StemCell Therapy

SAN FRANCISCO, May 5, 2020 /PRNewswire/ -- Invitae Corporation (NYSE: NVTA), a leading medical genetics company, today announced financial and operating results for the first quarter ended March 31, 2020.

"We started the year with a very strong quarter, delivering record growth in volume and first quarter revenues and giving us strong momentum as we began experiencing impacts from the pandemic. As healthcare has shifted, we have been able to quickly leverage our pre-existing strengths, notably our telehealth offerings and our ability to deliver genetic testing remotely," said Sean George, co-founder and chief executive officer of Invitae. "Looking ahead, our investments in diversified products, services, technologies and geographies mean we are well-equipped to drive growth across an increasing number of customer segments as we drive genetics into mainstream medicine."

First Quarter 2020 Financial Results

Total operating expense, excluding cost of revenue, for the first quarter of 2020 was $121.6 million. Non-GAAP operating expense, which excludes amortization of acquired intangible assets and acquisition-related stock-based compensation, was $101.9 million in the first quarter of 2020. Interest and other expense, net and net loss are preliminary and subject to change as we finalize acquisition-related adjustments. These adjustments will be incorporated in Invitae's Form 10-Q to be filed with the SEC on or before May 11, 2020.

Preliminary net loss for the first quarter of 2020 was $102.2 million, or $1.03 preliminary net loss per share, compared to a net loss of $37.7 million in the first quarter of 2019, or $0.47 net loss per share. Preliminary non-GAAP net loss was $79.8 million in the first quarter of 2020, or $0.80 preliminary non-GAAP net loss per share.

At March 31, 2020 cash, cash equivalents, restricted cash, and marketable securities totaled $301.0 million. Net decrease in cash, cash equivalents and restricted cash for the quarter was $61.0 million. Cash burn, including various acquisition-related expenses, was $98.5 million for the quarter; $66.2 million when excluding $32.3 million cash paid to acquire Diploid.

In April, the company completed a public offering of common stock, resulting in gross proceeds of $184.0 million and $173.0 million in net proceeds after deducting underwriting discounts and commissions and offering expenses.

COVID-19 ImpactGlobal stay-at-home orders, lockdowns and shutdown of non-emergency healthcare and elective procedures began impacting Invitae during the second half of March. Invitae took a number of steps in response, including:

The impact of the pandemic on testing volume has and is likely to continue to vary based on clinical area, geography and clinician type. In response, the company has taken a number of steps to reduce cash burn.

The company is continuing to closely monitor the impact of the COVID-19 pandemic and plans to continue to reduce previously communicated cash burn through the remainder of 2020.

Given the unknown duration and extent of COVID-19's impact on our business, and the healthcare system in general, Invitae has previously withdrawn its 2020 guidance.

Corporate and Scientific Highlights

Webcast and Conference Call DetailsManagement will host a conference call and webcast today at 4:30 p.m. Eastern / 1:30 p.m. Pacific to discuss financial results and recent developments. The dial-in numbers for the conference call are (866) 324-3683 for domestic callers and (509) 844-0959 for international callers, and the reservation number for both is 9557177. Please note, after dialing in, you will be prompted to enter the Conference ID and then the pound "#" sign to enter the call. Following prepared remarks, management will respond to questions from investors and analysts, subject to time limitations.

The live webcast of the call and slide deck may be accessed by visiting the investors section of the company's website atir.invitae.com. A replay of the webcast and conference call will be available shortly after the conclusion of the call and will be archived on the company's website.

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

Safe Harbor StatementThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to preliminary financial results, including preliminary net loss and net loss per share; the company's belief that it has been able to quickly leverage its telehealth offerings and its ability to deliver genetic testing remotely; he company's belief that it is well-equipped to drive growth across an increasing number of customer segments as it drives genetics into mainstream medicine; the impact of the COVID-19 pandemic on the company's business, and the measures it has taken or may take In the future with respect thereto; the impact of the company's acquisitions, partnerships and product offerings; and the company's beliefs regarding the growth of its business, its position and impact on the genetic testing industry, its success in executing on its mission and achieving its goals, and the benefits of genetic testing. Forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially, and reported results should not be considered as an indication of future performance. These risks and uncertainties include, but are not limited to: the impact of the COVID-19 pandemic on the company, and the effectiveness of the efforts it has taken or may take in the future in response thereto; the completion of the closing process, including finalization of acquisition-related adjustments and the magnitude thereof; the company's ability to continue to grow its business, including internationally; the company's history of losses; the company's ability to compete; the company's failure to manage growth effectively; the company's need to scale its infrastructure in advance of demand for its tests and to increase demand for its tests; the risk that the company may not obtain or maintain sufficient levels of reimbursement for its tests; the company's failure to successfully integrate or fully realize the anticipated benefits of acquired businesses; the company's ability to use rapidly changing genetic data to interpret test results accurately and consistently; security breaches, loss of data and other disruptions; laws and regulations applicable to the company's business; and the other risks set forth in the company's Annual Report on Form 10-K for the year ended December 31, 2019. These forward-looking statements speak only as of the date hereof, and Invitae Corporation disclaims any obligation to update these forward-looking statements.

Non-GAAP Financial MeasuresTo supplement Invitae's consolidated financial statements prepared in accordance with generally accepted accounting principles in the United States (GAAP), the company is providing several non-GAAP measures, including non-GAAP gross profit, non-GAAP cost of revenue, non-GAAP operating expense, including non-GAAP research and development, non-GAAP selling and marketing and non-GAAP general and administrative, as well as non-GAAP net loss and net loss per share and non-GAAP cash burn. These non-GAAP financial measures are not based on any standardized methodology prescribed by GAAP and are not necessarily comparable to similarly-titled measures presented by other companies. Management believes these non-GAAP financial measures are useful to investors in evaluating the company's ongoing operating results and trends.

Management is excluding from some or all of its non-GAAP operating results (1) amortization of acquired intangible assets and (2) acquisition-related stock-based compensation related to inducement grants. These non-GAAP financial measures are limited in value because they exclude certain items that may have a material impact on the reported financial results. Management accounts for this limitation by analyzing results on a GAAP basis as well as a non-GAAP basis and also by providing GAAP measures in the company's public disclosures.

Cash burn excludes (1) changes in marketable securities and (2) cash received from exercises of warrants. Management believes cash burn is a liquidity measure that provides useful information to management and investors about the amount of cash consumed by the operations of the business. A limitation of using this non-GAAP measure is that cash burn does not represent the total change in cash, cash equivalents, and restricted cash for the period because it excludes cash provided by or used for other operating, investing or financing activities. Management accounts for this limitation by providing information about the company's operating, investing and financing activities in the statements of cash flows in the consolidated financial statements in the company's most recent Quarterly Report on Form 10-Q and Annual Report on Form 10-K and by presenting net cash provided by (used in) operating, investing and financing activities as well as the net increase or decrease in cash, cash equivalents and restricted cash in its reconciliation of cash burn.

In addition, other companies, including companies in the same industry, may not use the same non-GAAP measures or may calculate these metrics in a different manner than management or may use other financial measures to evaluate their performance, all of which could reduce the usefulness of these non-GAAP measures as comparative measures. Because of these limitations, the company's non-GAAP financial measures should not be considered in isolation from, or as a substitute for, financial information prepared in accordance with GAAP. Investors are encouraged to review the non-GAAP reconciliations provided in the tables below.

INVITAE CORPORATION

Consolidated Balance Sheets

(in thousands)

(unaudited)

March 31,2020

December 31,2019

Assets

Current assets:

Cash and cash equivalents

$

90,220

$

151,389

Marketable securities

204,388

240,436

Accounts receivable

37,734

32,541

Prepaid expenses and other current assets

25,085

18,032

Total current assets

357,427

442,398

Property and equipment, net

41,085

37,747

Operating lease assets

37,588

36,640

Restricted cash

6,343

6,183

Intangible assets, net

163,378

125,175

Goodwill

177,432

126,777

Other assets

7,635

6,681

Total assets

$

790,888

$

781,601

Liabilities and stockholders' equity

Total liabilities and stockholders' equity

$

790,888

$

781,601

Certain line items have been condensed as we finalize acquisition-related adjustments. These adjustments will be incorporated in Invitae's Form 10-Q to be filed with the SEC on or before May 11, 2020.

INVITAE CORPORATION

Consolidated Statements of Operations

(in thousands, except per share data)

(unaudited)

Three Months EndedMarch 31,

2020

2019

Revenue:

Test revenue

$

63,078

$

39,619

Other revenue

1,170

934

Total revenue

64,248

40,553

Cost of revenue

40,422

21,254

Research and development

55,668

17,994

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Invitae Reports More Than $64 Million in Revenue Driven by More Than 154,000 Samples Accessioned in the First Quarter of 2020 - PRNewswire

The novel coronavirus behind the COVID-19 pandemic may have jumped from its original animal host into humans as early as October, according to the latest analysis of the changing viral genome.

Scientists analysing the genetic trees of 7,666 SARS-CoV-2 genomes collected from around the world estimated a common ancestor to the circulating COVID virus strains as having most likely appeared in China at some point between Oct. 6 and Dec. 11, 2019.

The genomic diversity of the global SARS-CoV-2 population being recapitulated in multiple countries points to extensive worldwide transmission of COVID-19, likely from extremely early on in the pandemic, they write in a paper just published in the peer-reviewed journal Infection, Genetics and Evolution.

This suggests that the virus was probably infecting people in multiple countries weeks or even months before the official outbreak began in January 2020 in Wuhan, China.

