StemCell Therapy

More than 13% of the global burden of disease is due to disorders such as depression, anxiety, schizophrenia and substance abuse. Almost three-quarters of this burden lies in low- and middle-income countries, because of extremely scarce health resources and investment. Many countries allocate less than 1% of the health budget to mental health. Poor or non-existent access to evidence-based care also leads to the need for long-term care and increased costs of care.

The economic burden is also significant. The global cost of lost productivity due to depression and anxiety disorders is an estimated US$1.15 trillion a year. Around 4.7 billion days of productivity are lost.

There is good evidence that these conditions are treatable. But the estimates of people in sub-Saharan Africa receiving treatment are jarring. Only 15% of South Africans with mental health conditions receive treatment. In Ghana and Ethiopia the estimates are less than 10%.

Weve spent decades researching mental health and health economics around the world. Our research has demonstrated that, for example, peer support for treating perinatal depression shows benefits that far outweigh any costs incurred in delivering the treatment. Weve also seen the Healthy Activity Programme Psychological Treatment in India provide better clinical outcomes at lower costs. In a recent study in Ghana weve shown that investments in population-level screening and subsequent treatment could yield benefits greater than the costs. The findings imply that every $1 invested over a 10 year period in depression, anxiety disorders and schizophrenia treatment would accrue about $7.4, $4.9 and $1.7 in returns respectively to society.

There are compelling arguments that neglecting mental health will make it extremely difficult to attain many other targets. These include Sustainable Development Goals related to poverty, HIV, malaria, gender empowerment and education.

For example, poverty rates are two times higher in people with mental health conditions compared to those without. People living with mental illness or substance use disorders are more likely to become infected with HIV. Poor mental health weakens immunity and adherence to treatments for malaria.

Clearly, there is a case for investing in mental health and more importantly, making interventions and services accessible to all. Having set out this case we also offer recommendations on how this might be achieved.

Political will and support from civil servants affect the proportion of GDP allocated to mental health. For Africa as a whole, government mental health expenditure per capita is $0.1.

Practical tips for mental health advocates to convince politicians have been offered in previous writings. These include placing arguments within the political context, working with the civil servants who advise politicians, and offering a multisectoral explanation of the wider picture of mental health.

Further, advocates must take advantage of crisis situations such as the COVID-19 pandemic to promote a long-term agenda for mental health, and lobby for major cross-government commissioned reviews. For example, the US Institute of Medicines report on neurological, psychiatric and developmental disorders led to increased prioritisation and research investment in mental health by major international donors.

Convening an African ministerial summit on mental health financing as a strategic follow-up to the Global Ministerial Mental Health Summit held in October 2018 would be a major boost.

We propose that governments invest in making training for and practice of mental health care attractive and relevant. This can be done by offering mentorship programmes, and use of digital and mobile technologies for delivering care. Short re-skilling programmes that focus on evaluation and management of common cases in the community and outpatient setup can be conducted annually for students and healthcare staff.

A national survey on mental health conditions is key for every country because under-recognition of the prevalence and impact of mental health needs is one reason they dont get enough attention. No African country is currently doing one. But Nigeria comes close. It has a survey conducted between 2001 and 2003 but only in Yoruba-speaking states which account for 22% of the population.

There are other areas for innovation. One could be a decentralised public health spending model that allocates resources according to performance, linking funding to specific mental health needs.

Governments could introduce financial incentives that favour community care. This means community-based rehabilitation initiatives would get more support. For example, in Rwanda, a national government incentive for subnational public and nonprofit faith-based health providers increased healthcare services by 20%.

There is also a need to rethink health and life insurance. These must reflect a move towards investing in preventative medicine and not the current curative policies.

Deliberate government leadership must promote local production of psychotropic medication as was done in the case of personal protective equipment in response to COVID-19 containment. Technology must also be used to deliver mental health services in times of public health emergencies.

Underpinning all our recommendations is sufficient and timely mental health financing. This requires a multi-sectoral strategy that shows the health and economic benefits of investing in mental health in Africa.

More:
Why Africa needs to invest in mental health - The Conversation CA

President Donald Trumps refusal to tell America the truth about the pandemic in a bid to save his political skin, on display at a potential super-spreader rally in Iowa on Wednesday night, is fostering a vacuum in national leadership and crucial public health mobilization as a winter of sickness and death looms.

Trump is touting his own recovery from Covid-19 with a cocktail of expensive experimental therapies available to almost no one else in the world as proof there is nothing to fear from a disease that has killed more than 216,000 Americans.

The President, 19 days before the election, is trying to pull the wool over voters eyes by arguing the pandemic is almost over, in the hope they wont hold him to account for his poor management of the crisis. On Wednesday, he used his own rebound and the symptom-free experience of his son Barron, who also tested positive to yet again downplay the virus.

Open your states! Trump said at a rally at which Air Force One formed a backdrop.

The cure cannot be worse than the problem itself, he said, and again wildly claimed that his own strength meant he probably didnt need the cutting-edge therapies he was given in the hospital at Walter Reed National Military Medical Center.

Maybe I would have been perfect anyway, Trump said.

The governments top infectious disease specialist, Dr. Anthony Fauci, who Trump has repeatedly attacked in recent days, said Wednesday that although he was glad the President had recovered, his case should not be seen as indicative of everyone who gets infected.

Thats sort of like saying somebody was speeding in a car at 95 miles an hour and didnt get in an accident, so I can go ahead and speed and not get in an accident, Fauci told CBS Evening News.

Fauci also criticized the concept of herd immunity, which relies on a majority of the population getting infected to build community resistance to the disease, after some White House officials appeared to partially embrace earlier this week. Trump is also advocating an approach where vulnerable people are shielded while allowing everyone else to get on with their lives nearly impossible to accomplish in practice.

What that will do is that there will be so many people in the community that you cant shelter, that you cant protect, who are going to get sick and get serious consequences, Fauci said Thursday on ABCs Good Morning America. He added that the idea that we have the power to protect the vulnerable is total nonsense.

In the real world, rather than Trumps fantasy version, the pandemic is getting worse quickly. Average daily infections are at more than 51,000. The disease that the President says should no longer dominate US life is killing more than 700 Americans a day. On Wednesday alone, newly registered infections reached nearly 60,000 with 985 new deaths. Coronavirus cases are rising in 35 states, according to Johns Hopkins University data.

The high baseline of cases that is the legacy of the failure to better suppress the virus is leaving epidemiologists in despair at the suffering that will inevitably follow as the weather cools and people move indoors.

The darkening picture would have surely dominated the second presidential debate on Thursday night. But the event was canceled amid a drama over the Presidents own diagnosis with the disease two weeks ago. Instead, Trump and Democratic nominee Joe Biden will hold dueling town halls on NBC and ABC.

Trumps tactic of minimizing the crisis is rooted in his quest to maximize turnout from his most loyal base voters, whom he and his conservative media allies constantly target with misinformation about the virus. His rallies and public acts send a visual message that life is back to normal, even as polls suggest that clear majorities of Americans disapprove of his handling of the crisis one of the dominant issues of the election.

Trump is not just risking the health of his supporters. People who get the virus at his rallies also can pass it on to others in wider society. But the Presidents word is still law among the voters who have disregarded reports that previous Trump rallies and events have spread the virus and are flocking to his events in a remarkable show of support for his reelection bid.

If Im gonna get sick and die, I guess its my turn, one rallygoer, Brenda Strothoff, told CNNs Jim Acosta in Des Moines on Wednesday night.

I feel like, yes, the Covid is kind of dangerous and it can be for some people, but for the most of us, were gonna go on with life, Strothoff said.

Another rallygoer, John Stanford, told Acosta that while he didnt want to give anybody the virus, he believed infection totals were inflated and that I figured the sooner we all get it, the sooner well be done with it.

The latest Trump rally in Des Moines, in front of a packed crowd that largely spurned masks and ignored social distancing, took place in a state where the virus is taking a deeper hold. Iowa has one of the highest testing positivity rates 18.8% in the union.

Still, the sentiments of Trumps supporters point to an important question: Has society got the balance right between fighting the pandemic and preserving as much of normal economic and social life as possible? Lockdowns and restrictions have inflicted a terrible impact on employment, family and cultural connections, and the countrys mental health and morale. A generation of schoolkids is at increasing risk of a learning deficit that could set them back years.

Trump has also taken to pointing out that European countries feted by the media for doing a better job than he has in containing the virus are now facing steep escalations in cases. Those nations, however, did experience a respite in the summer, are starting from a lower baseline of infections than the US autumn spike and saved significant numbers of lives with a more stringent approach.

And the fatalistic view of some Trump supporters also fails to acknowledge the tragedies suffered by more than 200,000 families who have lost loved ones many of whom did not have to die. It disregards the threat of hospitals being overwhelmed this winter, leading to agonizing choices for doctors and front-line workers, who are at extreme risk of taking on fatal virus loads themselves.

Reconciling these national, societal and moral dilemmas would in normal times land on the desk of the President: Its what hes elected to do. But Trumps obsession with his own political prospects is leaving such questions unaddressed. His absence is also exacerbating a leadership vacuum elsewhere; for instance, in the failure of his administration, House Democrats and suddenly thrifty Republican senators to agree on a new Covid-19 economic rescue plan.

An engaged President, reminding a weary nation of the need to commit to another round of restrictions on American life during a grim winter until vaccines become available, could save tens of thousands of lives.

If Trump wins reelection on November 3, it seems highly unlikely that he will feel a greater sense of accountability to make a more genuine effort to combat the virus. And if he loses, it seems unlikely he will be in the mood to commit to using his remaining weeks in power to tackle an issue that led to his loss.

Biden, who is leading Trump in national polls and in many swing states, may eventually be called upon to pick up the pieces, and he has anchored his campaign in criticism of the Presidents performance.

The rest of the world is wondering, what in the Lords name is happening? Biden said during a virtual fundraiser event on Wednesday.

What were living through today is not normal, the former vice president said, according to a pool report.

If the American people elect me, were going to have an enormous task in repairing the damage (Trumps) done. We have to be beating the virus, rebuilding the economy and figuring out how to restore American leadership around the world.

The Presidents negligence is not just having an immediate political impact. His constant undermining of social distancing measures and masks the only current ways of limiting the virus risks making a bad situation much worse.

Apparent hiccups with several trials being conducted by big pharmaceutical firms on vaccines and Covid-19 therapies are reemphasizing the importance of preventative measures. There was one optimistic sign on Wednesday, however, when the governments top infectious disease specialist, Fauci, predicted a safe and effective vaccine would be widely available by April.

But the Presidents dismissal of public health recommendations that are needed until then is causing despair among public health experts and front-line medics.

Its just a matter of time before we now see this terrible fall and winter surge. And this is going to be a horrible winter. We may see numbers that dwarf what we saw in March and April or during the summer, and I think we probably will, said Dr. Peter Hotez, dean of Baylor Medical Schools National School of Tropical Medicine.

And were also going to see a rise of mortality. This is going to be one of the most troubling times in our modern history in terms of the public being frightened, homeland security being affected, people worried about going outside, as the deaths mount, Hotez told CNNs Jake Tapper on Tuesday.

In a time of national peril, the White House is looked to to set priorities, to bring states together, to explain to Americans the extent of the challenge and to chart a route out of the emergency.

But Trumps coronavirus task force is invisible, as CNNs White House team reported Wednesday. Its leader, Vice President Mike Pence, is out campaigning and, like Trump and his family members, holding events that are almost certain to spread the virus. The groups most visible doctors, such as Fauci and Dr. Deborah Birx, havent appeared in public with the President for weeks.

At a time when other global leaders, including Frances Emmanuel Macron, Canadas Justin Trudeau and Britains Boris Johnson, are leveling with their people about the difficult days to come and desperately working to get new spikes of infection under control with new restrictions and partial lockdowns while trying to save their economies, Trump falsely told Americans Wednesday that they were rounding that final turn.

See the original post here:
Trump's lack of honesty on Covid hangs over his reelection bid - ABC17News.com

In summary

Proposition 14 asks voters to spend nearly $8 billion to continue the stem cell research program at a time when the coronavirus pandemic has decimated the state budget.

