TipRanks

Markets are volatile, there can be no doubt. So far this month, the S&P 500 has fallen 9% from its peak. The tech-heavy NASDAQ, which had led the gainers all summer, is now leading the on the fall, having lost 11% since September 2. The three-week tumble has investors worried that we may be on the brink of another bear market.The headwinds are strong. The usual September swoon, the upcoming election, doubts about another round of economic stimulus all are putting downward pressure on the stock markets.Which doesnt mean that there are no opportunities. As the old saw goes, Bulls and bears can both make money, while the pigs get slaughtered. A falling market may worry investors, but a smart strategy can prevent the portfolio from losing too much long-term value while maintaining a steady income. Dividend stocks, which feed into the income stream, can be a key part of such a strategy.Using the data available in the TipRanks database, weve pulled up three stocks with high yields from 7% to 11%, or up to 6 times the average dividend found on the S&P 500 index. Even better, these stocks are seen as Strong Buys by Wall Streets analysts. Lets find out why.Williams Companies (WMB)We start with Williams Companies, an Oklahoma-based energy company. Williams controls pipelines connecting Rocky Mountain natural gas fields with the Pacific Northwest region, and Appalachian and Texan fields with users in the Northeast and transport terminals on the Gulf Coast. The companys primary operations are the processing and transport of natural gas, with additional ops in crude oil and energy generation. Williams handles nearly one-third of all US commercial and residential natural gas use.The essential nature of Williams business really, modern society simply cannot get along without reliable energy sources has insulated the company from some of the economic turndown in 1H20. Quarterly revenues slid from $2.1 billion at the end of last year to $1.9 billion in Q1 and $1.7 billion in Q2. EPS in the first half was 26 cents for Q1 and 25 cents for Q2 but this was consistent with EPS results for the previous three quarters. The generally sound financial base supported the companys reliable dividend. Williams has been raising that payment for the past four years, and even the corona crisis could not derail it. At 40 cents per common share, the dividend annualizes to $1.60 and yields an impressive 7.7%. The next payment is scheduled for September 28.Truist analyst Tristan Richardson sees Williams as one of the midstream sectors best positioned companies.We continue to look to WMB as a defensive component of midstream and favor its 2H prospects as broader midstream grasps at recovery Beyond 2020 we see the value proposition as a stable footprint with free cash flow generation even in the current environment. We also see room for incremental leverage reduction throughout our forecast period on scaled back capital plans and even with the stable dividend. We look for modestly lower capex in 2021, however unlike more G&P oriented midstream firms, we see a project backlog in downstream that should support very modest growth, Richardson noted.Accordingly, Richardson rates WMB shares as a Buy, and his $26 price target implies a 30% upside potential from current levels. (To watch Richardsons track record, click here)Overall, the Strong Buy analyst consensus rating on WMB is based on 11 Buy reviews against just a single Hold. The stocks current share price is $19.91 and the average price target is $24.58, making the one-year upside potential 23%. (See WMB stock analysis on TipRanks)Magellan Midstream (MMP)The second stock on our list is another midstream energy company, Magellan. This is another Oklahoma-based firm, with a network of assets across much of the US from the Rocky Mountains to the Mississippi Valley, and into the Southeast. Magellans network transports crude oil and refined products, and includes Gulf Coast export shipping terminals.Magellan's total revenues rose sequentially to $782.8 in Q1, and EPS came in at $1.28, well above the forecast. These numbers turned down drastically in Q2, as revenue fell to $460.4 million and EPS collapsed to 65 cents. The outlook for Q3 predicts a modest recovery, with EPS forecast at 85 cents. The company strengthened its position in the second quarter with an issue of 10-year senior notes, totaling $500 million, at 3.25%. This reduced the companys debt service payments, and shored up liquidity, making possible the maintenance of the dividend.The dividend was kept steady at $1.0275 per common share quarterly. Annualized, this comes to $4.11, a good absolute return, and gives a yield of 11.1%, giving MMP a far higher return than Treasury bonds or the average S&P-listed stock.Well Fargo analyst Praneeth Satish believes that MMP has strong prospects for recovery. [We] view near-term weakness in refined products demand as temporary and recovering. In the interim, MMP remains well positioned given its strong balance sheet and liquidity position, and ratable cash flow stream Satish goes on to note that the dividend appears secure for the near-term: The company plans to maintain the current quarterly distribution for the rest of the year.In line with this generally upbeat outlook, Satish gives MMP an Overweight (i.e. Buy) rating, and a $54 price target that implies 57% growth in the coming year. (To watch Satishs track record, click here)Net net, MMP shares have a unanimous Strong Buy analyst consensus rating, a show of confidence by Wall Streets analyst corps. The stock is selling for $33.44, and the average price target of $51.13 implies 53% growth in the year ahead. (See MMP stock analysis on TipRanks)Ready Capital Corporation (RC)The second stock on our list is a real estate investment trust. No surprise finding one of these in a list of strong dividend payers REITs have long been known for their high dividend payments. Ready Capital, which focuses on the commercial mortgage niche of the REIT sector, has a portfolio of loans in real estate securities and multi-family dwellings. RC has provided more than $3 billion in capital to its loan customers.In the first quarter of this year, when the coronavirus hit, the economy turned south, and business came to a standstill, Ready Capital took a heavy blow. Revenues fell by 58%, and Q1 EPS came in at just one penny. Things turned around in Q2, however, after the company took measures including increasing liquidity, reducing liabilities, and increasing involvement in government-sponsored lending to shore up business. Revenues rose to $87 million and EPS rebounded to 70 cents.In the wake of the strong Q2 results, RC also started restoring its dividend. In Q1 the company had slashed the payment from 40 cents to 25 cents; in the most recent declaration, for an October 30 payment, the new dividend is set at 30 cents per share. This annualizes to $1.20 and gives a strong yield of 9.9%.Crispin Love, writing from Piper Sandler, notes the companys success in getting back on track.Given low interest rates, Ready Capital had a record $1.2B in residential mortgage originations versus our $1.1B estimate. Gain on sale margins were also at record levels. We are calculating gain on sale margins of 3.7%, up from 2.4% in 1Q20, Love wrote.In a separate note, written after the dividend declaration, Love added, We believe that the Board's actions show an increased confidence for the company to get back to its pre-pandemic $0.40 dividend. In recent earnings calls, management has commented that its goal is to get back to stabilized earnings above $0.40, which would support a dividend more in-line with pre-pandemic levels.To this end, Love rates RC an Overweight (i.e. Buy) along with a $12 price target, suggesting an upside of 14%. (To watch Loves track record, click here)All in all, Ready Capital has a unanimous Strong Buy analyst consensus rating, based on 4 recent positive reviews. The stock has an average price target of $11.50, which gives a 9% upside from the current share price of $10.51. (See RC stock analysis on TipRanks)To find good ideas for dividend stocks trading at attractive valuations, visit TipRanks Best Stocks to Buy, a newly launched tool that unites all of TipRanks equity insights.Disclaimer: The opinions expressed in this article are solely those of the featured analysts. The content is intended to be used for informational purposes only. It is very important to do your own analysis before making any investment.