All these ideas about trying to find a Patient Zero are pointless because there are so many patient zeros, genetics researcher Francois Balloux of the University College London Genetics Institute told CNN. It has been introduced and introduced and introduced in almost all countries.

However, despite this evidence of the virus already circulating globally much earlier than previously suspected, the scientists squashed the hopeful notion that sufficient numbers of people might already have been exposed to the virus to build up substantial herd immunity around the world.

This rules out any scenario that assumes SARS-CoV-2 may have been in circulation long before it was identified, and hence have already infected large proportions of the population, the scientists wrote in their paper, entitled Emergence of genomic diversity and recurrent mutations in SARS-CoV-2.

The latest analysis provides no evidence to support recent conspiracy theories asserting that the COVID-19 virus was deliberately created or released, intentionally or otherwise, from a lab. The authors reference earlier genetic analysis making clear that SARS-CoV-2 has natural origins, most likely having jumped into humans originally from bats.

SARS-CoV-2 shares 96 percent of its genome with a horseshoe bat virus called BatCoV RaTG13, which researchers say shows no evidence of recombination events. An intermediate animal host connecting this bat virus to human COVID has still not been definitively identified, but is thought to have been pangolins an endangered animal illegally traded in Asian wildlife markets and also widely used in non-scientific Chinese medicine.

Dr. Anthony Fauci,director of the United States National Institute of Allergies and Infectious Diseases, has also spoken out strongly against ideas of deliberate or even accidental release from a Chinese lab. Everything about the stepwise evolution over time strongly indicates that [this virus] evolved in nature and then jumped species, Fauci told National Geographic.

There is some good news from this latest genomic analysis because it shows only a limited rate of mutations among the multiple strains of SARS-CoV-2, which still have enough of their genes and proteins in common to mean that any vaccine or treatment drug should have long-term efficacy.

The study also helps identify the parts of the SARS-CoV-2 genome which are conserved meaning they stay the same despite other genetic variations helping vaccine researchers better identify targets for their differing approaches. The researchers write that it is important to stress that there is no evidence for the evolution of distinct phenotypes in SARS-CoV-2 at this stage.

According to the World Health Organization, there are now more than 100 COVID-19 candidate vaccines in development around the world.

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Covid pandemic might have begun as early as October, experts say - Alliance for Science

The novel coronavirus causing COVID-19 seems to hit some people harder than others, with some people experiencing only mild symptoms and others being hospitalized and requiring ventilation. Though scientists at first thought age was the dominant factor, with young people avoiding the worst outcomes, new research has revealed a suite of features impacting disease severity. These influences could explain why some perfectly healthy 20-year-old with the disease is in dire straits, while an older 70-year-old dodges the need for critical interventions.

These risk factors include:AgeDiabetes (type 1 and type 2)Heart disease and hypertensionSmokingBlood typeObesityGenetic factors

About 8 out of 10 deaths associated with COVID-19 in the U.S. have occurred in adults ages 65 and older, according to the U.S. Centers for Disease Control and Prevention (CDC). The risk of dying from the infection, and the likelihood of requiring hospitalization or intensive medical care, increases significantly with age. For instance, adults ages 65-84 make up an estimated 4-11% of COVID-19 deaths in the U.S, while adults ages 85 and above make up 10-27%.

The trend may be due, in part, to the fact that many elderly people have chronic medical conditions, such as heart disease and diabetes, that can exacerbate the symptoms of COVID-19, according to the CDC. The ability of the immune system to fight off pathogens also declines with age, leaving elderly people vulnerable to severe viral infections, Stat News reported.

Related: Coronavirus in the US: Latest COVID-19 news and case counts

Diabetes mellitus a group of diseases that result in harmful high blood sugar levels also seems to be linked to risk of more severe COVID-19 infections.

The most common form in the U.S. is type 2 diabetes, which occurs when the body's cells don't respond to the hormone insulin. As a result, the sugar that would otherwise move from the bloodstream into cells to be used as energy just builds up in the bloodstream. (When the pancreas makes little to no insulin in the first place, the condition is called type 1 diabetes.)

In a review of 13 relevant studies, scientists found that people with diabetes were nearly 3.7 times more likely to have a critical case of COVID-19 or to die from the disease compared with COVID-19 patients without any underlying health conditions (including diabetes, hypertension, heart disease or respiratory disease), they reported online April 23 in the Journal of Infection.

Even so, scientists don't know whether diabetes is directly increasing severity or whether other health conditions that seem to tag along with diabetes, including cardiovascular and kidney conditions, are to blame.

That fits with what researchers have seen with other infections and diabetes. For instance, flu and pneumonia are more common and more serious in older individuals with type 2 diabetes, scientists reported online April 9 in the journal Diabetes Research and Clinical Practice. In a literature search of relevant studies looking at the link between COVID-19 and diabetes, the authors of that paper found a few possible mechanisms to explain why a person with diabetes might fare worse when infected with COVID-19. These mechanisms include: "Chronic inflammation, increased coagulation activity, immune response impairment and potential direct pancreatic damage by SARS-CoV-2."

Related: 13 coronavirus myths busted by science

Mounting research has shown the progression of type 2 diabetes is tied to changes in the body's immune system. This link could also play a role in poorer outcomes in a person with diabetes exposed to SARS-CoV-2, the virus that causes COVID-19.

No research has looked at this particular virus and immune response in patients with diabetes; however, in a study published in 2018 in the Journal of Diabetes Research, scientists found through a review of past research that patients with obesity or diabetes showed immune systems that were out of whack, with an impairment of white blood cells called Natural Killer (NK) cells and B cells, both of which help the body fight off infections. The research also showed that these patients had an increase in the production of inflammatory molecules called cytokines. When the immune system secretes too many cytokines,a so-called "cytokine storm" can erupt and damage the body's organs. Some research has suggested that cytokine storms may be responsible for causing serious complications in people with COVID-19, Live Science previously reported. Overall, type 2 diabetes has been linked with impairment of the very system in the body that helps to fight off infections like COVID-19 and could explain why a person with diabetes is at high risk for a severe infection.

Not all people with type 2 diabetes are at the same risk, though: A study published May 1 in the journal Cell Metabolism found that people with diabetes who keep their blood sugar levels in a tighter range were much less likely to have a severe disease course than those with more fluctuations in their blood sugar levels.

Scientists aren't sure whether this elevated risk of a severe COVID-19 infection also applies to people with type 1 diabetes (T1D). A study coordinated by T1D Exchange a nonprofit research organization focused on therapies for those with type 1 diabetes launched in April to study the outcomes of T1D patients infected with COVID-19. When a person with T1D gets an infection, their blood sugar levels tend to spike to dangerous levels and they can have a buildup of acid in the blood, something called diabetic ketoacidosis. As such, any infection can be dangerous for someone with type 1 diabetes.

People with conditions that affect the cardiovascular system, such as heart disease and hypertension, generally suffer worse complications from COVID-19 than those with no preexisting conditions, according to the American Heart Association. That said, historically healthy people can also suffer heart damage from the viral infection.

The first reported coronavirus death in the U.S., for instance, occurred when the virus somehow damaged a woman's heart muscle, eventually causing it to burst, Live Science reported. The 57-year-old maintained good health and exercised regularly before becoming infected, and she reportedly had a healthy heart of "normal size and weight." A study of COVID-19 patients in Wuhan, China, found that more than 1 in 5 patients developed heart damage some of the sampled patients had existing heart conditions, and some did not.

In seeing these patterns emerge, scientists developed several theories as to why COVID-19 might hurt both damaged hearts and healthy ones, according to a Live Science report.

In one scenario, by attacking the lungs directly, the virus might deplete the body's supply of oxygen to the point that the heart must work harder to pump oxygenated blood through the body. The virus might also attack the heart directly, as cardiac tissue contains angiotensin-converting enzyme 2 (ACE2) a molecule that the virus plugs into to infect cells. In some individuals, COVID-19 can also kickstart an overblown immune response known as a cytokine storm, wherein the body becomes severely inflamed and the heart could suffer damage as a result.

People who smoke cigarettes may be prone to severe COVID-19 infections, meaning they face a heightened risk of developing pneumonia, suffering organ damage and requiring breathing support. A study of more than 1,000 patients in China, published in the New England Journal of Medicine, illustrates this trend: 12.3% of current smokers included in the study were admitted to an ICU, were placed on a ventilator or died, as compared with 4.7% of nonsmokers.

Cigarette smoke might render the body vulnerable to the coronavirus in several ways, according to a recent Live Science report. At baseline, smokers may be vulnerable to catching viral infections because smoke exposure dampens the immune system over time, damages tissues of the respiratory tract and triggers chronic inflammation. Smoking is also associated with a multitude of medical conditions, such as emphysema and atherosclerosis, which could exacerbate the symptoms of COVID-19.

A recent study, posted March 31 to the preprint database bioRxiv, proposed a more speculative explanation as to why COVID-19 hits smokers harder. The preliminary research has not yet been peer-reviewed, but early interpretations of the data suggest that smoke exposure increases the number of ACE2 receptors in the lungs the receptor that SARS-CoV-2 plugs into to infect cells.

Many of the receptors appear on so-called goblet and club cells, which secrete a mucus-like fluid to protect respiratory tissues from pathogens, debris and toxins. It's well-established that these cells grow in number the longer a person smokes, but scientists don't know whether the subsequent boost in ACE2 receptors directly translates to worse COVID-19 symptoms. What's more, it's unknown whether high ACE2 levels are relatively unique to smokers, or common among people with chronic lung conditions.