For the second time in 16 years, California voters will decide the fate of the states multi-billion dollar stem cell research program that established the state as a worldwide leader.

How the times have changed.

In November, as the pandemic drags on, Proposition 14 asks voters to spend nearly $8 billion to continue the program during a period when the research environment has significantly evolved and coronavirus has battered the states budget.

The bond measure would approve $5.5 billion in bonds to keep the states stem cell research agency running and grants flowing to California universities and companies.

At least $1.5 billion would be earmarked for brain and central nervous system diseases like Alzheimers and Parkinsons. The overall cost of the bonds and their interest totals about $7.8 billion, according to the state legislative analyst. The state would pay about $260 million annually for 30 years, or about 1 percent of Californias annual budget.

Proposition 14 is essentially a repeat with a bigger price tag and a few tweaks of Proposition 71, which California voters approved in 2004 after then-President George W. Bush prohibited, on religious grounds, all federal funding of any stem cell research using human embryos.

The bond measure would approve $5.5 billion in bonds to keep the states stem cell research agency running and grants flowing to California universities and companies.

That groundbreaking measure authorized $3 billion in state bonds to create the states stem cell research agency, the California Institute for Regenerative Medicine, and fund grants for research into treatments for Alzheimers disease, cancer, spinal cord injuries and other diseases.

The institute has nearly used up its original funding, so Prop. 71s author, real estate investor and attorney Robert N. Klein II, led a new effort to get Prop. 14 on the November ballot.

This time, embryonic stem cell research is in a much different place, with federal funding no longer blocked and more funding from the biotech industry.

Voters will want to consider what Californias previous investment in stem cell research has accomplished. Its a nuanced track record.

While many scientific experts agree that Prop 71 was a bold social innovation that successfully bolstered emerging stem cell research, some critics argue that the institutes grantmaking was plagued by conflicts of interest and did not live up to the promises of miracle cures that Prop. 71s supporters made years ago. Although the agency is funded with state money, its overseen by its own board and not by the California governor or lawmakers.

The agency had done a very good job of setting priorities for stem cell research, including research using human embryos, and doling out $300 million annually to build up California as a regenerative medicine powerhouse, according to a 2013 evaluation by the National Academies of Science, Engineering and Medicine.

But the report also found that because the institutes board is made up of scientists from universities and biotech firms likely to apply for grants, board members had almost unavoidable conflicts of interest.

Because human stem cells can develop into many types of cells, including blood, brain, nerve and muscle cells, scientists have long looked to them for potential treatments for currently incurable diseases and injuries. Researchers use two types of stem cells: embryonic stem cells, derived from unused human embryos created through in vitro fertilization, and adult stem cells, which are harder to work with but in some cases can be coaxed in a lab into behaving more like embryonic stem cells.

From the start, stem cell research has been ethically charged and politically controversial because human embryos are destroyed in some types of studies. Federal restrictions on the research have waxed and waned, depending on which political party holds power. While former President Bush restricted federal money for embryonic stem cell research, former President Obama removed those restrictions.

The Trump administration has restricted government research involving fetal tissue but not embryonic stem cells. However, anti-abortion lawmakers have called on the President to once again end federal funding for embryonic stem cell research.

California-funded research has led to one stem cell treatment for a form of Severe Combined Immunodeficiency known as the bubble baby disease. Children with the rare disease dont make enough of a key enzyme needed for a normal immune system. Without treatment, they can die from the disease if not kept in a protective environment. The U.S. Food and Drug Administration is now reviewing the treatment but has not yet approved it for widespread use.

Although many of the agencys early grants were for basic science, the institute also has supported 64 clinical trials of treatments for many types of cancer, sickle cell disease, spinal cord injuries, diabetes, kidney disease and amyotrophic lateral sclerosis, commonlyknown as Lou Gehrigs disease.

A June 2020 analysis by University of Southern California health policy researchers estimated that taxpayers initial $3 billion investment in the research institute helped create more than 50,000 jobs and generated $10 billion for the states economy.

Gov. Gavin Newsom has endorsed Proposition 14, and other supporters include the Regents of the University of California, the California Democratic Party, the Juvenile Diabetes Research Foundation, patient advocacy groups like the March of Dimes, and some local politicians and chambers of commerce.

Supporters have raised more than $8.5 million, including about $2 million from billionaire Dagmar Dolby, to pass the measure, according to California Secretary of State campaign finance reports.

The passage of Proposition 71 helped save my life, Sandra Dillon, a blood cancer patient, wrote in a San Diego Union-Tribune commentary supporting Proposition 14. She wrote that she had benefited from a drug developed with Institute-funded research that has been designated by the FDA as a breakthrough therapy.

It is unimaginable to think that Californians would vote to discontinue this amazing effort I dont know where I would be or what condition I would be in if it wasnt for the investment Californians made nearly two decades ago.

I think the agencys done good work, but this was never planned to be funded forever with debt.

Lawrence Goldstein, a UC San Diego professor of cellular and molecular medicine and stem cell researcher, said the grants were instrumental in furthering his research on treatments for Alzheimers disease and that Prop. 14 will help create new jobs. The agency has funded a great deal of very important stem cell medical research thats already produced terrific results and has the prospect of saving many more lives in the decade to come, he said.

Opponents include one member of the institutes board and a nonprofit that advocates for privacy in genetic research. They contend that the proposition seeks too much money and does not sufficiently address the conflicts of interest that cropped up after Prop. 71 was passed. They also note that private funding, including venture capital, for stem cell research has grown in recent years. Opponents had raised only $250 by late September, from a single contribution by the California Pro Life Council.

The editorial boards of some of Californias biggest newspapers also have opposed the measure, including the Los Angeles Times, the Orange County Register, the San Francisco Chronicle and the San Jose Mercury News/East Bay Times. The Fresno Bee, Modesto Bee, and San Luis Obispo Tribune newspaper editorial boards support Prop 14.

Jeff Sheehy, the only institute board member not to support Proposition 14, told CalMatters that the research environment has changed since voters initially approved state funding for stem cell research in 2004 and that California should prioritize other needs like education, health care, and housing.

I think the agencys done good work, but this was never planned to be funded forever with debt, Sheehy said. At this point the state cant afford it; were looking at a huge deficit.

Read the original here:
Prop. 14: In the COVID age, can California still afford its stem cell research program? - CALmatters

Californians are voting on a number of propositions that deal with a wide variety of issues this election season. Heres a closer look at Proposition 14, which deals with stem cell research. This is a summary of information taken from the official California voters guide and the website Ballotpedia.

Prop 14: Authorizes Bonds Continuing Stem Cell Research. Initiative Statute.

This ballot initiative would issue $5.5 billion in general obligation bonds for the California Institute for Regenerative Medicine (CIRM), which was created to fund stem cell research. In 2004, voters approved Proposition 71, which created CIRM, issued $3.00 billion in bonds to finance CIRM, and established a State constitutional right to conduct stem cell research.

As of October 2019, CIRM had $132 million in funds remaining. On July 1, 2019, CIRM suspended applications for new projects due to depleted funds.

This ballot initiative would require CIRM to spend no more than 7.5% of the bond funds on operation costs. The remaining bond funds would be spent on grants to entities that conduct research, trials, and programs related to stem cells, as well as start-up costs for facilities.

Dedicates $1.5 billion to research and therapy for Alzheimers, Parkinsons, stroke, epilepsy, and other brain and central nervous system diseases and conditions.

An Independent Citizens Oversight Committee (ICOC) is responsible for governing CIRM.

Arguments in Favor

Nearly half of all California families include a child or adult with medical conditions who could benefit from stem cell research, treatments, and cures.

Prop 14 provides continued funding to develop treatments, advance clinical trials, and achieve new scientific breakthroughs for Californias patients with Cancer, Diabetes, Heart Disease, Alzheimers, Parkinsons, HIV/AIDS, ALS, MS, Sickle Cell Disease, Lung Diseases, Kidney Disease, Bubble Baby Disease, Age-Related Blindness and Genetic Blindness, Epilepsy, Stroke, Schizophrenia, Autism, other Mental Health and Brain Conditions, and Infectious Diseases like COVID-19.

Californias original stem cell funding, which runs out this year, has already led to significant progress in the development of treatments and cures, including 92 FDA-approved clinical trials for chronic disease and injuries, over 2,900 medical discoveries, and demonstrated benefits for patients and research on chronic diseases including Cancer, Diabetes, Heart Conditions, Blindness, HIV/AIDS, ALS, Children with Immune Deficiencies, Paralysis, and Kidney Disease.

New revenues, economic activity and jobs are generated by this funding that will contribute to Californias economic recovery.

Chronic diseases, conditions and injuries are cutting lives short and costing Californians billions in healthcare costs. We must continue our investment, developing stem cell treatments to improve the health and reduce the suffering of millions of Californians.

Arguments Against

We cant afford to waste billions. In the middle of an economic crisis, with soaring unemployment and budget shortfalls in the tens of billions of dollars, we dont have money to burn.

And thats on top of the nearly $3 billion this troubled State agency has spent over the past 15 yearswith poor results. After an extensive analysis of spending by the State agency handing out billions in grants, the San Francisco Chronicle concluded that, The predicted financial windfall has not materialized. Only a few federally approved therapies have resulted.

Prop 14 funds a bureaucracy with serious problems. Some have questioned the integrity and independence of the State agency overseeing these funds.

Others can do this job better. The National Institute of Health provides $1.5 billion a year in grants to fund the same type of research. Private investors and companies, including many in California, have made great strides in using stem cells to cure diseasesusing private funds, not tax dollars.

Paying back Prop 14s costs of $7.8 billion could mean huge tax increases at a time when our economy is on its knees. Or laying off thousands of nurses and other heroes who do the real work of keeping California healthy.

Groups supporting Prop 14 include:

California Democratic Party

JDRF (Juvenile Diabetes Research Foundation)

University of California Board of Regents

Top donors to Yes on 14:

Robert N. Klein II ($3,625,000)

Dagmar Dolby ($2,059,000)

Juvenile Diabetes Research Foundation ($1,750,000)

Open Philanthropy Action Fund ($580,000)

Ann S. Tsukamoto ($500,000)

Groups opposed to Prop 14 include:

Editorial boards of The Orange County Register, The Bakersfield Californian, Mercury News & East Bay Times, San Francisco Chronicle, and Los Angeles Times

Top donors to No on 14:

None reported

Protect local journalism please subscribe to the print edition of the Fullerton Observer. Our online edition is free, but we depend on print subscriptions from readers. Annual subscription is only $35/year.It only takes a minute Click Here To Subscribe. Thank you for your support for the Fullerton Observer. Click here to view a copy of the print edition.

Read more:
Stem Cell Research on the Ballot: A Closer Look at Prop 14 - Fullerton Observer

SAN DIEGO, Oct. 12, 2020 (GLOBE NEWSWIRE) -- Sorrento Therapeutics, Inc. (Nasdaq: SRNE, "Sorrento") announced today that it has entered into an exclusive license agreement with Personalized Stem Cells, Inc. (PSC) to acquire global rights to its adipose derived mesenchymal stem cells (MSCs) for patients suffering from acute respiratory distress syndrome (ARDS) associated with COVID-19, which have been cleared for a Phase 1 clinical trial by the FDA.

The study is a single arm, non-randomized Phase 1 study of the safety and preliminary efficacy of an adipose-derived allogeneic MSC product candidate. The outcome data will be compared to contemporaneous non-enrolled patients at the same clinical site(s) as the enrolled patients. The primary objective is to evaluate the safety of intravenous infusion of allogeneic adipose stem cells in patients with COVID-19 and in respiratory distress. The secondary objective is to evaluate a set of safety and efficacy outcome variables to give guidance regarding the risk/benefit ratio in patients with COVID-19 respiratory distress.

More information on the Phase 1 trial can be found at:

https://clinicaltrials.gov/ct2/show/NCT04486001?term=coronastem&draw=2&rank=1

Sorrento will be assuming responsibility for executing the Phase 1 trial, which is targeted to enroll about 20 hospitalized COVID-19 patients in California. Pending the results of the Phase 1 trial, Sorrento expects to expand into Phase 2 trials in multiple relevant geographies as may be determined in consultation with applicable regulatory authorities.