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Catalyst Biosciences to Present at the Stifel Immunology and Inflammation Summit - Yahoo Finance

Immunology

TL1A and its receptor could reduce fibrosis and tissue remodeling in patients with severe lung disease – News-Medical.Net

September 26, 2020 medical

Reviewed by Emily Henderson, B.Sc.Sep 25 2020

Your lungs and airways need to be stretchy, sort of like balloons. Take a big breath, and they'll open right up.

Damaged lungs can't open properly. Patients with asthma, idiopathic pulmonary fibrosis and systemic sclerosis suffer from fibrosis and tissue remodeling, where a build-up of tissue and immune cells, and proteins that form a glue-like substance, keep the airways from expanding. As fibrosis gets worse, taking a breath feels like blowing up a balloon filled with concrete.

In a new study, researchers at La Jolla Institute for Immunology (LJI) report that a protein called TL1A drives fibrosis in several mouse models, triggering tissue remodeling, and making it harder for lungs and airways to function normally.

"Our new study suggests that TL1A and its receptor on cells could be targets for therapeutics aimed at reducing fibrosis and tissue remodeling in patients with severe lung disease," says LJI Professor Michael Croft, Ph.D., director of scientific affairs at LJI and senior author of the new study in The Journal of Immunology.

Croft's laboratory is focused on understanding the importance of a family of proteins, called tumor necrosis factors (TNF) and tumor necrosis factor receptors (TNFR), in inflammatory and autoimmune diseases. By investigating these molecules, researchers hope to track down the root causes of inflammation and stop tissue damage before it's too late.

Previous research had shown that a TNF protein called TL1A can act on immune cells involved in allergic reactions and drive those immune cells to make inflammatory molecules. The Croft Lab wondered-;if TL1A leads to inflammation, could it contribute to fibrosis in the lungs?

For the new study, Croft and his colleagues used genetic and therapeutic interventions, tissue staining, and fluorescence imaging techniques to study protein interactions in mouse models of severe asthma, idiopathic pulmonary fibrosis and systemic sclerosis. They first discovered that TL1A acts directly on a receptor on cells in the lungs and bronchial tubes, which leads to fibrosis and tissue remodeling.

We're all familiar with the idea of tissue remodeling. When a wound on the skin heals, the new area of skin is sometimes shiner, darker or tougher than the skin around it.

The tissue has been remodeled. When lungs and airways try to heal-;in response to an asthma attack, for example-; the cells in the area also change. The damaged area accumulates cells called fibroblasts, which make several glue-like proteins, including collagen. Too much collagen makes the lungs and airways less elastic-;and less functional.

As Croft describes it, tissue remodeling is like wound healing, "but wound healing that goes wrong and becomes so exaggerated that it blocks tissue from behaving in its normal way." With the new study, scientists now know that TL1A is driving this harmful remodeling in the lungs.

