2 receptors? For those with mild to moderate Covid-19, the infectious load in the GI tract may simply not be sufficient to cause symptoms, Maitra said.

Kidney: The cells lining the tubules that filter out toxic compounds from the blood are rife with ACE2 receptors. Last month, scientists studying 1,000 Covid-19 patients at a New York City hospital reported that 78% of those in intensive care developed acute kidney injury.

Smell: An analysis of 24 studies with data from 8,438 Covid-19 patients from 13 countries found this month that 41% had lost their sense of taste or smell, or both. That shouldnt be surprising, said Fabio Ferreli of Humanitas University in Milan: Perhaps the highest levels of ACE2 receptors are expressed in cells in the nasal epithelium. The sensory loss isnt due to nasal inflammation, swelling, or congestion, he said, but to direct damage to these epithelial cells. Loss of smell also impacts taste, but the virus may also have a direct effect on taste: The nference analysis found high levels of the ACE2 gene in tongue cells called keratinocytes, which contribute to the sense of taste.

There is another implication of the high expression of ACE2 in olfactory epithelium cells, scientists at Johns Hopkins concluded in a paper posted to the preprint site bioRxiv last month: ACE2 levels in the olfactory epithelium of the upper airways that are 200 to 700 times higher than in the lower airways might explain the viruss high transmissibility. It was weeks before experts recognized that the virus could spread from person to person.

Lungs: This is where a respiratory virus should strike, and SARS-CoV-2 does. The lungs type II alveolar cells among other jobs, they release a compound that allows the lungs to pass oxygen to the blood and take carbon dioxide from it are studded with ACE2 receptors. Once infected with the coronavirus, they become dysfunctional or die, and are so swarmed by immune cells that this inflammatory response can explode into the acute respiratory distress syndrome (ARDS) that strikes many patients with severe Covid-19, Walensky said.

There is new evidence that the virus also attacks platelet-producing cells, called megakaryocytes, in the lungs. In a study published on Thursday, pathologist Amy Rapkiewicz of NYU Winthrop Hospital found something she had never seen before: extensive clotting in the veins and other small blood vessels of patients hearts, kidneys, liver, and lungs. She suspects that the platelets produced by infected megakaryocytes travel through the bloodstream to multiple organs, damaging their vasculature and producing potentially fatal clots. You see that and you say, wow, this is not just a respiratory virus,' Rapkiewicz said.

Pancreas: In April, scientists in China reported that there was higher expression of the gene for ACE2 in the pancreas than in the lungs. Genetic data are an indirect measure of ACE2 receptors themselves, but could have been a tip-off to physicians to monitor patients for symptoms there. As it happens, the Chinese researchers also found blood markers for pancreas damage in Covid-19 patients, including in about 17% of those with severe disease.

Heart: Patients with severe Covid-19 have a high incidence of cardiac arrests and arrhythmias, scientists at the Perelman School of Medicine at the University of Pennsylvania recently found. Thats likely due to an extreme inflammatory response, but there might be more direct effects of the coronavirus, too. A large team of European researchers reported in April that arrhythmia (including atrial fibrillation), heart injury, and even heart failure and pulmonary embolism might reflect the fact that ACE2 receptors are highly expressed in cells along the inside walls of capillaries. When these vascular endothelial cells become infected, the resulting damage can cause clots, MGHs Walensky said, which in turn can cause Covid toe, strokes, and ischemic bowel (too little blood flow to the gut). Studies from around the world suggest that 7% to 31% of Covid-19 patients experience some sort of cardiac injury.

Gallbladder: Specialized cells in this organ, too, have high levelsof ACE2 receptors. Damage to the gallbladder (like the pancreas) can cause digestive symptoms.

With the number of Covid-19 patients closing in on 10 million, physicians fervently hope the virus has no more surprises in store. But theyre not counting on it.

Ive seen patients every day during this crisis, said Northwells McGinn. There have been times when Ive said, wait, the virus cant do anything new and then theres a young woman with a stroke or an older man with myocarditis, inflammation of the heart muscle. I keep thinking Im going to run out of material for the teaching videos he does on Covid-19, but it hasnt happened.

Correction: An earlier version of the video misstated how SARS-CoV-2 replicates inside cells it infects.

The rest is here:
Not just the lungs: Covid-19 attacks like no other 'respiratory' virus - STAT

Cancer metastasis is all about rogue cancer cells abandoning the original tumor and venturing through the blood in search for new breeding grounds. Sometimes, single cells take the risk, but other times cancer cells detach from the tumor as clusters.

Scientific evidence shows that clusters seem to be more successful at metastasis than single cells and recent work from the laboratory of Dr. Xiang Zhang sheds new light into what contributes to the clusters enhanced metastatic abilities.