Several early studies have suggested a link between obesity and more severe COVID-19 disease in people. One study, which analyzed a group of COVID-19 patients who were younger than the age of 60 in New York City, found that those who were obese were twice as likely as non-obese individuals to be hospitalized and were 1.8 times as likely to be admitted into critical care.

"This has important and practical implications" in a country like the U.S. where nearly 40% of adults are obese, the authors wrote in the study, which was accepted into the journal Clinical Infectious Diseases but not yet peer-reviewed or published. Similarly, another preliminary study that hasn't yet been peer-reviewed found that the two biggest risk factors for being hospitalized from the coronavirus are age and obesity. This study, published in medRxiv looked at data from thousands of COVID-19 patients in New York City, but studies from other cities around the world found similar results, as reported by The New York Times.

A preliminary study from Shenzhen, China, which also hasn't been peer-reviewed, found that obese COVID-19 patients were more than twice as likely to develop severe pneumonia as compared with patients who were normal weight, according to the report published as a preprint online in the journal The Lancet Infectious Diseases. Those who were overweight, but not obese, had an 86% higher risk of developing severe pneumonia than did people of "normal" weight, the authors reported. Another study, accepted into the journal Obesity and peer-reviewed, found that nearly half of 124 COVID-19 patients admitted to an intensive care unit in Lille, France, were obese.

It's not clear why obesity is linked to more hospitalizations and more severe COVID-19 disease, but there are several possibilities, the authors wrote in the study. Obesity is generally thought of as a risk factor for severe infection. For example, those who are obese had longer and more severe disease during the swine flu epidemic, the authors wrote. Obese patients might also have reduced lung capacity or increased inflammation in the body. A greater number of inflammatory molecules circulating in the body might cause harmful immune responses and lead to severe disease.

Blood type seems to be a predictor of how susceptible a person is to contracting SARS-CoV-2, though scientists haven't found a link between blood type per se and severity of disease.

Jiao Zhao, of The Southern University of Science and Technology, Shenzhen, and colleagues looked at blood types of 2,173 patients with COVID-19 in three hospitals in Wuhan, China, as well as blood types of more than 23,000 non-COVID-19 individuals in Wuhan and Shenzhen. They found that individuals with blood types in the A group (A-positive, A-negative and AB-positive, AB-negative) were at a higher risk of contracting the disease compared with non-A-group types. People with O blood types (O-negative and O-positive) had a lower risk of getting the infection compared with non-O blood types, the scientists wrote in the preprint database medRxiv on March 27; the study has yet to be reviewed by peers in the field.

In a more recent study of blood type and COVID-19, published online April 11 to medRxiv, scientists looked at 1,559 people tested for SARS-CoV-2 at New York Presbyterian hospital; of those, 682 tested positive. Individuals with A blood types (A-positive and A-negative) were 33% more likely to test positive than other blood types and both O-negative and O-positive blood types were less likely to test positive than other blood groups. (There's a 95% chance that the increase in risk ranges from 7% to 67% more likely.) Though only 68 individuals with an AB blood type were included, the results showed this group was also less likely than others to test positive for COVID-19.

The researchers considered associations between blood type and risk factors for COVID-19, including age, sex, whether a person was overweight, other underlying health conditions such as diabetes mellitus, hypertension, pulmonary diseases and cardiovascular diseases. Some of these factors are linked to blood type, they found, with a link between diabetes and B and A-negative blood types, between overweight status and O-positive blood groups, for instance, among others. When they accounted for these links, the researchers still found an association between blood type and COVID-19 susceptibility. When the researchers pooled their data with the research by Zhao and colleagues out of China, they found similar results as well as a significant drop in positive COVID-19 cases among blood type B individuals.

Why blood type might increase or decrease a person's risk of getting SARS-CoV-2 is not known. A person's blood type indicates what kind of certain antigens cover the surfaces of their blood cells; These antigens produce certain antibodies to help fight off a pathogen. Past research has suggested that at least in the SARS coronavirus (SARS-CoV), anti-A antibodies helped to inhibit the virus; that could be the same mechanism with SARS-CoV-2, helping blood group O individuals to keep out the virus, according to Zhao's team.

Many medical conditions can worsen the symptoms of COVID-19, but why do historically healthy people sometimes fall dangerously ill or die from the virus? Scientists suspect that certain genetic factors may leave some people especially susceptible to the disease, and many research groups aim to pinpoint exactly where those vulnerabilities lie in our genetic code.

In one scenario, the genes that instruct cells to build ACE2 receptors may differ between people who contract severe infections and those who hardly develop any symptoms at all, Science magazine reported. Alternatively, differences may lie in genes that help rally the immune system against invasive pathogens, according to a recent Live Science report.

For instance, a study published April 17 in the Journal of Virology suggests that specific combinations of human leukocyte antigen (HLA) genes, which train immune cells to recognize germs, may be protective against SARS-CoV-2, while other combinations leave the body open to attack. HLAs represent just one cog in our immune system machinery, though, so their relative influence over COVID-19 infection remains unclear. Additionally, the Journal of Virology study only used computer models to simulate HLA activity against the coronavirus; clinical and genetic data from COVID-19 patients would be needed to flesh out the role of HLAs in real-life immune responses.

Originally published on Live Science.

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Why COVID-19 kills some people and spares others. Here's what scientists are finding. - Livescience.com

Six weeks ago, with little fanfare, a network of geneticists launched an obscure but potentially game-changing initiative. Their aim: to learn why people with particular DNA profiles end up dying from the coronavirusor completely avoiding its effects. Ultimately, they want to devise ways for scientists to cook up new therapies that might alter how our nanosize genes operate as a way of reversing or accelerating the pathogens progress. Called the COVID-19 Host Genetics Initiative, the project now involves close to 700 scientists and researchers, worldwide, who are busily comparing DNA data from pandemic victims to literally millions of existing DNA profiles of millions of people.

To appreciate how our genes might be impacted by the onslaught of COVID-19, imagine this: that a tiny, invisible bug is hovering over the surface of a cell inside your bodysay a lung cell. You dont know it yet, but youve just been infected with SARS-Cov-2. Maybe it came from that jogger who whizzed past you on the sidewalk, or that tabletop you touched before rubbing your eyes. Whatever its source, there it is, circulating inside you: a fuzzy, sphere-shaped pathogen thats less than 1/1000 the width of a human hair. Prickly, with spikes on its outside, its searching for a place to plug into and enter your cell. Its a little like a key and a lock, where the key (the virus) wants to slip into the keyhole (a receptor on the cell) and then release a payload that will be up to no good.

Except that, in some people, the virus-key doesnt fit the lock and is blocked from entering the cell. In others, it slips right in, leading to illness and sometimes to rapid deterioration and even death. One potential differencesay geneticists who are working day and night to better understand how SARS-Cov-2 invades and attacks our cellsmight be because your DNA code differs from mine. Yours might inherently spurn the virus at the cellular level; mine might make me more susceptible.

So what determines who gets dangerously sick? We know that people who are older and have underlying diseases like diabetes and heart disease are at higher risk for having a bad response to COVID-19, explained Mark Daly, a 52-year-old geneticist and the director of the Institute for Molecular Medicine in Helsinki, Finland. Other factors include higher risk biases that involve ethnicity, class, vocation, geographic location, and the medical resources available at the time of treatment. And yet, according to Daly, this doesnt explain why relatively healthy people, including young people, are sometimes having severe and life-threatening reactions such as very high fevers, pneumonia, and difficulty with breathing that requires oxygen and sometimes a ventilator. Most likely this has something to do with differences in their genes.

Daly should know. With his Paul Reverelike ponytail, circular hippie glasses, and lean, determined face, hes a pioneer of modern genetics who was a key player during and after the Human Genome Project, the huge international effort in the 1990s and early 2000s that sequenced the first-ever human genome. And as the pandemic has been raging, Daly, a physicist, decided to help spearhead a remarkable hive-mind effort: the COVID-19 Host Genetics Initiative.

The project was announced on March 16 in a tweet posted by Dalys cohort Andrea Ganna: Goal: aggregate genetic and clinical information on individuals affected by COVID-19. The response was immediate. Within days, scientists from over 150 organizations in more than 30 countries on six continents agreed to join. Thats the ideal use of the hive mind: a conglomeration of big brains and, in this case, their disparate data sources, to solve one huge problem. Participants have come not only from Harvard and MIT (institutions with which Daly has ongoing affiliations) and the usual institutional suspects in North America, Europe, and the wealthier Asian countries, but also from the Qatar Genome Program, Vietnams SARS-Cov-2 Susceptibility Program, and CLHORAZbased in Burkina Faso.

View original post here:
What Do Your Genetics Have to Do With Your Chances of Dying From Coronavirus? - Vanity Fair

Well come clean the pints and pub grub lifestyle often associated with the great British local hasnt dovetailed all that smoothly with the NHS since its launch on 5 July 1948, even if the community spirit that underpins arguably this countrys greatest piece of modern policy-making is broadly shared by pubs.

Born from a long-standing ideal that healthcare should be readily available based on clinical need rather than ability to pay, health minister Aneurin Bevan unveiled the nascent NHS at Park Hospital in Manchester after the passage of the National Health Service Act in 1946.

Despite extensive cutbacks in recent years, today, total health spending in England stands at around 130bn more than the annual GDP of Ukraine or Morocco with the NHS employing more people across the UK than live in Birmingham. According to a report by the Department of Health in December 2005, the NHS deals with more than 1m patients every 36 hours.

The Ram Inn, in Brundall, Norfolk, has raised close to 1,000 by asking locals to leave their rainbow images for the pub to display in return for a donation to theNorfolk & Norwich Hospitals Charity.

