Russia did meddle in the Brexit, Scottish Independence and the 2019 General Election – Euro Weekly News

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Russia not only meddled in the Brexit vote, but also in the Scottish Independence referendum

A report on Russian interference into British politics was finally published Tuesday, more than a year after allegations surfaced that Moscow sought to meddle in Britains 2019 general election and following similar claims about its2016 Brexit vote to leave the European Union and a 2014 failed referendum on Scottish independence.

The report published today stated that: the Kremlinhas used espionage and diverse forms of subversion, including cyberattacks, disinformation campaigns and state-sponsored assassinations to undermine British democratic processes and divide alliances such as NATO and the EU.

Russia has been adamant and repeatedly denied any such wrongdoing, and has said that the allegations are completely unfounded.

Although the report was initially given to Boris Johnson last October , he said it couldnt be released until it had been reviewed for national security issues.

The opposition Labour Party has accused Johnsons government of failing to publish the report because it would lead to further questions about links between Russia and the pro-Brexit campaign in the 2016 referendum on European Union membership, he said: Whats in the report that Johnson does not want us to see?

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Russia did meddle in the Brexit, Scottish Independence and the 2019 General Election - Euro Weekly News

Brexit will split financial markets, says Bank of England appointee – Reuters

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LONDON (Reuters) - Brexit will make markets less efficient but it wont be disastrous for Britains economy, an appointee to the Bank of Englands Financial Policy Committee (FPC) said on Monday.

FILE PHOTO: A small toy figure is seen in front of a Brexit logo in this illustration picture, March 30, 2019. REUTERS/Dado Ruvic/Illustration

Britain left the European Union in January, with transition arrangements that afford continued full access to the bloc ending in December.

Jonathan Hall told the Treasury Select Committee that Brexit represented a longer term risk of increased fragmentation and complexity in financial services.

This would increase friction costs for the economy, the supervisory burden, Hall said in a questionnaire he completed for the lawmakers.

Faced with an economy slammed by the COVID-19 crisis, Hall, a former Goldman Sachs banker, is due to start a three-year term on the FPC, a body set up after regulators failed to spot the last financial crisis coming a decade ago.

Britains financial sector is quite different in size and complexity compared with its European peers, Hall told the online meeting.

Future direct EU access for financial firms in Britain will hinge on Britain remaining equivalent or aligned with rules in Europe, but Hall said Britain cant be a rule taker.

Its very important that the UK does remain the regulator for the financial market in the UK, he said.

Britains banks, some of whom needed rescuing by taxpayers in the last crisis, were in good shape when the COVID-19 shock hit markets in March, he said.

It was so far, so good and there is no evidence that tougher capital rules brought in after the last crisis were restricting the ability of banks to lend to help businesses recover from the impact of COVID, Hall said.

Britain is looking at ways for insurers, pension funds and others to invest in firms struggling to repay loans taken out during the pandemic.

You can imagine some kind of closed-end fund that has a very diversified pool of small and medium sized businesses. But does the public sector need to do anything to help that along given this needs to move faster? Hall said.

(This story replaces Hall quote in paragraph 3 on fragmentation after BOE clarified it referred to clearing houses with new paragraph 3 and 4 from a questionnaire to lawmakers)

Reporting by Huw Jones; Editing by Andrew Heavens, Ken Ferris and Alison Williams

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Brexit will split financial markets, says Bank of England appointee - Reuters

The Russia Report who paid for Brexit? – TheArticle

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8.4 million it was the biggest ever political donation in British history, and made by an insurance salesman made uneasy by immigration and who opposed Britains membership of the European Union. Arron Banks gave this enormous sum of money to the 2016 Brexit campaign.

If that money came direct from Bankss bank account, then it was perfectly legal. (Banks has not been found to have breached electoral law). Foreign donations to elections and referendum campaigns have to be declared and identified. One of the biggest failures of the 1997 Labour government was not to adopt clear laws limiting political donations. Britain failed to ban donations by rich individuals or rich trade unions who want to buy influence.

Instead money continues to flow into political parties from the super rich, in exchange for access, peerages, and contracts.

Bankss close associations with the Russian government are not disputed. His own published accounts of his involvement in the Brexit campaign recorded meetings with the Russian ambassador Alexander Yakovenko, a close Putin associate. A Russian spy, Alexander Udod, was tasked with getting close to Nigel Farage, Ukip and Aaron Banks. Udod was expelled from the UK in 2018 following the attempted murder of Sergei Skripal in Salisbury.

The Skripal killer squad came from the GRU, the Russian military intelligence agency, headed up to 2016 by Igor Sergun. He was a strong advocate of Brexit, not from any reasons of taking back control or other anti-EU arguments advanced over many years by British politicians and journalists of right and left but simply because Putin intenselydisliked the role of the EU as a supra-national body which imposed sanctions on Russia after Putins invasion and annexation of Crimea.

Putin also disliked the EU Commissions competition directorate using EU law to stop Gazproms monopolistic practices in EU energy supply chains. Putins foreign policy is easily summed up. Russia up. America down. Europe out.

Putin had funded other anti-EU politicians like Marine le Pen in France, the Alternative fr Deutschland in Germany and the anti-EU Lega party of Matteo Salvini in Italy. In a sense this was no more than the continuation of a long-standing Russian practice since the 1920s of providing money for politicians and organisations which sympathised with Russian foreign policy objectives.

In evidence to the House of Commons Select Committee on Culture, Media and Sport, Banks and his associate, Andy Wigmore, denied any Russian connection.

Banks had been in Moscow and at least three business deals were offered at the Russian embassy or by Russian agents to the pair. The Russian ambassador and the spy Udod were invited to parties hosted by Banks.

The Electoral Commission did refer Banks to the National Crime Agency but Theresa May did not order the intelligence agencies help provide evidence. She refused to accept that any question mark might be placed over the very narrow win for Brexit when 36 per cent of the total registered electorate voted to leave the EU. Jeremy Corbyn has been a life-long opponent of EU membership and had voted against every EU treaty in the House of Commons since 1983.

With the arrival of Boris Johnson and a 100 per cent Brexit cabinet, the political establishment began to instinctively retreat from the notion that Russia may have influenced Brexit. Labours new leader, Sir Keir Starmer, also wants to shut down Brexit, believing that to challenge it would alienate Labour Red Wall voters who voted out in 2016.

In a new bookGoing Dark, Julia Ebner, a researcher at Londons Institute for Strategic Dialogue, reports on Russias Internet Research Agency, a Putin trolling operation that reached one in three Americans between 2015 and 2017 when Putin tried to get Trump elected. The Internet Research Agency set up 3,841 fake twitter accounts to pump out Kremlin lines on Trump and also Brexit. The Russian state-controlled TV station, RT, and linked news agency, Sputnik, based in in Edinburgh, provided endless platforms for anti-EU commentators, economists and politicians.

Banks may have gone too far with the chutzpah of his latest demand that he be allowed to see and challenge the suppressed Russia report that the Intelligence and Security Committee of the House of Commons produced last year, and which is released today. Johnson delayed publication but after the farce of his failed efforts to impose Chris Grayling as ISC Chair, we will now get to read it. The ISC Chair is Julian Lewis, a pro-Brexit Tory MP who has spent his political life seeking to expose the baleful Russian interference in democratic politics.

In the end Banks will survive as it was his legal right to give money to a political campaign. The fate of Brexit will be settled not by uncovering the origins of that 8.4 million, but on whether in 12 or 24 months time Brexit has brought us freedom, as the Brexiters always claimed it would, or whether we are left out in the cold.

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The Russia Report who paid for Brexit? - TheArticle

The UK government ‘actively avoided’ investigating Russian interference in the 2016 Brexit referendum – Business Insider India

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The UK government failed to investigate potential Russian interference in the 2016 Brexit referendum, according to a long-awaited report into the Kremlin's influence in British politics and society.

The report by the Intelligence & Security Committee (ISC) suggests that ministers "had not seen orsought evidence of successful interference" in Brexit.

He said the ISC found it "astonishing" that the UK government didn't seek to "protect the referendum" by looking into potential Russian interference.

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"This situation is in stark contrast to the US handling of allegations of Russian interference in the 2016 presidential election, where an intelligence community assessment was produced within two months of the vote, with an unclassified summary being made public."

"Even if the conclusion of any such assessment were that there was minimal interference, this would nonetheless represent a helpful reassurance to the public that the UK's democratic processes had remained relatively safe," it says.

The UK government rejected this call in its response to the report.

The UK government was led by David Cameron in the run-up to the referendum before he was replaced as UK prime minister by Theresa May.

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The UK government 'actively avoided' investigating Russian interference in the 2016 Brexit referendum - Business Insider India

Not publicizing black & brown mugshots is not fixing the racial problem with the justice system it’s hiding it – RT

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News outlets and even police departments are ending the publication of jail booking photos, claiming they foster stereotypes because minorities are more often arrested. But hiding inequities in the system doesnt fix them.

The Sacramento Bee, the Orlando Sentinel, theHouston Chronicle and a number of other city papers across the US have curtailed the practice of publishing mugshot slideshows, image galleries showing booking photos of arrested individuals who havent yet been convicted of crimes.

With exceptions for celebrity mugshots, suspected serial killers, threats to public safety, and hate crime suspects, the move is intended to counter racial stereotypes about criminality.

The papers have a point about the galleries lack of context a wordless array of scowling black and brown faces may indeed give the false impression that this is what all criminals look like. Some of the most destructive and dangerous criminals, the ones stealing your (or your parents) retirement savings or bombing civilians in the Middle East are unlikely to ever appear in one of these rogues galleries (or, alas, to be arrested at all). And publishing a persons mugshot before theyre even tried for a crime does impinge on the prisoners constitutional right to the presumption of innocence.

But sweeping these racial disparities under the rug doesnt solve the underlying problem of black and brown peoples overrepresentation in the criminal justice system. Indeed, its quite telling that police departments are now climbing aboard the no-mugshots bandwagon, suggesting a big fat ulterior motive lurking beneath the virtuous surface. San Francisco police announced earlier this month they will no longer release mugshots to the public unless the individual poses a threat to the community, again as part of an effort to reduce racial stereotyping.

The department thus acknowledges black and brown people are disproportionately arrested for victimless crimes (i.e. those that dont pose a threat to the community) a relatively uncontroversial reality that has been public knowledge for years, though still something one doesnt expect to hear police admit.

Black people are more than two and a half times more likely to be arrested and six times more likely to be imprisoned on drug charges than whites, for example, even though blacks and whites use and even sell drugs at approximately the same rate. These arent hard drug users either there were more arrests for marijuana in 2018 than for real crimes like aggravated assault, arson, burglary, or sex crimes, despite over a dozen states having legalized the drug, and black people are even more disproportionately likely 3.7 times to be arrested for that drug.

But making a surface show of addressing stereotypes does not translate to actually dismantling racial and economic inequities in policing. Especially given the nationwide Black Lives Matter protests threatening their jobs, police who announce the end of published mugshots as a civil rights victory are more likely to be covering their arses than addressing systemic racism.

Like the mega-corporations who publicly grovel at BLMs feet (sometimes literally) in order to avoid being held to account for selling products or condoning labor practices that disproportionately harm poor and minority communities, police departments that stop publishing mugshots are seeking an easy way out of their PR problem.