Stem cells have been demonstrated to support resolution of symptoms in multiple disease settings and have the potential to reduce the long-term effects associated with pulmonary tissue damage for these patients. More information on the potential use and benefits of MSCs for patients with COVID-19 can be found in the recently published review at:

https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-020-02380-2

Stem cells represent a treatment modality with high potential to help in the fight against COVID-19 as a stand-alone therapy or in synergy with other product candidates in Sorrentos pipeline, including small molecules (abivertinib or salicyn-30) and neutralizing antibodies (STI-1499 or STI 2020).

Until a time where early treatments are more readily available, it is important to provide patients severely afflicted with COVID-19 multimodal solutions that can help increase survival, reduce the time spent in the hospital and reduce long-term sequelae. The long-term lingering effects of COVID-19 on the body can persist for months after patients leave the hospital, especially for patients that received ventilator support. Shortness of breath, difficulty doing simple tasks and pulmonary fibrosis are among the common complaints of long-term effects of the disease on COVID-19 patients leaving the ICU.

Dr. Robert Harman, CEO of PSC stated, We are delighted to be working with a company such as Sorrento, that has the vision and expertise to take our program through the next steps in the clinical development process. Sorrento saw the translational value of our decades of work in animal health and has acknowledged the extensive manufacturing and regulatory work we have done in bringing human cell lines to a Phase 1 FDA clearance. We are looking forward to collaborating on this initiative and beyond.

Dr. Henry Ji, Chairman and CEO of Sorrento stated, Stem cells were a missing piece in our comprehensive portfolio of potential solutions against COVID-19. We now cover multiple stages of the continuum of care from prevention to potential therapeutic solutions for the most advanced stages of the disease. With PSCs Phase 1 product candidate, we hope to move quickly through the next clinical trials, and, if successful, be able to provide a supportive therapy that may save the lives of the most advanced patients and may also ensure patients who have to undergo intensive care can benefit from a therapy with the potential to minimize the long-term effects of the disease due to the lung damage created by the virus early in the infection.

About Sorrento Therapeutics, Inc.

Sorrento is a clinical stage, antibody-centric, biopharmaceutical company developing new therapies to treat cancers and COVID-19. Sorrentos multimodal, multipronged approach to fighting cancer is made possible by its extensive immuno-oncology platforms, including key assets such as fully human antibodies (G-MAB library), clinical stage immuno-cellular therapies (CAR-T, DAR-T), antibody-drug conjugates (ADCs), and clinical stage oncolytic virus (Seprehvir, Seprehvec). Sorrento is also developing potential antiviral therapies and vaccines against coronaviruses, including COVIDTRAP, ACE-MAB, COVI-MAB, COVI-GUARD, COVI-SHIELD, COVI-AMG and T-VIVA-19; and diagnostic test solutions, including COVI-TRACK, COVI-STIX and COVI-TRACE.

Sorrentos commitment to life-enhancing therapies for patients is also demonstrated by our effort to advance a first-in-class (TRPV1 agonist) non-opioid pain management small molecule, resiniferatoxin (RTX), and ZTlido (lidocaine topical system) 1.8% for the treatment of post-herpetic neuralgia. RTX has completed a phase IB trial for intractable pain associated with cancer and a phase 1B trial in osteoarthritis patients. ZTlido was approved by the FDA on February 28, 2018.

For more information visit http://www.sorrentotherapeutics.com

Forward-Looking Statements

This press release and any statements made for and during any presentation or meeting contain forward-looking statements related to Sorrento Therapeutics, Inc., under the safe harbor provisions of Section 21E of the Private Securities Litigation Reform Act of 1995 and subject to risks and uncertainties that could cause actual results to differ materially from those projected. Forward-looking statements include statements regarding the safety and efficacy of an adipose-derived allogeneic MSC product in patients with COVID-19 and in respiratory distress; the clinical testing of an adipose-derived allogeneic MSC product; the expected enrollment of the Phase 1 trial; the potential commencement of any future clinical trials for an adipose-derived allogeneic MSC product; the ability of an adipose-derived allogeneic MSC product to work as a stand-alone therapy or in synergy with our other product candidates; the ability of an adipose-derived allogeneic MSC product to support healing and reduce the long-term effects associated with pulmonary tissue damage for COVID-19 patients; our ability to provide a supportive therapy for COVID-19 patents using an adipose-derived allogeneic MSC product; the ability of an adipose-derived allogeneic MSC product to potentially save lives of COVID-19 patients and to potentially minimize the long-term effects of COVID-19; our ability to cover all stages of the continuum of care for COVID-19; and our potential position in the antiviral industry. Risks and uncertainties that could cause our actual results to differ materially and adversely from those expressed in our forward-looking statements, include, but are not limited to: risks related to Sorrento's and its subsidiaries', affiliates and partners technologies and prospects and collaborations with partners, including, but not limited to risks related to seeking regulatory approval for any adipose-derived allogeneic MSC product; clinical development risks, including risks in the progress, timing, cost, and results of clinical trials and product development programs; risk of difficulties or delays in obtaining regulatory approvals; risks that clinical study results may not meet any or all endpoints of a clinical study and that any data generated from such studies may not support a regulatory submission or approval; risks that prior test, study and trial results may not be replicated in future studies and trials; risks of manufacturing and supplying drug product; risks related to leveraging the expertise of its employees, subsidiaries, affiliates and partners to assist Sorrento in the execution of its COVID-19 therapeutic product candidate strategies; risks related to the global impact of COVID-19; and other risks that are described in Sorrento's most recent periodic reports filed with the Securities and Exchange Commission, including Sorrento's Annual Report on Form 10-K for the year ended December 31, 2019, and subsequent Quarterly Reports on Form 10-Q filed with the Securities and Exchange Commission, including the risk factors set forth in those filings. Investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date of this release and we undertake no obligation to update any forward-looking statement in this press release except as required by law.

Media and Investor Relations

Alexis Nahama, DVM (SVP Corporate Development)

Telephone: 1.858.203.4120

Email: mediarelations@sorrentotherapeutics.com

Sorrento and the Sorrento logo are registered trademarks of Sorrento Therapeutics, Inc.G-MAB, COVI-GUARDTM, COVI-SHIELD, COVI-AMG, COVIDTRAP, T-VIVA-19, COVI-MAB, ACE-MAB, COVI-TRACK, COVI-STIX and COVI-TRACE are trademarks of Sorrento Therapeutics, Inc.

ZTlido is a trademark owned by Scilex Pharmaceuticals Inc.All other trademarks are the property of their respective owners. 2020 Sorrento Therapeutics, Inc. All Rights Reserved.

Go here to read the rest:
Sorrento Adds Mesenchymal Stem Cell Program (MSC) That Has Been Cleared for a Phase 1 Trial by the FDA to the Pipeline of COVID-19 Focused Rescue...

IRVINE, Calif., Oct. 9, 2020 /PRNewswire/ --AIVITA Biomedical, Inc., a private biotechnology company developing personalized vaccines for the treatment of cancer and COVID-19, announced today the publication of the peer-reviewed manuscript, "Retina organoid transplants develop photoreceptors and improve visual function in RCS rats with RPE dysfunction,"in the journal Investigative Ophthalmology & Visual Science. The study, led by researchers at AIVITA Biomedical and the Sue & Bill Gross Stem Cell Research Center of the University of California, Irvine, used 3D-retina organoids generated from human stem cells developed by AIVITA to provide insight into the potential use of transplanted retina organoids as a therapeutic option for blinding diseases.

In the study, transplanted retina organoid sheets were examined to determine if human stem cell-derived photoreceptors coulddevelop, survive and function in vivo without the support of healthy retina pigment epithelium (RPE). Visual function was examined through a variety of tests, including optokinetic testing (OKT), electroretinogram (ERG), and superior colliculus (SC) brain recording. These tests concluded that retina organoid transplantations demonstrated significant improvement in visual function compared to non-surgery and sham surgery controls, supporting the application of AIVITA's stem cell technologies in visual disease therapeutics.

"Leveraging our expertise in stem cell growth and differentiation, I'm excited to see the promise of our technology platform in potential therapeutics for vision loss," said Hans Keirstead, Ph.D., chief executive officer of AIVITA and a contributing author to the paper. "To our knowledge, this study is the first to show that it's possible for photoreceptors derived from stem cells to survive and function after transplantation when a host has a dysfunctional RPE."

This work is supported by funding from the California Institute for Regenerative Medicine (CIRM) and National Institutes of Health (NIH).

About AIVITA Biomedical AIVITA Biomedical is a privately held company engaged in the advancement of commercial and clinical-stage programs utilizing curative and regenerative medicines. Founded in 2016 by pioneers in the stem cell industry, AIVITA Biomedical utilizes its expertise in stem cell growth and directed, high-purity differentiation to enable safe, efficient and economical manufacturing systems which support its therapeutic pipeline and commercial line of skin care products. All proceeds from the sale of AIVITA's skin care products support the treatment of people with cancer.

SOURCE AIVITA Biomedical, Inc.

More here:
AIVITA Biomedical's Stem Cell Therapeutic in Vision Loss Published in Investigative Ophthalmology & Vision Science - PRNewswire

As governments fight the COVID-19 pandemic, Snopes is fighting an infodemic of rumors and misinformation, and you can help. Read our coronavirus fact checks. Submit any questionable rumors and advice you encounter. Become a Founding Member to help us hire more fact-checkers. And, please, follow the CDC or WHO for guidance on protecting your community from the disease.

As the world raced to find a treatment that would alleviate the global pressure of the coronavirus pandemic, U.S. President Donald Trump contracted the virus in early October 2020 and developed COVID-19, the respiratory disease caused by SARS-CoV-2. In the days following his diagnosis and public release from Walter Reed Hospital, where he received world-class treatment, Trump touted the powers of a miracle drug called Regeneron, which he promised to make available to the American people.

A video shared in tweet by the president on Oct. 7 claimed that Regeneron was a cure.

I spent four days there [at Walter Reed] and I went in, I wasnt feeling so hot. And within a very short period of time, they gave me Regeneron. Its called Regeneron. And other things too but I think this was the key. But they gave me Regeneron, and it was like, unbelievable. I felt good immediately. I felt as good three days ago as I do now.

So, I just want to say, we have Regeneron. We have a very similar drug from Eli Lilly, and theyre coming out and were trying to get them on an emergency basis. Weve authorized it. Ive authorized it. And if youre in the hospital and youre feeling really bad, I think were going to work it so that you get them and youre going to get them free.

Shortly after the president praised what he deemed a cure for his COVID-19 infection, some social media users pushed the claim that the drug Trump was given was developed using fetal tissue a practice in direct conflict with the administrations pro-life platform.

To clarify, Trump was treated with REGN-COV2, a novel anti-viral antibody cocktail created by Regeneron Pharmaceuticals, a New York-based company that has openly stated it uses stem cell and fetal tissues as part of its research and development on new pharmaceutical treatments. This knowledge, and open support from a pro-life president, incited social media pushback from users who argued that the companys use of stem cells and fetal tissues for scientific research goes against pro-life platforms and policies.

REGN-COV2 is a combination of two human-made proteins, or monoclonal antibodies, known as REGN10933 and REGN10987. These two monoclonal antibodies were specifically designed to block the ability of SARs-CoV-2 to infect human cells. The biotechnology company further went on to describe the development of REGN-COV2 as follows:

To develop REGN-COV2, Regeneron scientists evaluated thousands of fully-human antibodies produced by the companys VelocImmune mice, which have been genetically modified to have a human immune system, as well as antibodies identified from humans who have recovered from COVID-19. The two potent, virus-neutralizing antibodies that form REGN-COV2 bind non-competitively to the critical receptor binding domain of the viruss spike protein, which diminishes the ability of mutant viruses to escape treatment and protects against spike variants that have arisen in the human population.