The operators of the Garden House in Norwich have pledged to use 2,000 worth of tech vouchers received as winners of BT Sports latest Manager of the Month prize to treat staff at local NHS services.

East Anglian pub operator Chestnut has teamed up with Food4Heroes to provide tens of thousands of free meals to the regions front-line NHS staff during the Covid-19 emergency.

Camden Town Brewery has produced a Heroes version of its flagship Hells lager which will be sold online and handed out to 20,000 NHS hospital workers - with proceeds from sales going to NHS charities.

Rendezvous & Royal Oak in Weymouth, Dorset, has raised 13,200 for Dorset County Hospital after live streaming 20-act music festival Quayfest.

Cornish brewer and pub operator St Austell Brewery has joined forces with takeaway and delivery service Pub Grub to deliver 800 bottles of soft drink to frontline staff at Royal Cornwall Hospital.

Publican Sylvia Ferron of the Foaming Tankard in Birmingham has returned to full-time work on the NHS front line during the Covid-19 emergency just months after entering the on-trade.

SallyAbof Michelin star-holding Estrella Damm Top 50 Gastropub frontrunner Harwood arms in London has cooked 100 meals per day for NHS staff through charity Hospitality for Heroes

Furloughed Stonegate Pub Company general manager, Cee-Jay Williams of the Junction Tap in Woking, Surrey, is using a 3D printer to help the NHS tackle a shortfall of 80,000 plastic visor clips.

Publican Eduardo Dantas of Tia Maria Bar & Restaurant in Vauxhall, south London, was reduced to tears by Staff at Londons Kings College Hospital after they surprised him with a round of applause during one of his daily deliveries of 60 free meals.

Lisa Staples of the Crown Inn, Gayton, Norfolk, has set up a website Free NHS Rooms for publicans to list their rooms so that NHS workers can find living quarters near hospitals.

The onset of the Covid-19 pandemic which has seen NHS staff treat close to 200,000 confirmed cases across the UK thus far has led to an unprecedented wave of gratitude from the public, with pubs more than playing their part.

Though the on-trade has regularly shown its support for the NHS over the years notable mentions include 2020 Great British Pub Awards-winning Best Local, the Chandos Arms in north London, throwing a street party for the NHSs 70th anniversary in 2018 and Beavertown Brewery offering free beer to blood donors the current outpouring is arguably the greatest show of support pubs have shown this countrys health service.

From Rendezvous & Royal Oak in Weymouth, Dorset, raising 13,200 for Dorset County Hospital by live streaming a 20-act music festival, for example, to pubs delivering tens of thousands of free meals and even joining efforts to make personal protective equipment, the on-trade has branched into some surprising areas to help the NHS through the ongoing emergency.

Whats more, while turning blue is medically speaking a very bad sign, a number of Britains pubs have chosen to do so in tribute to front-line workers battling Covid-19 though it wont obviously fall on the NHS to resuscitate them when operators are cleared to reopen.

The honour of having your face painted onto the front of a pub is usually one reserved for lords, ladies or royalty, but such is Britains rich medical history that a number of its nurses and scientists have had their names or tributes emblazoned above the door of a one of the nations many watering holes.

While London pubs the Sir Alexander Fleming in Paddington named after the Scottish inventor credited with the discovery of penicillin and the Florence Nightingale in Waterloo have sadly shut up shop since the turn of the Millennium, the NHSs chief architect, Bevan, has been immortalised by beverage behemoth JD Wetherspoon, which named Cardiff pub the Aneurin Bevan in his honour.

Other on-trade tributes to medicine include the Old Doctor Butlers Head in Masons Avenue, London, which was named after physician William Butler, a doctor at the court of James I who is credited with inventing the popular 17th century medicinal drink Dr Butlers purging ale.

Whats more, the namesake of Grade II-listed pub the William Harvey in Ashford, Kent, discovered the circulation of blood and once lived in what is now the pub. Though the local hospital is also named after Harvey, the pub is said to have got there first.

In a less direct tribute, the Air Balloon pub in Gloucestershire is named in tribute to physician Edward Jenner who popularised vaccination with his work to tackle smallpox. Jenner, who spent a fair amount of his time away from his work enthusing over hydrogen balloons, took to the skies from Berkeley Castle in Gloucestershire in September 1784 before landing more than 20 miles away in Birdlip where the local pub is now named in tribute to his flight.

Its not an understatement to suggest that James Watson and Francis Crick discovering the structure of DNA and how it carries genetic information in 1953 laid the groundwork for almost 75 years of game-changing medical discoveries and treatment.

Yet while images of DNAs double helix structure are among the most recognisable and iconic in science, what isnt as commonplace is the fact the pairs discovery was first announced in Cambridge pub, the Eagle.

The Grade II-listed venue was the local watering hole for scientists working at the University of Cambridges Cavendish Laboratory such as Watson and Crick, who would claim the Nobel Prize in Physiology or Medicine in 1962 for their discovery.

The pairs work to unravel DNAs structure essentially clarified how genes work. By uncovering the molecular properties of genes, Watson and Cricks discovery meant that scientists could understand how they could be damaged, why mutations could cause harmful diseases and allowed experts to work out ways to fix them. For example, in April 2020, Rhys Evans became the first child in Britain to be cured of an inherited disorder as a result of gene therapy stemming from Watson and Cricks work.

While MPs voted to ban smoking in enclosed public spaces including pubs as of summer 2007, more than 30 years prior a publican in Yorkshire created Britains first licensed smokeless zone.

According to the Pub History Society, Essex-born publican John Showers declaring the New Inn in Appletreewick near Skipton, in North Yorkshire, the worlds first no smoking inn in the early 1970s generated global media attention and even a congratulatory letter from then health minister George Godber.

While the publicans initial objection to customers smoking on his premises focused on the amount of damage it caused his pubs carpets, floors and furniture on top of nicotine staining his walls and ceilings and the fire risk the death of a close friend from lung cancer saw Showers shift his ire from building damage to disease.

Showerss then sensational ban featured on television, radio and newspapers both at home and abroad, with the publican advertising the New Inn as Englands First Fresh Air Inn.

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NHS: what role have pubs played in medical breakthroughs? - MorningAdvertiser.co.uk

CAMBRIDGE, Mass. and NEW YORK, May 06, 2020 (GLOBE NEWSWIRE) -- Black Diamond Therapeutics, Inc. (Nasdaq: BDTX), a precision oncology medicine company pioneering the discovery and development of small molecule, tumor-agnostic therapies, today announced that its President and Chief Executive Officer, David M. Epstein, Ph.D., will present an update about the Companys business at the Bank of America Global Research Health Care Conference 2020. The presentation will take place on Tuesday, May 12, 2020, at 4:20 PM ET.

About Black DiamondBlack Diamond Therapeutics is a precision oncology medicine company pioneering the discovery of small molecule, tumor-agnostic therapies. Black Diamond targets undrugged mutations in patients with genetically defined cancers. Black Diamond is built upon a deep understanding of cancer genetics, protein structure and function, and medicinal chemistry. The Companys proprietary technology platform, Mutation-Allostery-Pharmacology, or MAP, platform, is designed to allow Black Diamond to analyze population-level genetic sequencing data to identify oncogenic mutations that promote cancer across tumor types, group these mutations into families, and develop a single small molecule therapy in a tumor-agnostic manner that targets a specific family of mutations. Black Diamond was founded by David M. Epstein, Ph.D., and Elizabeth Buck, Ph.D., and, beginning in 2017, together with Versant Ventures, began building the MAP platform and chemistry discovery engine. For more information, please visit http://www.blackdiamondtherapeutics.com.

Contacts:

For Investors:Natalie Wildenradtinvestors@bdtherapeutics.com

For Media:Kathy Vincent(310) 403-8951media@bdtherapeutics.com

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Black Diamond Therapeutics to Present at the Bank of America Global Research Health Care Conference 2020 - GlobeNewswire

CALGARY, May 6, 2020 /CNW/ - We are surrounded by data. Lots of it. It is particularly true for genomics data, and the interpretation of complex sets of information have a significant role in improving the speed and effectiveness of applying genomic data in a number of areas.

When the Enabling Bioinformatics Solutions funding competition was first announced, we identified agriculture and human health as two key areas that were generating large amounts of genomics data. Applicants were asked to submit proposals that would support the development of bioinformatic and computational approaches to help users overcome limitations in understanding, analyzing, and drawing conclusions from the genomic data being collected. An independent panel reviewed the proposals and we are pleased to announce that a total of $1.1 million has been awarded to 5 projects.

One of the successful projects is led by Tarah Lynch, Clinical Assistant Professor in the Department of Pathology & Laboratory Medicine at the University of Calgary. Her project will help store and organize the terabytes worth of data generated by new high-throughput sequencing technology.HTS is used to gather all the genetic information contained within a microorganism. This provides a high-resolution genetic fingerprint to characterize and compare isolates to each other which is important for surveillance and infection control (e.g. outbreak investigations or antimicrobial resistance trends).

The resulting database from the project can be used by researchers in public health and clinical settings and will be compatible with Alberta Precision Laboratories current databases. Tara Lynch said about her work, "This project focuses on building a strong foundation for genomics use in Alberta Precision Laboratories by creating infrastructure to organize, analyze and interpret genomic data from microorganisms such as bacteria and viruses. This project is co-led by collaborators in Calgary and Edmonton with the intention that these tools will be open source to extend their use for other genomic applications in the province."