Actually retraining officers to not immediately see a young black man standing on a corner in a poor neighborhood (that he happens to live in) as a drug dealer takes time and money, while merely not publishing that mans mugshot in the Sunday paper creates the same impression, as long as the police department takes care to notify the community about why it is no longer releasing arrest photos.

Unfortunately, that move does nothing to stop biased police practices, which can be shockingly difficult to dislodge. It took the intervention of a federal judge to convince New York Mayor Mike Bloomberg to curtail the NYPDs stop and frisk tactic, which at its height saw police harassing largely non-white (87 percent) New Yorkers, most of whom (88 percent) were innocent of any crime.

Given that its stated purpose was not to nab low-level drug offenders, but to get illegal guns off the street something achieved in just 0.1 percent of stops it was a profoundly ineffective policy.

Retraining police isnt easy, but it must be done if the US is to truly become a more racially equitable society. While corporate Democrat fronts like BLM are apparently content with cosmetic reforms and paying lip-service to social justice, black communities are devastated by the justice system, which often serves up anything but for those without the funds to buy it.

As for the newspapers, merely failing to report news that doesnt fit the narrative falls so short of real social justice as to be laughable. Is it any wonder journalism is a dying industry?

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The statements, views and opinions expressed in this column are solely those of the author and do not necessarily represent those of RT.

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Not publicizing black & brown mugshots is not fixing the racial problem with the justice system it's hiding it - RT

Rare genetic mutation leaves people at higher risk for multiple cancers – Penn: Office of University Communications

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Rare inherited mutations in the bodys master regulator of the DNA repair systemthe TP53 genecan leave people at a higher risk of developing multiple types of cancer over the course of their lives. Now, for the first time, a team led by researchers in theBasser Center for BRCAat theAbramson Cancer Center details the potential implications of a lower risk TP53 mutation, including an association with a specific type of Li-Fraumeni syndrome (LFS), an inherited predisposition to a wide range of cancers. The findings raise questions about how to appropriately screen patients for this mutation and whether the standard process of full-body scans for LFS patients should be modified for this group, since their risk profile is different than those with classic LFS. The researchers published their findingsinCancer Research, a journal of the American Association for Cancer Research.

Mutations in the TP53 gene are the most commonly acquired mutations in cancer. The p53 protein, made by the TP53 gene, normally acts as the supervisor in the cell as the body tries to repair damaged DNA. Different mutations can determine how well or how poorly that supervisor is able to direct the response. The more defective the mutation, the greater the risk. When TP53 mutations are inherited, they cause LFS, a disease that leaves people with a 90 percent chance of developing cancer in their lifetime. There are currently no therapies that target the p53 pathway.

Researchers determined that there is an inherited set of genetic material shared among people who have this mutation, suggesting its whats called a founder mutationa mutation that tracks within one ethnicity. In this case, that ethnicity is the Ashkenazi Jewish population.

Due to the wide variety of disease types associated with inherited TP53 mutations and the early age of cancer diagnoses, cancer screening is exceptionally aggressive. However, we do not yet know if all mutations require the same high level of screening, says the studys senior authorKara N. Maxwell, an assistant professor of hematology-oncology and Genetics in thePerelman School of Medicine and a member of the Abramson Cancer Center and the Basser Center for BRCA. It is therefore critical to study the specifics of individual TP53 mutations so we can understand how best to screen people who carry lower risk mutations.

Read more at Penn Medicine News.

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Rare genetic mutation leaves people at higher risk for multiple cancers - Penn: Office of University Communications

Cleveland Clinic Researchers Identify Genetic Factors that May Influence COVID-19 Susceptibility – Health Essentials from Cleveland Clinic

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A new Cleveland Clinic study has identified genetic factors that may influence susceptibility to COVID-19. Published today in BMC Medicine, the study findings could guide personalized treatment for COVID-19.

While the majority of confirmed COVID-19 cases result in mild symptoms, the virus does pose a serious threat to certain individuals. Morbidity and mortality rates rise dramatically with age and co-existing health conditions, such as cancer and cardiovascular disease. However, even young and otherwise healthy individuals have unpredictably experienced severe illness and death. These clinical observations suggest that genetic factors may influence COVID-19 disease susceptibility, but these factors remain largely unknown.

In this new study, a team of researchers led by Feixiong Cheng, Ph.D., of Cleveland Clinics Genomic Medicine Institute, investigated genetic susceptibility to COVID-19 by examining DNA polymorphisms (variations in DNA sequences) in the ACE2 and TMPRSS2 genes. These genes produce enzymes (ACE2 and TMPRSS2, respectively) that enable the virus to enter and infect human cells.

Because we currently have no approved drugs for COVID-19, repurposing already approved drugs could be an efficient and cost-effective approach to developing prevention and treatment strategies, Cheng said. The more we know about the genetic factors influencing COVID-19 susceptibility, the better we will be able to determine the clinical efficacy of potential treatments.

Looking at 81,000 human genomes from three genomic databases, they found 437 genetic variants in the protein-coding regions of ACE2 and TMPRSS2. They identified multiple polymorphisms in both genes that offer potential explanations for different genetic susceptibility to COVID-19 as well as for risk factors.

These findings demonstrate a possible association between ACE2 and TMPRSS2 polymorphisms and COVID-19 susceptibility, indicating that identification of the functional polymorphisms of these variants among different populations could pave the way for precision medicine and personalized treatment strategies for COVID-19.

However, all investigations in this study were performed in general populations, not with COVID-19 patient genetic data. Therefore, Cheng calls for a human genome initiative to validate the teams findings and to identify new clinically actionable variants to accelerate precision medicine for COVID-19.

This study was supported by the National Heart, Lung, and Blood Institute and the National Institute of Aging (both part of the National Institutes of Health) as well as Cleveland Clinics VeloSano Pilot Program. Serpil Erzurum, M.D., chair of Cleveland Clinics Lerner Research Institute, and Charis Eng, M.D., Ph.D., chair of the Genomic Medicine Institute, are co-authors of the study.

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Cleveland Clinic Researchers Identify Genetic Factors that May Influence COVID-19 Susceptibility - Health Essentials from Cleveland Clinic

Rhythm Pharmaceuticals Announces Appointment of David Meeker, MD, as Chief Executive Officer – BioSpace

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BOSTON, July 20, 2020 (GLOBE NEWSWIRE) -- Rhythm Pharmaceuticals, Inc. (Nasdaq:RYTM), a late-stage biopharmaceutical company aimed at developing and commercializing therapies for the treatment of rare genetic disorders of obesity, today announced that David Meeker, M.D., the Chairman of Rhythms Board of Directors, has been appointed as the President and Chief Executive Officer (CEO) of the company, effective immediately. Dr. Meeker succeeds Hunter Smith, the Companys Interim President and CEO and Chief Financial Officer (CFO), who will continue in his role as CFO.

I am delighted to announce Davids appointment as Rhythms new CEO, said Hunter Smith, CFO of Rhythm. Since he joined our Board in 2015, David has played a key role in shaping the clinical and commercial strategy for setmelanotide and in fostering our collaborative and patient-focused culture. As we continue to work toward the first potential approval of setmelanotide in pro-opiomelanocortin (POMC) and leptin receptor (LEPR) deficiency obesities later this year, Davids extensive experience leading commercial organizations and managing the launches of new medicines for rare genetic diseases, coupled with his proven ability to build strong relationships with patient and clinician communities, will be invaluable. The Rhythm team is energized by the opportunity to work more closely with David in an effort to deliver setmelanotide and potentially transform the care of people living with rare genetic disorders of obesity.

Rhythm is an exciting company that I have long admired, both for its scientifically-rigorous approach to drug development and its commitment to patients with rare genetic disorders of obesity, said David Meeker, M.D. With setmelanotide, we have the opportunity to bring one of the first meaningful therapeutic candidates to a segment of that community in dire need. Moreover, we hope our efforts will create visibility for rare genetic disorders of obesity, enabling better care for the people affected and catalyzing ongoing research efforts globally. The current management team has done a great job leading the organization through the transition and I am honored to take the CEO role.

Dr. Meeker has served as Chairman of Rhythm Pharmaceuticals since April 2017 and as a member of the Board since November 2015. Most recently, he served as President and CEO of KSQ Therapeutics. Previously, Dr. Meeker was the Executive Vice President and Head of Sanofi Genzyme, the specialty-care global business unit of Sanofi that focuses on rare diseases, multiple sclerosis, oncology and immunology. Dr. Meeker joined Genzyme in 1994 as Medical Director and, over the course of his tenure, served the company as Vice President of Medical Affairs, Chief Operating Officer, and Chief Executive Officer. He led Genzyme's commercial organization and global market access functions and managed the launch of several treatments for rare genetic diseases, including Aldurazyme, Fabrazyme and Myozyme. Prior to his tenure with Genzyme, Dr. Meeker was Director of the Pulmonary Critical Care Fellowship at the Cleveland Clinic and an Assistant Professor of Medicine at Ohio State University. Dr. Meeker earned his M.D. from the University of Vermont Medical School and completed the advanced management program at Harvard Business School.

About Rhythm PharmaceuticalsRhythm is a late-stage biopharmaceutical company focused on the development and commercialization of therapies for the treatment of rare genetic disorders of obesity. The U.S. Food and Drug Administration (FDA) has accepted for filing Rhythms New Drug Application (NDA) for setmelanotide for the treatment of POMC deficiency obesity and LEPR deficiency obesity with Priority Review of the NDA and assigned a Prescription Drug User Fee Act (PDUFA) goal date of November 27, 2020. Rhythm also submitted a Marketing Authorization Application (MAA) for setmelanotide to treat individuals living with POMC deficiency obesity or LEPR deficiency obesity to the European Medicines Agency (EMA) in June 2020. Rhythm is also evaluating setmelanotide for reduction in hunger and body weight in a pivotal Phase 3 trial in people living with Bardet-Biedl and Alstrm syndromes, with topline data from this trial expected in the fourth quarter of 2020 or early in the first quarter of 2021. Rhythm is leveraging the Rhythm Engine -- comprised of its Phase 2 basket study, TEMPO Registry, GO-ID genotyping study and Uncovering Rare Obesity program -- to improve the understanding, diagnosis and potentially the treatment of rare genetic disorders of obesity. For healthcare professionals, visitwww.UNcommonObesity.comfor more information. For patients and caregivers, visitwww.LEADforRareObesity.comfor more information. The company is based inBoston, MA.

Forward-Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements contained in this press release that do not relate to matters of historical fact should be considered forward-looking statements, including without limitation statements regarding the potential, safety, efficacy, and regulatory and clinical progress of setmelanotide, including anticipated timing of data readouts and our expectations surrounding potential regulatory approvals and timing thereof. Statements using words such as expect, anticipate, believe, may, will and similar terms are also forward-looking statements. These statements are neither promises nor guarantees, but involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements, including, but not limited to, the impact of our management transition, our ability to enroll patients in clinical trials, the design and outcome of clinical trials, the impact of competition, the ability to achieve or obtain necessary regulatory approvals, risks associated with data analysis and reporting, our liquidity and expenses, the impact of the COVID-19 pandemic on our business and operations, including our preclinical studies, clinical trials and commercialization prospects, and general economic conditions, and other important factors discussed under the caption Risk Factors in our Quarterly Report on Form 10-Q for the quarterly period ended March 31, 2020 and our other filings with the Securities and Exchange Commission. Except as required by law, we undertake no obligations to make any revisions to the forward-looking statements contained in this release or to update them to reflect events or circumstances occurring after the date of this release, whether as a result of new information, future developments or otherwise.

