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 -...

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

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.

Story continues

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

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...

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

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

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

Scientists have identified a new type of cell that appears in the bloodstream of rheumatoid arthritis patients shortly before joint inflammation flares.

A never-before-seen cell type could forewarn of rheumatoid arthritis symptoms.

The cells, dubbed PRIME cells, accumulate in the blood during the week prior to disease flare-ups, Howard Hughes Medical Institute Investigator Robert Darnell's team reports July 15, 2020, in the New England Journal of Medicine. The findings could lead to better prediction of when severe pain and swelling, called flares will occur, as well as provide new avenues for treatment.

PRIME cells are one thing you might want to target to arrest the flare before it happens, Darnell says. Thats the ideal of medical science to know enough about a disease that you can put your finger on whats about to make someone sick.

Rheumatoid arthritis is a disease of the immune system that causes inflammation in the joints, especially around the hands and feet. It can be debilitating and frequently strikes people in their 30s or 40s. The symptoms come in waves, with stretches of relative quiet interspersed with painful flares. Current therapeutics, chiefly steroids, can treat these symptoms, but theres no cure.

To study this sort of disease, where symptoms vary dramatically from week to week, its critical to track changes in the body over an extended time. But its hard for patients to trek to a clinic for frequent testing. So Darnell, a neuro-oncologist at the Rockefeller University, and his colleagues developed an at-home blood collection system. Patients with rheumatoid arthritis did simple finger sticks and sent their blood to his lab. Each participant also kept a record of symptoms to identify when flares occurred.

PRIME cells are one thing you might want to target to arrest the flare before it happens.

Robert Darnell, HHMI Investigator at The Rockefeller University

Armed with these records, the researchers tested the blood samples, looking for molecular changes preceding the onset of symptoms. By analyzing the RNA of cells in the bloodstream, Darnells team could identify which types of cells were present during symptom-free times and in the weeks preceding a flare.

In samples collected two weeks prior to a flare, researchers saw an increase in immune cells called B cells. Thats not surprising, Darnell says researchers already knew these cells attacked patients joints in rheumatoid arthritis.

But in samples collected one week before a flare, his team noticed something odd. They saw an increase in RNA that didnt match the genetic signature of any known type of blood or immune cell. That got us thinking there was something fishy going on, says study coauthor Dana Orange, a rheumatologist at Rockefeller. The RNA signature instead resembled that of bone, cartilage, or muscle cells cells not typically found in the blood.

Darnells team called the newfound cell type a PRIME cell, for pre-inflammation mesenchymal cell. (Mesenchymal cells are a type of stem cell that can develop into bone or cartilage.) In the patients, PRIME cells accumulated in the bloodstream a week before the flare but disappeared during the flare. This observation, combined with previous work from another lab in mice, suggests a possible role for PRIME cells in rheumatoid arthritis flares, Darnell says.

One of the teams next steps is to test in more patients whether the presence of these cells can predict a flare, Darnell says. The researchers are still recruiting patients for this study; currently the teams blood collection system is only available for use in research. Darnell also wants to study PRIME cells molecular characteristics. If the cells do indeed take part in causing flares, he says, understanding the unique aspects of PRIME cells might enable us to target them with a drug and get rid of them.

###

Citation

Dana E. Orange et al. RNA Identification of PRIME Cells Predicting Rheumatoid Arthritis Flares, New England Journal of Medicine. Published online July 15, 2020. doi: 10.1056/NEJMoa2004114

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Blood Test Could Reveal When Rheumatoid Arthritis Will Strike - Howard Hughes Medical Institute

In the simplest terms, precision medicine is the right test for the right patient at the right time. But the practice of precision medicine is not so simple.A physician must choose from an array of complicated tests that are appropriate for a diagnosis and the creation of a treatment plan for their patient in a timely manner.Thats a lot of separate data and time points to manage for one patient, so how do we connect these individual patients together with their own personalized sets of tests and outcomes to improve population health?

We can look to breast cancer, where precision medicine has played out for the past decade and has paved the way for standard biomarker testing guidelines, risk assessment and screening protocols, as well as treatment plans that are now widely recognized and used.This clinical application of precision medicine has resulted in the avoidance of unnecessary and ineffective testing and treatment, rapid identification of targeted treatments with good responses in similar populations, and the proactive screening of families at high risk for breast cancers.

Hormone receptor and HER2 testing has become routine for primary invasive carcinomas, and recurrent and metastatic breast tumors.Knowing the estrogen receptor, progesterone receptor, and HER2 test results within a few days of a biopsy allows an oncologist to determine if a patient might benefit from hormone or anti-HER2 therapy. For patients who did not have a hormone receptor or HER2-positive test result or who did not respond to a standard one size fits all treatment plan, comprehensive tumor profiling can provide a personalized set of targeted therapy options that are uniquely matched to the tumor mutations.Additionally, women with early stage, lymph nodenegative breast cancer can undergo a 21-gene profiling test to determine if they need chemotherapy, once again getting the right treatment for the patient.

Approximately 5% to 10% of breast cancers can be attributed to an increased risk from inheriting a pathogenic gene mutation in BRCA1 or BRCA2.Genetic counselors choose an appropriate test for each family member of the affected, and then follow-up with regular monitoring plans for those with inherited pathogenic mutations.Catching a disease early requires the right test at the right time, which is why large-scale population screening, such as BRCA testing, is recommended at earlier ages for high-risk families and populations.

The big picture comes together in precision medicine when clinical outcomes are linked to the biomarker testing choices, disease screening methods, and targeted treatment plans for large groups of patients as part of clinical trials and translational research.With the analysis of big data comes new and updated biomarker testing recommendations, patient care models, disease screening protocols, and treatment guidelines by professional medical societies.These guidelines reflect the most recent technological advances in laboratory science from the bench to the bedside, and this information is continually evolving with new studies leading to better survival rates, increased detection, and improved treatments for future patients.

Like all aspects of healthcare, the emergence of coronavirus disease 2019 (COVID-19) has impacted many different areas of precision medicine. The pandemic has certainly hindered surgeries, and therefore, testing on biopsy tissue. Consequently, oncologists are expecting a wave of more advanced cancers at diagnosis due to delayed biopsies and other issues, such as postponed preventative screening and medical appointments that were put off because patients with suspicious symptoms were afraid to see physicians during the COVID crisis. Providers have tried to ensure the safest environment possible for patients by adjusting how they operate. For instance, some commercial laboratory vendors that offer liquid biopsy testing have implemented mobile phlebotomy to do the necessary blood draw at the patients house rather than in the clinic, but tissue is still needed for the initial diagnosis. Undoubtedly, there will be ramifications from these delays, as the earlier cancer is detected, the better the outcome.