We were working with different animal models investigating why tumor clusters seemed to be better at forming lung metastases than single cells, when we unexpectedly discovered that the clusters ability to metastasize appeared to be associated with the presence of competent natural killer (NK) cells, said first author Hin Ching Flora Lo, graduate student in Baylors Integrative Molecular and Biomedical Sciences Graduate Program in the Zhang lab. Zhang is professor of molecular and cellular biology and the Lester and Sue Smith Breast Center at Baylor.

The researchers determined that activated NK cells, immune cells that specialize in surveillance and destruction of tumor cells, can eliminate both single cell and cluster metastasis, but they are more efficient at eliminating the former. The clusters have a selective advantage and, as a result, their contribution to metastasis is higher than that of single cancer cells.

We also explored what mediated the clusters resistance to NK cell killing and discovered that cancer clusters seem to tone down the activity of NK cells against them, Lo said. Clusters display on the cell surface more molecules that inhibit the activity of NK cells and fewer that increase their activity. As a result, when NK cells bind to clusters to destroy them, the combined effect is reduced killing activity.

This phenomenon may represent an additional survival advantage complementary to other previously known characteristics of cancer clusters, such as being resistant to chemotherapy.

Our study highlights the importance of NK cells in immunotherapy. Activated NK cells act fast, and efficiently kill tumor cells. They use a killing mechanism that is similar to the one T cells use, but recognition of the tumor cells is different, said Zhang, a member of Baylors Dan L Duncan Comprehensive Cancer Center and a McNair Scholar.

Thats one of the reasons we think that enhancing NK-mediated killing ability may provide a complementary approach in immunotherapy, Zhang said.

Interested in reading all the details of this study? Find it in the journal Nature Cancer.

Other contributors to this work include Zhan Xu, Ik Sun Kim, Bradley Pingel, Sergio Aguirre, Srikanth Kodali, Jun Liu, Weijie Zhang, Aaron M. Muscarella, Sarah M. Hein, Alexander S. Krupnick, Joel R. Neilson, Silke Paust, Jeffrey M. Rosen and Hai Wang. The authors are affiliated with Baylor College of Medicine, Courier Therapeutics, Texas Medical Center, University of Virginia, The Scripps Research Institute and the McNair Medical Institute.

This study was supported by the Breast Cancer Research Foundation, National Cancer Institute grants (CA227904, NCI CA148761, NCI CA190467), U.S. Department of Defense (DAMD W81XWH-16-1-0073 and W81XWH-18-1-0574) and the McNair Medical Institute. Further support was provided by CPRIT RP170172, CPRIT Core Facility Support Award (CPRIT-RP180672), The Samuel Waxman Cancer Research Foundation and NIH grants (P01 AI116501, R01 AI145108-01, IO1 IBX0104588A, R41 CA224520-01A1, P30 CA125123, S10 RR024574 and 1S10OD016167).

By Ana Mara Rodrguez, Ph.D.

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The single cell and the cluster, what makes one better than the other at cancer metastasis? - Baylor College of Medicine News

By softening a cells nucleus so that it can squeeze its way through dense connective tissues, a group of researchers believe theyve demonstrated a new way to help the body efficiently repair injuries. The team of researchers tested this theory by using a medication to inhibit enzymes in the nucleus of knees meniscus cells, which allowed the cells to move through environments that were previously impenetrable. This study is published inScience Advances.

The study focuses on cells in the meniscus, which is a thin layer of dense connective tissue in the human knee. However, the approach could prove effective beyond that specific area.

In this case, we studied how meniscus cell nuclei can be softened to promote their migration through meniscus tissues. We have also shown similar enhancement of cell migration in other types of connective tissues, such as tendons or the cartilage covering the ends of bones, says the studys first author,Su Chin Heo,anassistant professor of research of Orthopaedic Surgery, who works within theMcKay Orthopaedic Research Lab.

In the study, the teams saw that isolated meniscus cells that had been treated with the inhibitor drug trichostatin A were able to move through areas that were once thought to be impassible to reach defects in tissue. This is important becomes some of the repair methods used for injuries involve fibrous scaffolding, which can also be dense and impenetrable. These areas, too, could be infiltrated with the repair cells whose nuclei were softened, the study shows.

This story is by Frank Otto. Read more at Penn Medicine News.

Excerpt from:
To heal meniscus injuries, researchers go to the heart of a cell - Penn: Office of University Communications

Startling, never-before-seen images show that the new coronavirus hijacks proteins in our cells to create monstrous tentacles that branch out and may transmit infection to neighboring cells.

Thefinding, accompanied byevidence ofpotentially more effective drugs against COVID-19,was published Saturday in the journalCellby an international team of scientists.