Corporate Contact:David ConnollyHead of Investor Relations and Corporate CommunicationsRhythm Pharmaceuticals, Inc.857-264-4280dconnolly@rhythmtx.com

Investor Contact:Hannah DeresiewiczStern Investor Relations, Inc.212-362-1200hannah.deresiewicz@sternir.com

Media Contact:Adam DaleyBerry & Company Public Relations212-253-8881adaley@berrypr.com

A photo accompanying this announcement is available at https://www.globenewswire.com/NewsRoom/AttachmentNg/66fae683-bf9b-4498-9dff-20f74fa14502

David Meeker, M.D., President and Chief Executive Officer

Rhythm Pharmaceuticals Announces Appointment of David Meeker, M.D., as President and Chief Executive Officer

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Rhythm Pharmaceuticals Announces Appointment of David Meeker, MD, as Chief Executive Officer - BioSpace

MyoKardia and Fulcrum Therapeutics Announce Multi-Target Collaboration to Discover Novel Targeted Therapies for Genetic Cardiomyopathies -…

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BRISBANE, Calif. and CAMBRIDGE, Mass., July 21, 2020 (GLOBE NEWSWIRE) -- MyoKardia, Inc. (Nasdaq: MYOK), a clinical-stage biopharmaceutical company discovering and developing targeted therapies for the treatment of serious cardiovascular diseases and Fulcrum Therapeutics, Inc. (Nasdaq: FULC), a clinical-stage biopharmaceutical company focused on improving the lives of patients with genetically defined rare diseases, announced today that they have entered into a strategic collaboration and license agreement to discover, develop and commercialize novel targeted therapies for the treatment of genetic cardiomyopathies.

Under the agreement, MyoKardia will access Fulcrums unique, proprietary target discovery engine to identify therapeutics that control the expression of genes that are known to be underlying drivers of genetic cardiomyopathies. The collaboration focuses joint discovery efforts on certain undisclosed genetic targets. MyoKardia will be responsible for all development and commercialization activities for, and will have global rights to, any potential therapeutics identified through this collaboration.

Fulcrum will receive a payment of $12.5 million at the close of the transaction and may be eligible to receive research, development and commercial milestone payments and additional research reimbursement of up to $302.5 million for a first product to progress through development and commercialization. If MyoKardia chooses to develop and commercialize products directed to additional targets under the collaboration, Fulcrum may be eligible for up to $150.0 million in milestone payments. Fulcrum may also be eligible to receive tiered royalty payments in the mid-single-digit to low double-digit range on net sales for any products under the collaboration that are commercialized.

MyoKardia intends to select targets for further exploration under this collaboration informed by its integrated research and development engine, which includes capabilities in translational research, proprietary and novel disease models, clinical development, and patient engagement and identification. Potential diseases associated with such undisclosed targets are expected to share common characteristics with indications currently being pursued by MyoKardia: strong and genetically-validated mechanistic rationale, high unmet patient need, potentially efficient pathway to approval, and synergy with the commercial organization that MyoKardia is building.

This partnership is a natural extension of MyoKardias investments over the last eight years in building a world-leading cardiovascular research, translational, clinical and commercial organization. We believe this collaboration will enable us to leverage our unique strengths to expand thoughtfully in identifying new therapeutic candidates for the potential treatment of heritable cardiomyopathies, said Robert S. McDowell, Ph.D., MyoKardias Chief Scientific Officer. We have been impressed by Fulcrums ability to discover new biology around genetic muscle disorders. By working together, we hope to further our mission to treat patients suffering from serious cardiovascular disease.

This collaboration highlights the broad applicability of our product engine to discover and develop new treatments in genetically defined rare diseases with high unmet need, said Robert J. Gould, Ph.D., Fulcrums President and Chief Executive Officer. We are pleased to partner with MyoKardia, a leader in the field of precision cardiovascular medicine and look forward to leveraging their unique capabilities to rapidly advance potential treatments to serve patients in urgent need.

About MyoKardia MyoKardia is a clinical-stage biopharmaceutical company discovering and developing targeted therapies for the treatment of serious cardiovascular diseases. The company is pioneering a precision medicine approach to its discovery and development efforts by (1) understanding the biomechanical underpinnings of disease; (2) targeting the proteins that modulate a given condition; (3) identifying patient populations with shared disease characteristics; and (4) applying learnings from research and clinical studies to inform and guide pipeline growth and product advancement. MyoKardias initial focus is on small molecule therapeutics aimed at the proteins of the heart that modulate cardiac muscle contraction to address diseases driven by excessive contraction, impaired relaxation, or insufficient contraction. Among its discoveries are three clinical-stage therapeutics: mavacamten (formerly MYK-461); danicamtiv (formerly MYK-491) and MYK-224.

MyoKardias mission is to change the world for people with serious cardiovascular disease through bold and innovative science.

About Fulcrum TherapeuticsFulcrum Therapeutics is a clinical-stage biopharmaceutical company focused on improving the lives of patients with genetically defined rare diseases in areas of high unmet medical need. Fulcrums proprietary product engine identifies drug targets which can modulate gene expression to treat the known root cause of gene mis-expression. The company has advanced losmapimod to Phase 2 clinical development for the treatment of facioscapulohumeral muscular dystrophy (FSHD) and is advancing losmapimod to Phase 3 for the treatment of COVID-19. Fulcrum also anticipates a regulatory filing in the second half of 2020 with FTX-6058 for the treatment of sickle cell disease.

Please visit http://www.fulcrumtx.com.

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MyoKardia and Fulcrum Therapeutics Announce Multi-Target Collaboration to Discover Novel Targeted Therapies for Genetic Cardiomyopathies -...

Treating Colorectal Cancer in the COVID-19 Era – Medscape

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This interview was originally published as part of MDedge's Blood & Cancer Podcast series. In this episode, podcast host David H. Henry, MD, of Pennsylvania Hospital, Philadelphia, spoke with David J. Kerr, CBE, MD, DSc, professor of cancer medicine at the University of Oxford in England and past president of the European Society for Medical Oncology. Kerr recently cowrote an article outlining recommendations for treating colorectal cancer during the COVID-19 pandemic. In their discussion, Henry and Kerr review those recommendations and compare notes on the practice of cancer medicine in the United States and the United Kingdom. This transcript has been edited for length and clarity.

David H. Henry, MD: As a general hematologist/oncologist, I usually think of stage II colorectal cancer (CRC) as something not to treat unless it meets several conditions. What typically pushes you to treat a patient with stage II CRC with adjuvant therapy?

David J. Kerr, CBE, MD, DSc: I was a part of the QUASAR (Quick And Simple And Reliable) trial group that published a study in 2007 showing that there was a survival benefit for offering adjuvant chemotherapy to stage II patients. The benefit was modest, with an approximately 4% survival improvement, but I feel that's enough to at least discuss adjuvant chemotherapy with patients who are under 70 and fit. We find that maybe 60% of the younger patients are keen to go ahead with adjuvant treatment, even with that very modest survival improvement. Older patients tend to look at the pros and cons and more often than not say no. But I think it's legitimate and intellectually reasonable to have the discussion with the patient.

Henry: That's something that also occurs in adjuvant chemotherapy in breast cancer, where the benefit is around 2%.

Kerr: Exactly. The QUASAR trial had about 3000 patients in it, so its reliability comes from large numbers and tight confidence intervals. Around 75% of these patients were not considered high risk.

I've got a wee bit of an ax to grind about using pathologic markers of high risk in stage II. When its capacity to identify patients with, for example, vascular and lymphatic invasion has been studied, the degree of correlation between different pathology centers can be as low as 50%. We think that these risk factors are carved in stone, yet they're often more subjective than objective. Therefore, I tend not to be too swayed by them. That's why we've got a big research group looking at more objective molecular and other markers to define those truly at high risk.

Henry: In breast cancer, we do the Oncotype DX testing all the time. Do you think that's ready for us to use yet in CRC?

Kerr: Our QUASAR group validated the Oncotype DX for colon cancer. The problem is that the risk factors associated with this assay for colon cancer are not as strong as for breast cancer. Although it is used and is a validated discriminant, the hazard ratios are relatively small, around 1.5. Whereas some of the more recent work, particularly looking at digital pathology and artificial intelligence, appears a bit more powerful, with hazard ratios up to 3 and 4. There are much stronger discriminants out there.

Henry: Discussing another patient scenario: If you saw less than 12 lymph nodes or perforation, would that push you to offer this patient adjuvant therapy?

Kerr: That would be true for the latter, but these days, less so for the first one. In the past decade and possibly longer, I've seen a remarkable global improvement in the quality of surgery and the uniformity of pathology. It's unusual now for anybody in a significant cancer hospital to see a pathology report that's got less than 12 nodes. And although I agree that it's a recognized prognostic factor, it just doesn't count as much now.

Henry: Shifting to the COVID-19 era, what are you giving and for how long?

Kerr: We use a lot of oral capecitabine. In the original placebo-controlled QUASAR studies, we were using bolus 5-fluorouracil (5-FU)/leucovorin, the so-called Mayo Clinic regimen. When the X-ACT trial came out comparing capecitabine with that regimen, the capecitabine came out very nicely. It's a much more cost-effective way for us to deliver the drug. It keeps patients out of the hospital facility. It's not a trivial drug; we still need to watch over patients. But we wanted to try to reduce the comorbidity of chemotherapy in the time of COVID, keep patients out of hospital, and reduce the burden on our chemotherapy front-line staff that is, fiddling around with infusional pumps and so on. We wanted to take the hassle factor down as low as we could. We use 6 months of capecitabine in a conventional dose (2 weeks on, 1 week off), as was reported in the X-ACT study. We were pretty happy with that.

Henry: You've also recommended measuring for enzymes to see if there's fluoropyrimidine toxicity. Do you check that on your capecitabine patients?

Kerr: Increasingly in the United Kingdom, we do that in all of our patients receiving fluoropyrimidine treatment. 5-FU, which is one of the most widely used anticancer drugs in the world, is broken down and degraded by an enzyme called dihydropyrimidine dehydrogenase. If there are genetic variants that reduce the activity of the enzyme, then consequently you get higher-than-average levels of 5-FU in the bloodstream. With some of these genetic variants, it's associated with an almost 100% risk for death.

We run genetic screens in all of our patients. That allows us to identify rarely but importantly patients who would die if we gave them 5-FU, patients who are at a high risk for grade 4 toxicity, particularly neutropenia, septic neutropenic fever, grade 4 hematology drops, and so on. In the 6 months since we instituted this, we found a significant reduction in the number of patients being admitted to our wards because of fluoropyrimidine toxicity, so that's a nice thing. It's a test that we helped to invent. We've got a fantastic genetics outfit in Oxford, and we've done quite a bit of work in improving the sensitivity and specificity of the test.

Henry: Patients with Gilbert syndrome don't metabolize irinotecan very well. Is this is a different enzyme system than with Gilbert syndrome?