In addition to causing fibroblasts to make collagen, the researchers found that TL1A also helps fibroblasts to behave like smooth muscle cells.

A thin layer of smooth muscle cells naturally lines the bronchial tubes allowing them to dilate and constrict, but a thick layer of these smooth muscle cells-;that includes fibroblasts-;will keep the airways from expanding and contracting normally, making it even hard for a patient to breathe.

The scientists then studied lung tissue remodeling in mice that lacked the receptor for TL1A, called DR3, or were given a reagent that blocked TL1A activity. These mice showed less lung remodeling, less collagen deposition and reduced smooth muscle mass in the lungs.

These animal model data may support recent research in humans. Researchers have found that patients with severe asthma have excessive production of TL1A. This could explain why these patients are more vulnerable to lung fibrosis and remodeling.

This type of research needs to be expanded to really understand if there are subsets of patients with asthma or other inflammatory lung diseases who might express TL1A at higher levels than other patients-;which could potentially guide future therapies for targeting TL1A to reduce remodeling and fibrosis."

Michael Croft, PhD, Professor and Study Senior Author, Director of Scientific Affairs, La Jolla Institute for Immunology

Going forward, Croft and his team plan to investigate how the DR3 receptor is expressed on tissue cells and whether it is affected by other inflammatory factors. They also want to know how active TL1A is in human patients and how many inflammatory activities the protein might be responsible for.

Source:

Journal reference:

Herro, R., et al. (2020) TL1A Promotes Lung Tissue Fibrosis and Airway Remodeling. Journal of Immunology. doi.org/10.4049/jimmunol.2000665.

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TL1A and its receptor could reduce fibrosis and tissue remodeling in patients with severe lung disease - News-Medical.Net

Immunology

The Tisch Cancer Institute Earns Second Consecutive Designation from National Cancer Institute – Newswise

September 26, 2020 medical

Newswise New York, NY (September 24, 2020) The Tisch Cancer Institute at Mount Sinai (TCI) has been awarded $13 million as part of the renewal of its National Cancer Institute Cancer Center Designation, a prestigious distinction that is based on scientific excellence, robust clinical research, and beneficial community impact. The National Cancer Institute rated TCIs application as outstanding.

The five-year redesignation awardthe Institutes second consecutive designationwill support research programs and facilities, promote collaborative translational cancer research in a coordinated manner, and help disseminate cancer research findings to the community. The funding complements $53 million in current cancer research grants earned by TCI investigators.

The strategic plan that helped lead to the redesignation this year included cutting-edge clinical research developed by teams from several disciplines, allowing TCI to provide personalized care to the New York City metro areas diverse communities. Four areas in which TCI researchers and physicians excel, and which contributed to the redesignation, include:

TCI was first named an NCI-designated cancer center in 2015. Since then, the recruitment of leaders in cancer genomics, lung cancer, cancer immunology, and clinical research, and the exponential growth of clinical trials originated by Mount Sinai physicians, has helped bolster the cancer centers national prominence and continued to bring cutting-edge research from the lab to the bedside of Mount Sinai patients.

The NCI redesignation recognizes our plan to maximize our ability to make an impact in our community and at the national level over the next five years, expanding on our successes in four key areas: cancer immunology, cancer mechanisms, cancer clinical investigation, and cancer prevention and control, said Ramon Parsons, MD, PhD, Director of The Tisch Cancer Institute at Mount Sinai, Ward-Coleman Chair in Cancer Research, and Chair of Oncological Sciences at the Icahn School of Medicine at Mount Sinai. Our patients are the beneficiaries of our commitment to advancing scientific research in cancer and harnessing our findings into new therapies and prevention initiatives.

Some achievements in the four key areas include:

Our physicians have built up a repertoire of investigator-initiated trials and novel clinical research studies, which contributed to this redesignation and has become a strength of The Tisch Cancer Institute, said William K. Oh, MD, Deputy Director of The Tisch Cancer Institute, Chief of the Division of Hematology and Medical Oncology at the Mount Sinai Health System, and the Ezra M. Greenspan, MD, Professor in Clinical Cancer Therapeutics at the Icahn School of Medicine at Mount Sinai. Another strength that sets us apart is our research on cancer in World Trade Center responders, due to our unique position of having a monitoring program at Mount Sinai. Our research has led to insights into how inflammation leads to cancer as well as which cancers should be investigated in this vulnerable population.

The Tisch Cancer Institute at Mount Sinai investigates real-world, complex medical problems and solves them with teams of scientists and physicians that successfully integrate many disciplines, said Dennis S. Charney, MD, Anne and Joel Ehrenkranz Dean of the Icahn School of Medicine at Mount Sinai and President for Academic Affairs of the Mount Sinai Health System. The NCI redesignation underscores our exceptional leadership, extensive research facilities, and an institution-wide commitment to research with a focus on identifying and combatting disparities so that all patients receive the best care possible.