While it is true that Regeneron has used stem cells for some of its research, no human stem cells or human embryonic stem cells were used in the development of REGN-COV2, according to Alexandria Bowie, a spokesperson for the company. An April 2020 statement issued by Regeneron confirmed that research using stem cells helps its scientists model complex diseases, test new drug candidates, and lead to scientific insights that may help spur the creation of new medicines but the company contends that embryonic cells were not used in the production of REGN-CO2.

In short: we did not use human stem cells or human embryonic stem cells in the development of REGN-COV2, Bowie told Snopes in an email.

But its not quite that cut and dried.

In the research and development of pharmaceutical therapeutics, many companies turn to what is known as a cell line. These are cultures of human or animal cells that are derived from a living organism and cultured and propagated repeatedly, and, in some cases, used indefinitely. The development of REGN-COV2 utilized HEK293T a cell line that is derived from human fetal embryonic kidney tissues to create a pseudovirus that mimics a spike Protein found in SARS-CoV-2 in order to test the drugs ability to neutralize and ultimately treat the novel coronavirus.

HEK293s are considered immortalized cells (not stem cells) and are a common and widespread tool in research labs. This cell line was originally derived by adenovirus transformation of human embryonic kidney cells in 1977, explained Bowie, adding that HEK293 were further transformed at Stanford in the 1980s with SV40 large T antigen, a solution that is used by researchers to initiate and maintain DNA replication necessary for creating cell lines.

Fetal tissues were not directly used n the development of REGN-COV2, but cell lines from decades-old embryonic kidney tissues were. Fetal tissues are used to develop cell lines. Embryonic stem cells, on the other hand, are different than adult stem cells in that they are undifferentiated and regenerative cells, which means that they have not been assigned a key task in the human body. As such, researchers have uncovered ways to direct their use in creating human tissues that allow for a variety of uses, including testing new pharmaceuticals.

Opposition to the use of fetal tissue and embryonic stem cell research has been at the heart of the pro-life platform due to the way in which these cells are obtained and its association with using living fetuses either inside (in utero) or outside of the uterus (ex utero). Pro-life groups like March for Life have even gone so far as to pressure the Trump administration to halt funding for research that requires aborted fetal organs and tissues. In summer 2019, the president required any federally funded research using fetal tissue to undergo an ethics review, and has since stocked his cabinet with other similarly-minded officials.

REGN-COV2 is currently in late-stage clinical trials for various populations, including non-hospitalized and hospitalized patients as well as for the potential prevention in individuals who may have had close household exposure to COVID-19. According to a news release published on Sept. 29, the company announced that the antibody cocktail was shown to reduce the viral load and alleviate symptoms in non-hospitalized patients with COVID-19. REGN-COV2 also showed positive trends in reducing medical visits. However, it is important to note that the research included a relatively small sample size of just 275 patients.

The greatest treatment benefit was in patients who had not mounted their own effective immune response, suggesting that REGN-COV2 could provide a therapeutic substitute for the naturally-occurring immune response. These patients were less likely to clear the virus on their own and were at greater risk for prolonged symptoms, said Regeneron President and Chief Scientific Officer Dr. George D. Yancopoulos in a statement.

As of Oct. 12, Regeneron had submitted an emergency use authorization (EUA) to the U.S. Food and Drug Administration in early October, and noted REGN-COV2s early, promising clinical data paired with the continued, pressing unmet need of COVID-19 meets the FDA standard for emergency use authorization.

Regeneron told Snopes that it cant speculate on potential timing for an EUA. We will update when such is available.

See the article here:
Was Trump's Regeneron 'Cure' Developed Using Stem Cells and Fetal Tissues? - Snopes.com

A company born at the University of Louisville has raised an additional $115 million to further develop a therapy that could improve the lives of kidney transplant recipients.

The company, Talaris Therapeutics Inc., plans to use the series B funding to support a Phase 3 clinical trial the last step before applying for FDA approval. This follows a $100 million series A funding round announced last year to hire staff and initiate the trial.

Talaris recently began dosing patients in that trial of the unique cell therapy, called FCR001, which allows living-donor kidney transplant recipients to stay off immunosuppression drugs they would otherwise need for the rest of their lives.

Immunosuppressants help prevent rejection of the transplanted organ, but can cause side effects, including high blood pressure, diabetes, high cholesterol, neurological effects, increased risk of infection and decline in kidney function over time.

This technology could help transplant patients live fuller, healthier lives,said UofL Executive Vice President for Research and Innovation, Kevin Gardner.This UofL research, in the hands of strong industry partners and backed by investors, is a big step in advancing our health.

FCR001 consists of stem cells taken from the organ donor and processed at the Talaris facility, then infused into the organ transplant recipient. The goal is to create a durable dual immune system (part donor-derived and part recipient) in the transplant recipient. These two immune systems coexist, recognizing both the recipients own body as well as the donated organ as self.

The new funding also will advance aplanned Phase 2 trial of FCR001 in diffuse systemic sclerosis, a severe form of the rare autoimmune disease scleroderma.

Talaris, formerly known as Regenerex LLC, was founded by UofL researcher and innovator Suzanne Ildstad to commercialize the pioneering work of her team at the university. She now serves as Talaris chief scientific officer.

This financing moves us one step closer to helping organ transplant recipients no longer be dependent on immunosuppressive drugs, resulting in a greatly improved quality of life, Ildstad said of the earlier Phase 3 trial financing. The support and research infrastructure at UofL have been invaluable in our journey to this important juncture.

In an earlier Phase 2 trial, FCR001 allowed 70% of living donor kidney transplant patients durably to be weaned off all of their immunosuppression treatments.

The Phase 3 trial is expected to enroll 120 adult living donor kidney transplant recipients at multiple sites across the U.S. To date, the trial has been initiated at five clinical sites around the country.

Read more here:
UofL-born company secures an additional $115 million to advance cell therapy - uoflnews.com

Novellus Therapeutics Exclusively Licenses Induced Mesenchymal Stem Cells (iMSCs) to NoveCite

"Novellus's iMSCs have the potential to be a breakthrough in the field of cellular therapy for acute respiratory conditions because of their high potency as demonstrated in our pre-clinical studies, as well as our ability to cost-effectively provide high doses and repeat doses." said Myron Holubiak, CEO of Citius.

"We are excited to be developing iMSCs because of their promise to save lives and reduce long term sequelae in patients with devastating respiratory diseases such as ARDS caused by COVID-19," said Matt Angel, Chief Science Officer of Novellus. He continued, "Our iMSCs have multimodal immunomodulatory mechanisms of action that make them promising for treatment of acute respiratory diseases."

About Novellus Therapeutics LimitedNovellus is a pre-clinical stage biotechnology company developing engineered cellular medicines using its patented non-immunogenic mRNA, high-specificity gene editing, mutation-free & footprint-free cell reprogramming and serum-insensitive mRNA lipid delivery technologies. Novellus is privately held and is headquartered in Cambridge, MA. For more information, please visit http://www.novellustx.com.

About NoveCite, Inc.NoveCite, Inc. is a newly formed subsidiary of Citius Pharmaceuticals, a late-stage specialty pharmaceutical company dedicated to the development and commercialization of critical care products, with a focus on anti-infectives and cancer care. For more information, please visit http://www.citiuspharma.com.

Contact: [emailprotected]

SOURCE Novellus Therapeutics

Read more:
Novellus Therapeutics Exclusively Licenses Induced Mesenchymal Stem Cells (iMSCs) to NoveCite for COVID-19 Related Acute Respiratory Distress Syndrome...

Gosselies, Belgium, 14 October 2020, 7am CEST BONE THERAPEUTICS(Euronext Brussels and Paris: BOTHE), the cell therapy company addressing unmet medical needs in orthopedics and other diseases, today announces positive 24-month follow-up results for the Phase IIa study with the allogeneic cell therapy product, ALLOB, in patients undergoing lumbar spinal fusion procedures.

The 24-month data show a high percentage of successful lumbar vertebrae fusion of 90%. Patients also continue to experience important clinical improvements in function and pain, from as early as six months after treatment, up to the 24-month follow-up period.

Degenerative spine disorders have a major impact on the quality of life of patients. These impacts include decreases in the stability of the spine and pain in motion,said Dr. Alphonse Lubansu, M.D., Head of the Spinal Clinic, Erasme University Hospital, Universit libre de Bruxelles. The 24 month follow-up data of this Phase IIa clinical trial have demonstrated that patients treated with ALLOB in spinal fusion procedure show a high incidence in fusion, and benefit from a sustained, clinically meaningful improvement in function and pain throughout the 24 months following treatment together with a good safety profile. These results show that ALLOB in combination with the standard spine fusion surgery could be a promising treatment option to address the currently unmet needs of these patients.

This positive data forlumbar spinal fusion complementsthe strong Phase I/IIa results from ALLOB in patients with delayed union fractures,said Miguel Forte, MD, PhD, Chief Executive Officer of Bone Therapeutics. These studies provide promising clinical evidence for the potential ofBone Therapeuticsunique allogeneic cell therapy platform to address high unmet medical needs in orthopaedics and bone related disorders. We will now hold discussions with global regulators and our partners to explore a variety of options for the next stages of clinical development for ALLOB in different orthopedic indications, while pursuing the phase IIb study of ALLOB in difficult tibial fractures.In addition, theclinical results provide further evidence for the expansion of ALLOB and our platform of differentiated MSCs to other indications.

The multi-center, open-label proof-of-concept Phase IIa study was designed to evaluate the safety and efficacy of ALLOB administered, procedure in which an interbody cage with bioceramic granules mixed with ALLOB is implanted into the spine to achieve fusion of the lumbar vertebrae. The main endpoints of the 24-month follow-up analysis included safety and radiological assessments to evaluate vertebrae fusion (continuous bone bridges) and clinical assessments to evaluate improvement in patients functional disability as well as reduction in back and leg pain. The study evaluated 30 patients treated with ALLOB, 29 patients attended the 24-month visit.

Radiological data was collected from CT-scans at 24 months and assessed by three external readers. It showed a successful fusion of the lumbar vertebrae in 27 out of 30 patients (90%). In addition, the remaining 3 patients showed radiological evidence of bone formation. Treatment with ALLOB also resulted in a clear and statistically significant clinical improvement in function and reduction in pain over the 24-month follow-up period. Functional disability improved from the pre-treatment baseline to 24-month by a mean score of 60% (p<0.001) on the Oswestry Disability Index(1). Back and leg pain were strongly reduced by 57 to 62% (p<0.001) and 68 to 70% (p<0.001) respectively compared to pre-treatment baseline. Treatment with ALLOB was generally well-tolerated by the patients, consistent with previous reported results.

(1)The Oswestry Disability Index (ODI) is an index derived from the Oswestry Low Back Pain Questionnaire used by clinicians and researchers to measure a patients permanent functional disability. This validated questionnaire was first published by Jeremy Fairbank et al. in Physiotherapy in 1980. ODI score of 0%-20%: minimal disability; 21%-40%: moderate disability; 41%-60%: severe disability; 61%-80%: crippled; 81%-100%: bed bound.

About Spinal Fusion

Due to ageing populations and sedentary lifestyles, the number of people suffering from degenerative spine disorders continues to increase. Today, spinal fusion procedures are performed to relieve pain and improve patient daily functioning in a broad spectrum of degenerative spine disorders. Spinal fusion consists of bridging two or more vertebrae with the use of a cage and graft material, traditionally autologous bone graft or demineralised bone matrix placed into the intervertebral space for fusing an unstable portion of the spine and immobilizing a painful intervertebral motion segment. Over 1,000,000 spinal fusion procedures are performed annually in the US and EU, of which half at lumbar level and the market is growing at a rate of 5% per year. Although spinal fusion surgery is routine, non-fusion, slow progression to fusion and failure to eliminate pain are still frequent with up to 35% of patients not being satisfied with their surgery.