Once the impact of COVID-19 begins to minimize and activities settle into a new normal, efforts to expand precision medicine across many diseases will resume. As more physicians learn the lessons of how breast cancer incorporated biomarker testing, disease screening, and targeted therapies into standard practices, support for this promising approach to personalized care will continue to grow for the betterment of individuals, families, and populations.

Jen Buhay, PhD, is the precision medicine clinical program manager for The US Oncology Network, leading biomarker testing, education, and operational efforts to support personalized patient care for oncology.Previously, she led precision medicine initiatives in a community hospital setting and worked as a laboratory scientist for commercial and academic molecular diagnostic laboratories.Dr Buhay holds a PhD in Integrative Biology (molecular genetics and computational biology) from Brigham Young University, an MS in Biology from Eastern Kentucky University, and a BS in Animal Behavior from Juniata College.She is board-certified as a molecular biologist through the American Society for Clinical Pathology.

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Precision Medicine Will Drive New Standards of Care in the PostCOVID-19 World - Targeted Oncology

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GlobalGenetic Modification Market Report 2020 Sales Forecast to Grow Negatively in Western Regio post COVID 19 Impact Analysis Updated Edition Top...

What is this enemy?

Seven months after the first patients were hospitalized in China battling an infection doctors had never seen before, the world's scientists and citizens have reached an unsettling crossroads.

Countless hours of treatment and research, trial and error now make it possible to take much closer measure of the new coronavirus and the lethal disease it has unleashed. But to take advantage of that intelligence, we must confront our persistent vulnerability: The virus leaves no choice.

"It's like we're in a battle with something that we can't see, that we don't know, and we don't know where it's coming from," said Vivian Castro, a nurse supervisor at St. Joseph's Medical Center in Yonkers, just north of New York City, which struggled with its caseload this spring.

Castro had treated scores of infected patients before she, too, was hospitalized for the virus in April, then spent two weeks in home quarantine. As soon as she returned to the emergency room for her first shift, she rushed to comfort yet another casualtya man swallowing the few words he could muster between gasps for air.

"It just came back, that fear," she said. "I just wanted to tell him not to give up."

The coronavirus is invisible, but seemingly everywhere. It requires close contact to spread, but it has reached around the globe faster than any pandemic in history.

COVID-19 was not even on the world's radar in November. But it has caused economic upheaval echoing the Great Depression, while claiming more than 580,000 lives. In the U.S. alone, the virus has already killed more Americans than died fighting in World War I.

Even those figures don't capture the pandemic's full sweep. Nine of every 10 students worldwide shut out of their schools at one point. More than 7 million flights grounded. Countless moments of celebration and sorrowweddings and graduations, baby showers and funeralsput off, reconfigured or abandoned because of worries about safety.

In short, the coronavirus has rescripted nearly every moment of daily life. And fighting itwhether by searching for a vaccine or seeking to protect familytakes knowing the enemy. It's the essential first step in what could be an extended quest for some version of normalcy.

"There's light at the end of tunnel, but it's a very, very long tunnel," said Dr. Irwin Redlener, director of the National Center for Disaster Preparedness at Columbia University.

"There's a lot we don't know. But I think it's absolutely certain we're going to be adapting to a new way of life. That's the reality."

The new coronavirus is roughly 1,000 times narrower than a human hair. But scrutinized through an electron scope, it is clear this enemy is well-armed.

Coronaviruses, including the newest one, are named for the spikes that cover their outer surface like a crown, or corona in Latin. Using those club-shaped spikes, the virus latches on to the outer wall of a human cell, invades it and replicates, creating viruses to hijack more cells.

Find a way to block or bind the spikes and you can stop the virus.

Once inside a human cell, the virus' RNA, or genetic code, commandeers its machinery, providing instructions to make thousands of virus copies.

But the coronavirus has a weakness: an outer membrane that can be destroyed by ordinary soap. That neutralizes the virus, which is why health experts emphasize the need to wash hands.

Like organisms, viruses evolve, searching for traits that will ensure survival, said Charles Marshall, a professor of paleontology at the University of California and self-described "deep time evolutionary biologist."

"Coronaviruses fit into the standard evolutionary paradigm extremely well, which is if you've had some innovation, you get into some new environment ... you get into a human and you do well, you're going to proliferate," Marshall said.

There are hundreds of coronaviruses, but just seven known to infect people. Four are responsible for some common colds. But in 2002, a virus called SARS, for severe acute respiratory syndrome, spread from China to sicken about 8,000 people worldwide, killing more than 700. Another coronavirus called Middle Eastern respiratory syndrome, or MERS identified in 2012 spread to humans through camels.

The new coronavirus, though, has captivated scientists' attention unlike any in decades.

When researcher Thomas Friedrich logged on to his computer at the University of Wisconsin-Madison after a meeting in January, he found colleagues had been frantically posting messages to one another about the new virus.

"People were getting increasingly excited and beginning to brainstorm ideas," said Friedrich, who has spent years studying other infectious diseases.

Now much of Friedrich's lab is focused on the coronavirus, studying its spread in Wisconsin, and collaborating with scientists around the world examining the disease's behavior in monkeys.

Even early on it was clear this virus posed a major threat, he said. Human immune systems had never encountered it. And unlike Zika, whose spread can be controlled by targeting mosquitoes, or AIDS, which most often requires sexual contact, the new virus is readily transmitted through droplets in the air.

"It had all the hallmarks, to me, of a potential pandemic," Friedrich said. "Basically, everyone in the world is susceptible."

The new virus has breached borders and claimed victims with stealth and speed that make it difficult to track.

Scientists are fairly certain the disease originated in bats, which harbor many coronaviruses. To get to humans, it may have been passed through another animal, possibly consumed for meat. By late January, when Chinese authorities walled off the city of Wuhan, where the disease was first diagnosed, it was too late to stop the spread.

The most severe pandemic in recent history, the "Spanish flu" of 1918, was spread by infected soldiers dispatched to fight World War I. But aboard ships, it took weeks for the troops and the disease to cross oceans.

Now, with more than 100,000 commercial flights a day ferrying tourists, business travelers and students around the globe, the new virus spread rapidly and virtually invisibly, said medical historian Mark Honigsbaum, author of "The Pandemic Century: One Hundred Years of Panic, Hysteria and Hubris."

