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Archive for September, 2020

Global Stem Cell Banking Market Is Projected To Witness Vigorous Expansion By 2026 – Kewaskum Statesman News Journal

Sunday, September 13th, 2020

DBMR has added a new report titled Global Stem Cell Banking Market with data Tables for historical and forecast years represented with Chats & Graphs spread through Pages with easy to understand detailed analysis. this report provides exact information about market trends, industrial changes, and consumer behaviour etc. The report assists in outlining brand awareness, market landscape, possible future issues, industry trends and customer behaviour about industry which eventually leads to advanced business strategies. Being a verified and reliable source of information, this market research report offers a telescopic view of the existing market trends, emerging products, situations and opportunities that drives the business in the right direction of success. The report has been framed with the proper use of tools like SWOT analysis and Porters Five Forces analysis methods.

Global stem cell banking market is set to witness a substantial CAGR of 11.03% in the forecast period of 2019- 2026. The report contains data of the base year 2018 and historic year 2017. The increased market growth can be identified by the increasing procedures of hematopoietic stem cell transplantation (HSCT), emerging technologies for stem cell processing, storage and preservation. Increasing birth rates, awareness of stem cell therapies and higher treatment done viva stem cell technology.

Get Sample Report + All Related Graphs & Charts (with COVID 19 Analysis) @https://www.databridgemarketresearch.com/request-a-sample/?dbmr=global-stem-cell-banking-market&pm

Competitive Analysis:

Global stem cell banking market is highly fragmented and the major players have used various strategies such as new product launches, expansions, agreements, joint ventures, partnerships, acquisitions, and others to increase their footprints in this market. The report includes market shares of inflammatory disease drug delivery market for Global, Europe, North America, Asia-Pacific, South America and Middle East & Africa.

Key Market Competitors:

Few of the major competitors currently working in global inflammatory disease drug delivery market are: NSPERITE N.V, Caladrius, ViaCord, CBR Systems, Inc, SMART CELLS PLUS, LifeCell International, Global Cord Blood Corporation, Cryo-Cell International, Inc., StemCyte India Therapeutics Pvt. Ltd, Cordvida, ViaCord, Cryoviva India, Vita34 AG, CryoHoldco, PromoCell GmbH, Celgene Corporation, BIOTIME, Inc., BrainStorm Cell Therapeutics and others

Market Definition:Global Stem Cell Banking Market

Stem cells are cells which have self-renewing abilities and segregation into numerous cell lineages. Stem cells are found in all human beings from an early stage to the end stage. The stem cell banking process includes the storage of stem cells from different sources and they are being used for research and clinical purposes. The goal of stem cell banking is that if any persons tissue is badly damaged the stem cell therapy is the cure for that. Skin transplants, brain cell transplantations are some of the treatments which are cured by stem cell technique.

Cord Stem Cell Banking MarketDevelopment and Acquisitions in 2019

In September 2019, a notable acquisition was witnessed between CBR and Natera. This merger will develop the new chances of growth in the cord stem blood banking by empowering the Nateras Evercord branch for storing and preserving cord blood. The advancement will focus upon research and development of the therapeutic outcomes, biogenetics experiment, and their commercialization among the global pharma and health sector.

Cord Stem Cell Banking MarketScope

Cord Stem Cell Banking Marketis segmented on the basis of countries into U.S., Canada and Mexico in North America, Germany, France, U.K., Netherlands, Switzerland, Belgium, Russia, Italy, Spain, Turkey, Rest of Europe in Europe, China, Japan, India, South Korea, Singapore, Malaysia, Australia, Thailand, Indonesia, Philippines, Rest of Asia-Pacific (APAC) in the Asia-Pacific (APAC), Saudi Arabia, U.A.E, South Africa, Egypt, Israel, Rest of Middle East and Africa (MEA) as a part of Middle East and Africa (MEA), Brazil, Argentina and Rest of South America as part of South America.

All country based analysis of the cord stem cell banking marketis further analyzed based on maximum granularity into further segmentation. On the basis of storage type, the market is segmented into private banking, public banking. On the basis of product type, the market is bifurcated into cord blood, cord blood & cord tissue. On the basis of services type, the market is segmented into collection & transportation, processing, analysis, storage. On the basis of source, market is bifurcated into umbilical cord blood, bone marrow, peripheral blood stem, menstrual blood. On the basis of indication, the market is fragmented into cerebral palsy, thalassemia, leukemia, diabetes, autism.

Cord stem cell trading is nothing but the banking of the vinculum plasma cell enclosed in the placenta and umbilical muscle of an infant. This ligament plasma comprises the stem blocks which can be employed in the forthcoming time to tackle illnesses such as autoimmune diseases, leukemia, inherited metabolic disorders, and thalassemia and many others.

Market Drivers

Increasing rate of diseases such as cancers, skin diseases and othersPublic awareness associated to the therapeutic prospective of stem cellsGrowing number of hematopoietic stem cell transplantations (HSCTs)Increasing birth rate worldwide

Market Restraint

High operating cost for the therapy is one reason which hinders the marketIntense competition among the stem cell companiesSometimes the changes are made from government such as legal regulations

Key Pointers Covered in the Cord Stem CellBanking MarketIndustry Trends and Forecast to 2026

Market SizeMarket New Sales VolumesMarket Replacement Sales VolumesMarket Installed BaseMarket By BrandsMarket Procedure VolumesMarket Product Price AnalysisMarket Healthcare OutcomesMarket Cost of Care AnalysisMarket Regulatory Framework and ChangesMarket Prices and Reimbursement AnalysisMarket Shares in Different RegionsRecent Developments for Market CompetitorsMarket Upcoming ApplicationsMarket Innovators Study

Key Developments in the Market:

In August, 2019, Bayer bought BlueRock for USD 600 million to become the leader in stem cell therapies. Bayer is paying USD 600 million for getting full control of cell therapy developer BlueRock Therapeutics, promising new medical area to revive its drug development pipeline and evolving engineered cell therapies in the fields of immunology, cardiology and neurology, using a registered induced pluripotent stem cell (iPSC) platform.In August 2018, LifeCell acquired Fetomed Laboratories, a provider of clinical diagnostics services. The acquisition is for enhancement in mother & baby diagnostic services that strongly complements stem cell banking business. This acquisition was funded by the internal accruals which is aimed to be the Indias largest mother & baby preventive healthcare organization.

For More Insights Get FREE Detailed TOC @https://www.databridgemarketresearch.com/toc/?dbmr=global-stem-cell-banking-market&pm

Research objectives

To perceive the most influencing pivoting and hindering forces in Cord Stem Cell Banking Market and its footprint in the international market.Learn about the market policies that are being endorsed by ruling respective organizations.To gain a perceptive survey of the market and have an extensive interpretation of the Cord Stem Cell Banking Market and its materialistic landscape.To understand the structure of Cord Stem Cell Banking Market by identifying its various sub segments.Focuses on the key global Cord Stem Cell Banking Market players, to define, describe and analyze the sales volume, value, market share, market competition landscape, SWOT analysis and development plans in next few years.To analyze competitive developments such as expansions, agreements, new product launches, and acquisitions in the market.To share detailed information about the key factors influencing the growth of the market (growth potential, opportunities, drivers, industry-specific challenges and risks).To project the consumption of Cord Stem Cell Banking Market submarkets, with respect to key regions (along with their respective key countries).To strategically profile the key players and comprehensively analyze their growth strategiesTo analyze the Cord Stem Cell Banking Market with respect to individual growth trends, future prospects, and their contribution to the total market.

Customization of the Report:

All segmentation provided above in this report is represented at country levelAll products covered in the market, product volume and average selling prices will be included as customizable options which may incur no or minimal additional cost (depends on customization)

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About Data Bridge Market Research:

An absolute way to forecast what future holds is to comprehend the trend today!Data Bridge set forth itself as an unconventional and neoteric Market research and consulting firm with unparalleled level of resilience and integrated approaches. We are determined to unearth the best market opportunities and foster efficient information for your business to thrive in the market. Data Bridge endeavors to provide appropriate solutions to the complex business challenges and initiates an effortless decision-making process.

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Global Stem Cell Banking Market Is Projected To Witness Vigorous Expansion By 2026 - Kewaskum Statesman News Journal

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What Is Covid-19 Doing to Our Hearts? – The New Republic

Friday, September 11th, 2020

Brady Feeney hadnt even taken any classes at Indiana University when he fell ill with Covid-19. Three weeks after he moved to Bloomington, the incoming freshman was in the emergency room, struggling to breathe. Before his illness, Feeney had been a perfectly healthy teenager, with no preexisting conditions. In high school, he was a three-time all-state football player and won two state titles in Missouri. But after two weeks of hell fighting the virus, his mother said, his bloodwork indicated possible heart problems.

When SARS-CoV-2 first struck the United States, the medical community had two working assumptions: First, this was primarily a respiratory disease, and second, it seemed to hit older people much harder than younger people, with eight out of 10 confirmed Covid-19 deaths in the U.S. happening in adults 65 or older. But now, new research is challenging both of these assumptions.

Growing evidence suggests that SARS-CoV-2 doesnt only infect the lungs. It also affects the brain, kidneys, and heart. At first, doctors and researchers wondered if these issues beyond the lungs came just from the stress of having Covid-19 and being on a ventilator or life support. But increasingly, research indicates that the virus may be attacking other organs in the body directlyand this may be more common than previously thought, even among those who arent sick enough to be hospitalized. Some have suggested that Covid-19 is actually a blood vessel disease; the lungs are merely the way the virus enters the body, but from there it gets into the bloodstream and takes up residence in major organs, leaving patients with complex, long-lasting symptoms. Moreover, experts now believe, healthy young people can get mild cases of the coronaviruseven not knowing they were sickthat could leave them with lasting cardiovascular damage. Even those who seem to have recovered from the deadly respiratory illness are not free of its complications.

Heart failure could be the next chapter of the coronavirus illness, Dr. Gregg C. Fonarow, interim chief of UCLAs Division of Cardiology, recently argued in a co-authored editorial in the journal JAMA Cardiology. Even if in younger adults Covid-19 may not be fatal, there still may be important health consequences, he told me.

Myocarditis, or inflammation of the heart, is usually a rare condition that can occur with viral infections, including the flu. But from the start of the pandemic, doctors were seeing heart inflammation among patients hospitalized with serious cases of Covid-19, Fonarow said: Early research showed that 20 to 30 percent of those hospitalized had heart issues. Left untreated, myocarditis can damage the heart and lead to heart attacks and arrhythmias, among other complications.

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What Is Covid-19 Doing to Our Hearts? - The New Republic

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‘Mini organs’ offer treatment hope for children with intestinal failure study – The Northern Farmer

Friday, September 11th, 2020

Mini organs grown using stem cells from a patients tissue could offer hope for children with intestinal failure, a study suggests.

Scientists at the Francis Crick Institute, Great Ormond Street Hospital (GOSH) and UCL Great Ormond Street Institute of Child Health (ICH) have grown human intestinal grafts using stem cells from patient tissue.

The team hope the findings could one day lead to personalised transplants for children with intestinal failure.

Dr Vivian Li, senior author and group leader of the Stem Cell and Cancer Biology Laboratory at the Crick, said: Its urgent that we find new ways to care for children without a working intestine because, as they grow older, complications from parental nutrition can arise.

Weve set out a process to grow one layer of intestine in the laboratory, moving us a step closer to being able to offer these patients a form of regenerative medicine, which uses materials created from their own tissue.

This would reduce some of the risks that transplant patients face, such as their immune system attacking the transplant.

Children with intestinal failure cannot absorb the nutrients essential for their overall health and development, researchers said.

While they can be fed intravenously, via a process called parenteral nutrition, this is associated with severe complications such as line infections and liver failure, they added.

If complications arise, or in severe cases the children need a transplant, researchers said there is a shortage of suitable donor organs and problems can arise after surgery such as the body rejecting the transplant.

The proof-of-concept study, published in Nature Medicine on Monday, showed how intestinal stem cells and small intestinal or colonic tissue taken from patients can be used to grow the inner layer of small intestine in the laboratory with the capacity to digest and absorb peptides and digest sucrose in food.

The researchers took small biopsies of intestine from 12 children who either had intestinal failure or were at risk of developing the condition.

In the lab they then stimulated the biopsy cells to grow into mini-guts, also known as intestinal organoids, generating over 10 million intestinal stem cells from each patient over the course of four weeks.

The researchers also collected small intestine and colon tissue that would have been discarded from other children undergoing essential surgery to remove parts of their gut.

Using laboratory techniques cells were removed from these tissues leaving behind a skeleton structure which formed scaffolds.

The researchers placed the mini-guts onto these scaffolds where they grew on this structure to form a living graft.