About ALLOB

ALLOB is the Companys off-the-shelf allogeneic cell therapy platform consisting of human allogeneic bone-forming cells derived from cultured bone marrow mesenchymal stem cells (MSC) from healthy adult donors, offering numerous advantages in product quality, injectable quantity, production, logistics and cost as compared to an autologous approach. To address critical factors for the development and commercialisation of cell therapy products, Bone Therapeutics has established a proprietary, optimised production process that improves consistency, scalability, cost effectiveness and ease of use of ALLOB. This optimized production process significantly increases the production yield, generating 100,000 of doses of ALLOB per bone marrow donation. Additionally, the final ALLOB product will be cryopreserved, enabling easy shipment and the capability to be stored in a frozen form at the hospital level. The process will therefore substantially reduce overall production costs, simplify supply chain logistics, improve patient accessibility and facilitate global commercialisation. The Company will implement the optimized production process for all future clinical trials with ALLOB.

About Bone Therapeutics

Bone Therapeutics is a leading biotech company focused on the development of innovative products to address high unmet needs in orthopedics and other diseases. The Company has a, diversified portfolio of cell and biologic therapies at different stages ranging from pre-clinical programs in immunomodulation to mid-to-late stage clinical development for orthopedic conditions, targeting markets with large unmet medical needs and limited innovation.

Bone Therapeutics is developing an off-the-shelf next-generation improved viscosupplement, JTA-004, which is currently in phase III development for the treatment of pain in knee osteoarthritis. Consisting of a unique combination of plasma proteins, hyaluronic acid a natural component of knee synovial fluid, and a fast-acting analgesic, JTA-004 intends to provide added lubrication and protection to the cartilage of the arthritic joint and to alleviate osteoarthritic pain and inflammation. Positive phase IIb efficacy results in patients with knee osteoarthritis showed a statistically significant improvement in pain relief compared to a leading viscosupplement.

Bone Therapeutics core technology is based on its cutting-edge allogeneic cell therapy platform with differentiated bone marrow sourced Mesenchymal Stromal Cells (MSCs) which can be stored at the point of use in the hospital. Currently in pre-clinical development, BT-20, the most recent product candidate from this technology, targets inflammatory conditions, while the leading investigational medicinal product, ALLOB, represents a unique, proprietary approach to bone regeneration, which turns undifferentiated stromal cells from healthy donors into bone-forming cells. These cells are produced via the Bone Therapeutics scalable manufacturing process. Following the CTA approval by regulatory authorities in Europe, the Company is ready to start the phase IIb clinical trial with ALLOB in patients with difficult tibial fractures, using its optimized production process. ALLOB continues to be evaluated for other orthopedic indications including spinal fusion, osteotomy, maxillofacial and dental.

Bone Therapeutics cell therapy products are manufactured to the highest GMP standards and are protected by a broad IP (Intellectual Property) portfolio covering ten patent families as well as knowhow. The Company is based in the BioPark in Gosselies, Belgium. Further information is available atwww.bonetherapeutics.com.

For further information, please contact:

Bone Therapeutics SAMiguel Forte, MD, PhD, Chief Executive OfficerJean-Luc Vandebroek, Chief Financial OfficerTel: +32 (0)71 12 10 00investorrelations@bonetherapeutics.com

For Belgian Media and Investor Enquiries:BepublicCatherine HaquenneTel: +32 (0)497 75 63 56catherine@bepublic.be

International Media Enquiries:Image Box CommunicationsNeil Hunter / Michelle BoxallTel: +44 (0)20 8943 4685neil.hunter@ibcomms.agency / michelle@ibcomms.agency

For French Media and Investor Enquiries:NewCap Investor Relations & Financial CommunicationsPierre Laurent, Louis-Victor Delouvrier and Arthur RouillTel: +33 (0)1 44 71 94 94bone@newcap.eu

For US Media and Investor Enquiries:LHA Investor RelationsYvonne BriggsTel: +1 310 691 7100ybriggs@lhai.com

Certain statements, beliefs and opinions in this press release are forward-looking, which reflect the Company or, as appropriate, the Company directors current expectations and projections about future events. By their nature, forward-looking statements involve a number of risks, uncertainties and assumptions that could cause actual results or events to differ materially from those expressed or implied by the forward-looking statements. These risks, uncertainties and assumptions could adversely affect the outcome and financial effects of the plans and events described herein. A multitude of factors including, but not limited to, changes in demand, competition and technology, can cause actual events, performance or results to differ significantly from any anticipated development. Forward looking statements contained in this press release regarding past trends or activities should not be taken as a representation that such trends or activities will continue in the future. As a result, the Company expressly disclaims any obligation or undertaking to release any update or revisions to any forward-looking statements in this press release as a result of any change in expectations or any change in events, conditions, assumptions or circumstances on which these forward-looking statements are based. Neither the Company nor its advisers or representatives nor any of its subsidiary undertakings or any such persons officers or employees guarantees that the assumptions underlying such forward-looking statements are free from errors nor does either accept any responsibility for the future accuracy of the forward-looking statements contained in this press release or the actual occurrence of the forecasted developments. You should not place undue reliance on forward-looking statements, which speak only as of the date of this press release.

Read the rest here:
Bone Therapeutics' allogeneic cell therapy product, ALLOB, shows 90% fusion rate at 24 months in Phase IIa study in lumbar spinal fusion -...

Injuries are a plague on the athlete. When we consider injuries at the professional level it can completely derail someones career. For those athletes who manage to battle through those injuries during their career, retirement can be quite painful. Just ask eight-time Olympia champion Ronnie Coleman.

Considered by many to be the greatest bodybuilder of all-time, Ronnie Coleman pushed his physique to the limit. Growing a massive amount of muscle throughout his career, Ronnie Coleman proved to be a genetic anomaly.

But while he may have dominated during his career, the injuries Coleman suffered during his career have been life altering.

Undergoing a number of surgeries since retirement, Coleman has experienced a tremendous amount of pain. His hips and back have given him the most issues. The eight-time champ detailed the injuries, specifically to his back and the numbness in his legs, that have caused him issues.

I got 14 screws, I got 2 cages and 2 rods. Circulation is kind of hard when you got all that hardware in your back.

With such trying injuries, Ronnie Coleman has come to welcome the idea of undergoing a different kind of treatment. Coleman has recently discussed the idea of undergoing stem cell therapy.

Looking to return to form, Ronnie Coleman discussed in a recent video about how hes ready to start stem cell therapy. Coleman discussed potentially undergoing the therapy when he appeared on the Joe Rogan Podcast.

Heres hoping that the therapy will be enough to help Ronnie Coleman fully recover. See the full interview here.

For more news and updates, follow Generation Iron on Facebook, Twitter, and Instagram.

Managing Editor at Generation Iron, Jonathan Salmon is a writer, martial arts instructor, and geek culture enthusiast. Check out his YouTube, Instagram, Twitter, Facebook, and Sound Cloud for in-depth MMA analysis.

Continue reading here:
Ronnie Coleman Starts Stem Cell Therapy to Help Recovery - generationiron.com

The ' Stem Cell Therapy market' study Added by Market Study Report, LLC, provides an in-depth analysis pertaining to potential drivers fueling this industry. The study also encompasses valuable insights about profitability prospects, market size, growth dynamics, and revenue estimation of the business vertical. The study further draws attention to the competitive backdrop of renowned market contenders including their product offerings and business strategies.

The Stem Cell Therapy market research report offers significant information related to the key growth drivers, challenges & limitations, and various opportunities that will define the business scenario in the upcoming years.

Request a sample Report of Stem Cell Therapy Market at:https://www.marketstudyreport.com/request-a-sample/2422751?utm_source=Algosonline.com&utm_medium=AN

According to the research analysis, the Stem Cell Therapy market is estimated to generate commendable returns and showcase a y-o-y growth rate of XX% over the period of 2020-20205.

The advent of COVID-19 pandemic has compelled various businesses to re-establish their respective profit trajectory for the forthcoming years. The study offers a comprehensive assessment of the impact of coronavirus outbreak on the growth of Stem Cell Therapy market.

The document also analyzes the several segmentations and their impact on the growth of this market.

Major highlights from the Stem Cell Therapy market report:

Ask for Discount on Stem Cell Therapy Market Report at:https://www.marketstudyreport.com/check-for-discount/2422751?utm_source=Algosonline.com&utm_medium=AN

Stem Cell Therapy Market segments covered in the research report:

Regional segmentation: North America, Europe, Asia-Pacific, South America, Middle East and Africa

Product types: Autologous and Allogeneic

Applications spectrum: Musculoskeletal Disorder, Wounds & Injuries, Cornea, Cardiovascular Diseases and Others

Competitive outlook: Osiris Therapeutics, Molmed, JCR Pharmaceutical, NuVasive, Anterogen, Chiesi Pharmaceuticals, Medi-post, Pharmicell and Takeda (TiGenix

The key questions answered in the report:

For More Details On this Report: https://www.marketstudyreport.com/reports/global-stem-cell-therapy-market-2020-by-company-regions-type-and-application-forecast-to-2025

Related Reports:

1. Global Transglutaminase Market 2020 by Manufacturers, Regions, Type and Application, Forecast to 2025Read More: https://www.marketstudyreport.com/reports/global-transglutaminase-market-2020-by-manufacturers-regions-type-and-application-forecast-to-2025

2. Global Oral Spray Market 2020 by Manufacturers, Regions, Type and Application, Forecast to 2025Read More: https://www.marketstudyreport.com/reports/global-oral-spray-market-2020-by-manufacturers-regions-type-and-application-forecast-to-2025

Related Report : https://www.marketwatch.com/press-release/contactless-payment-market-share-current-and-future-industry-trends-2020-2026-2020-10-12?tesla=y

Contact Us:Corporate Sales,Market Study Report LLCPhone: 1-302-273-0910Toll Free: 1-866-764-2150 Email: [emailprotected]

See original here:
Comprehensive Analysis on Stem Cell Therapy Market based on types and application - AlgosOnline

A study of some of the sickest COVID-19 patients, such as those placed on ventilators, has identified gene variants that put people at greater risk of severe disease.

By Jocelyn KaiserOct. 13, 2020 , 1:25 PM

Sciences COVID-19 reporting is supported by the Pulitzer Center and the Heising-Simons Foundation.

Its one of the pandemics puzzles: Most people infected by SARS-CoV-2 never feel sick, whereas others develop serious symptoms or even end up in an intensive care unit clinging to life. Age and preexisting conditions, such as obesity, account for much of the disparity. But geneticists have raced to see whether a persons DNA also explains why some get hit hard by the coronavirus, and they have uncovered tantalizing leads.

Now, a U.K. group studying more than 2200 COVID-19 patients has pinned down common gene variants that are linked to the most severe cases of the disease, and that point to existing drugs that could be repurposed to help. Its really exciting. Each one provides a potential target for treatment, says genetic epidemiologist Priya Duggal of Johns Hopkins University.

In a standard approach to finding genes that influence a condition, geneticists scan the DNA of large numbers of people for millions of marker sequences, looking for associations between specific markers and cases of the disease. In June, one such genomewide association study in The New England Journal of Medicine (NEJM) found two hits linked to respiratory failure in 1600 Italian and Spanish COVID-19 patients: a marker within the ABO gene, which determines a persons blood type, and a stretch of chromosome 3 that holds a half-dozen genes. Those two links have also emerged in other groups data, including some from the DNA testing company 23andMe.

The new study confirmed the chromosome 3 regions involvement. And because 74% of its patients were so sick that they needed invasive ventilation, it had the statistical strength to reveal other markers, elsewhere in the genome, linked to severe COVID-19. One find is a gene called IFNAR2 that codes for a cell receptor for interferon, a powerful molecular messenger that rallies the immune defenses when a virus invades a cell. A variant of IFNAR2 found in one in four Europeans raised the risk of severe COVID-19 by 30%. Baillie says the IFNAR2 hit is entirely complementary to a finding reported in Science last month: very rare mutations that disable IFNAR2 and seven other interferon genes may explain about 4% of severeCOVID-19 cases. Both studies raise hopes for ongoing trials of interferons as a COVID-19 treatment.

A more surprising hit from the U.K. study points to OAS genes, which code for proteins that activate an enzyme that breaks down viral RNA. A change in one of those genes might impair this activation, allowing the virus to flourish. The U.K. data suggest there is a variant as common and influential on COVID-19 as the interferon genetic risk factor.