About the Mount Sinai Health System

The Mount Sinai Health System is New York City's largest academic medical system, encompassing eight hospitals, a leading medical school, and a vast network of ambulatory practices throughout the greater New York region. Mount Sinai is a national and international source of unrivaled education, translational research and discovery, and collaborative clinical leadership ensuring that we deliver the highest quality carefrom prevention to treatment of the most serious and complex human diseases. The Health System includes more than 7,200 physicians and features a robust and continually expanding network of multispecialty services, including more than 400 ambulatory practice locations throughout the five boroughs of New York City, Westchester, and Long Island. The Mount Sinai Hospital is ranked No. 14 onU.S. News & World Report's"Honor Roll" of the Top 20 Best Hospitals in the country and the Icahn School of Medicine as one of the Top 20 Best Medical Schools in country. Mount Sinai Health System hospitals are consistently ranked regionally by specialty and our physicians in the top 1% of all physicians nationally byU.S. News & World Report.

For more information, visithttps://www.mountsinai.orgor find Mount Sinai onFacebook,TwitterandYouTube.

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The Tisch Cancer Institute Earns Second Consecutive Designation from National Cancer Institute - Newswise

Genetics

Scientists discover genetic and immunologic underpinnings of some cases of severe COVID-19 – National Institutes of Health

September 26, 2020 medical

Media Advisory

Thursday, September 24, 2020

New findings by scientists at the National Institutes of Health and their collaborators help explain why some people with COVID-19 develop severe disease. The findings also may provide the first molecular explanation for why more men than women die from COVID-19.

The researchers found that more than 10% of people who develop severe COVID-19 have misguided antibodiesautoantibodiesthat attack the immune system rather than the virus that causes the disease. Another 3.5% or more of people who develop severe COVID-19 carry a specific kind of genetic mutation that impacts immunity. Consequently, both groups lack effective immune responses that depend on type I interferon, a set of 17 proteins crucial for protecting cells and the body from viruses. Whether these proteins have been neutralized by autoantibodies orbecause of a faulty genewere produced in insufficient amounts or induced an inadequate antiviral response, their absence appears to be a commonality among a subgroup of people who suffer from life-threatening COVID-19 pneumonia.

These findings are the first published results from the COVID Human Genetic Effort, an international project spanning more than 50 genetic sequencing hubs and hundreds of hospitals. The effort is co-led by Helen Su, M.D., Ph.D., a senior investigator at the National Institute of Allergy and Infectious Diseases (NIAID), part of NIH; and Jean-Laurent Casanova, M.D., Ph.D., head of the St. Giles Laboratory of Human Genetics of Infectious Diseases at The Rockefeller University in New York. Major contributions were made by Luigi Notarangelo, M.D., chief of the NIAID Laboratory of Clinical Immunology and Microbiology (LCIM); Steven Holland, M.D., director of the NIAID Division of Intramural Research and senior investigator in the NIAID LCIM; clinicians and investigators in hospitals in the Italian cities of Brescia, Monza and Pavia, which were heavily hit by COVID-19; and researchers at the Uniformed Services University of the Health Sciences in Bethesda, Maryland.

The wide variation in the severity of disease caused by SARS-CoV-2, the virus behind COVID-19, has puzzled scientists and clinicians. SARS-CoV-2 can cause anything from a symptom-free infection to death, with many different outcomes in between. Since February 2020, Drs. Su and Casanova and their collaborators have enrolled thousands of COVID-19 patients to find out whether a genetic factor drives these disparate clinical outcomes.

The researchers discovered that among nearly 660 people with severe COVID-19, a significant number carried rare genetic variants in 13 genes known to be critical in the bodys defense against influenza virus, and more than 3.5% were completely missing a functioning gene. Further experiments showed that immune cells from those 3.5% did not produce any detectable type I interferons in response to SARS-CoV-2.

Examining nearly 1,000 patients with life-threatening COVID-19 pneumonia, the researchers also found that more than 10% had autoantibodies against interferons at the onset of their infection, and 95% of those patients were men. Biochemical experiments confirmed that the autoantibodies block the activity of interferon type I.

Q Zhang et al. Inborn errors of type I IFN immunity in patients with life-threatening COVID-19. Science DOI: 10.1126/science.abd4570 (2020).

P Bastard et al. Auto-antibodies against type I IFNs in patients with life-threatening COVID-19. Science DOI: 10.1126/science.abd4585 (2020).

NIAID Director Anthony S. Fauci, M.D., NIAID Senior Investigator Helen C. Su, M.D., Ph.D., and Luigi Notarangelo, M.D., chief of the NIAID Laboratory of Clinical Immunology and Microbiology, are available for interviews.

To schedule interviews, please contact NIAID Office of Communications, (301) 402-1663, NIAIDNews@niaid.nih.gov.

NIAID conducts and supports research at NIH, throughout the United States, and worldwide to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website.

About the National Institutes of Health (NIH):NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

NIHTurning Discovery Into Health

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Scientists discover genetic and immunologic underpinnings of some cases of severe COVID-19 - National Institutes of Health

Genetics

Researchers elucidate the impact of genetic mutations in cocaine addiction – News-Medical.Net

September 26, 2020 medical

Reviewed by Emily Henderson, B.Sc.Sep 26 2020

Cocaine addiction is a chronic disorder with a high rate of relapse for which no effective treatment is currently available.