Due to specific culture conditions, the stem cells changed into many of the different types of cells that exist in the small intestine and the grafts were able to digest and absorb peptides, the building blocks of proteins, as well as digest sucrose into glucose sugars.

The authors said research was the first step in efforts to engineer all the layers of the intestine for transplantation in the hope that laboratory-grown organs could offer a safe and longer-lasting alternative to traditional donor transplants.

Senior author Professor Paolo De Coppi, consultant paediatric surgeon at GOSH, said the research was an important step forward in regenerative medicine.

He added: Although this research is in the lab right now, were concentrating on making this a realistic and safe treatment option.

Whats significant here is weve shown that scaffolds can be created using tissue from the colon, not only tissue from the small intestine.

Its an important step forward in regenerative medicine and were optimistic about what this means for patients, but more research lies ahead before we can safely and effectively translate this approach to treatment.

As well as proving that biopsies taken from children could be used to grow functioning intestinal grafts, the researchers said that the grafts can survive and mature when transplanted into mice.

Researchers said the next step was to start growing the other layers of the intestine such as muscle and blood vessels.

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'Mini organs' offer treatment hope for children with intestinal failure study - The Northern Farmer

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Tweet Chat Recap: Evaluating Treatment Approaches for Relapsed/Refractory DLBCL – Targeted Oncology

Friday, September 11th, 2020

Targeted Oncology was joined by Kami J. Maddocks, MD, associate professor of clinical internal medicine, Division of Hematology, The Ohio State University Comprehensive Cancer CenterJames, for the discussion of a 76-year-old man with relapsed/refractory diffuse large B-cell lymphoma (DLBCL) in a recent tweet chat. In this case scenario, the patient presented with stage IV high-risk disease and received R-CHOP (Rituximab [Rituxan], cyclophosphamide, doxorubicin, vincristine, prednisone), and radiotherapy.

Although the treatment appeared well-tolerated, the patient presented with similar symptoms as at diagnosis after completing 6 cycles with complete response to the therapy. According to the work-up, the patient is ineligible for transplant.

The patient was ineligible for stem cell transplantation (SCT), which Maddocks speculates may be due to the patients age, although other considerations could include comorbidities or intolerance to R-CHOP. Eligibility is the first thing she considers for her patients as it is currently the standard of care and the only curative approach for patients to receive salvage chemotherapy followed by consolidation with autologous SCT.

Maddocks told Targeted Oncology, In some patient cases, [the reason for ineligibility] is age even though there's no specific age cutoff, but we know that it's harder on the marrow as patients get older to collect stem cells and get that aggressive salvage chemotherapy. Patient comorbidities [can also impact eligibility], so heart conditions, lung conditions, renal insufficiency can be a problem. Performance status and then lastly, just if the patient had trouble getting to their initial chemotherapy with R-CHOP or had a lot of complications, then it's probably going to be harder for them to tolerate even more aggressive or intensive therapy.

In a twitter poll ahead of the chat, Targeted Oncology asked what the next best line of therapy for this patient might be, with 4 potential different treatment options. The option that drew the most attention, however, was the recently approved regimen of tafasitamab (Monjuvi) and lenalidomide (Revlimid).

Maddocks tweeted, All these options are potential therapeutic choices for this patient, but the combination of tafasitamab/lenalidomide is the only option approved in this setting. The treatment has a promising ORR [overall response rate], and CR [complete response], and the remissions for patients who respond are durable!

During the tweet chat, Maddocks reviewed each of the different treatment options in the poll, and why she selected this combination regimen as the next best line of therapy for this particular patient. Following the chat, she spoke with Targeted Oncology to share further insights on each of these therapeutic approaches and the importance of the FDAs approval of tafasitamab plus lenalidomide in this setting.

The combination of tafasitamab plus lenalidomide held the majority vote, which Maddocks agreed would be the next best line of therapy for this patient.

For patients who are not candidates or considered eligible for a salvage chemotherapy followed by autologous SCT, the tafasitamab/lenalidomide combination was recently approved in the setting of first relapse, and it's the only approved therapy in this setting, Maddocks said. Historically, we would give some sort of palliative chemotherapy approach if patients were candidates and interested in pursuing therapy, or consideration of clinical trial, but this is the only therapy approved in this setting.

The approval of tafasitamab in combination with lenalidomide includes an indication for patients who are not eligible for autologous SCT, as describes the patient in our case. This regimen was approved on the basis of the phase 2 L-MIND (NCT02399085) clinical trial, which explored this use of this regimen in 81 patients with relapsed/refractory DLBCL. Two-year follow-up demonstrated an ORR of 58.5%, which included CRs in 41.3% of patients and partial responses (PRs) in 17.5% of patients. In addition, 15.0% achieved stable disease, and the median duration of response was 34.6 months (95% CI, 26.1-34.6).1

I think this patient case is the perfect example of where this can fit into the treatment landscape, Maddocks explained. For patients who first relapse from the standard R-CHOP therapy, the toxicities were generally manageable, and with the response rate, this is a great option for patients at first relapse who are not going to be candidates for a transplant. I think maybe patients who go on to get palliative chemotherapy or maybe patients who get treatment with plans to go to transplant but just don't tolerate it and dont look like they're going to [undergo] aggressive therapy, this may be an option for those patients too, understanding that there is some role for CAR T in a set of those patients.

This study, which was presented during the 25th Congress of the European Hematology Association (EHA), demonstrated that the majority of toxicities were hematologic, and most were reversible. The most common grade 3 hematologic treatment-emergent adverse events (TEAEs) were neutropenia in 49.4% of patients, thrombocytopenia in 17.3%, and febrile neutropenia in 13.2%.1

These were able to be managed by holding the dose growth factor, and there was a population of patients who had to be dose-reduced on the lenalidomide. The starting dose was 25 mg, so the majority were able to maintain 20 mg if they were dose-reduced, although a few had to be reduced more than once, Maddocks said. The most common grade 3/4 or serious AEs were infection, probably not surprisingly, and overall, that's probably similar to what you see with other options in this setting. There was a small number of infusion reactions, but these were all grade 1 in the trial and were easily managed.

Non-hematologic TEAEs of grade 3 included pneumonia in 8.6% of patients and hypokalemia in 6.2%. Serious AEs reported included pneumonia in 8.6%, febrile neutropenia in 6.2%, and pulmonary embolism in 3.7%, as well as bronchitis, lower respiratory tract infection, atrial fibrillation, and congestive cardiac failure in 2.5% each.1

Given the safety profile of this combination of tafasitamab plus lenalidomide, this regimen is particularly suitable for a large proportion of patients with DLBCL, Gilles Salles, MD, PhD, lead author of L-MIND, toldTargeted Oncology. We do know that the median age of occurrence of DLBCL is in the late 60s, and there are many, many patients that are over 70 and that are not usually transplant eligible. Clearly this is a great opportunity for patients to receive this non-cytotoxic regimen.

Although this regimen is an exciting opportunity for patients with DLBCL and relapsed/refractory disease, 1 challenge that needs to be addressed is the potential use of tafasitamab plus lenalidomide in sequence with CAR T-cell therapy. There is very little experience, if any, of patients receiving the combination regimen after receiving CAR T-cell therapy. The combination and CAR T cells both target the same antigen, CD19, which can be problematic. As its known that some patients will lose CD19 expression on CAR T-cell therapy, the regimen may no longer be an effective treatment option.

For those patients that had failed CAR T-cell therapy, substantial proportions, about 30% of them, may have lost CD19 expression and then may not be eligible anymore for this regimen. There is, however, a substantial proportion of patients that retains CD19 and in whom tafasitamab/lenalidomide can be used as a treatment option, Salles commented.

A large proportion of patients will maintain CD19 expression following CAR T-cell therapy, so tafasitamab plus lenalidomide may still be effective in a percentage of patients.

Its hard to say because we dont have a lot of data, but we do know there are other CD19-directed therapies outside of CAR T cell development, Maddocks told Targeted Oncology. I think in the next few years, were going to see patients treated both pre- and post-CAR T with other CD19-directed therapies, and well have more information on this.

The combination of polatuzumab vedotin (Polivy) plus bendamustine (Bendeka) and rituximab (BR) was approved by the FDA as treatment of patients with relapsed/refractory DLBCL after 2 prior lines of therapy in June 2019 based on the findings from the phase 1b/2 GO29365 (NCT02257567) clinical trial. Although this option is also not FDA-approved for the treatment of patients after first relapse, Maddocks noted that this was the only treatment evaluated in a randomized trial. The study had included patients who were ineligible for transplant.

Significant improvements were observed with polatuzumab vedotin plus BR compared with BR alone in an international, multicenter, open-label study, particularly in regard to the ORR, CRs, progression-free survival (PFS), and overall survival (OS). CRs were observed in 40.0% of the patients with the combination versus 17.5% with BR alone. Survival rates favored the combination as well, with a median PFS of 9.5 months with the combination versus 3.7 months with BR alone (HR, 0.36; 95% CI, 0.21-0.63; P <.001) and a median OS of 12.4 months versus 4.7 months (HR, 0.42; 95% CI, 0.24-0.75; P =.002), respectively.2

The addition of polatuzumab did increase toxicity from the standpoint of cytopenias, but that didn't really translate to increased serious infections. It did add neuropathy as a side effect, but most of that was reversible, so I think this was a regimen that, by the addition of polatuzumab, was something that you could offer patients that did give them somewhat of a better overall response and was more durable than just giving them a palliative chemotherapy alone, Maddocks added. This is also a regimen that's been used in patients who were not able to achieve a remission to bridge them to CAR T or in some patients after CAR T, and so I can understand why this was definitely one of the more favorable choices.

In the study, grade 3/4 neutropenia was observed more frequently in the combination arm (42.6%) compared with the BR alone arm (33.3%), but the occurrence of grade 3/4 infections was comparable between the 2 groups (23.1% vs. 20.5%, respectively). In addition, the study authors noted that although many of the fatal AEs occurred after disease progression, 11 patients in the BR arm experienced fatal AEs compared with 9 in the combination arm, infection being the most common, which was the cause in 4 patients in each arm.2

Although the regimen appeared tolerable in this setting, Maddocks tweeted, it is more attractive than chemotherapy alone and understandable why it was chosen [as the second-best option in the Twitter poll].

Among the treatment options considered in our twitter poll ahead of the tweet chat, selinexor (Xpovio) only caught the attention of 16.7% of voters, similar to CAR T-cell therapy. However, both of these options are currently only approved in patients who have received at least 2 prior lines of therapy, which this case did not.

In regard to selinexor in particular, Maddocks tweeted, Looking at the single arm phase 2 data, it also has the lowest overall response rates of all the options listed with an ORR of 28%.

Selinexor received its approval from the FDA in June 2020, which is indicated for the treatment of adult patients with relapsed/refractory DLBCL, not otherwise specified, who have received at least 2 prior systemic therapies. This is the only oral single-agent therapy approved in this setting, and it is also the only nuclear export inhibitor approved by the FDA for use in hematologic malignancies.

The agent was approved on the basis of the phase 2b SADAL clinical trial, which demonstrated an ORR of 29% with 13% CRs and 16% PRs. The responses achieved in the study were durable, which led to a median duration of response of 9.2 months in the overall population (95% CI, 4.8-23.0) and 13.5 months in those who had achieved a CR (95% CI, 9.3-23.0).3

The most common treatment-related AEs were cytopenias and gastrointestinal/constitutional symptoms, which were generally reversible and manageable with dose modifications and/or standard supportive care approaches. The most common on-hematologic AEs, which were mostly grade 1/2, were nausea (52.8%), fatigue (37.8%), and anorexia (34.6%). The most common grade 3/4 AEs included thrombocytopenia (39.4%), neutropenia (20.5%), and anemia (13.4%). No treatment-related grade 5 AEs were observed.

CAR T-cell therapy, on the other hand, offers a unique option to this patient case even though it is still only approved in patients who have progressed or relapsed after 2 prior therapies or SCT. The TRANSCEND-PILOT-017006 (NCT03483103) study is evaluating the potential for CAR T-cell therapy lisocabtagene maraleucel (liso-cel) as treatment of patients with relapsed/refractory aggressive B-cell non-Hodgkin lymphoma who have received at least 1 prior therapy and are ineligible for SCT. While this does appear promising for introducing CAR T-cell therapy earlier on for patients with DLBCL, the treatment is not available off trial and is not a standard approach.

Maddocks told Targeted Oncology, It's very clear who's eligible for autologous transplant by age and comorbidities, but with CAR T, it's not so clear all the time who is going to be a candidate. There's not as great of data or information on who is going to be a candidate for that or not. Probably more patients are going to be a candidate for transplant, but there is still going to be patients that are comorbidities that they're not going to be a candidate for CAR T cells, and while they're approved in this setting and they can be very effective, there's also logistical issues, including that right now there's only certain centers, most often transplant centers, that are able to administer CAR T cells, so the patient has to have access to a center, they have to be able to get through the time that their leukapheresis cells are sent out and then sent back, and there's still barriers to cost and insurance in some patients, too.