In addition to the project led by Tara Lynch at the University of Calgary, 4 other projects were selected:

David Bailey, President and CEO of Genome Alberta sees Alberta as home to global leaders in both health and agriculture genomics and said "Investments in bioinformatics will allow researchers to better understand and derive meaning from large, complex, genomic data sets. This will not only maximize the utility of previously generated data, but also help grow Alberta's capacity for big-data analyses. This is extremely relevant for improving the quality of care for Albertans in the era of precision medicine, as well as advancing Alberta's agricultural productivity and economy."

The Enabling Bioinformatics Solutions funding was made possible through a partnership involving Genome Alberta, Genome Canada, the Government of Alberta, and Alberta Innovates.

BACKGROUNDER

1. An Open Platform for Rapid, Reproducible, Phenotype-Centric Variant Prioritization in Poorly Characterized Rare Genetic DiseaseTotal budget - $200,000Project lead: Jason de Koning, University of Calgary

In rare disease research, identifying the genetic variants that cause an individual patient's disease can be like looking for a needle in a haystack by making informed guesses about where the needle may be. This project is intended to help enable more systematic, reproducible, and objective guesses via probabilistic reasoning and systematic prioritization models. The translational software platform developed by Dr. Jason de Koning, PhD, and team will allow these models to be customized, evaluated, and shared. It will be based on a variety of state-of-the-art and highly discriminating predictors derived from open data sources. Predictions will be made in the context of what scientists think they know about a patient's disease, and on measures of confidence in those beliefs.

2. Computational tools for viral pathogenesis and epidemiology using third-generation sequencingTotal budget: $200,000Project lead: Quan Long, University of Calgary

Third-Generation Sequencing (TGS) technology offers an exciting breakthrough opportunity for virology researchers. TGS can sequence the whole genome (including methylation status) in a single read, thereby, offering unprecedented opportunities to answer clinical and scientific questions related to viral evolution, transmission and pathogenesis. Dr. Quan Long, PhD, and his team will develop novel tools for the TGS and apply them to human immunodeficiency viruses (HIV). These tools will enhance our understanding of HIV, and will be widely applicable to study other viruses.

3. From sequencer to results: enabling routine genomics use for clinical and public health microbiology in AlbertaTotal budget: $201,750Project Lead: Tarah Lynch, University of Calgary

Academic scientists in Alberta currently use high-throughput sequencing (HTS) to gather vast amounts of data, such as detailed sets of genomic information in plants and animals. For public health, the data from microbial genomes can be used to enhance virus outbreak surveillance, patient treatment plans and infection prevention programs in hospitals.Dr. Tarah Lynch, PhD, and her team are building a database to better organize and share HTS data across the province. The project also aims to improve the process used to interpret data and the way the analyzed data is displayed, ensuring it is in a format that is easier to interpret.

4. Sustaining bee population health for Alberta's agriculture system. BeeBiome Data PortalTotal budget: $384,288Project lead: Rodrigo Ortega-Polo, Agriculture and Agri-Food Canada

Bees are fundamental to Alberta's agriculture, but are suffering severe declines worldwide due to multiple factors. The bee gut microbiome is the complex community of microorganisms living within the bee digestive system, and it directly impacts bee health and immunity. Now that a large amount of data on the bee microbiome is available, there is an urgent need for those data to be more accessible so that information can be applied for scientific discoveries and can be translated for stakeholder use.The goal of this project is to advance the development of the BeeBiome Data Portal, which will allow analysis and sharing of information on the microorganisms and viruses associated with bees.The outcome of the project will be greater accessibility to bee microbiome data and its use for new scientific discoveries and for translation efforts. This increased accessibility will benefit the scientific community, stakeholders and policy makers by enabling data-driven approaches to decision making regarding bee health.

5. Better cattle breeding predictions for Alberta producersTotal budget - $160,00Project lead Graham Plastow, University of Alberta

Results from the latest run of the 1000 bull genomes project, together with phenotypes and genotypes on tens of thousands of Alberta beef cattle, provides a vast amount of information that could greatly improve the accuracy of genomic prediction for economically important traits. The main challenge is to develop statistically powerful and efficient methods for largescale analysis of this information. The goal of this project is to develop a computing algorithm for such analysis. We plan to evaluate the algorithm for accuracy and develop a cloud-based platform that automatically runs the process.This project will provide the Alberta beef industry and research institutions with a powerful tool for fast integration of sequence information into genomic research and applications. It should also improve the accuracy of genomic prediction compared to current methods.

About Genome AlbertaGenome Alberta is a publicly funded not-for profit corporation which invests primarily in large-scale genome sciences research projects and technology platforms focused on areas of strategic importance to the province (e.g. human health, forestry, plant and animal agriculture, energy, and environment). By working collaboratively with government, universities, and industry, Genome Alberta is a catalyst for a vibrant life sciences cluster with far reaching social and economic benefits for Alberta and Canada. To date, the organization has managed a research portfolio with approved budgets totaling more than $255 million. Please visit Genome Alberta's website for more information.

SOURCE Genome Alberta

For further information: Mike Spear, Director of Corporate Communications, Genome Alberta, [emailprotected], 403-813-5843

https://genomealberta.ca/

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Alberta Bioinformatics Expertise at Work in Health and Agriculture - Canada NewsWire

FILE: Medical researchers perform serology, testing blood samples to find out whether someone already had and recovered from COVID-19, in Stanford University's Clinical Virology Lab in March 2020.

FILE: Medical researchers perform serology, testing blood samples to find out whether someone already had and recovered from COVID-19, in Stanford University's Clinical Virology Lab in March 2020.

Photo: Steve Fisch/Stanford Medicine

FILE: Medical researchers perform serology, testing blood samples to find out whether someone already had and recovered from COVID-19, in Stanford University's Clinical Virology Lab in March 2020.

FILE: Medical researchers perform serology, testing blood samples to find out whether someone already had and recovered from COVID-19, in Stanford University's Clinical Virology Lab in March 2020.

Why so many people are convinced that they had COVID-19 already

The week before Thanksgiving, Barbara O'Donnell came down with a wretched cough.

"It was just really bad, and it was constant," says O'Donnell, 62. "I would turn purple," gasping for breath. She could barely walk up the hills near her home outside of Philadelphia. Though she is a smoker, she was healthy and strong - "I don't get the flu, ever" - and had never experienced anything like this before.

It "felt like my lungs were so full that I wasn't going to make it," she says.

Two weeks of resting at home, and the illness vanished as quickly as it came. Two months later, California reported the country's first case of covid-19 that wasn't acquired via travel or direct contact with someone who had been abroad. Three weeks after that, Philadelphia closed nonessential businesses and issued a stay-at-home order. O'Donnell's job, as a privately employed aide for an elderly patient in a nursing home, was put on hold - the nursing home permitted only its own staff on the premises.

Sitting in her apartment, the thought occurred to her: "What if it was here way before they think it was?" she wondered. Was that cough covid?

The virus was here before anyone thought it was, we now know. Health officials in Santa Clara County, south of San Francisco, recently determined that at least two people who died in early and mid-February tested positive for the virus. But that doesn't answer the question that has been spreading, afflicting anyone who recently - or even kind of recently - experienced any covid symptoms:

Did I have it? I think I had it.

"I've been getting emails from hundreds, maybe thousands of people telling me, 'I'm sure I had it,' " Eran Bendavid, an associate professor of medicine specializing in infectious disease who is studying covid-19 at Stanford University.

"I am 99 percent sure I had it," says Janet Truchard, 58, who woke up in her Las Vegas home on Jan. 15 "sick as a dog" with a fever, dry cough, migraine and chest pain. She visited several doctors who prescribed various courses of antibiotics, diagnosing her with sinusitis and then allergies. The cough persisted all the way through March 25, but a chest X-ray came back clear.

Thinkihadititis is a condition afflicting people who experienced covid-like illnesses that befell them long before coronavirus was a thing. It happens when bits of news and scientific findings lodge in the parts of the brain that incubate hope - Oh hey, maybe I already beat it! - and anxiety - Oh God, maybe I gave it to a bunch of people.

Like covid-19, Thinkihadititis has infected some high-profile patients. "Sopranos" star Michael Imperioli told Page Six he was "certain" he caught the virus in early February. A star of the reality series "Love Island" thinks she "had the 'rona" while the show was filming in South Africa in January. And Patti Stanger, star of the Bravo show "Millionaire Matchmaker," was stricken with shallow breathing, a fever, fatigue and nausea after a January vacation in Miami, despite flying with a face mask at the advice of her nail technician. She had to skip the Grammys and had a panic attack when her fever spiked to 102.

"I didn't get up for three weeks," she says. "I didn't eat a thing. I lived on bone broth and crackers."

Later on, when news broke that the coronavirus had arrived in America earlier than we ever knew, "I thought, I could be one of those people," she says.

"I started hearing from all these friends saying, 'I think I had it, I think I had it.'"

- - -

No one wants to have covid-19, but everyone wants to have had it.

And recent research suggests that many people have already had it without knowing. Epidemiologists have said that the number of infections greatly exceeds the official count of cases, potentially by a factor of 10 or more, since people can be asymptomatic carriers of the illness, and because not every victim has been tested.

The World Health Organization has cautioned against the assumption that those who have already had the illness can't get it again. Researchers are still learning about the protective benefits that the disease's antibodies might bestow on survivors.

But after two long months of bad news about the painful effects and unpredictable deadliness of covid-19 - the sudden crashes, the mysterious strokes, the wide-ranging attacks on the body - who could be blamed for wondering, optimistically, about whether they've already joined the ranks of the Recovered?