"By the time we woke up to the outbreak in Italy, it had been there for weeks if not months," he said.

Soon after the first case in Wuhan, Chinese tourists with the virus traveled to France. But doctors there reported recently that a fishmonger contracted the disease even earlier than that, from an unknown source. On January 21, the first confirmed U.S. case was reported in Washington state, in a man who had traveled to Asia.

"It's one person coming in from China and we have it under control. It's going to be just fine," President Donald Trump said at the time. Ten days later, he blocked entry to most travelers from China.

But genetic analysis of samples taken from New York patients showed most of the virus present arrived from Europe instead, and took root in Februarywell before anyone thought about quarantining after a trip to Madrid, London or Paris.

Since February, when Dr. Daniel Griffin began treating patients suspected of having COVID-19, he's cared for more than 1,000 people with the disease, first noted for attacking the lungs. But the infection certainly does not stop there.

"I am actually shocked," said Griffin, a specialist in infectious diseases at New York's Columbia University Medical Center. "This virus seems to leave nothing untouched."

Scientists are getting a handle on the many ways the disease affects the body, but it's a scramble.

The lungs are, indeed, ground zero. Many patients find themselves gasping for breath, unable to say more than a word or two.

Even after five days in the hospital, Vivian Castro, the nurse who became infected, said she returned home struggling for air.

"I climbed two flights of stairs to my room and I felt like I was going to die," she said.

The reason why becomes clear in autopsies of those who have died, some with lungs that weigh far more than usual. Under a microscope, evidence of the virus' destruction is even more striking.

When Dr. Sanjay Mukhopadhyay examined autopsy samples from a 77-year-old Oklahoma man, he noted changes to the microscopic sacs in the patient's lungs. In a healthy lung, oxygen passes through the thin walls of those sacs into the bloodstream. But in the Oklahoma patient, the virus had turned the sac walls so thick with debris that oxygen was blocked.

The thickened walls "were everywhere," preventing the lungs from sustaining the rest of the body, said Mukhopadhyay, of Ohio's Cleveland Clinic.

Autopsies reveal "what the virus is actually doing" inside patient's bodies, said Dr. Desiree Marshall, a pathologist at the University of Washington who recently examined the heart of a Seattle man who died from disease.

"Each autopsy has the chance to tell us something new," she said. And those insights from the bodies of the dead could lead to more effective treatment of the living.

The coronavirus, though, keeps raising fresh questions. It left the hearts of two men in their 40s, recently treated by Griffin, flaccid and unable to pump enough blood. Some younger people have arrived in emergency rooms suffering strokes caused by blood clotting, another calling card.

Kidneys and livers fail in some patients and blood clots put limbs at risk of amputation. Some patients hallucinate or have trouble maintaining balance. Some get a treatable paralysis in arms or legs. Many have diarrhea, but often don't mention it until Griffin asks.

Their explanation? "That's the least of my problems when I can't breathe."

Initially, doctors often put patients on ventilators if their blood oxygen levels dropped. But death rates were so high they now try other strategies first, like turning patients on their stomachs, which can help them breathe. The truth is that hospital workers are learning as they go, sometimes painfully.

"Every patient that I see, I think that could've been me," said Dr. Stuart Moser, a cardiologist hospitalized in New York in March after he was infected. He recalls fearing that he might be put on a ventilator and wondering if he'd ever see his family again. Now, back at work, he said much of what he and his colleagues have learned about the virus' myriad effects enables them only to treat patients' symptoms.

"It's difficult because they have so many problems and there are so many patients," Moser said, "and you just want to do the right thinggive people the best chance to get better."

In recent weeks, researchers have recruited 3,000 patients from around the world in a bid to solve a puzzling anomaly. Why does the coronavirus ravage some previously healthy patients, while leaving others relatively unscathed?

The project, called the COVID Human Genetic Effort, focuses on each person's unique genetic makeup to seek explanations for why some got sick while others stay healthy. It's one of several projects looking for genetic causes of susceptibility, including recent work by other labs suggesting a link between blood type and risk of serious illness.

"Step one is understanding and step two is fixing. There is no other way," said one of the project's leaders, Jean-Laurent Casanova, of The Rockefeller University in New York. He is paid by the Howard Hughes Medical Institute, which also helps fund The Associated Press Health and Science Department.

His project focuses on people 50 or younger who had no health problems before the coronavirus put them in intensive care. But the question of why the disease affects people so differently has broader implications.

It's not clear, for example, why the disease has had such a limited impact on children, compared to other age groups. People older than 65 are well over 100 times more likely to be hospitalized for the virus than people under 18. But so far, there's no explanation why.

Do children resist infection for some reason? Or is it that, even when infected, they are less likely to develop symptoms? If so, what does that mean about their chances for passing the infection along to others, like their grandparents?

These aren't just academic questions. Answers will help in assessing the risks of reopening schools. And they could eventually lead to ways to help make older people resistant to the disease.

In largely sparing children, the pandemic virus echoes the bugs that caused SARS and MERS, said Dr. Sonja Rasmussen, a professor of pediatrics and epidemiology at the University of Florida.

Scientists wonder if children might have some key difference in their cells, such as fewer of the specialized proteins that the coronavirus latch onto. Or maybe their immune systems react differently than in adults.

While the virus has mostly bypassed children, researchers have recently been troubled by a serious, albeit uncommon, condition in some young patients, that can cause inflammation in hearts, kidneys, lungs and other organs. Most patients recovered, but the potential for long-term damage remains uncertain.

"This is what happens with a new virus," Rasmussen said. "There's a lot we don't know about it. We're on that steep learning curve.''

With states and countries reopening in the face of an ongoing pandemic, it's even more crucial to find solutions. At least the last few months have spotlighted the most critical questions.

Can people who have been infected with the disease get it again?

Dr. Anthony Fauci, the U.S. government's top infectious disease expert, has said that having the disease once should confer some degree of immunity. But it's not clear how much or for how long, or what levels or types of antibodies people must have to protect them against future illness.

If some people harbor the virus without symptoms, how can we block transmission?

The reality is that many infected people will never feel symptoms or get sick. That means temperature checks and other strategies based on symptoms won't be enough to stop it. Instead, many experts believe, widespread testing is needed to find silent carriers, isolate them until they are no longer contagious, and track down those they may have infected. Masks and distancing can help prevent infection and slow the spread of the virus.

Will researchers find medicines that can be used to treat the disease?