Kerr: It is. But you're exactly right to mention it. It's encompassed within a whole field of pharmacogenetics, in that if we can understand what the genetic variants are that may cause somebody to either overmetabolize or undermetabolize a drug, it would allow us to individualize those.

Precision medicine has been taken over by the molecular biologists, which we like. But you and I both know, being sort of graybeards, that the thing that we control most about the delivery of any drug to any patient is its dose and schedule. And that will be determined by a host of other factors. We overdose patients, but we also underdose them. If we could individualize that better, that's got to be an important component of precision medicine.

Henry: It's certainly a step in the right direction. Sadly, I've given capecitabine to patients and one or two times had someone admitted for weeks with diarrhea that wouldn't stop tremendous toxicity by proper meter-squared dosing.

Here where I practice, there's been a bid to keep people out of the hospital and clinic by using alternate-week capecitabine. Would you be a fan of that?

Kerr: It's a clever idea for reducing patterns of toxicity. We've gone with the enzyme because we're pretty comfortable with it. But we're also prepared to dose-reduce in those patients over the age of 70. In terms of clinical pharmacology, we old folk tend to be a wee bit gentler with the chemotherapy anyway, maybe offering 80% of the conventional dose up front, for sensible reasons.

Henry: In the COVID-19 era, what are you giving your patients with stage III T3N1 disease?

Kerr: I think the T3N1 patients do as well as the stage II patients. We wouldn't be inclined to offer them anything different. I don't think there's any role for the use of oxaliplatin in the treatment of stage II disease. If we think that the clinical outcomes, natural history, and survival patterns are similar for T3N1, as has been shown repeatedly in large community studies, we treat them in the same way.

Now, wouldn't it be lovely just to give 3 months of capecitabine? But that feels a step too far now. We try to base everything on published evidence, and 6 months of capecitabine feels fine to me. My wife Rachel [Kerr, an oncologist specializing in gastrointestinal cancers at the University of Oxford] was part of the SCOT trial, which contributed to that lovely New England Journal of Medicine publication in 2018, in which there was good evidence that 3 months was as effective as 6 months. If we were seeing patients with T4N2 disease in normal circumstances, we would often offer 6 months of treatment rather than 3, splitting hairs a little. But in the time of COVID, we just wouldn't do it. We'd do 3 months.

Henry: Are you persuaded by the International Duration Evaluation of Adjuvant Therapy (IDEA) trial showing that FOLFOX (fluorouracil, leucovorin, and oxaliplatin) was beat out by CAPOX (capecitabine/oxaliplatin)?

Kerr: We cannot work in Oxford and not be terrified of Sir Richard Peto, who is the enemy of all subgroup analyses. Richard has beat us over the head with that. So I think there's a huge statistical instability in subgroup analysis.

It would be surprising if CAPOX is better than FOLFOX, because if you look at the data overall, they're indistinguishable. If anything, the needle slightly favors FOLFOX. In this particular case, the needle went the other way. I didn't pay too much attention to it. But during COVID-19, we recommend 3 months of CAPOX for reasons of reducing hassle of infusion and making life that bit safer and easier, hopefully for our patients as well as our frontline chemotherapy staff.

Henry: You offered recommendations for advanced cancer as well. I just had a patient with sigmoid colon cancer with a couple of very large metastases in the liver. We began her on CAPOX. Is that the regimen you're suggesting?

Kerr: It is. That's sort of our default go-to chemotherapy at the moment.

Henry: What are your thoughts about using bevacizumab? Not just during the COVID-19 era, but before it as well.

Kerr: We don't use bevacizumab. This is a stark difference between our two healthcare systems. I used to be quite involved in governmental health policy around cancer planning. Our National Institute for Health and Care Excellence (NICE) decided early on that the clinical benefits accrued by bevacizumab were too small to warrant its at that stage enormous cost. So we don't use bevacizumab at all.

Henry: That's very interesting, because we're looking at the same data across the Atlantic and practicing differently. I can't disagree with you. I've been underwhelmed with the difference, yet our patients sometimes say, "What's the most you could possibly give to me?" Of course, then we'd start clicking off the bevacizumab and sink the national healthcare budget.

Kerr: The study that provided initial data in metastatic CRC randomized patients to receive bevacizumab in addition to bolus 5-FU, irinotecan, and leucovorin, which is a regimen that's not widely used at all. It showed a very significant benefit for bevacizumab. I suspect that the bevacizumab was making up the gap for a somewhat inferior chemotherapy regimen.

In the big, 2000-patient studies looking at CAPOX or FOLFOX plus or minus bevacizumab, the benefits almost disappeared. There were some improvements in progression-free survival but nothing seen in overall survival at all. Therefore, in our taxation-based healthcare system, it's actually an easy decision to say, sorry, we need to pass on this one.

Henry: If you've gotten 3 months in and a patient's carcinoembryonic antigen is falling and their lesions are smaller, do you press on or give a break?

Kerr: We've done two large trials in the United Kingdom, both of which were published in The Lancet, in which we took patients who were responding to chemotherapy after 3 months and randomized them into stop-and-start or continuous chemotherapy. There was no difference in overall survival in either of those groups. These are old trials with somewhat inferior chemotherapy, but nevertheless it gave us an intellectual basis for offering chemotherapy holidays. It's a nice way to present it to patients.

If patients have got small-volume disease and are relatively well, indolent, and asymptomatic, we would give them a couple of months' holiday break and then scan again. If there's any evidence of progression, we'd restart the chemotherapy.

If patients present with large-volume disease that we know we'll lose control of as soon as we stop the chemotherapy, we'll probably move from CAPOX to single-agent capecitabine, with the same regimen, doing the scan again in a couple of months. If patients were on epidermal growth factor receptor inhibitors, then we would keep that biologic going, probably with single-agent capecitabine, dose reduced.

Henry: My patient a couple of weeks ago had a sigmoid primary, was not obstructed, in pain, or bleeding, and had a couple of liver lesions that I could feel and were a bit tender. What's your threshold for deferring start of chemotherapy in metastatic disease like that?

Kerr: You present interesting cases. With that patient, I think I'd want to do something. That feels intuitively right.

But say we have somebody who has had their primary out, so we're not worried about any obstructive problems, and they come with a couple of small liver or pulmonary metastases. If they're elderly, a bit frail, or comorbid, then I'd consider watching them for a couple of months to see what happened.

There's very little trial evidence to suggest when you and I should start chemotherapy. When I was younger, there were two trials that I knew of, one Italian and one northern European, both of which were very small. Each recruited only about 120 patients. The idea was you observe and give chemotherapy when your patients become symptomatic, or give chemotherapy straightaway and randomize to one or the other management plan. One trial was positive for early intervention and the other was negative. These are very small, difficult trials to run.

Also, I think you and I suffer from two things. First, there's a lack of clear trial information. Second, there's a lack of biological markers that allow us to tell the patient sitting in our consulting room that we think they're going to get indolent disease and we can wait, or we've seen small volume in the scans but it's nasty, so we need to get on with treatment. These are things that we and many other labs around the world are looking at. Can we get a marker for aggressiveness? Wouldn't that be a handy thing to have?

Henry: The last of your recommendations for advanced CRC dealt with chemotherapy after resection and metastases. I believe there are some data pointing to the fact that postoperative chemotherapy may make for better outcomes. But would you hold that or give it in the COVID-19 era?

Kerr: We wouldn't recommend it. I think the whole literature around both neoadjuvant and classically post-resection adjuvant chemotherapy is difficult. It's an area that we've contributed to in the past and which is littered with small trials, some almost single-center. There have been great results with intrahepatic arterial infusion, but those are difficult to apply at other centers, even Penn and Oxford. So it's a rather confused area. And if I have a degree of confusion about benefits in the time of COVID-19, we don't feel it's worthwhile considering.

Henry: I also wanted to ask about rectal cancer. We've been persuaded a lot by data on this side of the world about total neoadjuvant therapy, which I've always been a fan of in my oncology career. In breast cancer, you and the patient can see if it's working or not. And here, you can do the same thing and probably get more drug in, as opposed to waiting. Are you a fan of the total neoadjuvant therapy? And are you somewhat curtailing the radiation piece in the COVID-19 era?

Kerr: I think we are becoming fans of the total neoadjuvant therapy. It's taking a bit longer to be taken up across the United Kingdom. But the data look good; we agree about that.

As things stand now, we are trying to curtail everything. We're going from complex radio-chemotherapeutic regimens, from long-course to short-course treatment. We're looking to omit some of the drugs for example, taking oxaliplatin out rather than giving combination chemo-radiotherapy. Our colleagues in the radiation field again are looking to compress and simplify as best they can and as logically as they can.

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Treating Colorectal Cancer in the COVID-19 Era - Medscape

GnomeDX Files for FDA Emergency Use Authorization for Rapid Turnaround Real-Time RT-PCR COVID-19 Test Utilizing the Fluidigm Biomark HD Platform -…

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Test Intended to Expand Availability of COVID-19 Screening Resources in Central Ohio

Workflow with Real-Time PCR Using Fluidigm Microfluidics Technology and Reagents

Increasing Number of Labs Adopting the Fluidigm High-Throughput Testing Model

SOUTH SAN FRANCISCO, Calif.,and COLUMBUS, Ohio, July 20, 2020 (GLOBE NEWSWIRE) -- Fluidigm Corporation(Nasdaq:FLDM), an innovative biotechnology tools provider with a vision to improve life through comprehensive health insight, today announced thatGnome Diagnostics, LLC (GnomeDX), a leading pharmacogenomics testing company, is utilizingFluidigmmicrofluidics technology and reagents in a test developed to detect the SARSCoV2 virus, which causes COVID-19.

The Rapid Turnaround Real-Time RT-PCR COVID-19 Test, which can be performed via oropharyngeal, nasopharyngeal and nasal swab, is intended to meet growing testing needs for patients, health care workers and other critical populations across central Ohio. GnomeDX has filed for Emergency Use Authorization (EUA) for its extraction-free GnomeDX RT-PCR COVID-19 Test from theU.S. Food and Drug Administration(FDA).

Supporting our first responders and their patients are among key goals of our test development program, said Vicky Amann, Vice President for Lab Operations at GnomeDx. Our CLIA certified genomics lab is ideally suited to this challenge, and we are committed to support our community in any way we can to respond to the pandemic.

GnomeDX selected the Fluidigm integrated fluidic circuit technology, reagents and workflow because they provide high-performance sample throughput that is unmatched by microwell plate-based PCR assays for the SARS-CoV-2 virus, Amann added.

GnomeDX is a high-complexity lab certified under the Clinical Laboratory Improvement Amendments (CLIA) inthe United Statesand eligible under FDA guidanceto create its own diagnostic tests for COVID-19.GnomeDX has validated a workflow using assays developed by the Centers for Disease Control and Prevention designed to be run on theFluidigm Biomark HD system.

Because sample collection methods for the test include oropharyngeal and nasal swabs, it does not require invasive nasopharyngeal collection.

COVID-19 testing on the Biomark HD platform provides throughput and cost advantages that reduce the impact of capacityconstrained supply chains. Fluidigms microfluidics technology enables processing of more samples per batch and uses a fraction of expensive testing reagents per sample as compared to more traditional, microwell plate-based PCR technology.