JoAnna Fischer is sure she had covid-19. She lost her sense of smell, and for three months, she had a cough and chest pain so bad she needed supplemental oxygen. Her husband came down with a respiratory illness, and so did her cat.

One problem: Fischer fell ill all the way back in September, when she was living in northeast Pennsylvania. That's far earlier than epidemiologists believe the disease could have come to the United States.

"There is 0.0% probability that #SARSCoV2 was circulating with community transmission in the US in or before Nov 2019," tweeted Trevor Bedford, a computational biologist at Fred Hutchinson Cancer Research Center who has been tracking the virus' genetic code and spread.

Fischer isn't willing to give up her theory. "When you're thinking about how this thing spread so fast," the 63-year-old says, "it couldn't have just gotten here in December."

Bendavid, the Stanford professor, said one person who wrote to him believed they caught the virus in 2018. "That, I think, is stretching it," says Bendavid.

Thinkihadititis usually involves stretching the imagination to some degree. After all, covid-19 shares some symptoms with the seasonal flu and common allergies. Currently fewer than 20 percent of covid-19 tests are coming back positive, according to data reported to the Centers of Disease Control and Prevention, suggesting that the great majority of people who thought they had it - even in the middle of the pandemic - didn't actually have it.

To the extent that having already beat covid-19 is preferable to wondering if you're one of the people it's going to put in the hospital, Thinkihadititis may be a form of positive thinking. Humans are hardwired to anticipate positive outcomes, says Tali Sharot, a professor of cognitive neuroscience at the University College London who studies optimism and expectations.

"When there is something we want to believe, we are very good at interpreting the evidence in a way that would support that belief," says Sharot.

The reverse is also true. "Say there was a doctor saying that if you had it before, then the likelihood that you would get it again is higher, and it would be even more dangerous," says the professor. If that were the case, people "would probably look back to their illnesses and interpret certain symptoms as definitely not covid-19."

Whether it's a comfort or a source of anxiety, Thinkihadititis represents a state of limbo.

The good news? There's a cure.

Kind of.

- - -

"The only way to know is to get an antibody test," says Rachael Ayscue. "And I don't know anywhere around here that'll give one."

Ayscue, 47, lives in the suburbs of Raleigh, North Carolina. On Jan. 6, she felt sick, and before long she was coughing so much that it sometimes hurt to breathe. Then her daughter got sick, too. Raleigh didn't see its first confirmed covid case until March 3, but Ayscue wondered whether the tech workers of the Research Triangle had traveled to Asia over the holidays, and brought the virus back. (Epidemiologists believe the earliest American cases originated in Europe, not Asia.)

Antibody tests may provide relief from the fever of doubt. Also known as serology tests, they determine whether a patient's blood contains antibodies, which are proteins that help us fight off infection. The presence of antibodies means the patient's immune system has already been exposed to the virus.

Those tests are now becoming available nationwide, although experts warn that their accuracy can vary.

Since it began offering appointments for antibody tests, the telemedicine provider PlushCare saw "a pretty overwhelming response (from) people who are interested," especially in harder-hit areas like New York, says James Wantuck, the platform's chief medical officer and co-founder.

PlushCare's doctors remind patients that immunity is not a given and that they must continue social distancing and other protective measures. And if the tests come back negative, some patients - confident in their self-diagnosis and wary of possible testing inaccuracies - might not believe them.

"Some of the patients are certainly disappointed," says Wantuck. "I think everyone wants to have this in their rearview mirror or feel some sense of relief."

Fischer, the woman who got sick last September, says she couldn't be convinced so easily. "If I get tested," she says, "and I don't have the antibodies, I think I would ask for a different test."

Ayscue says she plans to get an antibody test if she can, but she doesn't need one to feel comfortable returning to life as usual. She does not hesitate to go to the grocery store, sometimes without a mask. She says she supports the protesters who have demonstrated against strict lockdown rules in North Carolina.

"I've chosen not to be afraid," she says.

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Why so many people are convinced that they had COVID-19 already - Chron.com

From Netdoctor

Gender differences exist in many health conditions, and COVID-19 is no different. It appears that with regards to the novel coronavirus, mens health is less robust.

This global phenomenon is particularly visible in some countries. In Thailand, males account for a massive 81% of COVID-19 related deaths, in England and Wales, its 61%.

What are the reasons for the considerable difference between the sexes? We spoke to Dr Anthony Kaveh, MD, physician anesthesiologist, and integrative medicine specialist.

Men are disproportionately affected by COVID-19 than women. From preliminary data, possible reasons include behavioural, baseline health, and genetic differences between men and women, says Dr Kaveh.

Lets look at what we know about COVID-19 infections among men and women. But first, a little about how and why the sexes are different.

Men and women have vastly different biological characteristics, that develop thanks to our chromosomes. A chromosome is a bundle of coiled DNA, found in the nucleus of almost every cell in the body. Humans have 23 pairs of chromosomes.

The sex chromosomes determine whether you develop as a male or female.

In humans, women have two larger X chromosomes (XX), whereas men have a single X chromosome and a much smaller Y chromosome (XY) that has relatively fewer gene copies.

When an embryo is developing in the womb, these chromosomes dictate the future sex of the baby.

One of the genes found on the Y chromosomes, the SRY gene, starts testicular development in an XY embryo. The testicles begin to make testosterone which directs the embryo to develop as a male.

In an XX embryo, there is no SRY gene, so instead, an ovary develops which makes female hormones.

This basic, biological variation between the sexes can affect COVID-19 infection rates.

Although essential for male health, testosterone levels are also linked to a range of medical conditions.

Men are five times more likely to suffer an aortic aneurysm and three times more likely to develop kidney stones. Men also tend to die at a younger age than women.

Oestrogen is a predominantly female hormone that provides protective effects from conditions, including heart disease. Men cannot benefit from its positive health effects, as they only produce low levels.

However, Dr Kaveh says that The immunologic effects of oestrogen in protecting against COVID-19 are theoretical and dont yet provide a mechanism to explain our observations.

Testosterone could have a role to play in COVID-19 infection rates. High levels of testosterone can suppress an immune response. Researchers found that women and men with lower levels of testosterone had higher antibody responses to an influenza vaccine.

The X chromosome has about 900 genes, the Y chromosome, just 55. Women have a genetic advantage with two X chromosomes because if there is a mutation in one, the other gene provides a buffer.

Men have more sex-linked diseases such as the blood clotting disorder, haemophilia, and suffer from an increased rate of metabolic disorders. The protective XX effect explains why male death rates are frequently higher.

The female immune system is stronger. Concerning COVID-19 infections, Dr Kaveh says Genetic factors are often considered, including the more active female immune system. While a more active immune system would make sense to protect against COVID-19, it would be expected to worsen the cytokine storm we observe in severe COVID-19 infection.

However, there is no evidence to support that cytokine storms, which are potentially lethal, excessive immune responses, are more common in women.

If more men are testing positive for COVD-19, could the simple reason be that more men are tested than women? In fact, it seems the opposite is true.

Within the context of our early statistics, women are tested more frequently than men, but men have more positive tests. This may reflect a male stoicism that leads to delayed care, says Dr Kaveh.

Men are not as likely as women to seek medical attention. The Centers for Disease Control and Prevention (CDC) reported that women were 33% more likely than men to visit a doctor, even excluding pregnancy-related visits.

Story continues

It seems like the reason for higher infection and death statistics in men is not due to a bias in testing.

Obesity, diabetes, hypertension, and smoking are also predictors of COVID-19 hospitalisation, but the breakdown is difficult to correlate, said Dr Kaveh.

People of either sex are more likely to suffer from complications from coronavirus if they have certain pre-existing health conditions, or engage in behaviours such as smoking and excessive alcohol consumption.

These health conditions and behaviours tend to be more common in men, which could affect the imbalance that we see in COVID-19 infections.

The association between risk factors and infection rate are not yet fully understood. For example, hypertension is more common in men until menopause, at which point female rates quickly rise, explains Dr Kaveh. In this case, we should be seeing an increase in the COVID-19 infection rate for women who have reached menopausal age, yet this is not the case.

Obesity, a risk factor for diabetes, affects women more than men globally. However, diabetes is slightly more prevalent in men. These comorbid conditions dont fully explain the COVID-19 observations, and neither does smoking, says Dr Kaveh.

Smoking is a risk factor for all respiratory diseases and also of lung cancer which is another COVID-19 risk factor.

In China, about 50% of men smoke and only 2% of women. These figures could contribute to the high ratio of male deaths which are more than double the rate of female deaths.

These differences in smoking and death rates are not as extreme in other countries. Risky behaviour cannot fully explain sex bias in COVID-19 infections.

As yet, it seems like there is no definitive answer as to why more men are suffering severe COVID-19 infections. More research is needed.

We are still very early in our global epidemiological observations of COVID-19. More complete data in the coming months will hopefully provide more clues to explain our observations, concluded Dr Kaveh.

Last updated: 30-04-2020

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Coronavirus deaths: why are more men dying from COVID-19 than women? - Yahoo Style

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New Delhi: Scientists at the Council of Scientific and Industrial Research (CSIR) will launch two separate trials to test if a drug used to treat sepsis and liver cirrhosis can stop Covid-19 infection from progressing in asymptomatic patients and whether the same drug can prevent recurrence of the infection in patients who have recovered.

The ongoing coronavirus pandemic has research teams across the world scrambling to find a treatment or vaccine for the disease that has no known cure. Since developing a new treatment from scratch can take years, researchers are looking to repurpose existing drugs to help patients fight the SARS-CoV-2 virus that causes Covid-19.