This particular patient case does represent a challenge, Maddocks said. Historically, this is not a patient that's going to be a candidate for an autologous SCT, and that's going to be the only curative approach. CAR T is not approved in this setting, which is the other curative approach we know outside of patients who are unable to get to autologous STC, or at least appears to be likely curative for a percentage of patients.

Overall, CAR T-cell therapy is not a viable treatment option for the patient depicted in our tweet chat discussion, although it can still offer curative opportunities to a select group of patients with DLBCL who are ineligible for transplant.

In conclusion, tafasitamab plus lenalidomide helps fulfill the unmet need of patients who are in first relapse but are ineligible for transplant, which is the only curative option for patients with relapsed/refractory DLBCL. Although CAR T cells appear hopeful in this space, more research needs to be done to further determine their role in the treatment paradigm.

When you look at relapsed DLBCL, in general, and have these options, it's exciting for our patients to be able to have these. All of these have come up in the last 1 to 2 years, CAR T being a little bit longer than the other 3 regimens, but they all have offered patients tolerable therapy in the setting of previously not having these options.

Reference

1. Salles G, Duell J, Gonzlez-Barca E, et al. Long-term outcomes from the phase II L-MIND study of Tafasitamab (MOR208) plus lenalidomide in patients with relapsed or refractory diffuse large B-cell lymphoma. Presented at: Presented at: EHA25 Virtual; June 11-21, 2020. Abstract EP1201.

2. Sehn LH, Herrera AF, Flowers CR, et al. Polatuzumab Vedotin in Relapsed or Refractory Diffuse Large B-Cell Lymphoma.J Clin Oncol. 2019;38(2):155-165. doi: 10.1200/JCO.19.00172

3. Kalakonda N, Cavallo F, Follows G, et al. A phase 2b study of selinexor in patients with relapsed/refractory (r/r) diffuse large B-cell lymphoma (DLBCL).Hematol Oncol. 2019;37(S2). doi: 10.1002/hon.31_2629

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Tweet Chat Recap: Evaluating Treatment Approaches for Relapsed/Refractory DLBCL - Targeted Oncology

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Roche receives FDA clearance for BK virus quantitative test on cobas 6800/8800 Systems to support better care for transplant patients – Yahoo Finance

Friday, September 11th, 2020

Basel, 8 September 2020 - Roche (SIX: RO, ROG; OTCQX: RHHBY) today announced U.S. Food and Drug Administration (FDA) 510k clearance for the cobas BKV Test on the cobas 6800 and 8800 Systems. The test was previously granted FDA Breakthrough Device designation demonstrating the improved treatment or diagnosis of life-threatening diseases or conditions for transplant patients. The test provides standardised, high-quality results that can help healthcare professionals better assess the risk of complications caused by the BK virus in transplant patients and identify effective treatment options.

BK virus (BKV) is a member of the polyomavirus family that can cause severe transplant-associated complications. Infection can occur without symptoms and happen early in life. After primary infection, the virus can remain inactive, only to possibly reactivate in immunocompromised individuals such as transplant recipients.

Our diagnostic tests can help clinicians greatly improve patient treatment plans and make quick adjustments for personalised healthcare, said Thomas Schinecker, CEO Roche Diagnostics. This FDA clearance allows Roche to offer healthcare professionals a transplant testing portfolio that includes Cytomegalovirus, Epstein-Barr virus and BK virus so they can simultaneously monitor and improve care for transplant patients who are at risk for these common infections or viral reactivations which can cause further illness or death.

The cobas BKV Test is a polymerase chain reaction (PCR) viral load test that runs on the fully automated and widely available cobas 6800 and cobas 8800 Systems. Along with the previously approved cobas EBV and CMV Tests, the cobas BKV Test has been calibrated to the World Health Organization (WHO) International Standard. This means that test results are reported in international units, making it possible for laboratories anywhere in the U.S. to obtain comparable results when measuring levels of BKV DNA.

About the cobas BKV TestThe cobas BKV Test was previously granted Breakthrough Device Designation by the FDA, together with the cobas EBV Test.

The cobas BKV Test is a real-time polymerase chain reaction (PCR) test with dual-target technology that provides quantitative accuracy and guards against the risk of sequence variations that may be present in the BK virus. The cobas BKV Test has robust coverage with a limit of detection of 21.5 IU/mL and an expanded linear range from 21.5 IU/mL to 1E+08 IU/mL in EDTA plasma.

The test offers an alternative to lab-developed tests (LDTs) or Analyte Specific Reagent (ASR) combinations, potentially minimising variability and complexity in testing, reducing workload and alleviating risk for laboratories. The test supports the goal of result standardisation across institutions by providing reproducible, high-quality results for clinical decision-making.

The fully automated cobas BKV Test and the cobas CMV and cobas EBV Tests can run on the cobas 6800/8800 Systems simultaneously, providing absolute automation with proven performance and flexibility, leading to time savings and increased efficiency.

About BK polyomavirus BK polyomavirus (BKV) is a member of the polyomavirus family that can cause transplant-associated complications including nephropathy in kidney transplantation and hemorrhagic cystitis in hematopoietic stem cell transplantation. Infection can occur early in life, often with no symptoms. After primary infection, the virus can remain inactive throughout life, only to possibly reactivate in immunocompromised individuals, such as patients who receive solid-organ transplants. For kidney transplant patients, BKV infection is considered the most common viral complication, causing polyomavirus nephropathy (PVN) in up to 10 percent of kidney transplant recipients, and about 50 percent of PVN-affected patients will experience transplant graft failure.1 BKV is also associated with hemorrhagic cystitis after allogeneic hematopoietic stem cell transplantation.2

About the cobas 6800/8800 SystemsWhen every moment matters, the fully automated cobas 6800/8800 Systems offer the fastest time to results with the highest throughput and the longest walk-away time available among automated molecular platforms. The systems provide up to 96 results in about three hours and 384 results for the cobas 6800 System and 1,056 results for the cobas 8800 System in an eight hour shift.*

Both systems make it possible for labs to perform up to three tests in the same run with no pre-sorting required. The systems also enable up to eight hours (cobas 6800 System) and four hours (cobas 8800 System) of walk-away time with minimal user interaction.*

These real-time PCR systems serve the areas of infectious disease, donor screening, sexual health, transplant, respiratory and antimicrobial stewardship.

Through an ever-increasing worldwide install base of cobas 6800/8800 Systems, labs are quickly and easily processing millions of tests per month to meet the changing demands of their communities, their customers, and the patients relying on the results of each assay. Globally, labs know and trust that a Roche assay guarantees high precision, accuracy, and traceability to World Health Organization standards.

Today, rapid advancements in healthcare technology, a shortage of skilled workers, industry-wide consolidation, and the proven need to be ready for the next outbreak have health systems looking to lay a reliable foundation for the future. With proven performance, absolute automation, and unmatched flexibility delivering unparalleled throughput 24/7cobas 6800/8800 Systems are designed to ensure a labs long-term sustainability and success now, more than ever.

Learn more now: http://www.cobas68008800.com or http://diagnostics.roche.com.*May vary based on workflow demands

About RocheRoche is a global pioneer in pharmaceuticals and diagnostics focused on advancing science to improve peoples lives. The combined strengths of pharmaceuticals and diagnostics under one roof have made Roche the leader in personalised healthcare a strategy that aims to fit the right treatment to each patient in the best way possible.

Roche is the worlds largest biotech company, with truly differentiated medicines in oncology, immunology, infectious diseases, ophthalmology and diseases of the central nervous system. Roche is also the world leader in in vitro diagnostics and tissue-based cancer diagnostics, and a frontrunner in diabetes management.

Founded in 1896, Roche continues to search for better ways to prevent, diagnose and treat diseases and make a sustainable contribution to society. The company also aims to improve patient access to medical innovations by working with all relevant stakeholders. More than thirty medicines developed by Roche are included in the World Health Organization Model Lists of Essential Medicines, among them life-saving antibiotics, antimalarials and cancer medicines. Moreover, for the eleventh consecutive year, Roche has been recognised as one of the most sustainable companies in the Pharmaceuticals Industry by the Dow Jones Sustainability Indices (DJSI).

The Roche Group, headquartered in Basel, Switzerland, is active in over 100 countries and in 2019 employed about 98,000 people worldwide. In 2019, Roche invested CHF 11.7 billion in R&D and posted sales of CHF 61.5 billion. Genentech, in the United States, is a wholly owned member of the Roche Group. Roche is the majority shareholder in Chugai Pharmaceutical, Japan. For more information, please visit http://www.roche.com.

All trademarks used or mentioned in this release are protected by law.

References[1] Jamboti, J. S. (2016) BK virus nephropathy in renal transplant recipients. Nephrology, 21: 647 654. doi: 10.1111/nep.12728. [2] Hirsch HH, Randhawa PS; AST Infectious Diseases Community of Practice. BK polyomavirus in solid organ transplantation-Guidelines from the American Society of Transplantation Infectious Diseases Community of Practice. Clin Transplant. 2019;33(9):e13528. doi:10.1111/ctr.13528

Roche Group Media RelationsPhone: +41 61 688 8888 / e-mail: media.relations@roche.com

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Coronavirus, Charity, and the Trolley Problem – Crooked

Friday, September 11th, 2020

I signed up to be a bone marrow donor in 2016, after an anonymous strangers marrow saved my father. It started out easy enough: The registry mailed me a kit to swab my cheeks, I mailed it back, and then I heard nothing for years. This wasnt unusual. Marrow transplantation requires finding complex and rare genetic matches; according to Be The Match, only about one out of every 430 people who sign up will ever go on to donate. I expected it would be a while before I got to pay my dads transplant forward. It did not occur to me that my opportunity might arise at the height of a global coronavirus pandemic.

The coronavirus created a tangle of moral dilemmas that most Americans never expected to face. At the extremes, weve resolved these dilemmas easily. Weve designated whole categories of labormostly underpaid, perennially underappreciatedessential because we accept that even with a plague lurking, people must eat and medicate and have working showers in which to cry. On the opposite end of the spectrum, weve trained our online shaming apparatus on the most reckless and selfish offendersthe wealthy New Yorkers who fled to the Hamptons, the house parties posted to Instagram with weak defensive captions (we only took our masks off for the body shots).

The longer we live in the shadow of an uncontained virus, the more agonizing the in-between dilemmas become. How long should people be expected to remain isolated from their loved ones? Is there a point at which the negative effects of physical distancing begin to outweigh the toll of the disease itself? On the one hand, we should do everything in our power to protect the most vulnerable in our communities. On the other hand, what should we tell the vulnerable seniors who feel they dont have endless spare months to let pass without embracing their grandchildren? Are our individual mitigation responsibilities lessened by the fact that we all made sacrifices to buy an incompetent president time to get this under control, and he squandered it? Are we that much more obligated to pick up the slack?

In some sort of sick philosophical joke, the moral waters get even murkier when you throw altruism into the mix. For all of the guidance reminding us of the impact of our selfish choices on strangersyou might not kill your own grandmother by going to that dive bar, but think of the bartenders roommates grandmothermoral experts have had far less to say about the boundaries around charitable acts. How should we think about helping strangers when doing so requires a dangerous level of social interaction? How should we measure the suffering of the people we want to help against the harm we risk causing to unseen others in the process? That quandary leads to another awful question that most people should never have to confront: When does human life become too risky to save?

Be The Match first notified me that it had identified me as a potential match in June, when coronavirus cases in Los Angeles, where I live, had just begun to spike. By the time I was confirmed as the patients best match and asked to proceed with a donation several weeks later, the city had become a full-blown hotspot. The idea of navigating the whole process in plague conditions made me nervous, but underneath the anxiety was a distinct whiff of relief. Like a lot of people, Id spent the last few months in a horrified daze, helpless to do anything but stay home, donate money, and cyberbully the mayor. Here, finally, was a task that felt equal to the urgency of the moment. Here was somethingsomeonereal. I just wasnt allowed to know who.

Be The Match will put donor and recipient in contact one year after the transplant, if both have consented; until then, everything is completely anonymous. I was told that my recipient was a man in the United States, along with his age (surprisingly young), and diagnosis (a type of blood cancer). Because matches are typically found within shared ancestries, I assume that he is, like me, an Ashkenazi Jew, and because he needed a bone marrow transplant, his situation must have been dire.

Fortunately, helping people like him has become simpler. When most people think of donating for a bone marrow transplant, they imagine general anesthesia; a very big needle; a painful recovery. This is one of the two ways to donate, but its grown much less common. Ninety percent of donors (including me) are instead asked to donate peripheral blood stem cells (PBSC), through a process called apheresis. While a donor is awake and watching Party Down, their blood flows through a tube attached to one arm, gets spun around in a centrifuge that separates out the extra blood-forming stem cells, and is returned through a tube into the other arm. This can take several hours, but its painless, and neednt even happen at a hospital. Usually.