We believe a significant increase in testing capacity remains critical to an effective global response to the COVID-19 crisis, said Chris Linthwaite, President and CEO of Fluidigm. As governments, medical institutions and private labs look for solutions, speed, scale and automation are paramount. Since the beginning of the pandemic, we have been supporting labs around the world as they build out testing infrastructure that meets these important criteria.

The Biomark HD platform can generate as many as 6,000 test results per day on a single instrument. More and more labs are adopting the Fluidigm model of COVID-19 testing, which offers much-needed high-throughput capability per system. We also support multiple approaches to sample collection, having recently filed for Emergency Use Authorization from theFDAfor an extraction-free saliva-based test to detect COVID-19.

We are honored to have been chosen by GnomeDX to provide a platform for its COVID-19 test to provide critically needed testing capacity in central Ohio.

In early June, Fluidigm filed for Emergency Use Authorization with theFDA for an extraction-free saliva-based test to detect the SARSCoV2 virus. The test was developed in collaboration with scientists at theMcDonnell Genome Instituteand theDepartment of Genetics at the Washington University School of MedicineinSt. Louis.

With respect to the Fluidigm test, Fluidigm has filed for Emergency Use Authorization with the FDA. The test has been validated by Fluidigm, but the FDAs independent review of this validation is pending. The FDA may require additional data, validation and/or testing, and may not ultimately provide authorization for EUA requests. An EUA, if granted, does not constitute FDA clearance or approval, but would allow use by authorized laboratories only while the EUA is in effect.

About FluidigmFluidigm(Nasdaq:FLDM) focuses on the most pressing needs in translational and clinical research, including cancer, immunology, and immunotherapy. Using proprietary CyTOF and microfluidics technologies, we develop, manufacture, and market multi-omic solutions to drive meaningful insights in health and disease, identify biomarkers to inform decisions, and accelerate the development of more effective therapies. Our customers are leading academic, government, pharmaceutical, biotechnology, and plant and animal research laboratories worldwide. Together with them, we strive to increase the quality of life for all. For more information, visit fluidigm.com. Fluidigm, theFluidigmlogo, Biomark, and CyTOF are trademarks and/or registered trademarks ofFluidigm Corporationinthe United Statesand/or other countries. All other trademarks are the sole property of their respective owners. Fluidigm products are provided for Research Use Only. Not for use in diagnostic procedures.

Available InformationWe use our website (fluidigm.com), investor site (investors.fluidigm.com), corporate Twitter account (@fluidigm), Facebook page (facebook.com/Fluidigm), and LinkedIn page (linkedin.com/company/fluidigm-corporation) as channels of distribution of information about our products, our planned financial and other announcements, our attendance at upcoming investor and industry conferences, and other matters. Such information may be deemed material information, and we may use these channels to comply with our disclosure obligations under Regulation FD. Therefore, investors should monitor our website and our social media accounts in addition to following our press releases,SECfilings, public conference calls, and webcasts.

About Gnome Diagnostics:GnomeDX is a personalized medicine genetic testing company. Its pharmacogenomic tests help physicians to prescribe the safest and most effective doses of therapeutics based on an individual's unique genetic profile. GnomeDX panel tests can also screen for inherited cardiovascular disease risk, promoting early detection and prevention. GnomeDXs goal is to improve the treatment outcomes for patients, minimize risk and side effects from prescription drugs, and help reduce the overall cost of health care. The GnomeDX Diagnostics testing unit intends to provide COVID-19 assays for safer workplaces and communities under the guidance of health care professionals. The GnomeDX Science unit provides molecular lab services for research and pharmaceutical drug development.

Forward-Looking Statements for FluidigmThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including, among others, statements regarding the potential implementation of Fluidigm microfluidics technology and products for COVID-19 testing and the anticipated features and benefits of, and applications and demand for, such products. Forward-looking statements are subject to numerous risks and uncertainties that could cause actual results to differ materially from currently anticipated results, including but not limited to risks relating to the potential adverse effects of the coronavirus pandemic on our business and operating results during 2020; our ability and/or the ability of the institutions utilizing our products and technology to obtain Emergency Use Authorization from the FDA and any other requisite approvals to use our products and technology for diagnostic testing purposes; potential changes in priorities or requirements for Emergency Use Authorizations; potential limitations of any Emergency Use Authorization; challenges inherent in developing, manufacturing, launching, marketing, and selling new products; risks relating to company research and development and distribution plans and capabilities; interruptions or delays in the supply of components or materials for, or manufacturing of, Fluidigm products; potential product performance and quality issues; intellectual property risks; and competition. Information on these and additional risks and uncertainties and other information affecting Fluidigm business and operating results is contained in Fluidigms Annual Report on Form 10-K for the year ended December 31, 2019, and in its other filings with the Securities and Exchange Commission. These forward-looking statements speak only as of the date hereof. Fluidigm disclaims any obligation to update these forward-looking statements except as may be required by law.

Contacts

Gnome Diagnostics, LLC

Paige VandiverVP, Operations614 431 6414paige@gnomedx.com

Fluidigm

Media:Mark SpearmanSenior Director, Corporate Communications650 243 6621mark.spearman@fluidigm.com

Investors:Agnes LeeVice President, Investor Relations650 416 7423agnes.lee@fluidigm.com

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GnomeDX Files for FDA Emergency Use Authorization for Rapid Turnaround Real-Time RT-PCR COVID-19 Test Utilizing the Fluidigm Biomark HD Platform -...

Emerging Diseases in Swine: Past, Present, and the Future – National Hog Farmer

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Live Event: August 13,2020 | 2:00 pm ET / 11:00 am PT

For thousands of years, viruses and other biological agents have always found ways to adapt to their environment and survive. What current and future tools do we have to monitor those adaptations? How can we shorten the time interval between changes in the virus and resulting clinical outcome? How closely can we predict when and how genetic mutations will manifest clinically?

In this edition of Science Talks, Drs. Stephanie Rossow and Phil Gauger will leverage their experiences to provide insight as to why and how pathogens emerge as new diseases in swine populations.

Joining us as speakers will be:

Dr. Phil Gauger, DVM, MS, PhDVDPAM ISU VDLAssociate Professor and Diagnostic PathologistIowa State University Diagnostic Lab

Dr. Phil Gauger is a 1994 graduate of Iowa State University College of Veterinary Medicine and was a partner in a mixed animal practice for 12 years. Dr. Gauger received a Masters in 2008 and PhD in 2012 in Veterinary Microbiology from ISU. He is currently an associate professor and veterinary diagnostician at the ISU Veterinary Diagnostic Laboratory in the Department of Veterinary Diagnostic and Production Animal Medicine and section leader of the molecular diagnostic testing at the ISU VDL.

Dr. Stephanie Rossow, DVM, PhDMinnesota Veterinary Diagnostic Lab, Department of Veterinary Population Medicine, UMNSwine Disease Diagnostician

Dr. Stephanie Ann Rossow received her DVM from Kansas State in 1986 and her PhD in Veterinary Anatomic Pathology from the University of Minnesota in 1996. Prior to her PhD, she enlisted in the U.S. Army Veterinary Corps. Dr. Rossow holds a BS from South Dakota State University with a major in Zoology and minors in Microbiology and Chemistry. She is a swine disease diagnostician at the University of Minnesota Veterinary Diagnostic lab in the Department of Veterinary Population Medicine and conducts research on infectious diseases of swine.

Kevin Schulz - ModeratorSenior Staff WriterNational Hog Farmer

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Emerging Diseases in Swine: Past, Present, and the Future - National Hog Farmer

Switching from lifespan to healthspan – Yahoo Sports

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Some pessimism has been circulating about lifespan recently. In the modern era, lifespan has increased every decade, and dying before you turn seventy would now be considered a premature death. Three score and ten is no longer a destination for a normal life, and average lifespans among people who are not underprivileged could easily top ninety in the near future.

The difference in quality of life is now more important than lifespan on its own because the health status of two seventy-year-olds can vary wildly. The concept to keep in mind is healthspan, defined as the years you spend without infirmity, chronic disease, and dementia. Right now healthspan is a hit and miss proposition.

While we are told that our genes determine how we age, this needs to be clarified. Research on identical twins reveals that its not your genes that determine your healthspan but your lifestyle, nutrition and gut microbiome that plays a much more important role. Identical twins are born with the same genes, a fact that will not change over the decades, but by age seventy, many identical twins are as unalike in their health status as two people chosen at random.

What makes the difference is known as gene expression. DNA is an inactive molecule, but its expression into active molecules (proteins), is influenced by all the factors that determine the difference between aging well or badly. The active side of genetics belongs to the field of epigenetics, which controls whether a gene is turned on or off. You carry around at the epigenetic level all the major experiences of your lifetime. As these accumulate, they automatically divide into experiences that promote a long healthspan and those that do the opposite.

Here is where a breakthrough is possible that could make an enormous difference. We said that you cannot change the genes you were born with, which has been gospel in genetics for decades. Even though you can not change the genes you are born with, you can change their expression, which is what matters. Also, 90 percent of your genes are not in your cells but in your gut microbiome. Trillions of bacteria in your digestive tract do more than digest food. They constitute an immense chemical factory sending messages to every part of the body. Humans have evolved in cooperation with these bacteria. They are not alien or separate from you; they are part of your evolution, affecting you every moment.

Chemical messages can be harmful, such as those that create inflammation or promote stress, or beneficial. Your microbiome is unique to you and constantly shifting. In essence, you are changing the vast majority of your genes through your lifestyle, for the gut microbiome amounts to 90 percent of your genes. The genes you were born with amount to only 10 percent of your total genome. The good news here is that you can change their expression.

Healthspan, therefore, depends on living in such a way that the entire genetic complement functions properly. The enemies of beneficial gene expression are now pretty well known:

Impure water, air, and food

Lack of hygiene and sanitation

Stress

Chronic inflammation

Depression and anxiety

Toxins like alcohol and tobacco

Sedentary lifestyle

Inherited predisposition (normally a minor factor if you are healthy)

These negative factors take years to develop before symptoms appear and a doctor must be visited. In the meantime, people shorten their healthspan simply through everyday choices. Its the small things accumulating over a long time that determine who is healthy at seventy and who isnt. Similarly, the choices that support the best functioning at the cellular level are well known.

Pure food, water, and air

Absence of additives and toxins

Moderate physical activity

Meditation

Lowered stress

Good level of mood

Close fulfilling relationships

Having a good support system

Overall happiness and well-being

These influences go far beyond preventive medicine and depending on a doctor to keep you healthy. You can lower your biological age by the choices you make, and your entire complement of genes will benefit. They express the benefit by exchanging chemical messages that promote their own lives at the cellular level. Those messages are chemical and therefore do not speak in the language humans share. But every aspect of consciousness, going beyond the physical, lies at the heart of healthspan.

Thats why a direct connection can be made between meditating, even for a short period, and the level of telomerase in your cells. Telomerase is a chemical that is vital to keeping DNA intact without fraying from age. It took years of intense research to uncover the role of telomerase, yet the bottom line is that your consciousness, not just your positive lifestyle choices, is key to what your cells are doing, including the one-celled microbes in your intestinal tract.