Other genes identified by Baillies team could ramp up the inflammatory responses to lung damage triggered by SARS-CoV-2, reactions that can be lethal to some patients. One, DPP9, codes for an enzyme known to be involved in lung disease; another, TYK2, encodes a signaling protein involved in inflammation. Drugs that target those two genes proteins are already in useinhibitors of DPP9s enzyme for diabetes and baricitinib, which blocks TYK2s product, for arthritis. Baricitinib is in early clinical testing for COVID-19, and the new data could push it up the priority list, Baillie says.

The chromosome 3 region still stands out as the most powerful genetic actor: A single copy of the disease-associated variant more than doubles an infected persons odds of developing severe COVID-19. Evolutionary biologists reported last month in Nature that this suspicious region actually came from Neanderthals, through interbreeding with our species tens of thousands of years ago. It is now found in about 16% of Europeans and 50% of South Asians.

But the specific chromosome 3 gene or genes at play remain elusive. By analyzing gene activity data from normal lung tissue of people with and without the variant, the U.K. team homed in on CCR2, a gene that encodes a receptor for cytokine proteins that play a role in inflammation. But other data discussed at last weeks meeting point to SLC6Z20, which codes for a protein that interacts with the main cell receptor used by SARS-CoV-2 to enter cells. I dont think anyone at this point has a clear understanding of what are the underlying genes for the chromosome 3 link, says Andrea Ganna of the University of Helsinki, who co-leads the COVID-19 Host Genetics Initiative.

The U.K. genetics study did not confirm that the ABO variants affect the odds of severe disease. Some studies looking directly at blood type, not genetic markers, have reported that type O blood protects against COVID-19, whereas A blood makes a person more vulnerable. It may be that blood type influences whether a person gets infected, but not how sick they get, says Stanford University geneticist Manuel Rivas. In any case, O blood offers at best modest protection. There are a lot of people with O blood that have died of the disease. It doesnt really help you, says geneticist Andre Franke of the Christian-Albrecht University of Kiel, a coleader of the NEJM study.

Researchers expect to pin down more COVID-19 risk genesalready, after folding in the U.K. data plumbed by Baillies team, the COVID-19 Host Genetics Initiative has found another hit, a gene called FOXP4 implicated in lung cancer. And in a new medRxiv preprint posted last week, the company Ancestry.com reports that a gene previously connected to the effects of the flu may also boost COVID-19 susceptibility only in men, who are more likely to die of the disease than women.

Geneticists have had little luck so far identifying gene variants that explain why COVID-19 has hit Black people in the United States and United Kingdom particularly hard. The chromosome 3 variant is absent in most people of African ancestry. Researchers suspect that socioeconomic factors and preexisting conditions may better explain the increased risks. But several projects, including Baillies, are recruiting more people of non-European backgrounds to bolster their power to find COVID-19 gene links. And in an abstract for an online talk later this month at the American Society of Human Genetics annual meeting, the company Regeneron reports it has found a genome region that may raise the risk of severe disease mainly in people of African ancestry.

Even as more genetic risk factors are identified, their overall effect on infected people will be modest compared with other COVID-19 factors, Duggal says. But studies like the U.K. teams could help reveal the underlying biology of the disease and inspire better treatments. I dont think genetics will lead us out of this. I think genetics may give us new opportunities, Duggal says.

See the original post:
Found: genes that sway the course of the coronavirus - Science Magazine

Background

Observational studies have identified height as a strong risk factor for atrial fibrillation, but this finding may be limited by residual confounding. We aimed to examine genetic variation in height within the Mendelian randomization (MR) framework to determine whether height has a causal effect on risk of atrial fibrillation.

In summary-level analyses, MR was performed using summary statistics from genome-wide association studies of height (GIANT/UK Biobank; 693,529 individuals) and atrial fibrillation (AFGen; 65,446 cases and 522,744 controls), finding that each 1-SD increase in genetically predicted height increased the odds of atrial fibrillation (odds ratio [OR] 1.34; 95% CI 1.29 to 1.40; p = 5 10-42). This result remained consistent in sensitivity analyses with MR methods that make different assumptions about the presence of pleiotropy, and when accounting for the effects of traditional cardiovascular risk factors on atrial fibrillation. Individual-level phenome-wide association studies of height and a height genetic risk score were performed among 6,567 European-ancestry participants of the Penn Medicine Biobank (median age at enrollment 63 years, interquartile range 55-72; 38% female; recruitment 2008-2015), confirming prior observational associations between height and atrial fibrillation. Individual-level MR confirmed that each 1-SD increase in height increased the odds of atrial fibrillation, including adjustment for clinical and echocardiographic confounders (OR 1.89; 95% CI 1.50 to 2.40; p = 0.007). The main limitations of this study include potential bias from pleiotropic effects of genetic variants, and lack of generalizability of individual-level findings to non-European populations.

In this study, we observed evidence that height is likely a positive causal risk factor for atrial fibrillation. Further study is needed to determine whether risk prediction tools including height or anthropometric risk factors can be used to improve screening and primary prevention of atrial fibrillation, and whether biological pathways involved in height may offer new targets for treatment of atrial fibrillation.

See original here:
Genetics of Height and Risk of Atrial Fibrillation: A Mendelian Randomization Study - DocWire News

This article about the polygenic score was produced in partnership with The Hechinger Report, a nonprofit, independent news organization focused on inequality and innovation in education. This is part 3 of the series Gifted Educations Race Problem.

Many factors boost a child's chance of success in school like having wealthy parents who can afford tutors. But recent research has raised another possibility one that is discomforting to many the idea that scientists might someday be able to spot the genetic markers associated with academic performance.

To do this, researchers are turning to a relatively new genetic approach called the polygenic score, which assesses a persons likelihood for a specific future based on a combination of genetic variables. Its a research technique that some scientists are using to assess obesity or cancer risk, for instance. Now, researchers are exploring this approach in non-medical contexts, like academic or athletic success.

The scientists studying genetic markers in education are trying to untangle how nature and nurture together explain school performance. In principle, genetic screening might enable teachers to tailor their approach to groups of students. Educators might then more effectively instruct kids together in one classroom, rather than separating students into accelerated and low-level courses, which can deprive Black and brown children and children from low-income families of academic opportunities.

But some researchers fear this gene screening work could be misapplied and used to further racist or eugenic thinking, even though race is a social, not a genetic, classification. Theres an ugly history of proponents of eugenics, who believe in reshaping humanity by breeding superior traits and removing inferior traits, justifying their thinking with genetics. And there are debunked racist theories that have endeavored to falsely connect race and intelligence.

For now, the science is almost entirely based on data collected from people with European ancestry, which limits the conclusions that can be drawn from it, so researchers feel that theyve at least temporarily sidestepped the issue.

But that doesnt mean they arent worried about it and about the other ways this research could exacerbate inequities in education. Screening is expensive, for instance, increasing the odds that privileged students will qualify for extra enrichment or support before their less privileged peers.

Indeed, the idea of predicting students academic performance based on their genes comes with such a raft of ethical questions and unknowns that scientists in the field are urging caution. Polygenic scores are a potentially useful new scientific tool. At the same time, there are clear reasons to be concerned, Stanford University social scientist Ben Domingue said. Were going to have the capacity, with a vial of spit, to be able to predict all these different things.

Scientists and ethicists are also concerned about commercializing this work while the research is still evolving. Already, several companies sell reports to consumers that incorporate polygenic scores for health or various physical characteristics despite the fact that the scores are not perfect forecasters of a persons future.

Researchers in the field want to see more critical discussion of how their work could be applied in educational settings. If we dont pay attention now, systems will be created, constructed around us, responding to our genetic difference, said Sophie von Stumm, a psychologist at the University of York, in the United Kingdom, who studies genetics and education. Its high time to have this discussion. Honestly, were late to the party.

Related: College graduation may be partly determined by your genes, genome study of siblings finds

The polygenic score that could help predict academic performance aims to assess genetic markers related to educational attainment. In other words, it combines hundreds of common genetic variants that are linked to the number of years a person stays in school. In 2016, this score could explain about 5 percent of the variation in the level of education completed.

In 2018, researchers studied data from more than a million people across countries and found they could strengthen the polygenic score to explain 11 percent of the variation in educational attainment. That value puts the score on par with factors like a mothers level of education attainment, which explains 15 percent of variation, and household income, which explains about 7 percent.

There are genes that affect educational attainment that is for certain now, said Aysu Okbay, an economist at Vrije Universiteit in the Netherlands who contributed to the 2016 and 2018 studies.

The scores ability to explain variation in years of schooling could improve with more data. Rough estimates indicate about 80 percent of the variation in educational attainment comes from environmental factors the rest is genetic. With enough data, some scientists believe, the polygenic score could get close to explaining 20 percent of the difference in peoples level of education.

If so, the score would be an incredibly powerful single factor for making predictions about an individuals academic future even though the combined environmental variables still eclipse the role of genes. Its really not a puny predictor at this point, Domingue said.

In February, Domingue and his colleagues found that the polygenic score could help identify which groups of high schoolers had been placed into advanced math classes. The score could also point to students most likely to stick with advanced math courses across all four years of high school.

But polygenic scores also come laced with caveats. So many, in fact, that Okbay and her colleagues published a massive list of public FAQs including how the study was designed and whether the research could lead to stigmatization of people with certain genes to help readers interpret their research.

For more of NBC News' in-depth reporting, download the NBC News app

Paige Harden, a clinical psychologist at the University of Texas at Austin and a co-author on the math study likens the polygenic score to a credit score. Neither the polygenic nor the credit score can really forecast what will happen to a particular person. Instead, they provide a rough sense of how people with that score will, on average, fare. The score is better at gauging a groups overall performance than an individuals performance.

Harden and others acknowledge that its still a mystery how the genetic variants behind the score contribute to how far a person gets in school. We dont know what the mechanisms are, Okbay said. We dont know whether its causal or not.

Some research suggests the genes associated with education are related to the nervous system and the brain, raising the possibility that theyre connected to cognitive functions things like strong memory, creativity and perseverance that serve people well in school.

But the relationship could be nuanced. Domingue pointed out that there could be genetic factors that make a person more likely to be a supportive parent, which, in turn, would correlate to better school performance in their children. Because the child and parent share DNA, the polygenic score could capture gene variants in the child that explain educational performance but actually reflect the parents behavior.

There is also an enormous shortcoming in the datasets used for this research: Virtually all are built with DNA from people of European ancestry. Although there are biobanks in the works in Asia and Africa that could address this omission, for the time being, the scores are essentially only applicable to people of European descent. Youre basically developing a tool thats only useful for one segment of the population, Harden said.

Related: Gifted classes may not help talented students move ahead faster

Given all of these limitations, most scientists believe it would be unlikely, and inappropriate, for educators to use polygenic scores to determine student placement in specific classes or schools. Will someone be mad enough to track or stream on the basis of genetic predispositions? von Stumm said. Fortunately, I think were far from that.

There could be other ways of using this genetic information. Once genetic variants are better understood and enough data is in hand, for example, it might be possible to identify children with a predisposition to learning disabilities and intervene early. In May, von Stumm and her colleagues published a paper exploring whether a toddlers polygenic score for educational attainment could identify children at risk for language or literacy delays later in life. The conclusion: Were not there yet.

Critics caution that there is too much to establish ethically and scientifically before we confront those scenarios. Someday well understand the genetic contribution to educational success or to life success but it will be our grandchildren who understand it. It wont be us, bioethicist Arthur Caplan at NYU Langone Health said.

And even if we understood this information, its not clear how to best use the scores in schools. Last year, Stanfords Domingue and two colleagues wrote about a hypothetical case study: What happens when a parent tries to use genetic data, like a polygenic score, to make the case that their child deserves additional classroom support?

I dont know that I have good answers to that, he said. But the scenario hints at another serious concern: inequality. Not everyone will be able to afford genetic screening, even when there are meaningful scores for people across ancestries.

Still, researchers are already using the polygenic score to explore long-standing conundrums like why children with very similar advantages follow different trajectories in life.

We are all subject to a big genetic lottery that corresponds to an environmental lottery, von Stumm said. She added that research into the links between genetics and academic attainment could push people to examine fairness in meritocratic societies, given that some people may carry genetic strengths that give them a slight but significant academic advantage, that, in turn, improves other aspects of their lives.