(Sarah Lazarus)

On August 13, two nurses met me at the San Bernardino blood bank where I was scheduled to donate later that month. We were all there for an assessment, to make sure my arm veins could handle the apheresis needles. It was a weird little ritual. The two women bent on either side of me, intently tapping along my upturned arms in total silence as if waiting for something to tap back. They then switched sides, tapped the opposite arm, and issued their verdict: Too small. I would need to donate through a central line placed in one of my larger veins, and that could only happen at a hospital. I would probably be sent to a medical center two hours south in La Jolla, they told me.

This was a complication, but not necessarily a big deal. Be The Match footed the bill for all of my donation-related expenses, including the fancy car service that seemed safer, COVID-wise, than using Lyft. (I am a genius who moved to Los Angeles without a drivers license. A worse essay for another time.) Donating at the La Jolla hospital would mean a longer commute, maybe even one night in a hotel, but that was about it.

Later that morning I was waiting for my next appointment at an urgent care center when Heather, my donor coordinator, called to tell me that La Jolla didnt have an opening on the right day. Neither did the next-closest option, she told me as I paced around the parking lot, and the patients team couldnt shift his treatment schedule.

So my question for you is, would you feel comfortable flying to Boise, Idaho?

I went back inside to the busy waiting room and reclaimed my seat. Across the room, a man in a UPS uniform freed his nose to rest obscenely on top of his mask. I hunched over my phone and googled, Boise coronavirus. My phone informed me that it was dying. The UPS man coughed. On a TV in the corner, the president admitted he was sabotaging the post office to steal the election. I googled, airports coronavirus. At last, a nurse called me back and started checking my vitals.

Your heart rate is really elevated, she said, frowning at the reading. Any idea why?

As of this writing, Be The Matchs COVID-19 FAQ page was last updated on April 6. Heres part of the section on air travel:

Q: Are there alternatives to donors traveling for donation?A: Possibly. If you feel uncomfortable traveling, we respect your decision. However, it is extremely important that you tell us right away so we can look for alternatives. Donation is time-sensitive, and any delay can have a negative impact on the recipients wellbeing. It may be possible to arrange for donation to occur somewhere within driving distance.

There was an alternative to Boise, it turned out, if I felt uncomfortable. I could donate at the La Jolla hospital a day later than originally planned. My cells would be cryogenically frozen and given to the patient a week or two later, instead of immediately. Heather told me that the patients team preferred me to stick with the original date, that a delayed transplant would be riskier for him, but, for confidentiality reasons, they couldnt tell me how much riskier.

We dont want you to feel pressured, Heather emphasized. You should only agree to travel if you feel comfortable.

Did I feel comfortable? It depended on the circumstances, which I wasnt allowed to know. The window of risks were willing to take expands as the stakes get higher; anyone who showed up to a Black Lives Matter protest this summer or signed up to be a poll worker this fall can attest to that. I wouldnt feel at all comfortable flying for the heck of it, but I would certainly do it to save a life. This fell somewhere on the vast spectrum in between, but I had no idea where.

How do you make a call about your personal risk tolerance when its also a choice about the course of a strangers cancer treatment? If the pandemic had taught us all a valuable lesson about the interconnectedness of our fates, I was now being beaten over the head with it. Stuck without enough facts to make an informed decision, I thought about my dads old hospital room in Baltimore, the airlock separating his ward from the rest of the building because any mundane microbe could kill the patients on the other side. I imagined a somber-looking doctor walking through those doors to give my vulnerable recipient the news.

Im afraid theres been a change of plans, he would say, removing his glasses. It seems your donor is a pussy-ass bitch.

I called Heather back and told her to arrange my donation in Boise.

In most respects, my pre-donation medical screening was extremely, almost ludicrously thorough. I submitted vials and vials of blood to check for a host of diseases and disorders. I peed in a cup to make sure I wasnt pregnant. I had more blood drawn, to make sure I really wasnt pregnant. After the second pregnancy test confirmed the results of the first pregnancy test, I got the following email from Heather:

The result of your repeat pregnancy test on 8/13 was negative, but we are still required to complete our pregnancy assessment with you today. The assessment consists of a single question Is there any chance you could be pregnant? Please respond via email when convenient.

I have not touched another person in five months, I wrote back.

Thank you for completing the pregnancy assessment, Heather replied.

In one respect, my pre-donation medical screening seemed oddly lax. I wasnt tested for coronavirus until the day before my flight, and only then because I panicked.

(Sarah Lazarus)

The PBSC donation process begins in earnest a few days before the stem cells are actually collected, with five rounds of filgrastim injections. Its a drug normally given to cancer patients to bring up low white-blood cell counts after chemo or radiation. In my case, it would send my healthy bone marrow into overdrive, to produce enough cells for the donation. The injections have a few side effects: bone pain, fatigue, headaches, nausea. Essentially, filgrastim makes you feel like you have the flua particularly special feeling in the year of our lord 2020. My side effects were mild and I knew to expect them, and I was managing them fine until an extra one showed up.

The night after receiving my second round of shots, I went for a walk around my neighborhood. It was a hot night, and I was tired and achy from the medication; this was not a fast walk. And yet within a few blocks I noticed that my breathing was quick and shallow, and my heart was pounding as if Id just run a sprint. When I tried to take a deep breath, it felt like there was an elastic band cinched around my chest.

Shortness of breath was not on my list of filgrastim side effects. Neither were the heart palpitations, which continued long after I went home and collapsed on my bed.

I put an empty Gatorade bottle on my stomach and watched it pulse up and down as I considered how fucked I was. I had assumed my fatigue and body aches were side effects; what if those were symptoms, too? I mentally tallied up my appointments from over the past week. I had been to five different medical facilities, been a passenger in three different cars. Of course I had caught it. How stupid to think I wouldnt catch it.

The timing was a nightmare. At some point while I was receiving the filgrastim injections, the patient began a course of high-dose chemo to kill off his own blood-forming stem cells in preparation for the transplant. If I had to back out of donating after that treatment began, the patient would die quickly.

For a few desperate minutes, I thought about keeping these symptoms to myself. I didnt have a fever. As long as I didnt develop one, maybe I could get to Boise and finish the donation leaving no one the wiser. What was the moral math, I wondered, of proceeding with travel plans that might seed multiple new outbreaks (but also might not) and lead to numerous deaths (but maybe none), knowing that if I didnt, one person would certainly die? Had anyone solved that particular trolley problem? My heart palpitations got worse. This was insane. I texted Heather everything and asked if she could arrange for a rapid coronavirus test the next day.

It was nearly 11 p.m. by this point, later in Heathers time zone. She made sure my shortness of breath wasnt an emergency, then said shed see how I was feeling in the morning to assess whether a test was necessary.

I went to bed and thought about what they would tell the patient. Would his doctors be allowed to explain why I couldnt donate? Would he think I had just bailed? Would he and his family hate me? What did it say about my motivations that I was fixated on this? Probably nothing good. I drifted off into a stress dream, and then it was dawn.

My breathing was still labored in the morning, and now, compounding my dread, I had a definite tickle in my throat that verged on a cough. Heather and the medical team decided this did indeed warrant a coronavirus test, and went about setting one up. In the meantime, Heather told me, I should proceed with my third day of filgrastim.

When my home nurse Maria arrived at 8 a.m. to do the honors, I stopped her outside to inform her that I might be a vector of death. She was unimpressed. (Ok, sweetie. Can I come in and wash my hands?) Soon afterwards, Heather called to let me know she had found a doctors office that would send someone to test me at my apartment, and deliver results within 24 hoursjust fast enough that I could still make my flight if I tested negative. Be The Match picked up the tab for this, too, but the receipt came to my email. The cost of a rapid PCR test, antibody test, and home visit came out to a cool $900.

The unaffordable testing nurse arrived an hour later cloaked in full PPE. She coached me on how to swab my own mouth and throat for the diagnostic test, then we made small talk while waiting for the little white antibody tray, which looked for all the world like yet another pregnancy test, to reveal either one or two lines. She had been doing these home visits for two weeks, she told me, and none of her patients had yet tested positive for an infection. For no good reason at all, this made me feel better. The antibody test came up negative. The nurse wished me luck with my other results and headed off to her next appointment, leaving me alone with my wonderful thoughts.

I had nothing to do for the rest of the day but wait. By late afternoon my throat felt better, and my breathing had become less conspicuous. At one point I started to pack a bag, wondered if I was jinxing it, and unpacked the bag. At 10 p.m., less than 12 hours after my throat swab, the results arrived in my inbox. NOT DETECTED. I texted Heather a screenshot and lay down on the floor, awash with relief.

(Sarah Lazarus)

The travel and donation themselves were mercifully uneventful. My parents, who were very pleased that I was donating and terrified that I was flying, had shipped me a steady stream of hand sanitizer, KN95 masks, surgical masks, disinfectant wipes, face shields, safety glasses, and gloves. I wore only some of this to the airport, unless you are my parents, in which case I wore all of it. In any event, I felt protected. My terminal at LAX was deserted, and Heather had booked me a first class seat on Delta, which limits capacity to 50 percent. After barely leaving my immediate neighborhood for half a year, the feeling of takeoff, even for a two-day trip to Boise, was sensational.

The next day I arrived at the hospital at 7:15 a.m. By 8:30 Id had a central line inserted above my collarbone, in a painless 15-minute procedure under local anesthesia. The song We Are Young was playing, and the doctors threading a tube into my neck were chatting quietly about a patient whod given them trouble over the weekend. (Im just saying, if youre cussing people out and trying to beat me up, you probably didnt have too bad of a stroke.) Ive had much less pleasant mornings.

By 9:30 I was in bed and hooked up to the apheresis machine, where I would remain for the next seven hours. At one point my calcium levels dropped too low and I threw up; this was the excitement peak of the day. I spent the rest of the time comfortably reading or watching Netflix, keeping an eye on the stem cells slowly collecting in the bag above my head, and carefully avoiding any RNC coverage that might cause the nausea to recur. At around 4:30 I was loosed from the machine, and after waiting a couple more hours while the lab made sure I had forked over enough cells, the nurse removed my central line and I was officially done.

I was exhausted that evening, but the next day felt well enough to go for a walk along the Boise River, where I took 50 terrible photos of a great blue heron. My shortness of breath, whatever it had been, was gone. The day after that I was just a little more fatigued than usual, and by day three I was back to my 2020-adjusted tiredness baseline.

Coronavirus complications aside, the actual donation process was remarkably easy; shockingly easy, when you consider the scale of what it means for the recipient. It was a time commitment for a few weeksIm lucky to have employers who were happy to give me the necessary leaveand involved some mild discomfort, but as a baby about both pain and scheduling, I would not hesitate to do this again.

I also came away with a clearer sense of how to approach the kind of altruistic acts that standard social-distancing guidelines say we shouldnt engage in. The people and organizations that facilitate charity, particularly sensitive medical charity, have existing support systems that theyve retrofitted to help mitigate the extra risks. Those systems may be imperfect and require some self-advocacy, but when combined with ones own diligence and added layers of protection (and, if one is lucky, a concerned Jewish mother), its possible to get help to the people who need it with risk levels not much higher than we tolerate in normal times. There is a way to be selfless without being self-sacrificing, or worse, becoming an inadvertent menace.

Even so, pandemic experiences like this one wont be universally feasible. One might live with immunosuppressed family members or roommates, or have care-taking responsibilities, or lack the spare emotional bandwidth, or have any number of circumstances more complex than my own. And thats finethere will still be people in need of a lifeline on the other side of this crisis, and that lifeline will be no less appreciated.

I asked my dad, Mitchell Lazarus, what he thought potential donors should know about the recipient experience. He sent me this:

The diagnosis is, literally, a death sentence: you will soon die. Word of a matching donor who has agreed to participate is a reprieve the only possible reprieve. I have felt relief many times in my life, but except possibly for the safe birth of my children, nothing like that. I was in a chemo chair when they came by and told me. I called my wife and said, I have a donor, and I started to cry.

Patients in the transplant ward talk a lot about our donors, despite not knowing who they are. Everybody everybody! tears up when talking about their donors.

True story: I was in the hallway on the transplant floor, talking with the woman in the room next to mine. A nurse walking by stopped and said, Mr. Lazarus, are you having trouble with allergies? (which would require attention). I said no, I was talking about my donor. No other explanation needed. She patted my arm and walked on.

I am a chimera. The rest of me has my own DNA, but my blood cells carry my donors DNA, not mine. Somebody elses blood pumps through my body, keeping me alive, not just through treatment, but every second of every day for the rest of my life. How can you not be grateful to someone who literally gave you the rest of your life?