Hundreds of studies are under way, testing existing medicines and experimental ones. So far, only onea common steroid called dexamethasonehas been shown to increase survival. An antiviral medicine, remdesivir, has been shown to shorten recovery time. Two othersthe malaria drugs chloroquine and hydroxychloroquinehave not proven safe or effective for treating COVID-19 in large-scale trials, but some studies are still testing them to see if they might help prevent infection or illness.

How long will it take to find a vaccine?

Scientists in more than 150 labs around the world are pursuing a vaccine and nearly two dozen candidates are in various stages of testing. But there's no guarantee any will pan out. Finding out if any offer true protection will require testing thousands of people in places where the virus is spreading widely. Some huge studies are expected to begin this month.

"It's almost the Manhattan Project of today, where an enormous amount of resources are being devoted to this," said Rene Najera, an epidemiologist at Johns Hopkins University and the editor of a vaccine history website run by The College of Physicians of Philadelphia.

In the U.S., the goal is to have 300 million doses of potential vaccines by January. But any that fail tests will have to be thrown out. The World Health Organization has called for equitable sharing of any eventual vaccine between rich and poor countries, but how that will happen is far from clear.

It's also uncertain how useful any vaccine will be if a sizable number of people, their skepticism fed by misinformation, refuse to be inoculated.

Even an effective vaccine will not address the likelihood that, given the large number of coronaviruses and increasing contact between people and the animals harboring them, the world is very likely to face other pandemics, said Honigsbaum, the medical historian.

That means uncertainty will linger as a hallmark of the new normal.

The knowledge gained about the coronavirus could prove invaluable in defusing that doubt and, eventually, in defeating the enemy. The real uncertainty, Redlener said, is whether people will use the lessons learned to protect themselves from the virusor downplay the threat at their peril.

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Profile of a killer: Unraveling the deadly new coronavirus - ModernHealthcare.com

A recent stem cell study has shown that SARS-CoV-2, the novel coronavirus, can infect heart cells via the same receptor present in the lungs. This may be responsible for the cardiac complications associated with COVID-19.

Experts initially thought that COVID-19 was a respiratory disease, with symptoms including cough, shortness of breath, and pneumonia. However, more recent evidence into COVID-19 shows that the disease can also cause neurological and cardiac symptoms.

Physicians have reported changes to the circulatory system in people with COVID-19, sometimes leading to blood clots, as well as cardiac complications, such as changes to the heart rhythm, damage to heart tissue, and heart attacks.

Although there is widespread agreement that COVID-19 is a risk to the heart, whether these symptoms are due to the virus directly or a consequence of other disease processes, such as inflammation, has been unclear.

Stay informed with live updates on the current COVID-19 outbreak and visit our coronavirus hub for more advice on prevention and treatment.

In a new study appearing in the journal Cell Reports Medicine, scientists have helped resolve this mystery by showing that SARS-CoV-2 can infect heart cells and change their function.

Their findings, from experiments in human stem cells, suggest that the cardiac symptoms of COVID-19 may be the direct result of the infection of heart tissue.

The scientists used a type of stem cell called induced pluripotent stem cells (iPSCs) to generate heart cells.

Scientists can create iPSCs from a persons skin cells and then reprogram them to become any cell type in the body. They provide a useful tool for research into human disease and a way to test new treatments.

In this study, the team programmed the iPSCs to become heart cells and later incubated them with SARS-CoV-2. Using microscopes and genetic sequencing techniques, the researchers found that SARS-CoV-2 could directly infect the heart cells.

They also showed that the virus can rapidly divide inside heart cells, which caused changes to the hearts ability to beat after a period of under 3 days.

We not only uncovered that these stem cell-derived heart cells are susceptible to infection by [the] novel coronavirus, but that the virus can also quickly divide within the heart muscle cells, explains first study author Dr. Arun Sharma, a research fellow at the Regenerative Medicine Institute of Cedars-Sinai Medical Center in Los Angeles, CA.

Additional experiments focused on the different genes expressed by heart cells before and after the virus infected them. These studies showed activation of the innate immune response and antiviral clearance pathways to help fight the virus.

However, how does the virus get into the heart in the first place? The researchers suggest that one way in which it gains access may be by using angiotensin-converting enzyme 2 (ACE2). This is the same receptor the virus uses to infect cells in the lungs.

Importantly, studies have shown that treatment with an ACE2 antibody can help stop SARS-CoV-2 from replicating and save cells in the heart.

By blocking the ACE2 protein with an antibody, the virus is not as easily able to bind to the ACE2 protein, and thus cannot easily enter the cell. This not only helps us understand the mechanisms of how this virus functions, but also suggests therapeutic approaches that could be used as a potential treatment for SARS-CoV-2 infection.

Dr. Arun Sharma

The researchers suggest that scientists could use stem cell-derived heart cells to screen new drugs and find compounds able to stop the infection of heart cells.

This key experimental system could be useful to understand the differences in disease processes of related coronaviral pathogens SARS and MERS, adds study author Dr. Vaithilingaraja Arumugaswami, an associate professor at the University of California, Los Angeles.

There are some limitations to this approach, however. These include the fact that stem cell-derived heart cells are not exactly the same as the real thing.

The researchers also studied the cells in a dish, an isolated system lacking the immune interactions that would occur in the human body.

Nevertheless, the experiments clearly showed that the cells became infected with SARS-CoV-2, which is in line with some clinical data showing the virus in the hearts of people who died from COVID-19.

For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here.

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COVID-19 could directly affect the heart - Medical News Today

Researchers at the University of Toronto have shown that an enzyme called RNA polymerase (Pol) II drives generation of the building blocks of ribosomes, the molecular machines that manufacture all proteins in cells based on the genetic code.

The discovery reveals a previously unknown function for the enzyme in the nucleolus, the site of ribosome manufacture inside of human cells, where the enzyme had not been seen before. Pol II is one of three RNA polymerases that together enable cells to transfer genetic information from DNA to RNA and then proteins.

Our study redefines the division of labour among the three main RNA polymerases, by identifying Pol II as a major factor in the control of nucleolar organizations underlying protein synthesis, said Karim Mekhail, a professor of laboratory medicine and pathobiology at U of T. It also provides a tool for other researchers to interrogate the function of certain nucleic acid structures more precisely across the genome.

The journal Nature published the results today.