Measuring a persons genetic advantage (or disadvantage) also allows scientists to control for it in their studies. That is, they can better study factors that society can change, such as spending on special programs, compulsory education and school interventions, without having their results biased by a sample of students who are genetically advantaged or disadvantaged.

And researchers can use the polygenic score to assess whether a school has failed students with high potential or if an intervention helped retain children who were otherwise likely to drop out. In the math paper published in February, Domingue, Harden, and their colleagues found that some schools better supported high school students with low polygenic scores than others, ensuring those kids stayed in school.

Harden hopes to see the science applied in ways that emphasize social justice and provide resources to programs that need them: Thats how I think we should be using the polygenic scores if we use them at all.

Sign up for The Hechinger Reports newsletter.

Read more here:
A new way of predicting which kids will succeed in school: Look at their genes - NBC News

Genome-wide association study identifies ABO blood protein

The identification of a gene cluster associated with progression to severe disease in patients with Covid-19 strengthens findings from earlier studies suggesting a prominent role for ABO blood group locus in disease severity.

In the genome-wide association study (GWAS) involving patients hospitalized with Covid-19 in Italy and Spain during the local peak of the pandemic, patients with blood group A had an increased risk for progression to severe disease, while patients with blood group O had a lesser risk for progression.

The strongest signal for severe disease, however, was the rs11385942 insertion-deletion GA or G variant at locus 3p21.31, according to researchers from the Severe Covid-19 GWAS Group.

Blood-group specific analysis showed a higher risk for severe disease among patients with blood group A and a lower risk with blood group O.

The groups findings, published Oct. 14 in the New England Journal of Medicine, were originally reported online in June.

In a newly published commentary, researcher Arthur Kaser, MD, of the University of Cambridge Institute of Therapeutic Immunology and Infectious Disease wrote that the genome-wide association study represents a major leap toward disentangling the molecular mechanisms that cause severe Covid-19.

Kaser was not involved with the study.

This genome association study will set directions for research, he wrote, adding that a focus on the immunologic synapse between T cells and antigen-presenting cells appears to be warranted in the search for therapies to address the hyperinflammatory state known as cytokine storm that occurs in some patients with severe Covid-19.

Researchers from the Severe Covid-19 GWAS Group pragmatically compared data from patients hospitalized with severe Covid-19 (defined as respiratory failure), with data from contemporarily recruited blood donors with mostly unknown SARS-CoV-2 status and from historically healthy controls from the same region.

Associations were identified between the risk of developing severe Covid-19 and a multigene locus at 3p21.31 and the ABO blood group locus at 9q34.2.

No association signal was shown for the human leukocyte antigen (HLA) region, which is a regulator of infection immunity and has been suggested as a potential driver of Covid-19 severity.

At locus 3p21.31, the association signal spanned 6 genes: SLC6A20, LZTFL1, CCR9, FYCO1, CXCR6 and XCR1.

The association signal at locus 9q34.2 coincided with the ABO blood group locus; in this cohort, a blood-groupspecific analysis showed a higher risk in blood group A than in other blood groups (odds ratio, 1.45; 95% CI, 1.20-1.75; P=1.48104) and a protective effect in blood group O as compared with other blood groups (odds ratio, 0.65; 95% CI, 0.53-0.79; P=1.06105), wrote Tom H. Karlsen of the University of Oslo, and colleagues from the Severe Covid-19 GWAS Group.

In his editorial, Kaser noted that among the 6 candidate genes at 3p21.31, LZTFL1 might be the most compelling, with the rs11385942 variant and all other fine-mapped association signals that exceeded genome-wide significance located within it.

LZTFL1 is widely expressed and encodes a protein involved in protein trafficking to primary cilia, which are microtubule-based subcellular organelles acting as antennas for extracellular signals, he wrote. In T lymphocytes, LZTFL1 participates in the immunologic synapse with antigen-presenting cells, such as dendritic cells (these cells prime T-lymphocyte responses).

Kaser noted that of the other 5 candidate genes, 4 (CCR9, FYCO1, CXCR6 and XCR1) have roles in T-cell and dendritic-cell function, while SLC6A20 is a transporter with intestinal expression regulated by the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2).

Earlier research has shown the Covid-19 hyperinflammatory response to resemble secondary hemophagocytic lymphohistiocytosis (HLH), which is a rare and often fatal hyperinflammatory response triggered by autoimmune disorders, certain cancers, and infections.

Kaser wrote that while secondary HLH remains poorly understood, Mendelian-inherited primary HLH points toward CD8+ T lymphocytes, natural killer cells and dendritic cells triggering a cytokine storm involving macrophages.

Other shared features between secondary HLH and severe Covid-19 are cytopenia, hyperferritinemia, disseminated intravascular coagulation, acute respiratory distress syndrome, multiple organ dysfunction, excessive expansion of T lymphocytes, and bone marrow histiocytic hyperplasia with hemophagocytosis with aggregates of interstitial CD8+ lymphocytes, he noted.

The Severe Covid-19 GWAS Group concluded that further exploration of the (study) findings both as to their usefulness in clinical risk profiling of patients with Covid-19 and toward a mechanistic understanding of the underlying pathophysiology, is warranted.

In his commentary, Kaser concluded that the clinical success of treating Covid-19 patients on mechanical ventilation with the corticosteroid dexamethasone provides strong evidence that death may be caused by a late hyperinflammatory phase.

A therapeutic agent that converts severe Covid-19 into a manageable, nonfatal infection would render this pandemic a lesser concern, he wrote.

Because it is impossible to predict mechanisms straight from genomic coordinates, experimental testing of the biology of implicated genetic risk pathways is a route, albeit a potentially challenging one, toward that goal.

Salynn Boyles, Contributing Writer, BreakingMED

Karlsen reported grants from Stein Erik Hagen (via Canica A/S) during the conduct of the study; personal fees from Gilead Sciences, personal fees from Novartis, personal fees from Engitix, and personal fees from Intercept outside the submitted work.

Kaser had no disclosures.

Cat ID: 497

Topic ID: 495,497,282,497,125,190,926,192,927,151,59,928,925,934

See the article here:
Genetic Variants Linked to Severe Covid-19 - Physician's Weekly

African cattle breeds are astonishingly diverse, and often quite beautiful. They range from the dark-red Ankole of southern Uganda, with their massive heat-dissipating horns, to the Boran which thrive in the dusty plains of northern Kenya, to Ethiopias sturdy Mursi cattle, with their prominent shoulder humps and hanging dewlaps. The Kuri that graze on the grasses of Lake Chad are adept swimmers; the Red Fulani can trudge vast distances along the margins of the Sahara; and the famously disease-resistant Sheko inhabit tsetse fly-infested forests of southwest Ethiopia.

All billion or so cattle today descend from ancient aurochs, an extinct species of wild cattle that once inhabited large swaths of Eurasia. These cattle were domesticated on at least two distinct occasions approximately 10,000 years ago during the Neolithic era: once in south Asia leading to the zebu or humped cattle and the other in the Middle East leading to the taurine or humpless cattle.

In Africa, the oldest archaeological evidence of domestic cattle dates back to between 6000 and 5000 BC in western Egypt. These taurine cattle, initially confined to the Saharan-Sahelian belt, eventually reached isolated pockets of land in West and East Africa.

Africas cattle today have adapted to the climate, forage conditions, diseases and pests prevalent in their habitat. The individuals best adapted to their environments were more likely to survive and reproduce. They were also more favoured by people. Over time this led to different breeds and species.

Today there are an estimated 800 million livestock keepers across the continent. Cattle provide nutritious, calorie-dense food, much-needed income, and nitrogen-rich manure for replenishing soils. There are few regions of Africa where cattle do not play a central role, both economically and culturally.

But it was not always this way. My colleagues and I from the International Livestock Research Institute (ILRI) recently published a paper detailing how African cattle acquired their adaptive capacities.

Sifting through the DNA of 16 indigenous African breeds, we discovered a thousand-year-old event in which the worlds two main subspecies of cattle namely taurine and zebus mixed. This allowed African cattle after spending thousands of years confined to certain regions in Africa to diversify and spread across the continent.

Our findings help to explain how African cattle spread throughout the continent. But since they were selected and bred for resilience, African cattle never became as productive, in terms of meat or milk, as breeds in more temperate climates. Our hope is that, by studying the history hidden in indigenous cattle genomes, we can help guide efforts to breed for productivity without losing the breeds native resilience and sustainability.

Our new genome sequencing work revealed that, about a thousand years ago, pastoralist herders in the Horn of Africa began breeding the Asian zebu cattle with local taurine breeds.

The zebu offered traits that allowed cattle to survive in hot, dry climates. The taurine traits provided cattle with the ability to endure humid climates, where vector-borne diseases that affect cattle, like trypanosomiasis (or sleeping sickness) are common.

This event, which we dubbed an evolutionary jolt, allowed African cattle after spending thousands of years confined to a shifting patchwork of sub-regions in Africa to spread across the continent and flourish into the breeds we see today.

But this resilience came at a cost. African cattle are often not as productive in terms of growth rates, meat or milk as their European and American cousins. Canadian Holsteins, for example, can deliver 30 litres of milk per day, several times what most African breeds are capable of. Traditional Ethiopian Boran, for example, produced only four to six litres of milk per day.

Today scientists at ILRI, in partnership with governmental institutions in Tanzania and Ethiopia, are again trying to deliver an evolutionary jolt to Africas cattle. This time, however, they want to speed up the evolutionary clock by identifying genetic markers that signal both adaptability and productivity. Screening embryos for these markers could help scientists replicate in the lab the slow work of evolution by favouring the traits that most benefit farmers.

Earlier efforts to improve cattle productivity on the continent focused on importing cattle breeds from elsewhere, without adequately recognising African breeds unique resilience. Nearly, all these attempts have failed or resulted in crossbreeds with both adaptability and productivity diluted.

This time, we are focusing on sustainable productivityproductivity that builds on rather than disregards the resilience of indigenous African breeds.

But while we have new tools and shortcuts which enables scientists to analyse vast swaths of genetic data and decide which breeds could work well together, there are some lessons we should still draw from the first evolutionary jolt.

The first is that we shouldnt be overly concerned about crossbreeding. Because of a sense of national pride and wanting to conserve indigenous African cattle breeds, there is at times a tendency on the part of some to treat them as iconic, untouchable manuscripts.

This ignores the long tradition of crossbreeding practised by African livestock farmers and pastoralists they were (and still are) constantly mixing and matching breeds to select the animals best suited to their needs.

Another lesson is that, as scientists experiment and cross-breed, it is vitally important to remember that the local breeds have adaptations not all of them immediately obvious (a tolerance for episodic drought, for example) that have enabled their success. It is important that we do not lose those adaptive traits in the randomness of crossbreeding.

This will take innovative crossbreeding programs that incorporate scientists, government ministries, private partners and farmers to ensure the conservation of genetic information across the long life cycle of cattle generations.

And finally, its essential to include the practical, accumulated experience of pastoralists in these processes.

David Aronson, Senior Communications Advisor with ILRI, contributed to the writing of this article

See the original post here:
An evolutionary jolt helped cattle to spread across Africa. Now genetics must make them more productive - The Conversation Africa

The El Dorado Rotary Club hosted Tammy McKamie, a genetic certified nurse at the Christus St. Michael Health System in Texarkana, on Monday at their regular meeting, where she spoke about the health benefits of genetic testing.

McKamie, who has worked as a medical professional for nearly 40 years, is the only credentialed genetic certified nurse in Texas, and also serves patients from Arkansas. On Monday, she discussed her specialization in genetics and the role ones genes may play in determining whether they develop cancer during their lives.

While 90% of those who develop cancer do so because of environmental and lifestyle factors, such as smoking or being exposed to carcinogenic chemicals, McKamie said some people are at a heightened risk due to genetic factors.

Almost every person is born with 23 pairs of chromosomes, half of which are inherited from their biological mother and the other half of which are inherited from their biological father.