The drug to be used for the trials is known as Sepsivac, which was developed by the CSIR in partnership with pharmaceutical company Cadila in 2007.

Also read: Govt plans to test whether ashwagandha, mulethi, guduchi will help fight Covid-19

In an earlier interview, Ram A. Vishwakarma, director, CSIR-Indian Institute of Integrative Medicine (IIIM) in Jammu, told ThePrint that his team is set to test whether the drug can reduce the risk of death in critically-ill Covid-19 patients.

This trial has now started at the PGIMER, Chandigarh, while AIIMS, Delhi, and AIIMS, Bhopal, will launch the trial later.

There will be another trial of patients who have tested positive, but have no symptoms. These people will be given this drug as a vaccine, so that their disease does not progress, and they do not end up in hospitals, Vishwakarma told ANI Wednesday.

A third trial of the drug will be for people who have already been cured as it is now known that the virus can stay in patients for upto a month.

people who have been released from hospital will be given this as a vaccine, so that they dont redevelop this infection, he said.

Vishwakarma explained to ThePrint that to fight viruses there are usually two approaches developing a drug against the virus itself or creating an immunomodulator, which helps the immune system in fighting off the virus.

Sepsivac falls in the second category, Vishwakarma said.

The drug is synthesised by culturing a bacteria called Mycobacterium w in a large scale, which is inactivated by heat. A number of proteins on the surface of the bacteria triggers a desirable immune response, he said.

Sepsis is a condition that happens due to an overactive or inflammatory immune response that occurs when a pathogen enters the blood plasma, leading to organ dysfunction that can be fatal.

Caused by gram-negative bacteria, sepsis has a pathology similar to that of Covid-19, Vishwakarma said.

Initially our body tries to defend itself against viruses by using its innate immune system. After 4-5 days, when the body cannot fight off the pathogens, it employs a higher level of defence which is what causes the cytokines storm, he said.

Cytokines are small proteins secreted as a result of different types of interactions between cells. In the novel coronavirus infection, this heightened release of cytokines is common in critically ill patients.

This high level of immune response starts to damage the bodys organs. That is what is causing the multi-organ failure that we are seeing in Covid-19 patients, Vishwakarma said.

Also read: Modi govt advises homoeopathy, Unani to prevent coronavirus that has no known cure yet

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CSIR to test sepsis drug in asymptomatic Covid patients and those who have recovered - ThePrint

A shortage of COVID-19 test kits and the need for broader testing in Vermont has mobilized a task force of researchers from UVM College of Nursing and Health Sciences, Larner College of Medicine, Vermont Integrative Genomic Resource and the University of Vermont Medical Center. The scientific team is working to bridge the gap in available test supplies in Vermont and nationwide by developing new methods of testing patient samples and sharing their new workflows with other scientists and labs.

UVM alumna Diana Gerrard, a medical laboratory scientist in UVM Medical Centers genomic medicine department, is a critical task force team member. An expert on molecular pathology, Gerrard graduated from UVM in 2019 with a doctorate in Cellular, Molecular and Biomedical Sciences.

We talked with Gerrard about her work and how laboratory scientists in Vermont contribute valuable knowledge in the race to stop the spread of the disease.

As the need for COVID-19 testing increased in our community, we knew that we needed to be ready at the frontlines of testing. We also knew that we needed to think critically and creatively about how we would test people as we faced shortages in testing kits.

In my role at UVM Medical Center, I evaluate and validates new assays (tests for measuring the components of a substance or sample). My usual work involves investigating assays surrounding cancer. These assays allow us to determine specific genetic mutations underlying a persons cancer, which can inform a more specific clinical care plan for their treatment. While I do not usually work with viruses, the tests used to screen COVID-19 are molecular-based assays and my leaders brought me on the local task force to utilize my expertise in molecular biology and familiarity with assay evaluations and validations for the medical center.

In general, the COVID-19 test can be broken up in two parts: the first step involves extraction of the viral material from the patient samples collected. The second step is to detect the COVID-19 viral genome, the specific genetic sequences that give the virus its identity.

Our team of researchers identified an alternative resource to use for the first step that would allow us to work around the shortage of extraction kits. My role has been validating this change in the clinic and piecing that together with different methods for step two. This involves implementing the workflow in our clinical laboratory getting the space, resources and instrumentation up and running in order to perform the testing and performing a validation process that allows us to determine our limit of detection (the lowest amount of virus detected in a given sample).

There has been a national shortage of testing kits using the Center for Disease Controls method, so our group published a preprint of the changes we made to the first step of the process. This change uses kits widely available in a majority of biomedical science research laboratories, and clinical groups have contacted us to inquire about our workflow and clinical evaluation of these kits.

Laboratory scientists working on COVID-19 nationally have formed a collaborative community. We are working hard and fast while maintaining high standards in our testing and so we have relied on each other to give feedback during both the trials and successes of testing.

I completed my PhD in the Cellular Molecular Biomedical Sciences program in the laboratory of Dr. Seth Frietze in the Biomedical and Health Sciences Department at the College of Nursing and Health Sciences. I developed my molecular biology expertise during my PhD, and this has trained me for the technical responsibilities during the COVID-19 response. Additionally, my doctoral training has allowed me to develop the rigor needed to work actively for long hours and think critically and collaboratively.

All of us working on the front lines of the response to COVID-19 are at risk for contracting the virus; however, serving our community is exactly what fuels us. We are sure to take appropriate and careful measures while working with the virus by wearing appropriate personal protective equipment. Additionally, we are sure to take the same precautions regarding hand hygiene as everyone else in our work and home life, not only to stay well for ourselves but also so that we can continue to serve and support our community.

Read this article:
Working to Improve COVID-19 Testing - UVM News

Matt Hancock has said there are early signs showing that the antiviral drug hydroxychloroquine may be a very effective treatment, implying the government is acquiring significant stocks of it. This is the correct approach. Trustworthy research has found it disrupts the endocytosis process ruffling of cell membrane to ingest particles and nutrients from its surrounding environment meaning it blocks the entry of Covid-19.

In the same way, hydroxychloroquine can also starve cancer given cancer cells grab extracellular nutrients to feed themselves. Looking forward, we need to modernise our cancer care in the UK. We sadly have some of the worst stats for cancer recovery in Europe. Our cancer survival rates are not just worse than America, Scandinavia, Canada, or Australia, for some cancers, they are even worse than Brazil or Costa Rica.

Conventional NHS therapy must move with the science, this includes repurposing existing drugs, traditionally used for other conditions, which are proving to disrupt the metabolic pathways of cancer cells. There is a huge untapped medicine cabinet of generic drugs and herbs that could help treat cancer, and many other conditions such as motor neurone disease and schizophrenia. Despite facing a record-breaking 17 billion annual drugs bill, the NHS still retains an outdated, rigid attitude to innovation. This drugs bill is rising around 8% a year, as the NHS struggles in negotiations with Big Pharma to keep costs down.

In the US, the costs of cancer care have also surged by 40% in the past decade. There is existing evidence suggesting that, together, these repurposed drugs disrupt the metabolic pathways of cancer cells to slow down or prevent their reproduction. They are among several cheap drugs with proven anti-cancer properties that are not available to NHS cancer patients. Many thousands of published scientific studies already show they can disrupt tumour growth by reducing cancer cell nutrition, and the Medical Research Council (MRC) is running clinical trials to begin to collect more data on the benefits of these repurposed drugs. But the results are at least a decade away, and the dose of aspirin being used in this MRC trial is not one that is commercially available anyway.

To improve cancer care in the NHS, we need a parallel support system for people that links in with NHS treatment, but allows them to access the best of other science-based treatments, of personalised medicine such as circulating tumour DNA analysis and cancer stem-cell treatment with integrated oncology. We also must find a mechanism and a structure for the regulators to allow out-of-patent drugs to be used again. Lets learn from best cases around the world.

We rightly cherish our NHS, even more so now than we ever did. Our carers deserve a new settlement once the pressure is lifted, as do other key workers like bin collectors, delivery drivers and cleaners. But in the long term we must ask ourselves seriously why, if the NHS is the envy of the world, in over 70 years no other country has copied it? We should take the opportunity to radically improve long-term healthcare in the UK and reform the NHS and social care system together once Covid passes.

The NHSs traditional levelling-down attitude that if something cant be offered to everyone then it shouldnt be offered at all is bad for innovation, bad for short-term care and bad for people who would otherwise benefit. Did you know around half of people get better after a cancer diagnosis? A shocking statistic mostly for people with one of the first three stages of cancer. I am aiming to join this 50% as I have Stage 4 breast cancer. Given just two years to live, Ive since made remarkable progress through one of these clinical trials using repurposed drugs.

Covid-19 has meant Ive ended up an accidental health tourist locked down in Thailand where Im watching from a distance whats happening in the UK. I am determined to play my part in increasing the survival figure by raising awareness of simple science-based things that help you to biohack your body, take control of your own health and beat the statistics. As my hero Marie Curie said: Nothing in life is to be feared, it is only to be understood. Now is the time to understand more, so that we may fear less.

Katharine Harborne is a chartered environmental scientist, artist and a former prospective parliamentary candidate for the Brexit Party, and former Conservative councillor in the London Borough of Richmond.

Read more:
Boris is back, and we need him to end the coronavirus crisis and heal the NHS - Telegraph.co.uk

Personalized Stem Cells Incorporated (PSC) in Poway said the therapy could reduce the most serious complications of the infection in the lungs.

SAN DIEGO A San Diego biotech company is seeking emergency FDA approval for an experimental trial of stem cell therapy for coronavirus patients.