Mekhail and his colleagues found that inside the nucleolus, Pol II enables the expression of ribosomal RNA genes a key step in the creation of ribosomes, essential molecular complexes that make proteins in all cells. Pol II, they showed, generates R-loops hybrid DNA-RNA structures that directly shield ribosomal RNA genes from molecular disruptors called sense intergenic non-coding RNAs (or sincRNAs).

Those disruptors are produced by Pol I in intergenic, non-protein-coding sequences of DNA between genes, and they become more active in various conditions: disruption of Pol II, under environmental stress, and in Ewing sarcoma.

Pol II puts the brakes on Pol I and prevents sincRNAs from sinking the nucleolus, said Mekhail, who holds the Canada Research Chair in Spatial Genome Organization. Thats how we united the name and action of the disruptors in our discussions of this work.

Mekhail and his team developed a new technology to test the function of R-loops at specific locations on chromosomes, which they dubbed the red laser system.

The existing tool in the field would obliterate R-loops across the whole genome, but we wanted to test the function of R-loops associated with a given genetic locus, said Mekhail. We were able to turn an old technology into a modern laser-guided missile, which we are still working to further improve.

Two U of T students were co-lead authors on the study Karan (Josh) Abraham and Negin Khosraviani and Mekhail said they made exceptional and complementary contributions to the research.

Abraham, an MD/PhD student, began work on the project in 2014.

I pursued this work having observed enrichment of Pol II at ribosomal DNA genes in the nucleolus, which was compelling, said Abraham, who will finish his medical training next year. Its incumbent upon every scientist to challenge existing models should the evidence support an alternate one.

A doctoral student who joined the lab in 2018, Khosraviani said teamwork and time management were critical.

We could not have completed this research without the help and dedication of our entire lab. Coordination with local and international collaborators was also essential.

Mekhails team worked with colleagues across U of T and affiliated hospitals on the study, and with international collaborators at the University of Texas at San Antonio and the University of Miami.

Next steps based on this research could include exploration of sincRNAs and nucleolar disorganization as biomarkers for various cancers, and whether tumours with those features respond to drugs that target intergenic Pol I or II.

COVID-19 has been devastating, but other diseases have not stopped, said Mekhail, who temporarily closed his physical lab space during the pandemic but has continued working with his team to analyze and publish results. For example, cancer is still rampant and affecting peoples lives. We have to do what we can and look forward to building on the progress weve made as soon as possible.

This research was supported by the Canadian Institutes of Health Research, Canada Research Chairs, U.S. National Institutes of Health, Ontario Ministry of Research and Innovation, Ontario Graduate Scholarship Program, and Natural Sciences and Engineering Research Council of Canada.

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U of T scientists uncover key process in the manufacture of ribosomes and proteins - News@UofT

Biotech company Moderna, one of many organizations developing a vaccine for COVID-19, published results from an early-stage test of its experimental mRNA vaccine in the New England Journal of Medicine July 14. Vanderbilt University Medical Center staff scientist and protein chemistry expert Sanjay Mishra explains what the results of the phase 1 trial mean.

They were testing for two things the proof of concept, and whether there are any side effects.

The results that just came out in the New England Journal of Medicine are interim. We have to be really clear about it.

This particular batch of results is from 45 adults between the ages of 18 and 55 who were not screened for infection [for COVID-19]. So we would call them healthy adults, although no serology or PCR (polymerase chain reaction) tests were done before the trial began.

They were given one of the three doses 25, 100 or 250 micrograms. More than half the participants had discomfort, like fatigue, chills, headaches, myalgia (muscle pain) and pain at the injection site. After 28 days, the exact same dose was given a second time. After the second dose, these events of discomfort were far more common. But in general, you can say there was nothing severe reported. And then on the 29th day, blood was drawn.

These blood samples were tested for their antibody response. They found that the antibody responses, as you would expect, were higher with the higher dose. They were slightly higher than what you would expect to see in patients who had been recovering from a coronavirus infection.

They tested these things in three different ways. One of these is where you are testing the quantity of antibodies made. Then they also tested the efficacy of these antibodies in the serum through two different methods. All in all, it does seem that there is binding and neutralization of the virus.

But the second batch of results, which is from the older patients, has still not been announced. So that would be coming farther down the line. After that, they hope to come up with the third batch of results, which will include the durability of immunity from both of these age groups in one batch.

[You need to understand the coronavirus pandemic, and we can help. Read The Conversations newsletter.]

The results are promising. At least they proved the concept. The results show that when you give this vaccine, the body makes antibodies. But we dont know whether those antibodies will lead to immunity in the body because all of the results that we have are observed outside the body [in blood samples].

And so that proof will come from a larger data set in the next stage. Then we would know whether the people who have received these vaccines are at least 50% less likely to become infected [to meet FDA guidelines for vaccine efficacy]. So they are good results, they are promising results, but they are pretty early in the game, so to speak.

Vaccines are meant to train the immune system to attack the disease-causing virus. In the case of SARS-CoV-2, there is a spike protein, or the S-protein, which is the flag that the immune system needs to recognize as the signature of the virus. So the goal of a vaccine is to train your immune system to recognize the S-protein, and then trigger the immune response. This S-protein is the standard in all coronaviruses, thats why theyre called coronaviruses, because the corona is the crown.

Traditionally, the vaccines involved either a weakened virus, or a preparation of the virus that would have contained (in this case) the spike protein. In the cleanest method you would have produced the spike protein in the lab and then you would have used that as the immunization candidate.

All those methods are time-consuming and require extensive quality control. And usually there is a lot of headache in scaling up from lab to production. Modernas vaccine and another candidate vaccine bypasses this process by using mRNA , or messenger RNA. It is genetic coding material which will help your body produce that protein. This way you dont have to deal with the production of the protein in the lab and risk creating an impure protein sample, which can be clinically difficult to standardize and then can be dangerous as well.

So in this case, what youre giving is not the protein or part of the virus, but a synthetic messenger RNA in a lipid droplet.

I feel cautiously optimistic. The study provides promising data on the safety and immunogenicity, or the ability to provoke an immune response. It is a good starting point for training the immunity of the body. But if I can paraphrase Robert Frost, we still have miles to go before we sleep.

Vaccine development is complex and theres a lot more work that needs to be done before this can become an actual marketable candidate.

This first batch of data is from the 18- to 55-year-old group. We do not know what the dosing would be for the older age group, which is the most vulnerable to COVID-19. As we age, we do not produce as many antibodies, which generally leads to poor vaccine response. So the question is: Will they have to go for a higher dose, which is usually the case in flu vaccines. The higher dosage, which is 250 micrograms, has led to somewhat more severe side effects in this study. So then how would that be balanced? It is still difficult to say.