Scientists from the Institut Pasteur, the CNRS, Inserm and the Paris Public Hospital Network (AP-HP) recently demonstrated that two gene mutations involved in the conformation of nicotinic receptors in the brain appear to play a role in various aspects of cocaine addiction. The results of the study were published in Progress in Neurobiology.

There are approximately 18 million users worldwide, and cocaine is implicated in more than 50% of overdose deaths in the United States and 25% in France. It is also one of the only drugs for which there is no approved pharmacological treatment.

Cocaine acts primarily in the brain by blocking the dopamine transporter, thereby increasing the concentration of this "pleasure" molecule in the reward system. But cocaine can also act directly on the nicotinic receptors1 in the brain.

Several human genetics studies have recently suggested that a mutation in the gene encoding the 5 subunit of nicotinic receptors, hereafter referred to as '5SNP', already known to increase the risk of tobacco dependence,2 may conversely also confer "protection" against cocaine addiction.

This mutation is highly present in the general population (approximately 37% of Europeans and up to 43% of the Middle Eastern population carry it), so it is important to determine how it affects cocaine addiction and, more generally, to better understand the role of the 5 nicotinic subunit in the effects of cocaine.

Scientists of the Integrative Neurobiology of Cholinergic Systems Unit (Institut Pasteur/CNRS) began by evaluating the role of the 5 nicotinic subunit and the impact of the 5SNP mutation on various processes involved in the development of cocaine addiction in animal models. The results obtained were then used to characterize more specifically its impact on humans.

The scientists observed that the 5SNP mutation reduces the voluntary intake of cocaine upon first exposures.

These preclinical data suggest that the mutation protects against cocaine addiction by modulating an early phase in the addiction cycle."

Morgane Besson, Study Lead Author, Institut Pasteur

Working in collaboration with the Paris Public Hospital Network (AP-HP) and Inserm, the scientists then confirmed this significant effect in approximately 350 patients with cocaine addiction: those with the mutation exhibited a slower transition from first cocaine use to the emergence of signs of addiction.

At the same time, the authors showed that a total absence of the 5 nicotinic subunit increased the risk of relapse after withdrawal in preclinical models. This led the scientists to identify another mutation in another nicotinic subunit, 4, associated with a shorter time to relapse after withdrawal in addicted patients.

Taken together, these results elucidate the role played by both a highly frequent mutation in the 5 nicotinic subunit and the subunit itself in various stages of cocaine addiction. The research suggests that drugs modulating nicotinic receptors containing this 5 subunit could represent a novel therapeutic strategy for cocaine addiction.

Source:

Journal reference:

Forget, B., et al. (2020) Alterations in nicotinic receptor alpha5 subunit gene differentially impact early and later stages of cocaine addiction: a translational study in transgenic rats and patients. Progress in Neurobiology. doi.org/10.1016/j.pneurobio.2020.101898.

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Researchers elucidate the impact of genetic mutations in cocaine addiction - News-Medical.Net

Genetics

NIH researchers find genetic link in patients with severe COVID-19 – fox6now.com

September 26, 2020 medical

United launches rapid COVID-19 testing program for some travelers

United Airlines plans to offer COVID-19 tests for passengers flying from San Francisco International Airport to Hawaii.

LOS ANGELES - Scientists at the National Institutes of Health (NIH) say they have found how genetics play a critical role in who develops severe cases of COVID-19 and why more men than women die from the illness.

Much is still being learned about the novel coronavirus that has claimed the lives of more than 200,000 people in the U.S. Nearly 1 million deaths have been recorded worldwide to date, according to data tracked by Johns Hopkins University.

Researchers have rushed to study the unpredictable and wide variations in illness severity that the virus causes in different people. Determining whether a genetic factor contributes to the virus severity and health outcomes of COVID-19 patients is highly important for researchers to develop a solution to the crisis.

Results published as part of the COVID Human Genetic Effort, an international project consisting of more than 50 genetic sequencing hubs and hundreds of hospitals, found that more than 10% of people who develop a severe case of the coronavirus have misguided antibodies which attack the immune system.

FILE - A medical laboratory scientist runs a clinical test in the Immunology lab at UW Medicine looking for antibodies against SARS-CoV-2. (Photo by Karen Ducey/Getty Images)

Researchers found that another 3.5% of people who develop severe COVID-19 carry a specific genetic mutation which negatively impacts immunity from the disease.

Consequently, both groups lack effective immune responses that depend on type I interferon, a set of 17 proteins crucial for protecting cells and the body from viruses," according to a news release by the NIH.

The health agency said the absence of these proteins appear to be common among a subgroup of people who are at risk of life-threatening effects of COVID-19.

After examining 1,000 patients with life-threatening pneumonia caused by the coronavirus, researchers found that 10% of patients had the misguided antibodies, otherwise known as autoantibodies, which defended against the interferon proteins needed to protect the cells. Of those patients with harmful antibodies, 95% were men.