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More importantly, however, is the message that healthspan should be everyones top priority when thinking about present and future health. What makes you young and keeps you young is the healthy functioning, right this minute, of your cells and microbiome. How do you actually know that your lifestyle is contributing towards healthy aging or in other words are you biologically becoming younger or older than your chronological age? Viome is a company that recently launched a health intelligence service that gives you insight into your microbial health, cellular health, immune system health, mitochondrial health, stress response health and your biological age. (Editors note: For disclosure, the authors are founders and adviser, respectively, to Viome.) Your microbiome is living solely for your benefit, and by giving them some attention in return, you are caring for your future far beyond what a doctor can do after symptoms appear.

Naveen Jain also contributed to this story.

DEEPAK CHOPRA MD, FACP, founder of The Chopra Foundation, a non-profit entity for research on well-being and humanitarianism, and Chopra Global, a modern-day health company at the intersection of science and spirituality, is a world-renowned pioneer in integrative medicine and personal transformation. Chopra is a Clinical Professor of Family Medicine and Public Health at the University of California, San Diego and serves as a senior scientist with Gallup Organization. He is the author of over 89 books translated into over forty-three languages, including numerous New York Times bestsellers. His 90th book, Metahuman: Unleashing Your Infinite Potential, unlocks the secrets to moving beyond our present limitations to access a field of infinite possibilities. Time magazine has described Dr. Chopra as one of the top 100 heroes and icons of the century.

Naveen Jain is the founder of Viome and many other successful companies. Viome's Health Intelligence service assesses your gut microbiome health, cellular health, mitochondrial health, immune system health, and your stress response health. Viome can even reveal your biological age. Naveen is the author of the award-winning book Moonshots Creating the World of Abundance, has been awarded E&Y "Entrepreneur of the Year", and "Most Creative Person" by Fast Company.

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Switching from lifespan to healthspan - Yahoo Sports

Positive Phase 3 Study Results for TRIKAFTA (elexacaftor/tezacaftor/ivacaftor and ivacaftor) in People Ages 12 and Older With Cystic Fibrosis Who Have…

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BOSTON--(BUSINESS WIRE)--Vertex Pharmaceuticals Incorporated (Nasdaq: VRTX) today announced results of a global Phase 3 study of TRIKAFTA (elexacaftor/tezacaftor/ivacaftor and ivacaftor) in people with cystic fibrosis (CF) ages 12 years and older who have one copy of the F508del mutation and one gating mutation (F/G) or one copy of the F508del mutation and one residual function mutation (F/RF). The study met its primary endpoint of mean absolute within-group change in percent predicted forced expiratory volume in 1 second (ppFEV1) from baseline through 8 weeks of treatment, demonstrating a statistically significant 3.7 percentage point (p<0.0001) improvement in ppFEV1 in patients treated with TRIKAFTA compared to their baseline after a 4-week run-in of treatment on ivacaftor or tezacaftor/ivacaftor. The study met all secondary endpoints, including a statistically significant mean within-group reduction of 22.3 mmol/L from baseline in sweat chloride (p<0.0001). The regimen was generally well-tolerated, and safety data were consistent with those observed in previous Phase 3 studies with TRIKAFTA.

The study is a post-marketing commitment in the U.S. and the results will be submitted to the U.S. Food and Drug Administration. In the U.S., TRIKAFTA is already approved for use in people with CF ages 12 years and older who have at least one copy of the F508del mutation, which includes the populations evaluated in this study. In June, Vertex received a positive opinion from the Committee for Medicinal Products for Human Use (CHMP) for the initial triple combination regimen application for people with CF ages 12 years and older with one F508del mutation and one minimal function mutation (F/MF) or two F508del mutations (F/F). Data announced today from this study will be submitted to the European Medicines Agency to support a potential indication expansion of the EU label, once European Commission approval has been granted for the initial triple combination application. Full study results will be submitted for presentation at a future medical meeting and/or publication.

The results of this study demonstrate that the triple combination provides significant additional benefit compared to existing CFTR modulator therapy for F/G and F/RF patients and adds to the robust body of evidence supporting the benefit of this medicine for patients with at least one F508del mutation, said Carmen Bozic, M.D., Executive Vice President, Global Medicines Development and Medical Affairs, and Chief Medical Officer at Vertex. We look forward to submitting these data to the EMA in support of a potential indication expansion of the EU label following initial approval.

About the 445-104 Study

The data announced today are from a global Phase 3, randomized, double-blind, parallel-group study to evaluate the efficacy and safety of TRIKAFTA in people with CF ages 12 years and older who have one copy of the F508del mutation and one gating mutation (F/G), or one copy of the F508del mutation and one residual function mutation (F/RF). All participants had a 4-week run-in period of either ivacaftor or tezacaftor/ivacaftor. Following the run-in, patients were randomized to receive TRIKAFTA or to remain on their prior regimen of ivacaftor or tezacaftor/ivacaftor for 8 weeks. Baseline was measured at the end of the run-in period, prior to the start of the 8-week treatment period. A total of 132 participants received TRIKAFTA and 126 patients were in the control group that received either ivacaftor or tezacaftor/ivacaftor.

The primary endpoint of the study, the mean absolute within-group improvement from baseline in ppFEV1 through 8 weeks of treatment with TRIKAFTA, demonstrated a statistically significant improvement of +3.7 percentage points in ppFEV1 (p<0.0001).

The study met all secondary endpoints, including, in the order of statistical testing hierarchy, statistically significant mean absolute within-group change in sweat chloride of -22.3 mmol/L (p<0.0001) from baseline through 8 weeks in patients treated with TRIKAFTA, and between-group mean changes of +3.5 percentage points in ppFEV1 (p<0.0001) and -23.1 mmol/L in sweat chloride (p<0.0001) in patients treated with TRIKAFTA compared to the control group of those who received ivacaftor or tezacaftor/ivacaftor.

Overall, safety data were similar to those observed in previous Phase 3 studies of TRIKAFTA, and the regimen was generally well tolerated. The majority of adverse events were mild or moderate. The most common adverse event that occurred in 15% or more patients, regardless of treatment arm, was headache. Serious adverse events were observed in 3.8% (n=5) of the patients who received TRIKAFTA and in 8.7% (n=11) of the patients who received ivacaftor or tezacaftor/ivacaftor. In the study, 2 patients taking ivacaftor or tezacaftor/ivacaftor and 1 patient taking TRIKAFTA discontinued treatment due to adverse events.

About Cystic Fibrosis

Cystic Fibrosis (CF) is a rare, life-shortening genetic disease affecting approximately 75,000 people worldwide. CF is a progressive, multi-system disease that affects the lungs, liver, GI tract, sinuses, sweat glands, pancreas and reproductive tract. CF is caused by a defective and/or missing CFTR protein resulting from certain mutations in the CFTR gene. Children must inherit two defective CFTR genes one from each parent to have CF. While there are many different types of CFTR mutations that can cause the disease, the vast majority of all people with CF have at least one F508del mutation. These mutations, which can be determined by a genetic test, or genotyping test, lead to CF by creating non-working and/or too few CFTR proteins at the cell surface. The defective function and/or absence of CFTR protein results in poor flow of salt and water into and out of the cells in a number of organs. In the lungs, this leads to the buildup of abnormally thick, sticky mucus that can cause chronic lung infections and progressive lung damage in many patients that eventually leads to death. The median age of death is in the early 30s.

About TRIKAFTA

TRIKAFTA (elexacaftor/tezacaftor/ivacaftor and ivacaftor) is a prescription medicine used for the treatment of cystic fibrosis (CF) in patients ages 12 years and older who have at least one copy of the F508del mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Patients should talk to their doctor to learn if they have an indicated CF gene mutation. It is not known if TRIKAFTA is safe and effective in children under 12 years of age. TRIKAFTA is designed to increase the quantity and function of the F508del-CFTR protein at the cell surface. The approval of TRIKAFTA was supported by positive results of two global Phase 3 studies in people ages 12 years and older with CF: a 24-week Phase 3 study in 403 people with one F508del mutation and one minimal function mutation (F/MF) and a 4-week Phase 3 study in 107 people with two F508del mutations (F/F).

U.S. INDICATION AND IMPORTANT SAFETY INFORMATION FOR TRIKAFTA (elexacaftor/tezacaftor/ivacaftor and ivacaftor) TABLETS

TRIKAFTA is a prescription medicine used for the treatment of cystic fibrosis (CF) in patients aged 12 years and older who have at least one copy of the F508del mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Patients should talk to their doctor to learn if they have an indicated CF gene mutation. It is not known if TRIKAFTA is safe and effective in children under 12 years of age.

Patients should not take TRIKAFTA if they take certain medicines, such as: antibiotics such as rifampin or rifabutin; seizure medicines such as phenobarbital, carbamazepine, or phenytoin; St. Johns wort.

Before taking TRIKAFTA, patients should tell their doctor about all of their medical conditions, including if they: have kidney problems, have or have had liver problems, are pregnant or plan to become pregnant because it is not known if TRIKAFTA will harm an unborn baby, or are breastfeeding or planning to breastfeed because it is not known if TRIKAFTA passes into breast milk.

TRIKAFTA may affect the way other medicines work, and other medicines may affect how TRIKAFTA works. Therefore, the dose of TRIKAFTA may need to be adjusted when taken with certain medicines. Patients should especially tell their doctor if they take: antifungal medicines including ketoconazole, itraconazole, posaconazole, voriconazole, or fluconazole; antibiotics including telithromycin, clarithromycin, or erythromycin; other medicines including rifampin, rifabutin, phenobarbital, carbamazepine, phenytoin, and St. Johns wort.

TRIKAFTA may cause dizziness in some people who take it. Patients should not drive a car, operate machinery, or do anything that requires alertness until they know how TRIKAFTA affects them.

Patients should avoid food or drink that contains grapefruit while they are taking TRIKAFTA.

TRIKAFTA can cause serious side effects, including:

High liver enzymes in the blood, which is a common side effect in people treated with TRIKAFTA. These can be serious and may be a sign of liver injury. The patients doctor will do blood tests to check their liver before they start TRIKAFTA, every 3 months during the first year of taking TRIKAFTA, and every year while taking TRIKAFTA. Patients should call their doctor right away if they have any of the following symptoms of liver problems: pain or discomfort in the upper right stomach (abdominal) area; yellowing of the skin or the white part of the eyes; loss of appetite; nausea or vomiting; dark, amber-colored urine.

Abnormality of the eye lens (cataract) in some children and adolescents treated with TRIKAFTA. If the patient is a child or adolescent, their doctor should perform eye examinations before and during treatment with TRIKAFTA to look for cataracts.

The most common side effects of TRIKAFTA include headache, diarrhea, upper respiratory tract infection (common cold) including stuffy and runny nose, stomach (abdominal) pain, inflamed sinuses, increase in liver enzymes, increase in a certain blood enzyme called creatine phosphokinase, rash, flu (influenza), and increase in blood bilirubin.

These are not all the possible side effects of TRIKAFTA. Please click here to see the full Prescribing Information for TRIKAFTA.

About Vertex

Vertex is a global biotechnology company that invests in scientific innovation to create transformative medicines for people with serious diseases. The company has multiple approved medicines that treat the underlying cause of cystic fibrosis (CF) a rare, life-threatening genetic disease and has several ongoing clinical and research programs in CF. Beyond CF, Vertex has a robust pipeline of investigational small molecule medicines in other serious diseases where it has deep insight into causal human biology, including pain, alpha-1 antitrypsin deficiency, and APOL1-mediated kidney diseases. In addition, Vertex has a rapidly expanding pipeline of genetic and cell therapies for diseases such as sickle cell disease, beta thalassemia, Duchenne muscular dystrophy and type 1 diabetes mellitus.