Fluorescence microscopy image of human epithelial cells taken from the colon and infected with SARS-CoV-2, the virus, that causes COVID-19. The infected cells produce tentacles, known formally as filopodia ( in white) extending out from the cell surface containing viral particles (M protein in red).(Photo: Dr. Robert Gross, University of Freiburg)

By focusing on the fundamental behavior of the virus how it hijacks key human proteins and uses them to benefit itself and harm us the team wasable to identify a family of existing drugs called kinase inhibitors that appear to offerthe most effective treatment yet forCOVID-19.

"We've tested a number of these kinase inhibitors and some are better than remdesivir," said Nevan Krogan, one of more than 70authors of the new paper, and director of the Quantitative Biosciences Instituteat the University of California, San Francisco.

While remdesivir has yet to beapproved for use against COVID-19,U.S.regulatorsare allowing "emergency use" of the drug inhospitalized patients.

Krogan said tests ofkinase inhibitors showed some, including Gilteritnib and Ralimetinib, required lower concentrations thanremdesivir in order tokill off 50% of the virus.

The new study, whichinvolvedexperiments using cells from humans and othersfrom African green monkeys, shows that the virus known as SARS-CoV-2is especially adept at disrupting vital communications. These communicationstake place both withincells and from one cell to another.

Electron microscopy image of cells from the kidney of a female African green monkey that have been infected with SARS-CoV-2, the virus that causes COVID-19. Infected cells produce tentacles known formally as filopodia (orange) extending out from the cell surface to enable budding of viral particles (blue) and infection of nearby cells.(Photo: Dr. Elizabeth Fischer, NIAID/NIH)

"This paper shows just how completely the virus is able to rewire all of the signals going on inside the cell. That's really remarkable and it's something that occurs very rapidly (as soonas twohours after cells are infected)," said Andrew Mehle, an associate professor of medical microbiology and immunology at the University of Wisconsin-Madison.

The communicationssystemknown ascell signaling, allowscells to grow, and to detect and respond to outside threats. Errors in cell signaling can lead to such illnesses as cancer and diabetes.

RELATED:"Something we've never seen before: Scientists still trying to understand baffling, unpredictable coronavirus"

Mehle, who was not involved in the study, said the work shows that scientists are contending with a daunting enemy in thenew conronavirus. "These are highly efficient, evolutionarily-tuned machines that will make it very challenging to develop therapeutics," he said.

From early in the pandemic, Krogan and his colleagues have taken adifferentapproach from that of manyresearchers seeking treatments for the new virus.

Many scientists have been screeningthousands of drugs already approved for other uses to determine if theycan also be used to treat COVID-19.

"We're not doing that," Krogan said. "We're saying 'Let's understand the underlying biology behind how the virus infects us, and let's use that against the virus.'"

In thesearch for treatments, many scientists have homed inonkey proteins in the virus especially the Spike protein, which allowsthe viral cellsto attach themselves to human cells.

Fluorescence microscopy image of of human epithelial cells taken from the colon and infected with SARS-CoV-2, the virus that causes COVID-19.Viral N protein (red) hijacks human Casein Kinase II (green; co-localization in yellow) to putatively produce branching filopodia protrusions (white outline boxes) to enable budding of viral particles and infection of nearby cells.(Photo: Dr. Robert Gross, University of Freiburg)

Krogan and his team looked in the opposite direction, focusingon the human proteins, instead of those in the virus. Dozens ofhuman proteins play a critical role in the disease processbecause the virusneeds themto infect people and to make copies of itself.

There is an important advantage to developing treatments aimed atthe human, rather than the viral, proteins. Viral proteins can mutate causing them to develop resistance to the drugs targeted to them. Human proteins are far less likely to mutate.

In April,Krogan and his colleaguespublished a study in the journal Nature showing that332 human proteinsinteract with 27 viral proteins.

Feixiong Cheng, a PhD researcher who runs a lab at Cleveland Clinic Genomic Medicine Institute, called themapping ofinteractions between theseproteins "a novel" and "powerful" strategy for findingexisting drugs that might helpCOVID-19 patients.

RELATED:Two classes of drugs found that may treat COVID-19

In the new study, Krogan's international teamlooked deeper into the biology, focusing onhow the new coronavirus changes a complex process called phosphorylation. Thisprocess acts as a series ofon-off switches for differentcell activities, includinggrowth, division, deathand communicationwith one another.

"What they've done is really a fantastic next step," said Lynne Cassimeris, a professor of biological sciences at Lehigh University, explaining that the work builds on the previous paper and applies knowledge of cell biologygained over the last30 years.