RELATED: Could your symptoms be COVID-19? The signs range from mild to severe

Health officials say that becoming infected with COVID-19 can lead to a wide variety of symptoms, ranging from mild to severe. The most common symptoms are fever, a dry cough, shortness of breath and fatigue.

But as the months-old virus continues its spread, additional symptoms are being identified and they can be unpredictable.

The U.S. Centers for Disease Control and Prevention highlights 11 key symptoms of COVID-19 on its website:

Fever or chillsCoughShortness of breath or difficulty breathingFatigueMuscle or body achesHeadacheNew loss of taste or smellSore throatCongestion or runny noseNausea or vomitingDiarrhea

The agency notes that the list does not include all possible symptoms of COVID-19, and said that it would continue to update the list as more becomes known about the virus.

Kelly Taylor Hayes contributed to this story.

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NIH researchers find genetic link in patients with severe COVID-19 - fox6now.com

Genetics

Zelis and Concert Genetics Launch Genetic Testing Claim Editing Solution – Business Wire

September 26, 2020 medical

BEDMINSTER, N.J. & NASHVILLE, Tenn.--(BUSINESS WIRE)--Zelis, the healthcare industrys leading claims cost and payments optimization platform with superior technology and solutions to price, pay and explain claims, and Concert Genetics, a technology company dedicated to advancing precision medicine, have launched a claim editing solution for the complex and rapidly-growing area of genetic testing.

The solution embeds Concerts claim editing capabilities, which are powered by robust genetic testing market data and machine learning, into Zelis existing claim editing platform. This leading-edge platform already contains more than 18 million edits sourced to national coding standards. The partnership adds specialized content in genetic testing that other platforms lack, enabling Zelis and Concert to improve coding and billing accuracy of these complex and ambiguous genetic test claims before they are paid.

Our clients are experiencing higher costs due to the complexity of managing the variability of genetic testing codes and volume of new tests entering the market, said R. Andrew Eckert, Zelis CEO. Combining our payment integrity expertise with Concerts precision technology will enable us to proactively identify inaccurate claims and continue to support our clients with innovative solutions to reduce costs.

This solution comes at a critical time, as the availability and demand for genetic tests grow with the global genetic testing market expected to reach $17.6 billion by 2025, from $7.5 billion in 2017.1 Additionally, the total number of available genetic testing products has surpassed 150,000, up from around 10,000 in 2012. Meanwhile, much of the growth in volume is represented by multi-gene panel tests, which are particularly difficult for health plans to process in an efficient and accurate way because they are billed using multiple billing codes in widely varying combinations. Some categories of genetic tests are billed in thousands of different code combinations.

The pace of advancement in the science and clinical application of genetics is remarkable, and the healthcare system has had difficulty keeping up, said Rob Metcalf, CEO of Concert Genetics. Concert has assembled the data and digital infrastructure to enable transparency, connectivity, and value in this space, and we are pleased to partner with Zelis to make our technology available to its clients.

A key enabler of this claim editing solution is its ability to match complex claims with multiple billing codes back to its catalog of tests on the market. The combined solution is available to Zelis clients effective immediately.

About Zelis

Zelis is the healthcare industrys leading claims cost and payments optimization platform with superior technology and solutions to price claims, pay claims and explain claims, all at enterprise scale on a claim-by-claim basis. Zelis leverages proprietary technology, robust analytics, extensive payment and provider networks, and innovative claim savings channels to deliver to the industry superior administrative and medical cost savings. Zelis was founded on a belief that there is a better way to determine the cost of a healthcare claim, manage payment related data, and make the claim payment. Zelis provides the industrys only comprehensive, integrated platform to take a claim through the entire pre-payment to payments lifecycle. Zelis ~1000 associates serve more than 700 payor clients, including the top-5 national health plans, Blues plans, regional health plans, TPAs and self-insured employers, and more than 1.5 million providers. Zelis delivers more than $5B of claims savings, $50B of provider payments and 500 million payment data communications annually.

About Concert Genetics

Concert Genetics is a software and managed services company that advances precision medicine by providing the digital infrastructure for reliable and efficient management of genetic testing. Concerts market-leading genetic test order management platform leverages a proprietary database of the U.S. clinical genetic testing market today more than 150,000 testing products and genetic testing claims from more than 100 million lives. Learn more at http://www.ConcertGenetics.com.

1 Allied Market Research report, Genetic Testing Market by Type (Predictive Testing, Carrier Testing, Prenatal & Newborn Testing, Diagnostic Testing, Pharmacogenomic Testing, and Others), Technology (Cytogenetic Testing, Biochemical Testing, and Molecular Testing), and Application (Chromosome Analysis, Genetic Disease Diagnosis, Cardiovascular Disease Diagnosis, and Others): Global Opportunity Analysis and Industry Forecast, 20182025

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Zelis and Concert Genetics Launch Genetic Testing Claim Editing Solution - Business Wire

Genetics

Capturing marine biodiversity with the power of genetics – Australian Antarctic Division

September 26, 2020 medical

Scientists at the Australian Antarctic Division are studying small drops of the enormous Southern Ocean to find out which animals live within it using new genetic methods.