Founded in 1989 in Cambridge, Mass., Vertex's global headquarters is now located in Boston's Innovation District and its international headquarters is in London, UK. Additionally, the company has research and development sites and commercial offices in North America, Europe, Australia and Latin America. Vertex is consistently recognized as one of the industry's top places to work, including 10 consecutive years on Science magazine's Top Employers list and top five on the 2019 Best Employers for Diversity list by Forbes. For company updates and to learn more about Vertex's history of innovation, visit http://www.vrtx.com or follow us on Facebook, Twitter, LinkedIn, YouTube and Instagram.

Special Note Regarding Forward-looking Statements

This press release contains forward-looking statements as defined in the Private Securities Litigation Reform Act of 1995, including, without limitation, statements made by Dr. Carmen Bozic in this press release, statements regarding the potential benefits of TRIKAFTA and our plans to submit data and full study results, and our expectations regarding potential approval for the triple combination regimen and a potential expansion of the EU label. While Vertex believes the forward-looking statements contained in this press release are accurate, these forward-looking statements represent the company's beliefs only as of the date of this press release and there are a number of risks and uncertainties that could cause actual events or results to differ materially from those expressed or implied by such forward-looking statements. Those risks and uncertainties include, among other things, that data from the company's development programs may not support registration or further development of its compounds due to safety, efficacy or other reasons, risks related to approval and commercialization of our medicines, and other risks listed under Risk Factors in Vertex's annual report and subsequent quarterly reports filed with the Securities and Exchange Commission and available through the company's website at http://www.vrtx.com. Vertex disclaims any obligation to update the information contained in this press release as new information becomes available.

(VRTX-GEN)

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Positive Phase 3 Study Results for TRIKAFTA (elexacaftor/tezacaftor/ivacaftor and ivacaftor) in People Ages 12 and Older With Cystic Fibrosis Who Have...

Researchers develop credit-card sized tool to understand how cancer cells invade host tissues – News@UofT

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A group of researchers from the University of Toronto hasdeveloped a credit-card sized tool for growing cancer cells outside the human body, which they believe will enhance their understanding of breast cancer metastasis.

The device, described in a paperpublished on July 15inScience Advances, reproduces various environments within the human body where breast cancer cells live. Studying the cells as they go through the process of invasion and metastasis could point the way toward new biomarkers and drugs to diagnose and treat cancer.

Metastasis is what makes cancer so deadly, said the publication's corresponding authorAaron Wheeler, a professor in the Institute of Biomedical Engineering in the Faculty of Applied Science & Engineering, whose lab is located in theDonnelly Centre for Cellular and Biomolecular Researchin U of T's Faculty of Medicine.

If cancer cells would simply stay in one spot, it would be easy to excise them and cure the disease. But when cancer metastasizes, cancer cells move through the body, making the disease difficult to treat.

We decided to apply our expertise in microfluidics to develop a new tool to aid in studying how cancer cells begin to invade into surrounding tissues in the first steps in metastasis.

Normally metastasis is studied in a petri dish cell culture or in whole animals. However, these model systems present problems in terms of cost, efficiency, or lack of representation.

An oversimplified system like cells in petri dishes doesnt mimic what happens in the body, while in an animal model, its difficult to isolate and study parameters that govern the invasiveness of a cell, saidBetty Li, a senior Institute of Biomedical Engineering PhD student and leadauthor of the paper.

Our system gives us control over all the specific parameters that we want to look at, while allowing us to make structures that better resemble what happens to the body.

The device consists of patterned metal electrodes which can move extremely small droplets around through the use of electric fields. By selectively changing the water-repelling properties of the surface at various points, researchers can pinch off the water droplets and form precise shapes.

In the paper, the researchers describe how they used a collagen matrix coated with a layer of basal membrane extract to mimic the structure of the breast tissue seen by breast cancer cells during the first step of metastasis.

By placing cancer cells outside of these tissue mimics, researchers could observe the invasion process in detail, including measurements of speed and location.

One interesting thing we observed is that not all cancer cells within the same population have the same invasiveness, Li said.Some invaded into the tissue mimics while others did not, which prompted us to look at what gives the invaded cells such an advantage.

Li and her team extracted cancer cells at various distances from the invasion point and subjected these cells to genetic sequencing.

We identified 244 different genes that are differentially expressed between the cancer cells that invaded versus the ones that didnt invade, Li said. This means that using the tool we developed, researchers in the future can develop therapeutics that target some of these genes to halt the cancer metastasis.

We think this type of tool will be quite useful to the community, as cell invasion is important in cancer and also a host of other (non-pathological) processes, like tissue growth, differentiation and repair, Wheeler said.

This research was funded by the National Sciences and Engineering Research Council of Canada, the Canada Foundation for Innovation,the Province of Ontario, and by U of T's Medicine by Design initiative, which receives funding from the Canada First Research Excellence Fund.

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CVM Researcher Develops Tool To Improve Chronic Wasting Disease Resistance In White-Tailed Deer – Texas A&M University Today

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Chronic wasting disease is a fatal syndrome found in white-tailed deer populations.

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Christopher Seabury, an associate professor of genomics at the Texas A&M University College of Veterinary Medicine & Biomedical Sciences (CVM), has confirmed that certain aspects of the white-tailed deers response to chronic wasting disease (CWD) are moderately to highly heritable, or passed from parent to offspring, and can be predicted using a custom genomic tool designed by Seabury and his team.

This custom tool, a novel array designed by Seabury, can be used to predict a white-tailed deers responses to CWD exposure with high accuracy and specificity, meaning that the array is likely to become widely deployed for use in a genetic evaluation program aimed at reducing the prevalence of CWD.

Such a program would allow deer farmers, wildlife managers and regulatory agencies to selectively breed the least susceptible deer, thereby building healthier, more CWD-resistant populations. This tool and program could support herd health of both farmed and free-ranging deer populations; although the initial application of this technology is currently focusing on U. S. farmed white-tailed deer.

CWD is a fatal syndrome that causes weight loss, ataxia (as part of a degenerative disease of the nervous system), listlessness and other neurologic symptoms in both farmed and free-ranging U.S. mule deer, elk, moose and white-tailed deer populations.

CWD is recognized as a prion disease, meaning that an infectious misfolded protein (PrPCWD) is instrumental for behavioral changes, emaciation and progressive neurological disease leading to death. Another relevant prion disease known as Scrapie (PrPSc) affects both sheep and goats, and was first recognized in sheep as early as the 18th century.

Importantly, the prevalence of scrapie has been reduced by approximately 85% through afederal eradication program administered by USDA APHIS.

CWD is currently present in at least 26 U.S. states, multiple Canadian provinces and several areas in Eurasia, but its geographic distribution is expanding despite the implementation of surveillance programs that aim to contain and depopulate CWD-positive herds.

Some naturally occurring genetic variation within thePRNP gene which encodes the normal cellular prion protein has previously been associated with enhanced risk for CWD. However, this study clearly demonstrates that while some genetic variation within the PRNPgene has large effects on risk for CWD, selective breeding based uponPRNPinformation alone is insufficient to facilitate a rapid reduction in the overall prevalence of CWD in farmed U.S. white-tailed deer.

Seaburys research published in G3: Genes, Genomes, Genetics used molecular genetic techniques and machine learning to analyze DNA samples from deer with and without CWD.

He and his team confirmed the G96S genetic variant of thePRNPgene as having large effects on risk, while also demonstrating for the first time that genetic variation in other genes collectively explains more differential susceptibility and variation in disease progression thanPRNPalone; thereby necessitating a whole-genome approach to selective breeding.

The novel test designed and validated by Seabury in this study involves a custom Affymetrix Axiom single nucleotide polymorphism (SNP) array, which is used to collect genome-wide DNA profiles from white-tailed deer; for both association mapping and machine learning.

One of the most important things from this initial study is the mean genomic prediction accuracy, which hovers around 81 percent, Seabury said. This means that we can predict with about 81 percent accuracy the phenotype of a tested animal, and that we can accurately estimate the genetic merit of each animal, as it relates to CWD, by producing something called genomically-estimated breeding values.

This novel strategy for producing genomic predictions for risk of CWD in white-tailed deer could be used to mitigate CWD risk in both farmed and free-ranging deer populations.

White-tailed deer are very adaptable and prolific; often reappearing in free-ranging areas where depopulation or herd reduction was attempted to control CWD, Seabury said. Additionally, in regions where indigenous anthrax occurs, and has caused wide-spread dead-loss among white-tailed deer, managers have often reintroduced white-tailed deer by translocation. Wouldnt you like to be able to select deer for replacement that you felt would reduce the populations overall risk for CWD?

Seaburys next goal includes making the test an affordable and reliable tool that deer farmers and wildlife agencies can use to ensure healthier populations of white-tailed deer.

I want to achieve a final array designed to be so cheap that it can be widely used and implemented, Seabury said. Im going to strive to redesign the array to maximize the prediction accuracy, but also minimize the costs.

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The Prostate Cancer Foundation and Robert F. Smith Announce New Effort to Address Health Disparities for African American Men – BioSpace

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LOS ANGELES, July 21, 2020 /PRNewswire/ --TheProstate Cancer Foundation(PCF) and Robert F. Smith, founder, chairman and CEO of Vista Equity Partners, announce a new effort to reduce deaths from prostate cancer, one of the largest health disparities facing African American men today.

"As African American men are at an increased risk for being diagnosed or dying from prostate cancer, understanding their risk profile and applying this knowledge earlier with strategic detection, care, and decisions about cancer risk management is of utmost importance to address health inequity in the U.S.," said Smith. "This is why I made a personal commitment to help accelerate research, encourage African American men to participate in the study and subsequent testing, and develop new detection strategies that have the power to transform how we diagnose and treat this disease and help save lives."

The research Smith is supporting will lead to the development of the Smith Polygenic Risk Test for Prostate Cancer, a non-invasive, early detection test that will identify a man's lifetime prostate cancer risk using a combination of more than 250 genetic variants obtained from a single sample of saliva or blood. The Smith Test is expected to cost less than $90 USD and will be made available in PCF's dedicated Veterans Affairs (VA) network of Centers of Excellence, including the Robert Frederick Smith Center of Precision Oncology Excellence at the VA Chicago.

The test is part of a larger PCF research initiative to improve the understanding of genetic risk in African American men and transform early detection and imaging strategies, risk management, and clinical-decision making by men at highest lifetime risk of prostate cancer. The research, led by Dr. Chris Haiman, ScD, a genetic epidemiologist at the University of Southern California, and international colleagues is aimed at accelerating the reduction of prostate cancer disparities for African American men by 2030.

Prostate cancer affects more than three million men in the U.S., with one in nine men diagnosed with prostate cancer in his lifetime. African American men are disproportionately impacted. They are 76 percent more likely to develop prostate cancer than Caucasian men, and are more than twice as likely to die from the disease compared to men of other ethnicities. Earlier, strategic detection is a key step in finding a cure and ending the health disparity faced by men of African descent.