On each one of these chromosomes, there are thousands of genes. If I add up all the genes in this DNA, were going to have about 20,000 genes, and each one of those has a purpose, McKamie said.

Some of those genes purposes are to protect the individual from developing cancer, she said, a medical breakthrough that was discovered in 1994 during research for the Human Genome Project.

God gave us genes to protect us from cancer, McKamie said. We have two of each gene that theyve discovered so far. One gene may protect you from multiple cancers, so if ones defective, you may be at risk for multiple cancers.

Rotarian Art Noyes asked whether genetic predisposition to cancer may have been related to actress Angelina Jolies decision to undergo a double mastectomy (breast removal) several years ago.

Yes, Angelinas mother had ovarian cancer, so she had this genetic testing years ago, McKamie said. She did the genetic testing and she had a genetic mutation in one of these genes. Angelina had never had cancer, but she had the genetic predisposition toward it.

In Jolies case, McKamie said, there was likely a mutation of the BRCA 1 or 2 gene, which can heighten ones susceptibility to several types of cancers, including breast cancer, ovarian cancer, prostate cancer, colorectal cancer and other types.

For those who opt not to undergo preventative surgeries, like Jolies mastectomy, knowing of any genetic defects can still help medical professionals that care for them, since they will be aware of their increased risk level. Those who do have a genetic predisposition to some types of cancer should undergo earlier and more frequent screenings so that any cancer that does develop can be treated sooner, McKamie said.

If you started out with this defect, we would not wait til 40 (years old) to do a mammogram we would start much earlier, she said. Everybody knows that if you detect cancer early, youre more likely to survive it.

McKamie said a defect in the BRCA 1 or 2 gene can heighten a womans risk of developing breast cancer significantly. For someone without a gene defect, the risk at 40 years old is about 0.5%; at 50 years old, about 2%; and at 70 years old, about 7%. For a woman who does carry a hereditary risk, the likelihood that they will develop breast cancer by age 40 increases to 10 to 20%, depending on which BRCA gene the defect is in; by age 50, the risk is 33 to 50%, and by 70 the risk is 58-87%, McKamie said. For men, the risk of breast cancer increases from 1% for the general population to 7% for those with a genetic defect.

People take it for granted that everythings working but if you knew that one of these was defective and you were at a higher risk for cancer, you might be more healthy, more conscious, McKamie said.

At Christus St. Michael, McKamie offers consultations for those who would like to undergo genetic testing to determine whether they might be at a heightened risk for developing cancer. First, she will take a detailed family medical history and explain to her patient how ones genes might increase their risk for cancer. Following that, she will draw one tube of blood from the patient and send it to a laboratory, with a typical turnaround time of two to three weeks, she said.

This testing is now even evolved to the point to where if you have cancer, the physicians will use it to determine the best type of drug to use to treat you, McKamie said. I get a lot of consults from our cancer physicians and oncologists because they need to know what type of drug to use to treat this person.

McKamie noted that Medicare pays 100% for this sort of genetic testing, and most other medical insurance companies follow their lead; additionally, should any out-of-pocket costs emerge once a patients sample reaches the testing lab, a representative from the lab will call the patient to ensure they still want the testing done.

Before a patient comes to Texarkana for a screening, McKamie will screen them over the phone to ensure they will qualify for coverage for the genetic testing, she said. Those who are interested in a consult can contact her at 903-614-2654 or [emailprotected]

[Cancer diagnostics and treatment] just really evolved, and it continues to evolve, McKamie said. This is the way of the future now.

Read the original:
Nurse advises Rotary of the benefits of genetic testing - El Dorado News-Times

Amazon Prime Day is here, and have you seen these deals? They're bigger and better than ever, and we can't say we mind all that much. For two days only, you can score everything from fitness deals to beauty buys and kitchen gadgets. But, we'd be remiss if we didn't talk about the fact that it's October (seriously, how?) and gift-giving season is almost here. If you've got someone in your life who could use a cool present, consider this 23andMe Health + Ancestry Service ($99, originally $199).

This genetic-testing kit is beloved by millions, and will give you a unique and in depth look into your genetics. You can save $100 if you buy it today, which is major. Whether you want to check some people off your gifting list or are curious for yourself, now's the time to buy this insanely cool kit.

Read more:
The 23andMe Genetic Kit Is an Insanely Cool Gift You May Just Want to Give Yourself - It's on Sale For Prime Day! - Yahoo News

Germline genetic testing is essential in order to identify optimal treatments for patients with cancer, as well as detecting inherited mutations via cascade testing that could affect family members, according to John M.Carethers, MD, MACP, who emphasized that improvements to genetic testing technology and testing costs has increased not only the accuracy of, but access to these assays.

The technology in sequencing has moved from the old gels to capillary to ChIP [chromatin immunoprecipitation]-based, and has revolutionized the way we approached it. The depth of [genetic testing] coverage [has evolved], said Carethers. Sequencing technologies totally revolutionized this [process].

He added, There are some unusual situations in which additional technologies have to be used to figure out some of the ones that typical ChIP technologies don't fully explain. That has markedly changed the way we approach [testing] these days.

In an interview withOncLiveduring the 2020 Institutional Perspectives in Cancer (IPC) webinar on Precision Medicine, Carethers, a professor of Internal Medicine and Human Genetics at the University of Michigan, discussed recent developments in multi-gene panel testing.

OncLive: How are predictive and somatic genetic tests being utilized in clinical practice?

Carethers: In terms of germline testing, the benefit is knowing which disease you carry, and that information can also spread to other family members to understand whether they [are at an increased risk of getting a cancer diagnosis]. Sometimes, at least in my experience, [germline testing] does alleviate some anxiety. Some people get more anxious once they know they have a germline mutation, but in general, it does at least explain the reason why they're seeing certain diseases in the family. Thats the general benefit for germline testing.

The benefit of somatic testing is knowing the type of mutations that occur in the tumor; there may be a therapeutic drug or compound that is in current use that could benefit the patient. For instance, I had a patient with unresectable esophageal cancer. She was dying and her esophagus was almost completely obstructed with the tumor. She had a feeding tube put into her stomach and lost a lot of weight; she was literally counting out the days until she died. With some thought, we decided to take a sample of the tumor and do somatic testing.

She had some mutations that werent typically found in esophageal cancer, and we did have drugs [to treat her]. She was actually put on those drugs and the tumor shrunk dramatically to the point that she could eat again, she gained weight, and she lived another 5 years. Normally, she wouldn't have lasted more than a few months. The benefits of somatic testing is understanding the genetic makeup of the tumor in which you might be able to use some compounds that exist to benefit the patient. Thats the real goal of somatic testing.

There is an unusual situation for somatic testing, as well. For instance, in colon cancer, we know about Lynch syndrome, but there is also a Lynch-like syndrome. In Lynch-like syndrome, there is no germline [mutation], but the tumor has 2 somatic mutations of a mismatch repair deficient tumor. They can look like a Lynch syndrome tumor, and maybe even behave a little bit like a Lynch syndrome tumor, but they're really not caused by a germline mutation. Sometimes, somatic genetics can help us understand tumor genesis as well as ways to treat the tumor.

What changes have we seen recently in multigene panel testing? How are test results interpreted and how do they help guide treatment strategies?

There are patients who will walk in with the classic phenotype and then there are patients walking in who don't have the classic phenotype, yet they carry that mutation in the same gene. Multigene testing allows us to account for phenotypic variation.

Someone may walk in with colon cancer, the next person in the family might walk in with endometrial cancer, and the next person in the family may walk in with a skin tumor, but they all line up with the same mutation in Lynch syndrome. However, if you saw the skin tumor first, would you have thought of Lynch [syndrome]? [What about] if you saw the endometrium or the colon cancer? It depends on the specialty and the type of disease presentation they show up with. In many cases, though, the disease could be subtle.

For instance, there was a family I followed, which comprised the grandmother, mother, and daughter. The grandmother, who was well into her late 60s, had a Lynch syndrome mutation and got her colon removed appropriately. The mother was in her 40s with no cancers, but the daughter who was 21, developed colon cancer. It looked like it skipped a generation, yet, they all carry the same mutation. There's phenotypic variation, even with this exact same mutation in the family, because we're all genetically different to some, so there's probably modifiers and other things going on. However, if I can see that in this one family who I know [harbor that specific] mutation [then I know that] if multiple people walk into the clinic and have variations in their family histories and in their personal history of cancer, that we are seeing a wide phenotypic variation.

Now, instead of testing 1 gene at a time, we will test 30 or 50 genes at a time, and you can pick up some of these less penetrant genes that are causing the phenotypic variation. Sometimes there are major penetrant genes in these families.

What other barriers to germline testing need to be addressed?

We're always learning. Every year or so we add a few more genes to our repertoire and then, maybe they get on some of these panels. E3 ubiquitin ligase WWP1 is associated with PTEN hamartomatumorsyndrome, which is not on any panels, but the paper was published in the New England Journal of Medicine. We keep learning as we discover more and more of these genes. The more genes that we find tend to occur in less and less people, based on our current knowledge, but some of these patients present with these rare phenomena.

We're also finding out that some of these mutations arent specifically a change in the DNA sequencethere are methylation, or rearrangement, or even a deletion. You have to use other techniques in addition to sequencing to figure those families out or those families will be left in the lurch.

The downside of doing multigene panel testing is that now, if you push for more whole-exome and whole-genome sequencing, we have a lot more variants. One commercial lab got [results] back to me 2 months ago from a patient we had tested 4 years ago. They said, We finally have enough people [where we could determine that] his variant is not significant. It was good news. We are now more sure of variants because they now have more families in their database at the commercial lab. Sometimes it takes years to figure it out, unless we have functional analysis for all variants. Thats a big challenge right now.

Where do you hope to see the future of genetic testing head?

In a good way, genetic testing will probably [have a lower] cost and there [will be an] ease of doing it [with] whole-exome and whole-genome sequencing. It will even overtake panel testing over time because the machines are better and faster. The key, though, is having a database that you can go back and forth and analyze. Youre going to need the analytics and tools. What happens with the patient? Do I carry this [information] on a flash drive? Is it in a database I have to have access to?

It's not an easy answer and I'm not sure if the health system that a particular patient goes to is going to store all this information3 billion base pairs of informationand go back to it each time. Each place is going to have to have the right analytic tools to go back and [retrieve that information]. There are going to be some challenges with that, even though that's the way the technology is going.

The more challenging pieces [are related to] direct-to-consumer (DTC) testing. You don't always know what you're getting on those tests. We can test you for common diseases, such as diabetes and hypertension, but we also test you for BRCA1/2. In reality, very few of the DTC [tests] are doing sequencing or panel testing like we do clinically. Many of them are using single nucleotide polymorphisms (SNPs) that give you a suggestion. Many of these start from ancestry companies,and they recently moved into [testing for] these diseases because people are interested. I don't blame them for doing this, but the information they give might only [include] a fraction of the actual disease variants. If someone finds an SNP in BRCA1/2 or Lynch syndrome, you might need to see a doctor. [Based on your family history or phenotype,] we may have to send a ChIP test to verify [the results].

In some cases, people will test just to be curious, and they think they're going to have something, but there is zero evidenceno personal history and no family history. There are going to be some challenges with the DTC [testing] because we don't always know the type of test theyre getting and the information is not going to be as precise and could present challenges in the clinics. Some people are going to get upset because we're going to say, No, you don't need testing, or [patients will ask], Why does this test say I might have it but your test says I don't? We have to explain all this and those are going to be challenges.

What else would you like to add regarding the evolution of genetic testing?

There is phenotypic variability in the presentation of many of these syndromes. The standard now is multigenetic panel testing to try to assuage the phenotypic variation; we do pick up [genes in] people who we didn't necessarily think had that disease. I've been surprised too many times, so I'm not surprised anymore. A lot of these inherited conditions have phenotypic variability. If you have any suspicion or your primary care physician has any suspicion, feel free to send [a test] to our clinic because we can investigate that and do testing that's relatively cheap if there's a good cause to investigate that. It may save their life and the lives of their loved ones.

Read the original:
Focusing on the Future of Genetic Testing in Oncology - OncLive