At some point during the 24 hours after I was unhooked from the machine, a volunteer courier arrived at the hospital in Boise. He or she or they retrieved the bag of my donated cells, flew with it to wherever the recipient is located, and hand-delivered it to his hospital. The patient almost certainly received the transplant before I made it back to Los Angeles. If all goes well, my stem cells will navigate their way into his bone marrow, where theyll settle in, multiply, and start producing healthy blood cells. If all goes well, this perfect stranger will eventually have my blood type, and potentially even my childhood immunitieshe might soon, in other words, have my immune system. If all goes well, may that sucker protect us both.

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Coronavirus, Charity, and the Trolley Problem - Crooked

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Global Induced Pluripotent Market By 2026 Emerging Technology, Opportunities, Analysis And Future Threats With Key Players Like Thermo Fisher…

Friday, September 11th, 2020

Induced Pluripotent MarketIs Expected To Rise To An Estimated Value Of Usd 2.33 Billion By 2026, Registering A Substantial Cagr In The Forecast Period Of 2019-2026. This Rise In Market Value Can Be Attributed To The Increasing Prevalence Of Chronic Diseases And Ailments Requiring The Development Of Modern Technologically Advanced Therapeutic Options.

The strategies encompassed in the Induced Pluripotent report mainly include new product launches, expansions, agreements, joint ventures, partnerships, acquisitions, and others that boost their footprints in this market. This gives more accurate understanding of the market landscape, issues that may affect the industry in the future, and how to best position specific brands. The base year for calculation in the report is taken as 2017 whereas the historic year is 2016 which will tell you how the Induced Pluripotent market is going to perform in the forecast years by informing you what the market definition, classifications, applications, and engagements are.

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Few of the major competitors currently working in the induced pluripotent market are Bristol-Myers Squibb Company; CELGENE CORPORATION; Astellas Pharma Inc.; Thermo Fisher Scientific; Cell Applications, Inc.; Axol Bioscience Ltd.; Organogenesis Holdings; Merck KGaA; FUJIFILM Holdings Corporation; Fate Therapeutics; KCI Licensing, Inc.; Japan Tissue Engineering Co., Ltd.; Vericel; ViaCyte, Inc.; STEMCELL Technologies Inc.; Horizon Discovery Group plc; Lonza; Takara Bio Inc.; Promega Corporation and QIAGEN.

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Headaches, confusion and delirium with COVID-19: How SARS-CoV-2 attacks the brain – Firstpost

Friday, September 11th, 2020

The ACE2 receptor that the virus targets is rare in the brain. But new research shows that the virus could enter brain cells via this method too.

The coronavirus targets the lungs foremost, but also the kidneys, liver and blood vessels. Still, about half of patients report neurological symptoms, including headaches, confusion and delirium, suggesting the virus may also attack the brain.

A new study offers the first clear evidence that in some people, the coronavirus invades brain cells, hijacking them to make copies of itself. The virus also seems to suck up all of the oxygen nearby, starving neighboring cells to death.

Its unclear how the virus gets to the brain or how often it sets off this trail of destruction. Infection of the brain is likely to be rare, but some people may be susceptible because of their genetic backgrounds, a high viral load or for other reasons.

If the brain does become infected, it could have a lethal consequence, said Akiko Iwasaki, an immunologist at Yale University who led the work.

The study was posted online Wednesday and has not yet been vetted by experts for publication. But several researchers said it was careful and elegant, showing in multiple ways that the virus can infect brain cells.

Scientists have had to rely on brain imaging and patient symptoms to infer effects on the brain, but we hadnt really seen much evidence that the virus can infect the brain, even though we knew it was a potential possibility, said Dr. Michael Zandi, consultant neurologist at the National Hospital for Neurology and Neurosurgery in Britain. This data just provides a little bit more evidence that it certainly can.

Zandi and his colleagues published research in July showing that some patients with COVID-19, the illness caused by the coronavirus, develop serious neurological complications, including nerve damage.

In the new study, Iwasaki and her colleagues documented brain infection in three ways: in brain tissue from a person who died of COVID-19, in a mouse model, and in organoids clusters of brain cells in a lab dish meant to mimic the brains three-dimensional structure.

Brain scans of coronavirus patients from a study published in July. The new study offers the first clear evidence that in some people, the coronavirus invades brain cells, hijacking them to make copies of itself, and the virus also seems to suck up all of the oxygen nearby, starving neighbouring cells to death. By [Apoorva Mandavilli/Ross W. Paterson, Rachel L. Brown, et al./Brain, Oxford University Press] 2020 The New York Times

The coronavirus is much stealthier: It exploits the brain cells machinery to multiply, but doesnt destroy them. Instead, it chokes off oxygen to adjacent cells, causing them to wither and die.

The researchers didnt find any evidence of an immune response to remedy this problem. Its kind of a silent infection, Iwasaki said. This virus has a lot of evasion mechanisms.

These findings are consistent with other observations in organoids infected with the coronavirus, said Alysson Muotri, a neuroscientist at the University of California, San Diego, who has also studied the Zika virus.

The coronavirus seems to rapidly decrease the number of synapses, the connections between neurons.

Days after infection, and we already see a dramatic reduction in the amount of synapses, Muotri said. We dont know yet if that is reversible or not.

The virus infects a cell via a protein on its surface called ACE2. That protein appears throughout the body and especially in the lungs, explaining why they are favoured targets of the virus.

Previous studies have suggested, based on a proxy for protein levels, that the brain has very little ACE2 and is likely to be spared. But Iwasaki and her colleagues looked more closely and found that the virus could indeed enter brain cells using this doorway.

Its pretty clear that it is expressed in the neurons and its required for entry, Iwasaki said.

Her team then looked at two sets of mice one with the ACE2 receptor expressed only in the brain, and the other with the receptor only in the lungs. When they introduced the virus into these mice, the brain-infected mice rapidly lost weight and died within six days. The lung-infected mice did neither.

The structure and cross-sectional view of the novel coronavirus SARS-CoV-2. Image: Wikimedia

Despite the caveats attached to mouse studies, the results still suggest that virus infection in the brain may be more lethal than respiratory infection, Iwasaki said.

The virus may get to the brain through the olfactory bulb which regulates smell through the eyes or even from the bloodstream. Its unclear which route the pathogen is taking, and whether it does so often enough to explain the symptoms seen in people.

I think this is a case where the scientific data is ahead of the clinical evidence, Muotri said.

Researchers will need to analyse many autopsy samples to estimate how common brain infection is and whether it is present in people with milder disease or in so-called long-haulers, many of whom have a host of neurological symptoms.

Forty percent to 60% of COVID-19 patients experience neurological and psychiatric symptoms, said Dr. Robert Stevens, a neurologist at Johns Hopkins University. But the symptoms may not all stem from the virus invading brain cells. They may be the result of pervasive inflammation throughout the body.

For example, inflammation in the lungs can release molecules that make the blood sticky and clog up blood vessels, leading to strokes. Theres no need for the brain cells themselves to be infected for that to occur, Zandi said.

But in some people, he added, it may be low blood oxygen from infected brain cells that triggers strokes: Different groups of patients may be affected in different ways, he said. Its quite possible that youll see a combination of both.

Some cognitive symptoms, like brain fog and delirium, might be harder to pick up in patients who are sedated and on ventilators. Doctors should plan to dial down sedatives once a day, if possible, in order to assess COVID-19 patients, Stevens said.

Apoorva Mandavilli. c.2020 The New York Times Company

Link:
Headaches, confusion and delirium with COVID-19: How SARS-CoV-2 attacks the brain - Firstpost

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Post-COVID heart damage alarms researchers: ‘There was a black hole’ in infected cells – Yahoo Movies UK

Friday, September 11th, 2020

Shelby Hedgecock contracted the coronavirus in April and thought she had fought through the worst of it the intense headaches, severe gastrointestinal distress and debilitating fatigue but early last month she started experiencing chest pain and a pounding heartbeat. Her doctor put her on a cardiac monitor and ordered blood tests, which indicated that the previously healthy 29-year-old had sustained heart damage, likely from her bout with COVID-19.

I never thought I would have to worry about a heart attack at 29 years old, Hedgecock told Yahoo News in an interview. I didnt have any complications before COVID-19 no preexisting conditions, no heart issues. I can deal with my taste and smell being dull, I can fight through the debilitating fatigue, but your heart has to last you a really long time.

Hedgecocks primary-care physician has referred her to a cardiologist she will see this week; the heart monitor revealed that Hedgecocks pulse rate is wildly irregular, ranging from 49 to 189 beats per minute, and she has elevated inflammatory markers and platelet counts. She was told to go to the emergency room if her chest pain intensifies before she can see the specialist. A former personal trainer who is now out of breath just from walking around the room, Hedgecock is worried about what the future holds.

She is far from alone in her struggle. Dr. Ossama Samuel is a cardiologist at New Yorks Mount Sinai Hospital, where he routinely sees coronavirus survivors who are contending with cardiac complications. Samuel said his team has treated three young and otherwise healthy coronavirus patients who have developed myocarditis an inflammation of the heart muscle weeks to months after recovering from the virus.

Shelby Hedgecock in a hospital bed. (Shelby Hedgecock)

Myocarditis can affect how the heart pumps blood and trigger rapid or abnormal heart rhythms. It is particularly dangerous for athletes, doctors say, because it can go undetected and can result in a heart attack during strenuous exercise. In recent weeks, some collegiate athletes have reported cardiac complications from the coronavirus, underscoring the seriousness of the condition.

Last month, former Florida State basketball center Michael Ojo died from a heart attack in Serbia; Ojo had recovered from the coronavirus before he collapsed on the basketball court. An Ohio State University cardiologist found that between 10 and 13 percent of university athletes who had recovered from COVID-19 had myocarditis.When the Big Ten athletic conference announced the cancellation of its season last month, Commissioner Kevin Warren cited the risk of heart failure in athletes. Researchers have estimated that up to 20 percent of people who get the coronavirus sustain heart damage.

Samuel said he feels an obligation to warn people, particularly since some of the patients he and Mount Sinai colleagues have seen with myocarditis had only mild cases of the coronavirus months ago.

We are now seeing people three months after COVID who have pericarditis [inflammation of the sac around the heart] or myocarditis, Samuel said. He said he believes a small fraction of coronavirus survivors are sustaining heart damage, but when a disease is so widespread it is concerning that a tiny fraction is still sizable.

Samuel said he worries particularly about athletes participating in team sports, since many live together and spend time in close quarters. Teammates may all get the coronavirus and recover together, Samuel said, but the one who really gets that crazy myocarditis could be at risk of dying through exercise or training.

Story continues

Its a concern about what do you do: Should we do sports in general, should we do it in schools, should we do it in college, should we just do it for professionals who understand the risk and they're getting paid? Samuel asked. I hope we dont scare the public, but we should make people aware.

Samuel is recommending that patients recovering from COVID-19 with myocarditis avoid workouts for three to six months.

Todd McDevitt, who runs a stem-cell lab at Gladstone Institutes, which is affiliated with the University of California at San Francisco, recently published images that show how the coronavirus can directly invade the heart muscle. McDevitt said he was so alarmed when he saw a sample of heart muscle cells in a petri dish get diced by the coronavirus that he had trouble sleeping for nights afterward.

Todd McDevitt. (Facebook)

McDevitt said his teams research was spurred by their desire to understand if the coronavirus is entering heart cells and how it is affecting them. He was surprised to see the heart muscle samples he was studying react to a very small amount of the coronavirus, usually within 24 to 48 hours. He said the virus decimated the heart cells in his petri dishes.

Cell nuclei the hubs of all the genetic information, all of the nuclear DNA in many of the cells were gone, McDevitt said. There was a black hole literally where we would normally see the nuclear DNA. Thats also pretty bizarre.

While McDevitts study has not yet been peer-reviewed it is still in pre-print he said he felt compelled to share the findings as soon as possible. He said his team also sampled tissues from three COVID-19 patient autopsies and found similar damage in the heart muscles of those patients, none of whom had been flagged for myocarditis or heart problems while they were alive.

This is probably not the whole story yet, but we think we have insights into the beginning of when the virus would get into some of these people and what it might be doing that is concerning enough that we should probably let people know, because clinicians need to be thinking about this, McDevitt said in an interview. We dont have any means of bringing heart muscle back. ... This virus is [causing] a very different type of injury, and one we haven't seen before.

McDevitt said the chopped-up heart muscles he and his colleagues saw are so concerning because when the microfibers in the muscle are damaged, the heart cant properly contract.

If heart muscle cells are damaged and they cant regenerate themselves, then what youre looking at is someone who could prematurely have heart failure or heart disease due to the virus, McDevitt said. This could be a warning sign for a potential wave of heart disease that we could see in the future, and its in the survivors thats the concern.