"It's an amazing leap. We know that the virus has to be manipulating these human proteins. Now we have a list of what is changing over time."

Cassimeris said that mapping these changesallows researchers to seek drugs thatcan intervene at specific points.

The scientists found that on-off switcheschanged significantly in 40 of the 332 proteins that interact with the new coronavirus.

Thechanges occur because the viruseither dialsup or down49 enzymes called kinases. The dialing up or down ofkinases cause them to alter40 of the proteins that interact with virus.

Imagine the kinases as guards protecting our health until the new coronavirus turns them against us. In each case, however, the new study identified treatments that can stopthe virus from turningguards into assailants.

The virus most powerfully hijacks a kinase called CK2, which plays a key role in the basic frameof thecell as well asitsgrowth, proliferation and death.

This led the scientists to investigatea drug called Silmitasertib. Tests found this druginhibits CK2and eliminatesthe new coronavirus.

Electron microscopy image of cells from the kidney of a female African green monkey, which have been infected with SARS-CoV-2, the virus that causes COVID-19. Infected cells produce tentacles known formally as filopodia (blue) extending out from the cell surface to enable budding of viral particles (orange) and infection of nearby cells.(Photo: Dr. Elizabeth Fischer, NIAID/NIH)

They also found that the virus has a dramatic effect on a pathway a group of kinases that forma cascade a little like falling dominoes. The virus hijacksthis cascade so that the end result becomesa dangerous overreaction by ourimmune system.

The study's findingon this pathwaymay help to explainthe extreme overreaction acytokine storm that causes the immune system to kill both healthy anddiseased tissue, leadingtomore than half of the deaths from COVID-19.

RELATED:UW joins drug trial aimed at stopping haywire immune response

Here too, the scientists were able to identify treatments, including the experimental cancerdrug Ralimetinib, whichmay preventthe immune system overreaction.

Authors of the new study also found that the virus harms a family of kinasescalled CDKs. Theseplay roles incell growth and in the response toDNAdamage. An experimental drug called Dinaciclib may be effective in thwarting thisviral assault.

Finally, Krogan and his colleagues found that the virus also hijack a kinase that helps cells stay healthy in different environments and cleans out damaged cells.A small molecule called Apilimod targets this kinase and has been able to hinderthe virus in lab tests.

Krogan, who is also an investigator at the Gladstone Institutes at UCSF, said the strategy of examining the human kinases affected by the virus has provedfruitful.

"The kinases are a very druggable set of proteins in our cells," he said.

Email him at mark.johnson@jrn.com; follow him on Twitter: @majohnso.

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Study reveals images of the coronavirus forming tentacles in cells -- but monstrous discovery helps identify new treatment - Milwaukee Journal...

Lingjia Yu,1 Qi Fei,1 Jisheng Lin,1 Yong Yang,1 Yisheng Xu2

1Department of Orthopedics, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, Peoples Republic of China; 2Orthopedics Department, Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou, Guangdong 510120, Peoples Republic of China

Correspondence: Yong YangDepartment of Orthopaedics, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, Peoples Republic of ChinaEmail spineyang@126.comYisheng XuOrthopedics Department, Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou, Guangdong 510120, Peoples Republic of ChinaEmail xuyishengdr@gzucm.edu.cn

Purpose: Bone tissue infections are a difficult problem in orthopedic surgery. Topical application of vancomycin and tobramycin powder has been proved to significantly reduce infection rates. However, the osteogenic effect of the topical application of these two antibiotics is unclear. In this study, the osteogenic effect of local delivery antibiotics on bone regeneration was investigated in vitro.Methods: Bone marrow stromal cells (BMSCs) were incubated in the presence of vancomycin (14.28g/mL), tobramycin (28.57g/mL), or vancomycin combined with tobramycin (vancomycin 14.28g/mL and tobramycin 28.57g/mL). Cell viability, proliferation, and migration were analyzed. The alizarin red staining as well as the alkaline phosphatase staining was investigated. Then, the quantitative real-time (qRT)-PCR of osteogenic mRNA expression levels were also evaluated.Results: The results showed that vancomycin combined with tobramycin has no adverse effect on the viability and proliferation of BMSCs. The topical application of vancomycin alone may interfere with the bone regenerative processes. However, the tobramycin can promote the osteogenic differentiation of BMSCs and also rescue the osteogenic potential of BMSCs inhibited by vancomycin both in vitro.Conclusion: From this in vitro study, local application of vancomycin combined with tobramycin does not affect the osteogenic potential of BMSCs.

Keywords: vancomycin, tobramycin, osteogenesis, bone regeneration

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The Osteogenic Effect of Local Delivery of Vancomycin and Tobramycin o | IDR - Dove Medical Press