"Reducing prostate cancer disparities is at the heart of PCF's mission to end prostate cancer once and for all. This test will democratize access to genetic testing and machine learning algorithms for prostate cancer risk. It will have a historical impact in public health, racial health justice, and cancer research. We are profoundly grateful to partner with Robert to close the health equity gap and spare more men the hardship of a late-stage prostate cancer diagnosis," said Dr. Jonathan W. Simons, CEO of PCF.

Most genomic studies of prostate cancer have focused on men of European ancestry, and there is a vital need for additional resources to develop and optimize a polygenic risk score in those disproportionately affected. This new Smith-PCF initiative will increase the representation of African American men in the study and vastly expand the research to allow Dr. Haiman to quadruple the size of his study cohort, a key step to providing worldwide access to the Smith Polygenic Risk Test as soon as possible.

About the Prostate Cancer FoundationThe Prostate Cancer Foundation (PCF) is the world's leading philanthropic organization dedicated to funding life-saving cancer research. Founded in 1993 by Mike Milken, PCF has raised more than $830 million in support of cutting-edge research by more than 2,200 research projects at 220 leading cancer centers in 22 countries around the world. Thanks in part to PCF's commitment to ending death and suffering from prostate cancer, the death rate is down by 52% and countless more men are alive today as a result. The Prostate Cancer Foundation research now impacts more than 70 forms of human cancer by focusing on immunotherapy, the microbiome, and food as medicine. Learn more at http://www.pcf.org.

Connect with PCF: Facebook | Twitter | LinkedIn

MEDIA CONTACT: Donald Wilson for the Prostate Cancer Foundation(310) 428-4730press@pcf.org

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Bitcoin Surges to $9.3K for First Time in a Week Is it a Fakeout? – Cointelegraph

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The price of Bitcoin (BTC), the top-ranked cryptocurrency by market capitalization, surged past $9,300 on July 21 for the first time in over a week. Following a low-volatility range, traders are seemingly turning cautiously bullish in the near-term.

Since late June, Bitcoin has been stuck in a relatively tight range between $9,000 and $9,250. It struggled to see a major price movement causing the volume to slump. After a quick upsurge from $9,150 to over $9,300, traders predict that a volatility spike is imminent.

The price surge coincided with a U.S. stock market rally, driven by a new round of stimulus. U.S. Treasury Secretary Steven Mnuchin said a $1 trillion stimulus deal is in the works.

The performance of top cryptocurrencies in the last 24 hours. Source: Coin360.io

Some traders say a break to the upside is likely, but declining volume is concerning

Several technical analysts say that the recent rally of Bitcoin could lead to a bigger rally in the short-term. Bitcoin faces key resistance levels at $9,550 and $9,800, and BTC saw steep rejections from both areas previously.

Crypto trader Philip Swift pinpointed that the two-month range of Bitcoin since May occurred above the 200-day moving average (MA), indicating that the uptrend of Bitcoin could be intact.

The trader said:

Promising little pump this morning. I suspect this will be the week we finally break out of the dreaded range.

The range of Bitcoin since May was above the 200-day moving average. Source: Philip Swift

Arthur Hayes, the CEO of BitMEX, also expressed his excitement towards Bitcoins minor rally. Hayes said BTC awoke from thee slumber, referring to its low volatility in the past week.

Arthur Hayes tweets about Bitcoins first breakout in over a week. Source: Arthur Hayes Twitter

Michael van de Poppe, a full-time trader at the Amsterdam Stock Exchange, hinted that Bitcoin is cautiously optimistic. He said:

We've got our breaker and bullish move here, as the market is showing strength. I don't think $BTC will accelerate, as it's just still hopping around.

Binance Futures data shows that the majority of traders on the platform are majority long on Bitcoin and Ether (ETH).

Data from Datamish suggests there are substantially more long contracts than shorts in the entire Bitcoin futures market as well. Longs amount to 22,496 BTC, worth around $209 million. In contrast, shorts stand at a mere 5,555 BTC, worth less than $52 million.

Although the 200-day MA technically suggests an uptrend, historical data shows it could easily break down below it. Previous peaks witnessed in July 2019 and February 2020 both rejected above the 200-day MA.

Data from Santiment also shows that the volume of Bitcoin has declined in recent weeks. When an uptrend coincides with declining volume, it could hint at a fakeout.

Researchers at Santiment wrote:

BTC's overall trading volume continues to slide, and with so much focus on altcoins currently, Bitcoin's trading volume hitting a daily value of $12.25B Saturday marked the lowest single-day value since October 5, 2019 (a 9.5-month low).

The trading volume of Bitcoin continues to decline. Source: Santiment

The market remains mixed as BTC grinds through the new week. Technical indicators and macro fundamental factors, like Bitcoins hash rate and low exchange inflows, suggest an uptrend. But the low volume of BTC throughout the past two months remains a variable.

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Bitcoin Surges to $9.3K for First Time in a Week Is it a Fakeout? - Cointelegraph

Bitcoin And Other Crypto-Assets Excluded From Central Bank Experiments – Forbes

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A picture taken on January 15, 2020 shows the facade of the Banque de France building in Paris. The ... [+] bank is working with the European Central Bank to re-imagine how new technologies can change the way money works.

The central bank of France is on the verge of conducting a series of sweeping experiments whose lessons could be used to change the way money works. Cryptocurrency wont be included. In a statement from the Banque de France, the nations central bank, which works together with the European Central Bank to determine the monetary policy of the continent, the institution today released the names of eight participants in the experiments and the scope of the work.

Participants are consulting giant Accenture ACN , settlement giant Euroclear, the HSBC bank, French firm, Iznes, etheruem platform LiquidShare, little-known startup, ProsperUS, crypto bank Seba, and Forge, Societe Generales digital capital markets spinoff. The broad parameters of the experiments include everything from testing regulation using digital currency to improve cross-border payments, an analysis of how a central bank digital currency should be made available, and importantly, to explore new methods of exchanging financial instruments (excluding crypto-assets) for central bank money.

The statement from one of the words leading central banks shows how the vaunted institutions are scrambling to learn the best that cryptocurrency, and its underlying blockchain technology have to offer, but only within limits. Neither blockchainthe shared ledger that lets bitcoin existnor the more sanitized word to describe the larger group of technologiesdistributed ledger technology were mentioned by name in the statement. As such, the work also helps define the limits of what any actual adoption of the technology might look like.

The strong mobilization around this call for candidates testifies to the interest of the actors of finance and technology for this approach aiming to explore the potential contributions of a digital money issued by the central bank to improve the functioning of financial markets, in particular interbank regulations, according to a Google GOOGL translation of the statement. A representative of the Banque de France declined to share any additional context.

Over the coming days, the Banque de France will begin conducting experiments with each of the candidates, according to the statement, with some of the projects expected to take as long as multiple months. Candidates were asked to respond to the banks call for applications for CBDC experiments by May 15. The experiments could have far-reaching implications to the decision-making processes for the central bank, which in addition to helping define Europes monetary policy and implement it in France, regulates Frances banks and insurance companies and ensures risk management.

Beyond the confines of France though, lessons learned from the central bank digital currency experiments will be contributed to the international work being led by the Eurosystem, the monetary authority of the European Union. Earlier this month, the bank joined Germanys central bank, the Deutsche Bundesbank, and the European Central Bank in co-hosting a new innovation center in Europe within the framework of the Innovation Hub of the Bank for International Settlements.

In May, European Central Bank executive board member, Yves Mersch, confirmed in a speech at industry conference Consensus, that the European Central Bank was one of at least 66 central banks exploring how lessons learned from blockchain could change the very fabric of what we consider money.

For example, Chinas central bank, the Peoples Bank of China, has taken a giant first-mover advantage in the space, starting its CBDC experiments years ago, and currently testing a working implementation. If successful, one side-effect of CBDCs could be borderless transactions, possibly giving people the choice to store Chinese Renminbi in addition to, or instead of dollars, as a global reserve currency,

Based on what we know of the nearly pervasive experiments around the world looking into the nature of CBDCs, some of the other possible changes to the way money works could include giving citizens accounts at central banks, allowing them to occasionally bypass commercial banks and receive direct access to stimulus checks and more. Another possible, but controversial side-effect of central bank digital currencies could enable online payments while maintaining the privacy citizens have historically enjoyed with cash.

Skeptics of the CBDC concept argue that so long as central banks continue to have the authority to print or issue nearly unlimited amounts of the currency the underlying problems of inflation will continue to drive people to more distributed, deflationary alternatives such as bitcoin, which has a set amount. Other skeptics point to the unlikelihood that central banks will ever actually allow citizens the same privacy they have in the real world, online, and could use the technology as a way to track their own citizens spending habits.

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Bitcoin And Other Crypto-Assets Excluded From Central Bank Experiments - Forbes

Survey: 60% of Bitcoin Investors Will Die With Their BTC If Price Stays Below $10,000 | News – Bitcoin News

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About 60% of bitcoin investors are willing to hold their coins until they die if the price fails to breach the key $10,000 level.

Now thats according to a Twitter poll by Peter Schiff. The gold-bug asked bitcoin hodlers: How much longer does the price of #Bitcoin have to stay below $10,000 before you will throw in the towel and sell?

With about 7 hours left for the poll to expire (at Press time), nearly 26,000 people have responded. At least 58% said they will hold the top crypto for as long as it matters, even if that means taking it to their graves.

Another 15%, or 3,900 people, said it will be a year before they decide to sell. Around 14% of the respondents said they will hodl for another three years and 13% for the next decade before opting to exit their positions.

It seems unfathomable that anyone would willingly die holding onto dear bitcoin because the price stagnated below the psychological $10,000 threshold. Rather, it is more plausible that Schiffs poll result illustrates the faith with which investors hold in regard to BTC, even as the price struggles.

Bitcoin bulls have struggled to gain momentum since the Bitcoin network scheduled supply cut of May 11 the event looked upon by many as a potential turning point for a bullish breakout. Previous such events have led to a major rally. Twice the price of BTC broke above $10,000 and twice it was rejected, at one point to as low as $8,600.

Today, BTC is trading at $9,248, down 0.9% over the last 24 hours, according to markets.Bitcoin.com data. The immediate target is to break above $10,000 and stay there. Analysts consider this level as important for sparking BTCs long-awaited price rally.

According to Chainlysis, a crypto data analytics company, most BTC investors do not want sell their assets because they regard it as digital gold. Of the 18.6 million BTC mined as of June 2020, around 60% is held by entities either people or businesses that have never sold more than 25% of the bitcoin theyve ever received.

The firm says only 3.5 million bitcoin or 19% of total circulating supply is actively traded throughout the world. Another 20% of the existing bitcoin supply has not moved from its current set of addresses in five years or longer what Chainalysis called lost bitcoin.

What do you think about the result of Peter Schiffs poll? Let us know in the comments section below.

Image Credits: Shutterstock, Pixabay, Wiki Commons

Disclaimer: This article is for informational purposes only. It is not a direct offer or solicitation of an offer to buy or sell, or a recommendation or endorsement of any products, services, or companies. Bitcoin.com does not provide investment, tax, legal, or accounting advice. Neither the company nor the author is responsible, directly or indirectly, for any damage or loss caused or alleged to be caused by or in connection with the use of or reliance on any content, goods or services mentioned in this article.

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Survey: 60% of Bitcoin Investors Will Die With Their BTC If Price Stays Below $10,000 | News - Bitcoin News