The ocean encircling an entire continent and joining the worlds oceans supports a polar food web that is globally unique and teeming with life.

Ongoing monitoring of Southern Ocean biodiversity will be crucial for scientists to assess the impact of a rapidly changing climate on the marine ecosystem.

Its hugely important to actually monitor how things are changing, said AAD genetics researcher Dr Leonie Suter. Its a pretty big deal.

How best to capture that information has been the subject of a two-year research project, detailed in the journal of Molecular Ecology.

The Continuous Plankton Recorder (CPR) has been capturing snapshots of the ocean for the last century.

Its a device dropped into the water and towed behind a ship at a constant speed on a narrow path, for 450 nautical miles at a time.

It works by trapping plankton between fine sheets of silk, the contents of which is examined back in the laboratory by taxonomists who microscopically identify, log and analyse whole organisms.

CPR surveys have been run by the Australian Antarctic Program across vast swathes of the Southern Ocean since 1991, involving ships from several nations.

A staggering amount of data has been amassed around 47,000 samples analysed from more than 1000 CPR tows for a total of approximately 240,000 nautical miles.

Now a new method harnessing the power of genetic sequencing, called environmental DNA metabarcoding, promises to extend our information about biodiversity.

If DNA is like a biochemical barcode unique to every species, eDNA metabarcoding records the traces of those organisms left in their surroundings.

Environmental DNA is pretty much the DNA that is shed by any organism into the environment, said Dr Leonie Suter.

So in the marine environment, imagine a fish shedding a scale or doing a poo, or spawning, or dying and slowly decaying.

With genetic methods, we can extract this DNA from quite small water samples and from that determine what actually lives in the environment.

Unlike conventional methods, analysing eDNA doesnt require an entire organism to establish a snapshot of whats in the water.

The team analysed water samples taken from the Southern Ocean between Tasmania and Macquarie Island.

For comparable results, where 1500 litres of seawater was filtered through the Continuous Plankton Recorder over five nautical miles, the eDNA method relied on just two litres taken at a single location, piped cleanly and directly from the ocean onto the Aurora Australis research vessel.

All youre really doing is turning a tap and in your lab collecting two litres of water that you can filter on site. This filter is then used for genetic analysis, said Dr Suter.

So you dont need to even go on the deck of the ship or anything, youre in a quite safe environment. You turn your tap and collect your sample to find out what lives in the ocean, which is quite amazing.

Dr Suter said this eDNA metabarcoding method is a relatively new concept in the Southern Ocean.

The open ocean is quite different to other environments. The water body is just so big, she said.

It all dilutes quite quickly, there are currents and other factors that spread the eDNA out quite quickly. So we werent sure how well this would work.

When eDNA and CPR samples were both processed genetically, eDNA detected about two thirds of the species that were detected with CPR.

This is quite amazing considering the difference in sampled water volume. Both methods detected similar species that contributed to community differentiation across different environments, said Dr Suter.

When eDNA metabarcoding was compared to morphological analyses (whole organisms) of CPR samples, eDNA detected up to 1.5 times more species.

The overlap of species detected with the two methods was small, suggesting that eDNA is more of a complementary method to traditional CPRs.

Because the open ocean is prone to quickly degrading the quality of minute eDNA samples, multiple eDNA samples at different times of the day should be collected to establish a more complete picture.

Dr Suter said more refining of sampling and processing could lead to an unprecedented biodiversity monitoring capacity in the open ocean for future research.

Its personally a really big achievement for me because Ive got three little kids at home, said Dr Suter, also the lead author.

I started working on this when my twins were four months old. So its been pretty big for me to achieve this work. And obviously its not just my work. Its a big team effort.

Im really proud that we managed to get it out.

In addition, the team is now developing targeted Antarctic krill markers to test how abundant the species is in the Southern Ocean and inform the future management of the krill fishery.

The AADs new icebreaker RSV Nuyina will also be equipped for ongoing monitoring of eDNA.

Whenever the ship goes out we hope to be collecting water samples to analyse and start creating a long-term monitoring program, said Dr Suter.

This content was last updated 2 days ago on 25 September 2020.

Genetics

ADHD is partially genetic, but there are other risk factors that play a key role – Insider – INSIDER

September 26, 2020 medical

Some mental health conditions have genetic components, and the same can be said for attention deficit hyperactivity disorder (ADHD).

Research have some insight into the genetic component of the condition. However, there are more to potential causes of ADHD aside from just your genes.

Here's what scientists know so far about the heritability of ADHD and how it compares to other risks that contribute to the condition.

Though it's unclear how significant a role genetics plays, studies have shown that having a parent or sibling can drastically increase one's risk of developing ADHD.

For example, a 2016 study published in Neuropsychiatric Disease and Treatment found that in the sample of 79 children with ADHD, 41.3% had mothers with ADHD and 51% had fathers with ADHD.