McDevitt said he believes the risk of heart disease is serious and one people should consider as they assess their own risk of getting the coronavirus.

I am more scared today of contracting the virus, by far, than I was four months ago, he said.

In lab experiments, infection of heart muscle cells with SARS-CoV-2 caused long fibers to break apart into small pieces, shown above. (Gladstone)

The medical journal the Lancet recently reported that an 11-year-old child had died of myocarditis and heart failure after a bout of COVID-induced multisystem inflammatory syndrome (MIS-C). An autopsy showed coronavirus embedded in the childs cardiac tissue.

A recent study from Germany found that 78 percent of patients who had recovered from the coronavirus and who had only mild to moderate symptoms while ill with the disease had indications of cardiac involvement on MRIs conducted more than two months after their initial infection.Lead investigator Eike Nagel said it is concerning to see such widespread cardiac impact; six in 10 of the patients Nagels team studied experienced ongoing myocardial inflammation.

We found an astonishingly high level of cardiac involvement approximately two months after COVID infection, Nagel said in an email. These changes are much milder than observed in patients with severe acute myocarditis.

The scale of the cardiac impact on relatively healthy, young patients surprised many doctors. Nagel said the findings are significant on a population basis, and that the impact of COVID-19 on the heart must be studied more.

Dr. Gregg Fonarow. (UCLA)

Dr. Gregg Fonarow, chief of UCLAs Division of Cardiology and director of the Ahmanson-UCLA Cardiomyopathy Center, said the picture is evolving, but the new studies showing cardiac impact in even young people with mild cases of COVID-19 have raised troubling new questions.

We really do need to take seriously individuals that have had the infection and are having continued symptoms, [and] not just dismiss those symptoms, Fonarow said. There could be, in those who had milder or even asymptomatic cases, the potential for cardiac risk.

Fonarow said it is important to understand whether a more proactive screening and treatment approach is needed to better address the needs of patients who have recovered from the coronavirus and who may still have weakened heart function. Fonarow said he found McDevitts research to be potentially significant because it proves from a mechanistic standpoint that there can be direct cardiac injury from the virus itself.

Even if it were going to impact, say, 2 percent of the people that had COVID-19, when you think of the millions that have been infected, that ends up in absolute terms being a very large number of individuals, Fonarow said in an interview. You dont want people to be unduly alarmed, but on the other hand you dont want individuals to be complacent about, Oh, the mortality rate is so low with COVID-19, I dont really care if Im infected because the chances that it will immediately or in the next few weeks kill me is small enough, I dont need to be concerned. There are other consequences.

_____

Read more from Yahoo News:

See the original post here:
Post-COVID heart damage alarms researchers: 'There was a black hole' in infected cells - Yahoo Movies UK

Read More...

‘There was a black hole’ in infected cells – Sports Grind Entertainment

Friday, September 11th, 2020

Shelby Hedgecock contracted the coronavirus in April and thought she had fought through the worst of it the intense headaches, severe gastrointestinal distress, and debilitating fatigue but early last month she started experiencing intense chest pain and a pounding heartbeat. Her doctor put her on a cardiac monitor and ordered blood tests, which indicate the previously healthy 29-year-old had sustained heart damage, likely from her bout with COVID-19.

I never thought I would have to worry about a heart attack at 29 years old, Hedgecock told Yahoo News in an interview. I didnt have any complications before COVID-19 no pre-existing conditions, no heart issues. I can deal with my taste and smell being dull; I can fight through the debilitating fatigue, but your heart has to last you a really long time.

Hedgecocks primary care physician has referred her to a cardiologist she will see this week; the heart monitor revealed Hedgecocks pulse rate is wildly irregular, ranging from 49 to 189 beats per minute, and she has elevated inflammatory markers and platelet counts. Hedgecock was told to go to the emergency room if her chest pain intensifies before she can see the specialist. A former personal trainer who is now out of breath just from walking around the room, Hedgecock is worried about what the future holds.

Hedgecock is far from alone in her struggle. Dr. Ossama Samuel is a cardiologist at New Yorks Mount Sinai Hospital, where he routinely sees coronavirus survivors who are contending with cardiac complications. Samuel said his team has treated three young and otherwise healthy coronavirus patients who have developed myocarditis an inflammation of the heart muscle weeks to months after recovering from the virus.

Myocarditis can affect how the heart pumps blood and trigger rapid or abnormal heart rhythms. It is particularly dangerous for athletes, doctors say, because it can go undetected and can result in a heart attack during strenuous exercise. In recent weeks, some collegiate athletes have reported cardiac complications from coronavirus, underscoring the seriousness of the condition.

Story continues

Last month, former Florida State basketball center Michael Ojo died from a heart attack in Serbia; Ojo had recovered from coronavirus before he collapsed on the basketball court. An Ohio State University cardiologist found that between 10 and 13 percent of university athletes who had recovered from COVID-19 had myocarditis. When the Big Ten athletic conference announced the cancellation of its season last month, Commissioner Kevin Warren cited the risk of heart failure in athletes. Researchers have estimated that up to 20 percent of people who get coronavirus sustain heart damage.

Samuel said he feels an obligation to warn people, particularly since some of the patients he and other Mount Sinai colleagues have seen with myocarditis had only mild cases of coronavirus months ago.

We are now seeing people three months after COVID who have pericarditis [inflammation of the sac around the heart] or myocarditis, Samuel said. He said he believes a small fraction of coronavirus survivors are sustaining heart damage, but when a disease is so widespread it is concerning that a tiny fraction is still sizable.

Samuel said he worries particularly about athletes participating in team sports since many live together and spend time in close quarters. Teammates may all get coronavirus and recover together, Samuel said, but the one who really gets that crazy myocarditis could be at risk of dying through exercise or training.

Its a concern about what do you do: Should we do sports in general, should we do it in schools, should we do it in college, should we just do it for professionals who understand the risk and theyre getting paid? Samuel asked. I hope we dont scare the public, but we should make people aware.

Samuel is recommending patients recovering from COVID-19 with myocarditis avoid workouts for three to six months.

Todd McDevitt, who runs a stem-cell lab at the University of California at San Francisco-affiliated Gladstone Institutes, recently published images that show how coronavirus can directly invade the heart muscle. McDevitt said he was so alarmed when he saw a sample of heart muscle cells in a petri dish get diced by the coronavirus that he had trouble sleeping for nights afterward.

McDevitt said his teams research was spurred by their desire to understand if the coronavirus is entering heart cells and how it is affecting them. McDevitt was surprised to see the heart muscle samples he was studying react to a very small amount of coronavirus, usually within 24-48 hours. He said the virus decimated the heart cells in his petri dishes.

Cell nuclei the hubs of all the genetic information, all of the nuclear DNA in many of the cells were gone, McDevitt said. There was a black hole literally where we would normally see the nuclear DNA. Thats also pretty bizarre.

While McDevitts study has not yet been peer-reviewed it is still in pre-print he said he felt compelled to share the findings as soon as possible. He said his team also sampled tissues from three COVID-19 patient autopsies and found similar damage in the heart muscles of those patients, none of whom had been flagged for myocarditis or heart problems while they were alive.

This is probably not the whole story yet, but we think we have insights into the beginning of when the virus would get into some of these people and what it might be doing that is concerning enough that we should probably let people know because clinicians need to be thinking about this, McDevitt said in an interview. We dont have any means of bringing heart muscle back. This virus is [causing] a very different type of injury and one we havent seen before.

McDevitt said that the chopped up heart muscles he and his colleagues saw is so concerning because when the microfibers in the muscle are damaged, the heart cant properly contract.

If heart muscle cells are damaged and they cant regenerate themselves, then what youre looking at is someone who could prematurely have heart failure or heart disease due to the virus, McDevitt said. This could be a warning sign for a potential wave of heart disease that we could see in the future, and its in the survivors thats the concern.

McDevitt said that he believes the risk of heart disease is serious and one people should consider as they assess their own risk of getting the coronavirus.

I am more scared today of contracting the virus, by far, than I was four months ago, McDevitt said.

The Lancet recently reported an 11-year-old child had died of myocarditis and heart failure after a bout of COVID-induced multi-system inflammatory syndrome (MIS-C). An autopsy showed coronavirus embedded in the childs cardiac tissue.

A recent study from Germany found that 78 percent of patients who had recovered from coronavirus and who had only mild to moderate symptoms while ill with the disease had indications of cardiac involvement on MRIs conducted more than two months after their initial infection.Lead investigator Eike Nagel said it is concerning to see such widespread cardiac impact; six in 10 of the patients Nagels team studied experienced ongoing myocardial inflammation.

We found an astonishingly high level of cardiac involvement approximately two months after COVID infection, Nagel said in an email. These changes are much milder than observed in patients with severe acute myocarditis.

The scale of the cardiac impact on relatively healthy, young patients surprised many doctors. Nagel said the findings are significant on a population basis, and that the impact of COVID-19 on the heart must be studied more.

Gregg Fonarow, chief of UCLAs Division of Cardiology and director of the Ahmanson-UCLA Cardiomyopathy Center, said the picture is evolving, but the new studies showing cardiac impact in even young people with mild cases of COVID have raised troubling new questions.

We really do need to take seriously individuals that have had the infection and are having continued symptoms [and] not just dismiss those symptoms, Fonarow said. There could be, in those who had milder or even asymptomatic cases, the potential for cardiac risk.

Fonarow said it is important to understand whether a more proactive screening and treatment approach is needed to better address the needs of patients who have recovered from coronavirus and who may still have weakened heart function. Fonarow said he found McDevitts research to be potentially significant because it proves from a mechanistic standpoint that there can be direct cardiac injury from the virus itself.

Even if it were going to impact, say, 2 percent of the people that had COVID 19, when you think of the millions that have been infected that ends up in absolute terms being a very large number of individuals, Fonarow said in an interview. You dont want people to be unduly alarmed, but on the other hand you dont want individuals to be complacent about, Oh, the mortality rate is so low with COVID-19, I dont really care if Im infected because the chances that it will immediately or in the next few weeks kill me is small enough, I dont need to be concerned. There are other consequences.

_____

Read more from Yahoo News:

Read more:
'There was a black hole' in infected cells - Sports Grind Entertainment

Read More...

The reason your face mask might be causing dry eye – The List

Friday, September 11th, 2020

Eye doctors say MADE, like maskne orfogged-up glasses, are not reasons to skip a mask. "The real reason for bringing this to people's attention is to say, 'Hey, if you notice this, this is why it's happening and let's help you manage your dry eye while you continue to wear your mask," Lyndon Jones, the director of the Center for Ocular Research and Education at Canada's University of Waterloo tells The Washington Post.

To keep MADE at bay, doctors suggest you find a face mask that fits properly, so that air has less of a chance of escaping from the top. Also, step away from the computer every 20 minutes to give your eyes a break. And speak to an eye specialist when you feel an early onset of MADE, which includes discomfort and blurred vision.

Much as we hate all the associated problems that come with wearing face masks, there is a compelling reason you need to keep them on. The CDC says clinical studies have shown that face masks are an important ally in the pandemic, because they catch potentially infectious droplets before they spread through coughing, sneezing, talking, or raising your voice. This means masks, along with social distancing, are still the best way to keep the virus from spreading.

See original here:
The reason your face mask might be causing dry eye - The List

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Can we stand together and overcome adversity and genetics? – Laurel Outlook

Friday, September 11th, 2020

I would like to refer to the excellent article by Barbara Karst in the Outlook September 3rd edition. I take exception to one statement.

Racism is not an inherent attitude. It has to be taught by someone - parents, grandparents, and others who are racist/ bigoted. This statement brings into play the continuing discussion; does man learn through nurture or nature? Do we only learn from the experiences encountered from the time of conception on, or is there residual knowledge passed on to us via genetics?

I would like to refer you to the works of Dr. E. O. Wilson, major proponent of sociobiology, Robert Ardrey and his four book series, The Nature of Man, and to the work of Dr Raymond Dart after his 1924 discovery of the Australopithecus Africanus. Their assertion is we learn by both nurture AND nature. Dr. Darts bold, blunt and controversial statement is both man and animals retain knowledge through instinct. The strongest instinct being the instinct to survive.

There are many facets to the act of survival. Currently most common is the discussion of the herd instinct, or the social need for community. This need for community is so strong, we use the deprivation of community as a form of punishment. We imprison, or remove from society our criminals. Solitary confinement is not only considered a punishment but has proven to be a form of torture. Religions shun or excommunicate controversial individuals. We instinctually repel or fear that which is new or not understood for it may threaten our survival.

To be succinct, we are all bigots. Strength in numbers, or the herd can provide security. We look alike. We talk alike. We think alike. I will be safe. I will survive and in times of stress, we revert to that which we presume will again protect us.