There are 178 COVID-19 vaccines in various stages of development and 14 are leading to human trials, including from AstraZeneca and others. There are more potential candidates from Merck, Johnson & Johnson and others. There is a similar vaccine that is already being tested by Pfizer and BioNTech, and that has also shown positive results at the lower doses.

Continued here:

Video: An infectious disease expert explains the results from Moderna's latest vaccine trials - The Conversation US

Researchers are also examining how parts of the body, other than the brain, may play a role in disease development. Studies have looked into the effect various medications individuals are already taking, such as insulin, and theyre finding promising results.

A study looking at inhaled insulin showed some cognitive and amyloid-tau distribution improvements, but the type of inhaler seemed to make a big difference. Other approaches include studying gingivitis and other markers of inflammation, which Giordani says may help track the disease process earlier on as well.

Giordani also detailed the importance of understanding how the disease manifests in different groups of individuals. For example, the network of tau distribution (another Alzheimers disease pathological hallmark) in the brain of women is very different than men as the disease starts, he said, as Alzheimers disease has been found to affect more women than men.

Researchers have also been interested in studying the disease in the LGBTQ community. Older individuals with dementia from the [LGBTQ] community tend to live alone. They tend not to be partnered, they dont tend to have children who can take care of them, [and] so this can lead to very significant difficulty, Giordani explained.

Finally, Giordani described a new dementia classification called LATE, for individuals who develop dementia in their 80s and later. This is a disease that looks like Alzheimers disease, but its related to a different protein, he described, which in turn causes them to not respond well to Alzheimers treatment drugs.

No matter who you are, risk reduction may be the key to avoiding Alzheimers disease, Giordani claims. Researchers have discovered that adopting four to five low-risk factors or preventative habits lowers the risk significantly, even for individuals with a high genetic risk.

Exercise activities, social and emotional support, maintaining our general health, challenging our brain and watching our diet: these are five things we can all do to protect our brain, Giordani said.

The Michigan Alzheimers Disease Centers next virtual lecture is July 21, featuring Scott Roberts, Ph.D., discussing Can Alzheimers Disease be Prevented? Sign up on the centers website.

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Shifting from Treatment to Prevention in Alzheimer's Research - Michigan Medicine

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New Delhi: It is six months into the pandemic and scientists across the world have been publishing research findings nearly every day to improve understanding into the novel coronavirus.

Here are some of the latest research findings on Covid-19.

Scientists have identified a host of genetic factors that may influence susceptibility to Covid-19 and help guide personalised treatments for the infection.

While a majority of confirmed Covid-19 cases result in mild symptoms, the virus can unpredictably cause severe illness and death. Clinical observations suggest that genetic factors may influence disease susceptibility, but these factors remain largely unknown.

In the study, researchers have examined variations in DNA sequences in the ACE2 and TMPRSS2 genes, which produce enzymes that enable the virus to enter and infect human cells.

Looking at 81,000 human genomes from three genomic databases, they have identified over 60 variations 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 variants and Covid-19 susceptibility, and indicate that a systematic investigation of these variants among different populations could pave the way for precision medicine and personalised treatment strategies for Covid-19.

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Also read: Low-cost hepatitis C drugs reduce death rate in Covid-19 patients, researchers claim

Even mildly obese people are at greater risk of suffering from severe Covid-19 infection or even dying from it, according to a new study.

Published in the European Journal of Endocrinology, the findings showed that BMI over 30 was associated with a significantly higher risk of respiratory failure, admission to intensive care and death in Covid-19 patients, regardless of age, gender and other associated diseases.

Current guidelines in the UK and the US identify those having BMI above 40 to be at greater risk of Covid-19. However, researchers have said that these recommendations were based on smaller studies and limited data.

The new study analysed the outcomes of almost 500 patients hospitalised with Covid-19. They found that obesity was associated with a significantly higher risk of severity and death. The researchers also found that any BMI higher than 30 was associated with adverse outcomes.

A common drug heparin, already approved by the US Food and Drug Administration (FDA), can help block the SARS-CoV-2 virus from infecting human cells, a study has found.

Heparin, usually used as a blood thinner, is also available in non-anticoagulant varieties.

A study published in the Antiviral Research states that the drug can bind tightly with the surface spike protein, potentially blocking infection.

The drug may be administered using a nasal spray or nebulizer to lower the odds of infection. Similar strategies have already shown promise in curbing other viruses, including influenza A, Zika, and dengue, researchers have said.

Scientists have developed a surface coating which, when painted on common objects such as door knobs, light switches and shopping carts, can inactivate SARS-CoV-2 within an hour.

The team from Virginia Tech hopes to further improve this antiviral coating so that it inactivates the virus in minutes. Usually, the virus can survive on surfaces, especially metals, for several days.

When the coating is painted on glass or stainless steel, the amount of virus is reduced by 99.9 per cent in one hour, researchers have said in a study published in the ACS Applied Materials & Interfaces.

The researchers have said that the coating does not peel off even after being scraped with a razor blade. It also retains its ability to inactivate the virus after multiple rounds of being exposed to it.

Scientists have created a new non-invasive method to detect SARS-CoV-2 viruses from gargled solution.

The method, which is currently undergoing improvements and might be available as standard diagnostic tool for Covid-19 in the future, uses mass spectrometry to detect proteins of the virus.

Currently, the polymerase chain reaction (PCR) is the most prominent test method being used to detect whether someone suffers from Covid-19 infection. This tests looks for genetic material of the virus, and is unable to differentiate between live viruses and viral residues.

Mass spectrometry allows molecules to be precisely identified based on their mass and charge.

The procedure to obtain samples for the PCR tests is invasive, requiring paramedics to take swab samples from the back of the throat and nasal cavity.

For the new test, the virus can be detected from gargled samples. The test currently takes about 15 minutes. However it may take a few months to be completely ready.

Also read: Disruption in healthcare services due to Covid may increase HIV, TB deaths, says Lancet study

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Study identifies gene variations that increase susceptibility to Covid-19 - ThePrint

The future of healthcare just landed in Florida. This is a story about the ingenuity of Israeli technology and a partnership with the premier active adult community on planet earth. The combination is turning the central Florida heartland into a world-class medical destination and adding energy to the local economy.

People are living longer and as we age its normal to suffer from more and more ailments. That in turn affects quality of life and places an increasing burden on the healthcare ecosystem.