Another study, published in 2017 in Revista Colombiana de Psiquiatra, found that siblings of someone with ADHD had a 26% to 45.2% chance of also having ADHD making it a greater likelihood than if no siblings had ADHD.

Another 2014 studyof 59,514 twins found the heritability of ADHD the likelihood of a genetic component for the condition to be 88%. However, genetics are likely not the sole factor for whether or not a person develops ADHD.

"Since siblings also share a social, physical, and rearing environment, this in itself does not prove genetic rather than potentially shared environmental causes," says Robert King, MD,

Pediatric Developmental and Behavioral Medicine Psychiatrist and Medical Director of the Tourette's/OCD Clinic at Yale Child Study Center.

There is no one gene that causes ADHD, and there is no test you can take to determine your risk of developing it. In fact, ADHD is most likely a condition associated with multiple genes, not just one, says King.

But researchers have hypothesized that one gene in particular, the DRD4 gene, may play a part in ADHD. The DRD4 gene affects dopamine receptors in the brain, which in turn can influence brain function and mental disorders associated with brian function, including ADHD. However, how strong a role DRD4 plays in ADHD, specifically, remains unclear.

King says that researchers have found other rare genes that are associated with different aspects of brain development, but clarifies that "although these are of interest in suggesting new research leads, they are found only in a very small number of cases of ADHD and are not useful as any sort of diagnostic test."

Another factor that makes genetic studies for ADHD so complicated is the fact that ADHD is often co-occurring with other mental health conditions like anxiety, depression, and tic disorders, King says, and these disorders may also be partly genetic.

King says that aside from genetics, various other factors predispose somebody to ADHD, and some of them are preventable. Some examples of ADHD risk factors are:

While genetics are not the only factor in whether or not someone develops ADHD, there certainly is a genetic component, which has been proven through years of scientific research. However, there is not one specific gene that is directly associated with ADHD.

There are multiple non-genetic risk factors that may contribute to an individual's ADHD, as well. Regardless of what caused somebody's ADHD, there are multiple treatment options available that can help manage ADHD symptoms and improve quality of life.

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ADHD is partially genetic, but there are other risk factors that play a key role - Insider - INSIDER

Genetics

Genetic variation not linked with differences in COVID-19 morbidity and mortality – News-Medical.Net

September 26, 2020 medical

Reviewed by Emily Henderson, B.Sc.Sep 24 2020

A comprehensive search of genetic variation databases has revealed no significant differences across populations and ethnic groups in seven genes associated with viral entry of SARS-CoV-2.

African Americans and Latinos in the United States and ethnic minorities in the United Kingdom are disproportionately affected by COVID-19. They are more likely to develop severe symptoms and also show significantly higher mortality compared with other regional and ethnic groups.

To investigate if this disparity could be caused by genetic variation, a team of three researchers - including Assistant Professor Ji-Won Lee of Hokkaido University's Graduate School of Dental Medicine - surveyed publicly available databases of genomic variants, including gnomAD, the Korean Reference Genome Database, TogoVar (a Japanese genetic variation database) and the 1000 Genomes Project. They studied variants across multiple regional and ethnic groups in seven genes known to play roles in viral entry into host cells and recognition of viral RNA in host cells.

SARS-CoV-2 has spiked protein (S protein) on its envelope, which encloses the virus. Before the virus can enter host cells, the S protein has to bind with the ACE2 receptor on the cell surface. It is then broken into two pieces by the enzymes TMPRSS2 and cathepsin B and L. After the virus enters the cells, the viral RNA binds with proteins such as TLR3, TLR7 and TLR8, triggering an innate immune response.

According to the results, there were genetic variants in these seven proteins, with the largest number of variants in ACE2. However, very few of these variations alter the functions of these proteins. Since the overall variation frequency was extremely low (less than 0.01 percent), the scientists determined there is no significant difference across populations or ethnic groups in the functions of the seven proteins involved in infection.

The team's findings suggest that differences in morbidity and mortality are not the result of genetic variations in genes for viral entry across populations. Rather, it is more likely that preexisting medical conditions, individual medical histories, environmental factors and healthcare disparities play a significant role in affecting the morbidity and mortality of COVID-19. However, due to the limited size of the population databases used in this study, additional research using more diverse human genome databases is required. Additionally, other studies have shown that genetic factors may contribute to serious cases.

Also taking part in the study were In-Hee Lee of Boston Children's Hospital (Computational Health Informatics Program) and Sek Won Kong of Harvard Medical School (Department of Pediatrics). The team's findings were published online on August 25, 2020, in the medical journal Infection, Genetics and Evolution.

Source:

Journal reference:

Lee, I., et al. (2020) A survey of genetic variants in SARS-CoV-2 interacting domains of ACE2, TMPRSS2 and TLR3/7/8 across populations. Infection, Genetics and Evolution. doi.org/10.1016/j.meegid.2020.104507.

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Genetic variation not linked with differences in COVID-19 morbidity and mortality - News-Medical.Net