Ironically, the study of genetics has shown us the necessity for diversity. We have learned the inbreeding of animals and humans can cause numerous physical and mental deficiencies. We can also inbreed our society intellectually. The art of learning is augmented through the nurturing of our young and the continued exploration of creation throughout our lives.

In this time of social and economic uncertainty, will we revert to the herd? Retreat to our embattlements and separate into isolated communities fearful of the unknown? Or do we have the courage and strength of character to stand together in an ever expanding herd and face the unknown? Strength of numbers, nature, expansion of knowledge, nurture, they can work together.

Jim Tikalsky of Laurel

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Can we stand together and overcome adversity and genetics? - Laurel Outlook

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Brighton researchers lead study on genetics and asthma – The Argus

Friday, September 11th, 2020

A STUDY has shown for the first time that genetics may play a part in how well children respond to treatment for asthma.

Researchers at Brighton and Sussex Medical School (BSMS) say their findings indicate that childrens asthma symptoms could be better controlled with personalised treatments.

Dr Tom Ruffles, honorary consultant in paediatric respiratory medicine, worked with a study team led by Professor Somnath Mukhopadhyay, chairman in paediatrics at the Royal Alexandra Childrens Hospital and BSMS.

Dr Ruffles and Professor Mukhopadhyay presented the results from their trial at the virtual European Respiratory Society International Congress.

According to Dr Ruffles, asthma affects one in 11 children in the UK and a child is admitted to hospital because of their asthma every 18 minutes.

He told the conference: Asthma is a common condition in children that causes coughing, wheezing and difficulty breathing.

We have a number of medicines that are generally effective in treating children with asthma, but they dont work equally well for all children.

We think that genetic differences could have an effect on whether these medicines work and thats what we wanted to examine in this study.

Previous research suggests the majority of children with asthma will benefit from standard treatment with a medicine called salmeterol and their regular steroid inhaler.

However about one in seven children have a small genetic difference which means using this medication could actually result in them having more asthma symptoms.

The BSMS study involved 241 young people aged between 12 and 18 who were all being treated for asthma.

Participants were randomly assigned either to receive treatment according to existing guidelines, or treatment according to particular genetic differences their genotype an approach known as personalised medicine.

Children in the personalised medicine group were treated with an alternative asthma medicine called montelukast.

Researchers followed the children for a year to monitor their quality of life, with a score between one and seven according to how their symptoms were and whether their normal activities were limited by their asthma.

They found that for children with a particular gene who were given personalised treatment, they experienced an improvement in their quality of life score.

Professor Mukhopadhyay said: These results are very promising because they show for the first time, that it could be beneficial to test for certain genetic differences in children with asthma and select medication according to those differences. In this study we saw only a modest effect, but this may be partly because the childrens asthma was generally very well controlled and only a few children experienced any serious symptoms during the 12-month period.

Larger trials, with a focus on those with poorer asthma control, may help us determine the true benefit for children of prescribing in this way.

Link:
Brighton researchers lead study on genetics and asthma - The Argus

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Harbour BioMed and Hualan Genetic Announced Collaboration to Develop Multiple Innovative Antibody Programs – PRNewswire

Friday, September 11th, 2020

CAMBRIDGE, Mass.,ROTTERDAM, Netherlands, SUZHOU,China and XINXIANG, China, Sept. 11, 2020 /PRNewswire/ -- Harbour BioMed (HBM), a global, clinical-stage, innovative biopharmaceutical company today announced a strategic partnership agreement with Hualan Genetic Engineering Co., Ltd (Hualan Genetic) to develop HBM's three proprietary innovative monoclonal and bispecific antibodies.

Under the terms of the agreement, Hualan Genetic will be responsible for preclinical and process development in exchange for exclusive rights for the development, manufacturing, and commercialization of these innovative antibody drugs in Greater China (Mainland China, Hong Kong, Taiwan and Macau). HBM will retain the rights for advancing the clinical development and commercialization in rest of the world. Both parties will collaborate on clinical developments and drug manufacturing. HBM will receive an upfront payment of USD 8.75M and royalties based on sales in Greater China.

Using its proprietary H2L2 and HCAb fully human transgenic mouse platforms, HBM has developed a series of novel antibody candidates against oncology and immunological diseases. Many of these candidates have already progressed to preclinical and clinical stages. HBM has developed an immune cell engager platform HBICE, and one productof this collaboration with Hualan Genetic is HBICE bispecific antibody.

Hualan Genetic has been dedicated to R&D and the production of monoclonal antibodies, recombinant human coagulation factors, recombinant hormone drugs. To date, the company has 19 recombinant protein products under development and 7 monoclonal antibody products that received approval for the clinical trial, among which several are under Phase III clinical study. Hualan Genetic is a novel biopharmaceutical company specializing in R & D, production and sales with product indications covering a dozen major diseases, including breast cancer, melanoma, lung cancer, colorectal cancer, and diabetes mellitus.

"We are pleased to join forces with Hualan to accelerate the development of novel therapeutics based on our HCAb platform that gives us the flexibility to design and develop innovative therapeutics. This collaboration brings together complementary capabilities to address patients' needs across the world." said Dr. Jingsong Wang, Founder, Chairman & Chief Executive Officer of HBM. "As a global biopharma, we have been collaborating with several industry and academic partners around the world to leverage complementary capabilities in both research and development to advance the next generation of therapeutics in oncology and immunology." he added.

Dr. Wenqi An, General Manager of Hualan Genetic, said, "Business of antibody drugs is one of the core strategic directions for the future development of Hualan Genetic. Previously, Hualan Genetic has successfully completed R&D of 7 monoclonal antibody drugs and established an antibody-drug production line with a scale of 10,000L. Hualan Genetic is on the development path transiting from the production of biosimilars to R&D of products concentrated on the latest antibody technologies (such as HBICE bispecific antibody). Hualan is very pleased to cooperate with HBM to accelerate our buildup ofinnovative product pipeline and accomplish the upgrade from biosimilars to bio-innovative drugs."

About Harbour BioMed

Harbour BioMed is a global, clinical stage biopharmaceutical company developing innovative therapeutics in the fields of immuno-oncology, immunologic diseases, and COVID-19. The company is building its proprietary pipeline through internal R&D programs, collaborations with co-discovery and co-development partners and select acquisitions.

The company's internal discovery programs are centered around its two patented transgenic mouse platforms (Harbour Mice) for generating both fully human monoclonal antibodies, heavy chain only antibodies (HCAb) and HBICE immune cell engager technology for developing bispecific antibodies. Harbour BioMed also licenses the platforms to companies and academic institutions. The company has operations in Cambridge, Massachusetts; Rotterdam, the Netherlands; and Suzhou & Shanghai, China. For more information, please visit: http://www.harbourbiomed.com

About Hualan Genetic

Hualan Genetic has been dedicated to R&D and production of monoclonal antibodies since its foundation in 2013. From generics to biologics, Hualan Genetic has started its independent innovation development path transiting from production of biosimilars to R&D of products with the latest antibody technologies (such as innovative drugs of bispecific antibody and heavy-chain-only antibody). The company has advanced and complete R&D testing platform, pilot test workshop, scale production workshop and inspection testing platform, with four 2,500L and two 500L cell culture production lines of EU and WHO standard design, and various fully automatic filling lines, which can realize production, filling and packaging and lyophilization for various products of different scales at the same time. Hualan also provides CRO and CMO services of biomacromolecules including monoclonal cell strain screening, assessment, process R&D, drug analysis, preparations development, submission and approval for production, filling and packaging and labeling.

Media and Investor Contact:

Harbour BioMed Atul Deshpande PhD, MBA Chief Strategy Officer and Head, US Ops. Phone: +1-908-210-3347 E-mail: [emailprotected]

Hualan Genetic International Business Director Kevin Cai E-mail: [emailprotected]

SOURCE Harbour BioMed

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Harbour BioMed and Hualan Genetic Announced Collaboration to Develop Multiple Innovative Antibody Programs - PRNewswire

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Genetic Links to Drug and Alcohol Use Among Young People With Mental Health Risks – Medscape

Friday, September 11th, 2020

Young people who are genetically predisposed to risk-taking, low extraversion and schizophrenia are more likely to use alcohol, cigarettes, cannabisor other illicit drugs, according to a new University College London-led study.

The researchers say that the findings, published in Addiction Biology, are in line with the notion that people who are more vulnerable to psychopathology or certain personality traits are more inclined to try several types of drugs or use them to 'self-medicate'.

The study used data from the Avon Longitudinal Study of Parents and Children (n=4218) and applied traitstateoccasion models to delineate the common and substancespecific factors based on four classes of substances (alcohol, cigarettes, cannabis and other illicit substances) assessed over time (ages 17, 20 and 22 years). The researchers generated 18 polygenic scores indexing genetically influenced mental health vulnerabilities and individual traits.

The results implicated several genetically influenced traits and vulnerabilities in the common liability to substance use, most notably risk taking (bstandardised, 0.14; 95% CI, 0.10-0.17), followed by extraversion (bstandardised, 0.10; 95% CI, 0.13 to 0.06)and schizophrenia risk (bstandardised, 0.06; 95% CI, 0.02-0.09).

Educational attainment (EA) and body mass index (BMI) had opposite effects on substancespecific liabilities such as cigarette use (bstandardised EA, 0.15; 95% CI, 0.19 to 0.12 and bstandardisedBMI, 0.05; 95% CI, 0.02-0.09) and alcohol use (bstandardisedEA, 0.07; 95% CI, 0.03-0.11 and bstandardisedBMI, 0.06; 95% CI, 0.10 to 0.02).

These findings point towards largely distinct sets of genetic influences on the common versus specific liabilities.

Co-lead author Dr Tabea Schoeler (UCL Psychology and Language Sciences) said: Treatment and prevention programmes that target risk-taking behaviours among young people, while also focusing on adolescents with early signs of schizophrenia, could be beneficial in reducing the risk of developing substance use problems.

Iob E, Schoeler T, Cecil CM, Walton E, McQuillin A, Pingault JB. Identifying risk factors involved in the common versus specific liabilities to substance use: A genetically informed approach. Addict Biol. 2020 Jul 23 [Epub ahead of print]. doi: 10.1111/adb.12944. PMID: 32705754. View full text

This article originally appeared on Univadis, part of the Medscape Professional Network.

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Genetic Links to Drug and Alcohol Use Among Young People With Mental Health Risks - Medscape

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Genetic sleuths flesh out the story of how coronavirus got its start in Washington – GeekWire

Friday, September 11th, 2020

An epidemiological family tree shows how different strains of the coronavirus that causes COVID-19 spread out across different regions of the world. The red circle highlights WA1, the first confirmed case reported in Washington state and the United States. Click on the image for a larger view. (Nextstrain Graphic)

Detailed genetic analyses of the strains of virus that cause COVID-19 suggest that the outbreak took hold in Washington state in late January or early February, but went undetected for weeks.

Thats the upshot of two studies published by the journal Science, based on separate efforts to trace the genetic fingerprints of the coronavirus known as SARS-CoV-2.

The studies draw upon analyses of more than 10,000 samples collected in the Puget Sound region as part of the Seattle Flu Study during the early weeks of the outbreak, plus thousands more samples from other areas of the world.

One of the studies was conducted by a team including Trevor Bedford, a biologist at Seattles Fred Hutchinson Cancer Research Center who has been issuing assessments of the virus and its spread since the earliest days of the outbreak. The first version of the teams paper went online back in March and was revised in May, months in advance of todays peer-reviewed publication.

The other study comes from researchers led by the University of Arizonas Michael Worobey, who also published a preliminary version of their results in May.

There are subtle differences between the two analyses. For example, Bedford and his colleagues say its most likely that the majority of the infections in Washington state arose from a single case that was introduced in late January or early February.

Worobeys team, however, suggests multiple travelers returning from China during that time frame may have brought the virus to Washington and California.

Bedford and his colleagues say theres not yet enough evidence to rule out the hypothesis that the community spread of coronavirus started with the first reported case, known as WA1, which dates to Jan. 19. But the other teams analysis, which involved running simulations of the virus spread, argues against that scenario.

Worobey and his colleagues also argue against the possibility that the virus came to Washington state via British Columbia, which was an alternate scenario suggested by the data. Instead, they say its more likely that the virus made the jump directly from China.

At the time, foreign travelers were barred from coming to the U.S. from China, but tens of thousands of U.S. citizens and visa holders continued to make the trip even after the ban took effect. Worobey and his co-authors say a similar scenario led to separate introductions of the virus to the U.S. East Coast from China via Europe.

Both studies suggest that closer surveillance of COVID-19 cases, based on the model established by the Seattle Flu Study, could have lessened the impact of the pandemic in the U.S. But in a news release, Worobey said theres a silver lining to the researchers gloomy conclusions.

Our research shows that when you do early intervention and detection well, it can have a massive impact, both on preventing pandemics and controlling them once they progress, Worobey said. While the epidemic eventually slipped through, there were early victories that show us the way forward: Comprehensive testing and case identification are powerful weapons.