Why does it have to be that way?

Goldie Hawn, Academy Award winning actress and workout enthusiast, whos in her 70s said, There is no turning back the clock. So, the question in life becomes: What are you going to do while youre here?

Helping people get the most out of their life requires new tools and ways of thinking. Thats exactly whats happening at the Center for Advanced Healthcare at Brownwood in The Villages, located in Wildwood.

Were delivering strategic solutions for patient-centered care, designed to improve the aging process by increasing cognitive and physical performance said Dr. Shai Efrati, MD, founder and research director at the Sagol Center in Israel, part of a leading teaching hospital affiliated with the University of Tel Aviv, and now associated with The Villages Health. The realization of his vision is Aviv Clinic, the worlds largest hyperbaric oxygen therapy center.

Dr. Efrati had an idea while still in medical school. He believed that there isnt enough actionable information for doctors on the front lines. And for patients, their medical records are just too hard to figure out. A new way to approach healthcare was needed; open source sharing of practical data on a massive scale, while keeping personal information confidential along with a complete holistic program using the latest research, technology, and education all conceived and built around patients.

Fast forward to today. Located smack in the center of rolling hills, giant oak trees, and lots of agriculture, Aviv is offering a multi-faceted treatment program. Their therapies are designed to improve the aging process by increasing cognitive and physical performance.

Aviv has chosen the ideal setting. The Villages is home to more than 130,000 people and 75,000 golf carts spread across parts of three counties Sumter, Lake and Marion about 50 miles northwest of Orlando and 80 miles north of the Tampa Bay area.

Villagers are very active and have long taken a proactive approach to their healthcare. This is the perfect place to open our first clinic in the US., said Dave Globig, CEO. We want to change the world by giving people the opportunity to be the best version of themselves. Our goal is to help people live healthier lives by improving their aging experience

Thats a bold goal! How are they doing that?

Dana Nemenyi, Head of Marketing and Sales at Aviv Clinic, gave me a tour of their new 30,000 square foot facility, which blew me away! Theres a medical lab, physical and brain testing labs, classrooms for education, and even a waiting area with a caf.

Nemenyi told me that she joined Aviv to be a part of bringing cutting-edge healthcare to the US. I love helping people and believe the total client-for-life philosophy will change lives. She explained that Dr. Efrati created the concept of a personally and individually tailored protocol to enhance performance in the aging brain and body.

The heart of the program is evidence-based hyperbaric oxygen therapy coupled with a tech-enabled healthcare program. Clients go through an extensive health assessment, including comprehensive cognitive, physical and nutritional testing along with genetic sequencing to create a baseline and personalized plan.

Dive sessions come next. Aviv has state-of-the-art hyperbaric oxygen therapy suites designed to be pressurized to two atmospheres, causing oxygen levels in the bodys tissues to rise to 10-15 times over that of what we normally experience. This is a well-established treatment for a variety of medical conditions affecting brain and physical health.

There are four suites, each seating fourteen people. Stepping inside reminded me of a first-class cabin on a sleek jet filled with innovative technology, and customizable seating. Plus, an iPad provides personalized cognitive training and interactive entertainment options too. Clients go through sixty sessions, or dives, of two hours each over twelve weeks.

Also, each client is fitted with a customized Aviv wearable device, worn throughout the day to collect millions of data points and connected to an Aviv mobile app. This allows Aviv to monitor vital stats and provide feedback real-time. At any time, clients can view assessment results and track progress using the app, as well as communicate with the Aviv healthcare team or schedule appointments.

If all of this wasnt enough, Aviv clients are part of their family for a lifetime. They have access to physicians and other healthcare professionals as well as certified coaches such as registered dietitians.

Whats happening in The Villages, smack in the center of Florida, is nothing short of amazing. The multi-specialty Center for Advanced Healthcare facility that Aviv is part of is already attracting patients from all across Florida and beyond.

The innovation thats occurring here even is remarkable. The coupling of health tech, big data, wireless telecom, custom wearables, and analytics is improving lives and leading to reduced healthcare costs. The result more resilient lifestyles and increased life spans.

Read earlier columns from Florida Trend's sales and marketing coach, Ron Stein.Ron is the founder of FastPath Marketing and More Customers Academy. He works with tech-enabled companies, helping them find the fastest path to revenue with executive advising, business development coaching and consulting, as well as marketing and selling training. As an accomplished tech industry business leader and entrepreneur, Ron has served in top-level sales, marketing and business development roles ranging from emerging companies to global tech giants, including as the CEO of a venture-backed wireless startup. Ron is on the advisory board of the University of Floridas two internationally recognized tech business incubators and writes a popular column on how to grow revenue in the award-winning Florida Trend business magazine. Learn more atwww.FastPathMarketing.com.Ron can be reached at 727-642-4246 or byemail.

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How personalized medicine is revolutionizing healthcare in Florida and beyond - Florida Trend

Those who have one blood type are at higher risk of contracting COVID-19, and those in another are at a lower risk, a new study says.

The four blood types areA, B, AB and O.

The findings by a team of European scientists were published in the New England Journal of Medicine.

Blood Type O had the lowest frequency of disease positivity and Blood Type A the highest, the study revealed.

A total of 1,980 patients described as having "severe" respiratory disease in seven Italian and Spanish hospitals participated in the research. Those results were compared to approximately 2,000 healthy individuals.

"Our genetic data confirm that blood group O is associated with a risk of acquiring Covid-19 that was lower than that in non-O blood groups, whereas blood group A was associated with a higher risk than non-A blood groups," a report on the research states."

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COVID-19: Those With This Blood Type Have Higher Chance Of Contracting Virus, Study Shows - New Rochelle Daily Voice

By Lin Chia-nan / Staff reporter

A team of researchers yesterday unveiled the key genetic mutations of nonsmoking lung cancer patients, aiming to develop early diagnostic tools and precision medicine for the disease.

The study was a product of Taiwans participation in the US-led National Cancer Moonshot program since 2016, when Academia Sinica signed a memorandum of understanding with the US National Cancer Institute, Institute of Chemistry director Chen Yu-ju () told a news conference in Taipei.

While nearly 80 percent of lung adenocarcinoma patients in the US are chain smokers, more than half of the patients in Taiwan are nonsmokers, she said, adding that 93 percent of female patients do not smoke.

Photo: Chang Chia-ming, Taipei Times

It is a feature shared by many other East Asian countries, but the reason was unclear, she said, adding that the study was the first in East Asia to unravel the mystery.