Trevor Bedford, Alex Greninger, Pavitra Roychoudhury, Lea Starita and Michael Famulare are the lead authors of Cryptic Transmission of SARS-CoV-2 in Washington State. Jay Shendure and Keith Jerome are the senior authors and there are scores of co-authors, including investigators with the Seattle Flu Study.

In addition to Worobey, the authors of The Emergence of SARS-CoV-2 in Europe and North America include Jonathan Pekar, Brendan Larsen, Martha Nelson, Verity Hill, Jeffrey Joy, Andrew Rambaut, Marc Suchard, Joel Wertheim and Philippe Lemey.

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New California law gives consumers more agency over data they share with genetic testing firms – Business Insider

Friday, September 11th, 2020

California lawmakers passed a law that allows consumers to revoke consent for genetic testing companies like 23andMe and Ancestry to use their data, mandating the companies to destroy the DNA samples within 30 days, STAT reported in its weeklynewsletter.

California law boosts genetic data privacy. Business Insider Intelligence

For context, direct-to-consumer (D2C) DNA testing firms often give customers the opportunity to opt into research by consenting to pass along their samples: For instance, 8 million of 23andMe's network of 10 million users haveopted in to participate in research. States are taking the helm at passing D2C genetic testing regulation, while federal lawmakers remain mumcreating a patchworked legal landscape for genetic testing companies to operate in.

Privacy laws have yet to be enacted on a federal level, so state lawmakers are stepping in: Florida recently passedlegislation prohibiting insurance companies from accessing members' genetic insights, which could impact the type and cost of coverage. But as states take charge putting forth their own laws, genetic testing companies will be faced with new obstacles, and it's unclear how they'll navigate adhering to the changing legal ecosystem.

In reference to the new law passed in California, Justin Yedor, a Los Angeles-based data privacy attorney, wascitedin Bloomberg asking, "are [D2C companies] going to provide these rights strictly for Californians or are they going to extend them to all consumers regardless of jurisdiction?" Contending with new rules passed on a state-by-state basis could cause hangups in operations, exacerbating the alreadysofteningD2C genetic testing market.

While a hodgepodge of legislation across the US will be a hurdle, increased privacy laws could assuage consumers' fears and translate into more sales.In a recent YourDNA survey,40%of consumers who had never taken a DNA test cited privacy concerns as the driving reason for why they've shied away. But if companies are transparent about granting consumers more autonomy over their data and how it's handled, they may be more likely to take the plunge.

Still, we think high-flying genetic testing firms will lean more heavily on their healthcare-focused initiatives as they navigate the shifting D2C realm: Some DNA testing firms likeColorandYouScriptthe latter of which is now owned by Invitaeare powering hospitals' precision medicine initiatives, for example.

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Invitae Appoints Kimber Lockhart to its Board of Directors – BioSpace

Friday, September 11th, 2020

SAN FRANCISCO, Sept. 11, 2020 /PRNewswire/ --Invitae Corporation (NYSE: NVTA), a leading medical genetics company, today announced the appointment of Kimber Lockhart to its Board of Directors, effective September 10, 2020.

"We are excited to welcome Kimber Lockhart to our board of directors, bringing expertise in scaling fast-growth businesses that will provide valuable insight as we continue to grow," said Sean George, co-founder and chief executive officer of Invitae. "Her expertise as a product, engineering and infrastructure leader, combined with her perspective on leveraging technology to improve healthcare for patients, will be a valuable addition to our board as we continue to pursue our mission to bring genetics to mainstream medicine to improve healthcare for billions of people around the world."

"I'm happy to join the board of directors at Invitae at this exciting time in the company's continued growth," said Lockhart. "Invitae's approach is unique and the company's capabilities combined with its dedication to its mission to make comprehensive genetic information services widely available has the potential to transform healthcare for patients worldwide."

Lockhart is an experienced technology leader, scaling technology platforms to support rapid business growth. Since 2015, Lockhart has served as chief technology officer at One Medical, a national leader in technology-enabled primary care, where she was previously vice president of engineering from 2014 to 2015. Prior to joining One Medical, Lockhart served in various engineering leadership roles at online file-sharing service Box from 2009 to 2014. Previously, Lockhart was co-founder and CEO of Increo Solutions, provider of document rendering and collaboration technologies, which was acquired by Box in 2009. She holds a B.S. in Computer Science from Stanford University.

About Invitae

Invitae Corporation (NYSE: NVTA) is a leading medical genetics company whose mission is to bring comprehensive genetic information into mainstream medicine to improve healthcare for billions of people. Invitae's goal is to aggregate the world's genetic tests into a single service with higher quality, faster turnaround time, and lower prices. For more information, visit the company's website atinvitae.com.

Contact:Laura D'Angeloir@invitae.com(628) 213-3369

View original content to download multimedia:http://www.prnewswire.com/news-releases/invitae-appoints-kimber-lockhart-to-its-board-of-directors-301128086.html

SOURCE Invitae Corporation

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BRCA1 and BRCA2 Gene Mutations: I Have a Mutation, What Are My Options? – University of Michigan Health System News

Friday, September 11th, 2020

If a patient learns that they do carry a mutation in their BRCA1 or BRCA2 genes, a genetic counselor can discuss potential options with them.

A common option for women is to undergo increased screening, including getting a breast exam from a health care provider every six months, and also a yearly mammogram and breast MRI.

There are also medications that people with BRCA gene mutations can take to reduce the risk of developing breast cancer, she says.

Doctors call these medications chemoprevention, but that makes it sound like chemotherapy, which its not, Milliron says. It is a medication that you do take for several years, and I think it's really important to have that discussion about the pros and cons and what to expect with a specialized health care provider. Women have to be at least age 35 and finished with family planning before they can consider taking a medication to reduce the risk of developing breast cancer because there is a risk of causing birth defects.

The medication that is usually given to premenopausal women is called tamoxifen, and studies point to more clear benefit for women with BRCA2 mutations. There are additional, related medications that are usually prescribed to postmenopausal women if tamoxifen is not a good option for those women.

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Some women chose to have both breasts removed a prophylactic/risk reducing bilateral mastectomy which has been shown to reduce the risk of developing breast cancer by about 90% to 95%, Milliron notes.

This is obviously a very, very personal choice, Milliron says. If you look at the statistics of the women who choose increased screening with mammogram and breast MRI, and the women who choose risk reducing or prophylactic bilateral mastectomy, there is no difference in the chance of passing away from breast cancer between those two groups. So that is something that I think is very important for patients to know and to understand.

These decisions can be influenced by watching family or friends go through cancer treatment, as can family dynamics as well as cultural and religious considerations, she adds.

Ovarian cancer is a different story than breast cancer, however.

I've been a genetic counselor for 22 years, and that is the only thing that has not yet changed about my job is that we still do not have a screening tool for ovarian cancer that works, Milliron says. So for a woman who has a BRCA1 gene mutation, we usually talk about having the ovaries and the fallopian tubes removed between 35 and 40. And then for a woman who has a BRCA2 gene mutation, we usually talk about having them removed between 45 and 50.

While the statistics vary slightly between studies, research shows this surgery can reduce the risk of developing ovarian cancer and fallopian tube cancer by 80 to 95%.

Birth control pills are also a potential option for women with these mutations to reduce their risk of developing ovarian cancer.

That may influence their breast cancer risk, however, so that's a conversation that we have to have, Milliron adds.

Men who carry a BRCA1 or BRCA2 gene mutation, are at increased risk for prostate cancer. And these can be more aggressive and develop at younger ages. For them increased screening starting about age 40 to 45 is recommended, including prostate-specific antigen, commonly referred to as PSA, testing and a digital rectal exam yearly.

The Rogel Cancer Center is very lucky to have a prostate cancer risk assessment clinic, Milliron says. So many times men are somewhat forgotten in the BRCA1, BRCA2 picture.

You can learn more about cancer genetics on the Rogel Cancer Centers website.

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Deformities linked to inbreeding found in L.A. County cougar – Los Angeles Times

Friday, September 11th, 2020

The discovery was heartbreaking for biologists, who consider the mountain lions of Southern California to be among the most threatened mammals in North America: a young male with the distortions of inbreeding a tail kinked like the letter L and only one descended testicle.

The cougar found in the Santa Monica Mountains in March represented the first documented physical manifestations of extremely low genetic diversity within an isolated population of less than two dozen mountain lions still roaming the rugged canyonlands just north of Los Angeles.

Since then, scientists have found two more lions with similar deformities. Announcement of the findings was delayed by the coronavirus pandemic, officials said.

This is something we hoped to never see, said Jeff Sikich, a biologist with the Santa Monica Mountains National Recreational Area and an expert on local mountain lion populations. We knew that genetic diversity was low here, but this is the first time we have actually seen physical evidence of it.

Mountain lions are not a formally threatened species in California. But state officials earlier this year concluded that six isolated and genetically distinct cougar clans from Santa Cruz to the U.S.-Mexico border make up a sub-population that may warrant listing as threatened under the state Endangered Species Act. Such a step could limit highway construction and development on thousands of acres of real estate.

The California Department of Fish and Wildlife reviewed the species status in response to a petition submitted by the Center for Biological Diversity and the nonprofit Mountain Lion Foundation, which argued that the populations constitute an evolutionary significant unit that should be listed as state endangered.

The California Fish and Game Commission is expected to make a final decision sometime next summer.

Recent scientific studies suggest theres an almost 1-in-4 chance that Southern California mountain lions could become extinct in the Santa Monica and Santa Ana mountain ranges within 50 years.

Thats partly because of how difficult it is to diversify the gene pool for the dozen adult lions still prowling in the Santa Monica Mountains: The 101 freeway is a near impenetrable barrier to gene flow for mountain lions. In the Santa Ana Mountains, the 15 freeway limits the movement of a family of 20 cougars.

Sometimes, the animals manage to cross the freeways without getting hit.

Just like climate change, extinction risk for Southern Californias mountain lions is not a future threat its already here, said Brendan Cummings, the centers conservation director. As California continues to encroach into wildlife habitat, they have become a test case as to whether were capable of living in this large state with wild animals.

A team led by Sikich discovered the problem on March 4 while placing a GPS radio-collar on P-81, a mountain lion weighing 95 pounds and estimated to be about 1 years old.

A few days later, another male mountain lion, also with a kinked tail, was recorded on a remote camera in the same area. Scientists believe the two cougars may be related and perhaps siblings.

Review of remote camera footage taken in the eastern Santa Monica Mountains between the 405 and Hollywood freeways suggests that a third mountain lion in the area also appears to have a kinked tail.

They underscore the results of extensive genetic analyses conducted over the past two decades: Cougars in the Santa Monica and Santa Ana mountains south of Los Angeles have the lowest levels of genetic diversity ever documented in the West, said Seth Riley, wildlife branch chief for the Santa Monica Mountains National Recreation Area.

The only population with lower levels was in south Florida a few decades ago, when Florida panthers were teetering on the edge of extinction. The really interesting, and worrying, thing, Riley said, is that they saw the same type of kinked tails and cryptorchidism among Florida panthers.

Cryptorchidism is a condition in which one or both testes fail to descend from the abdomen into the scrotum.

In the face of such a dire prognosis what biologists call an extinction vortex conservationists are stepping up calls for construction of a $60-million wildlife overpass that would cross the 101 Freeway in Agoura Hills, one of the last places where natural habitat abuts the highway on both sides.

The bridge could help diversify the gene pool among the lions remaining in the Santa Monicas south of the freeway as well as in the Simi Hills and Santa Susana Mountains to the north, they say.

Because the bridge would cross the freeway, Caltrans is overseeing design and construction but the transportation agency is not providing funding. Instead, roughly 80% of the funds are expected to come from private philanthropy and corporate donations.

As of September, the fundraising campaign led by the National Wildlife Federation had brought in about $15.4 million, including $3 million from the Santa Monica Mountains Conservancy, $2.2 million from the State Coastal Conservancy, $1 million from the Annenberg Foundation, $250,000 from the Leonardo DiCaprio Foundation and $100,000 from Boeing Co.

The project is currently in the final design phase, officials said. If fundraising stays on track, construction could begin in late 2021.

Farther south, however, conservationists are open to the idea of trans-locating mountain lions across the 15 freeway, even as they work with the California Department of Transportation on a relatively low-cost plan to improve freeway underpasses that would allow cougars freedom to roam.

These lions kinked tails are a genetic cry for help, telling us we must make it easier for them to move around and find mates, said Tiffany Yap, a biologist at the Center for Biological Diversity. More wildlife crossings are part of it, but we need to stop sprawl developments that cut these beautiful cats off from each other.

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Deformities linked to inbreeding found in L.A. County cougar - Los Angeles Times

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