Along with the US Clinical Proteomic Tumor Analysis Consortium, they studied tumor progression of patients in Taiwan and the US, she said.

Both studies were published in the journal Cell on Thursday last week and featured on its cover, showing an image of stargazers looking at a constellation that represents cancerous growth.

In Taiwan, up to 74 percent of female never-smokers (younger than 60 years old) showed higher mutation signatures of APOBEC a family of proteins related to RNA editing, Chen said.

The team also identified a correlation between high APOBEC signatures and good responses to immunotherapy treatment, making APOBEC a potential biomarker for early diagnosis, she added.

Some environmental carcinogens might be drivers in early carcinogenesis, as indicated by the teams findings about the metabolism and detoxification of carcinogens in females older than 70, Chen said.

Through the study, the team hopes to raise public awareness of the potential carcinogenesis of food additives, such as nitrosamine, which is used in fermented tofu and preserved radish, nitrated polycyclic aromatic hydrocarbons (nitro-PAHs) found in vehicle exhaust, cooking and secondhand smoke, as well as hereditary factors, Chen said.

As lung cancer symptoms mostly appear in late stages, most people have limited options other than immunotherapy and chemical therapy, which are costly, said National Taiwan University Hospital Division of Thoracic Surgery head Chen Jin-shing (), who provided clinical samples for the study.

The study helps with the development of screening tools through blood testing, which would allow high-risk groups for lung cancer to avoid carcinogenic substances or behaviors, he said.

The study is the first phenomenal outcome of Taiwans Cancer Moonshot, with more expected to come, said former vice president Chen Chien-jen (), now a distinguished research fellow at the institutions Genomics Research Center.

However, the program has only received four years of funding, which is to end next year, Chen Yu-ru said.

The funding has shrunk annually, she added, while expressing the hope that the government would continue to support the program.

Comments will be moderated. Keep comments relevant to the article. Remarks containing abusive and obscene language, personal attacks of any kind or promotion will be removed and the user banned. Final decision will be at the discretion of the Taipei Times.

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Study reveals key genetic mutations of nonsmokers -

Published inNature,the National Lung Matrix Trial (NLMT) is the worlds largest precision medicine clinical trial for non-small-cell lung cancer (NSCLC) patients, funded by Cancer Research UK (CRUK) and supported by the charitys Stratified Medicine Programme Phase 2 (SMP2) screening platform.

A 25 million collaboration with Pfizer, AstraZeneca and other pharmaceutical companies, and with support from the NHS, the NLMT matches different treatments to different groups of patients based on genetic changes in their cancer.

Using an innovative trial design that incorporates multiple treatment arms, NLMT allows for a more flexible and informed approach than traditional clinical trials. Each arm tests a different targeted treatment matched to a different genetic subtype of NSCLC.

The trials adaptive approach makes it possible for new drugs and combinations to be added as soon as they become available or retired quickly and easily if evidence suggests they arent effective.

Patients who sign up to take part in NLMT are genetically screened by the Cancer Research UK's SMP2 to understand more about their tumour type, and whether they possess the relevant genetic signatures to be matched to a targeted treatment.

Since the trial opened to recruitment in May 2015 until November 2019, 288 patients have been recruited to the 19 targeted treatment cohorts on the trial.

Results revealed key learnings on the use of precision medicine, such as how the appropriate pre-clinical work is essential in defining appropriate biomarker-drug combinations to test in the clinic, on ensuring that the best drugs available are used to hit the genomic targets, the scale of attrition from large screening platforms, and the importance of analysing and publishing outcome data of an ongoing study.

The attrition rate was high with only a 5% of SMP2 patients receiving treatment on NLMT. As trials often come towards the end of the patient journey, cancer progression might make patients too unwell to be recruited onto trials. Targeted therapy trials should take place much earlier in the cancer journey and use blood based genomic testing for fast turn-round of the information needed to match patients to drugs.

Lead authorProfessor Gary Middleton, Medical Oncologist at the University of Birmingham, said: This study provides data on how the next wave of trialling targeted therapies to treat complex cancers should be designed. This is the first trial of its kind, the novel Bayesian design allows outcome data from open cohorts that are still recruiting to be reported alongside closed cohorts, whereas previous umbrella studies have only published the results of completed arms and cohorts.

"We found genomically complicated tumours are hard to treat with targeted therapy, especially with monotherapy. The models we test drugs on are too simplistic - they dont represent the genomic complexity of the tumour, or the trajectory of how they rapidly evolve. We need models that take into account the complexity and trajectory of a human tumour to decide if a drug is going to work.

Professor Pam Kearns, Director of Birminghams Cancer Research UK Clinical Trials Unit and University of BirminghamsInstitute of Cancer and Genomic Sciences, said: The National Lung Matrix Trial is a landmark complex innovative design trial and represents a step-change in our understanding of how to develop precision medicine in challenging to treat cancers.

Dr Ian Walker, Director of Research at Cancer Research UK, said: The National Lung Matrix trial is a flagship programme for Cancer Research UK and continues to provide significant insights into how we should treat genomically diverse cancers, such as lung. Not only will it shape the thinking for future studies delivering complex precision medicines, but it has also demonstrated how molecular diagnostic testing and clinical research can work in a truly integrated manner within the National Health Service across the UK to allow patients to access the latest new treatments.

NLMT patient Paul Inett, 72 years old, said: I was diagnosed with stage four metastatic lung cancer in late April 2015 that had spread to glands in my chest. I was referred to Professor Gary Middleton at the Queen Elizabeth Hospital Birmingham and was recruited onto the National Lung Matrix Trial. Fortunately my biopsy showed a genetic marker that matched to one of the treatment arms on the trial and received a targeted cancer drug. This ground breaking research saved my life. Im now able to live a relatively active life including spending time with my family and taking exercise classes at my local gym.

Next steps in the NLMT are to continue recruiting patients. A new combination arm has just been added to the study and opened earlier in June. There will also be further publications from the individual arms and cohorts, and translational laboratory work.

For more information please contact Sophie Belcher, Communications Manager, University of Birmingham, on +44(0) 7815607157. Alternatively, contact the Press Office out of hours on +44 (0)7789 921165.

About the University of BirminghamThe University of Birmingham is ranked amongst the worlds top 100 institutions. Its work brings people from across the world to Birmingham, including researchers, teachers and more than 6,500 international students from over 150 countries.

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Flagship Cancer Research UK precision medicine trial highlights the need for a new approach in treating genomically complicated cancers - University...