Personalized Stem Cells Incorporated (PSC) in Poway said the therapy could reduce the most serious complications of the infection in the lungs.

PSC CEO, Dr. Bob Harman, said the company is asking to test the treatment on a group of 20 hospitalized COVID-19 patients in the first phase of a clinical trial.

"Stem cell doses will be ready for clinical trial use in May, depending on FDA approval," Harman said.

Harman said they've already scaled up production of stem cells in anticipation of FDA approval.

PSC Medical Director, Dr. Christopher Rogers, stated, "I believe this is the most promising therapy being explored by medical scientists at this time and stem cells may potentially reduce the most serious complications of coronavirus infection."

The FDA has a new program called the Coronavirus Therapeutic Accelerator Program (CTAP) to help speed up the launch of FDA clinical trials for hopeful COVID-19 therapies.

PSC was asked by the White House Coronavirus Task Force to apply to the FDA CTAP program for expedited review of their application.

PSC hopes to rapidly complete the CoronaStem 1 study and then proceed into a larger Phase 2 clinical trial and potentially into FDA compassionate use programs to reach more patients.

More information can be found on the PSC website.

See more here:
San Diego biotech firm seeks approval for stem cell research against COVID-19 - CBS News 8

Patientswith newly diagnosed transformed Fanconi anemia (FA) have poor outcomes andshould achieve complete remission (CR) prior to allogeneic hematopoietic stemcell transplantation (alloHSCT), according to results from a study published inthe American Journal of Hematology.

Stefano Giardino, MD, of the hematopoietic stem cell transplantation unit at the Istituto Giannina Gaslini in Italy, and colleagues retrospectively analyzed outcomes of 74 patients with transformed FA (36 male; median age, 14 years); 35 patients had myelodysplastic syndrome, 35 had acute leukemia, and 4 patients had high-risk cytogenetic abnormality. All patients underwent alloHSCT from 1999 to 2016.

The primary end points were overall survival (OS) and event-free survival (EFS). Secondary endpoints included the incidence of grade 2 to 4 acute graft-vs-host disease (AGVHD) and chronic graft-vs-host disease (CGVHD), non-relapse mortality (NRM), and incidence of relapse. To identify potential factors that may influence outcomes, the researchers assessed the type of diagnosis, preHSCT cytoreductive therapies and related toxicities, disease status prior to HSCT, donor type, and conditioning regimen.

Ata median follow-up of 7 years, 5-year OS and EFS were 42% and 39%,respectively; 5-year cumulative incidence relapse and NRM rates were 21% and40%, respectively. Patients in CR during transplant had better OS than those whostill had active disease (OS, 71% vs 37%, respectively; P =.04). No other factors had a significant effecton patient outcomes.

Of22 patients who received cytoreductive therapy prior to HSCT, 40.9% experienceda grade 3 to grade 4 toxicity event; this did not appear to effect survivalafter HSCT (3 year OS, toxicity preHSCT 48% vs no toxicity 51%; P =.98).At 100 days, the cumulative incidence of grade 2 to 4 AGVHD was 38%, and the cumulativeincidence of 5-year CGVHD was 40%.

At5 years, NRM was 40%, while incidence of relapse was 21%. Transplant-relatedevents were the cause of mortality in 81% of patients (34 of 42 deaths).

Limitationsof the study included the retrospective design and incomplete data for somevariables. The authors highlighted the large number of patients for this raredisorder as the primary strength.

Inorder to optimize the chances of the only curative option for FA in malignanttransformation, a sequential cytoreductive therapy followed by HSCT appears areasonable approach in FA patients with AL, if a previously identified donor israpidly available, wrote the authors. However, since the risk oftreatment-related complications is high, these patients should be managed inhighly specialized centers and transplant approaches aimed at reducing theoccurrence of [GVHD] and transplant-related complications should be prioritized.

Reference

Giardino S, Latour RP, Aljurf M, et al. Outcome of patients with Fanconi anemia developing myelodysplasia and acute leukemia who received allogeneic hematopoietic stem cell transplantation: a retrospective analysis on behalf of EBMT group [published online April 8, 2020]. Am J Hematol. doi: 10.1002/ajh.25810

Read this article:
Outcomes of Stem Cell Transplantation in Patients With Newly Diagnosed Transformed Fanconi Anemia - Hematology Advisor

by Lieba Nesis

Having the opportunity to speak with Dr. Camillo Ricordi, one of the foremost experts on stem cell research, was nothing short of extraordinary. The 63-year-old scientist is director of the Diabetes Research Institute at the University of Miami. While his specialty is pancreatic islet transplantation for Type 1 Diabetes, when coronavirus came calling he sprung into action. Since January he has been working 16 hours a day 7 days a week to help his colleagues in China, Italy and the US battle the deadly affliction. He is now conducting a clinical trial with 24 patients to test the efficacy of stem cells in critically ill COVID-19 patients. The cells which are injected directly into the lung hone in on the injury and inflammation producing an army of 200 million cells to fight the complications of the illness. Here are excerpts of my conversation with this heroic doctor who is on the front lines of this drudgerous battle.

I began by asking Ricordi if he was caught unawares by the virus: to which he responded there were simulations and warnings from individuals such as Bill Gates since 2014. However, he acknowledged until you get hit you dont think its real. Ricordi believes the virus emanated from a Wuhan lab which the NY Post and Newsweek claim was financially backed by the NIH, the CDC and the WHO, with Dr. Fauci contributing $7.4 million to the Wuhan Virology Lab. Ricordi cited the position of 200 scientists who had expressed concern of potentiating virus research in bats due to the possibility of a catastrophic leak. Ricordi is in agreement with Nobel Prize Winner Luc Montagniers assertion that the virus was engineered by inserting genes from HIV into the coronavirus in a misfired bid to find an AIDS vaccine. The bat which has a high number and rate of virus mutations was the perfect medium for creating a marginally lethal, yet highly contagious disease. With the viruses high level of changeability Ricordi was dubious as to whether the precise source of origination would ever be discovered. He also expressed concern as to the efficacy of a vaccine, since it might protect against COVID-19 but be ineffectual when a different strain called COVID-20 and 21 appeared.

One of the tricks to fighting this disease is building a strong immune system through an anti-inflammatory diet and supplements such as Vitamin C, D, Omega 3, Zinc and Resveratrol, according to Ricordi. While he is optimistic the disease will diminish during the summer months, he is equally confident a second and stronger wave will hit in the winter if lockdown procedures are relaxed-akin to what has occurred in Japan where a second state of emergency was declared on April 6th. Ricordi mentioned that China destroyed a paper proving the virus was engineered replacing it with documentation confirming natural origin leading him to conclude the disease was in fact manipulated. Ricordi is of the opinion that a cocktail will eventually be used to successfully treat the disease. Remdesivir and Hydroxychloroquine, he conceded, show immense promise if used in correct dosages and at the incipient stages of the illness before the patient becomes critically ill.

Ricordi is the most often quoted expert on stem cell research where he has successfully prevented the acceleration of aging as well as kidney and eye disease in patients with Type 1 diabetes. He has currently diverted a number of resources from diabetes to the study of COVID-19 where he has injected his 4th critically ill COVID patient with stem cells in a double blind study-the results of which will be ready in two months. The cells which were retrieved from the placenta of a baby can be used to treat more than 10,000 patients. The injections are administered intravenously with the natural first filter being the targeted area of the lungs (unlike in diabetes where a catheter has to be inserted to ensure cell transmission to the pancreas) The FDA approved his trial in a record weeks time and the 24 critically ill patients who receive the cells should see effects in weeks. Ricordis optimism is backed by science since colleagues in Israel reported zero deaths after using stem cells in 6 critically ill coronavirus patients. China had similarly favorable outcomes with no deaths in 80 seriously ill patients. Furthermore, injecting the cells is a benign procedure that takes only 10 to 15 minutes to perform. Unlike other treatments, the availability of cells abound with more than 3.8 million births in the US last year providing viable placentas. Moreover, the benefits of building a large scale emergency response repository in the form of cell banks to treat Alzheimers, severe lung damage, diabetes, and kidney disease in between pandemics would be revolutionary.

Stem cells have not been heretofore utilized due to the FDAs stringent safety requirements. Furthermore, there are significant costs associated with clinical trials where environmental sterility and quality control are carefully monitored. Ricordi raised funds from private individuals-90 percent of whom were of Italian descent. In his next larger trial he will be addressing how to stop progression of the disease in less severe cases. Ricordi stressed the importance of wearing masks and socially distancing due to the viruses airborne nature; noting that contained spaces such as cruise ships, planes, hospitals and nursing homes were especially problematic. Ricordi is currently meeting with architects to discuss how to construct pandemic resistant buildings which use ultraviolet lights in bathrooms and avoid recycled air. Our entire future will be reinvented said Ricordi, as telemedicine and home monitoring of patients will soon become commonplace. He also predicted there will be future pandemics as the distance between animals and humans continues to narrow with monkeys and bats encroaching on human habitats and vice versa-due to limited space. Moreover, Ricordi remarked bioweapons and vaccines were a disaster waiting to happen. As Ricordi rushed to attend a pivotal meeting he casually mentioned his daughter was working as an ICU nurse in California-another reason this heroic warrior felt such an urgent calling to discover an imminent cure.

Link:
Exclusive Interview with Renowned Coronavirus Researcher Dr. Camillo Ricordi - The Jewish Voice

Fifteen years ago, Scholar Muthamia was getting ready to welcome her second child. The pregnancy had no complications at all and when her son Ferdinand Mutugi Njuguna was born, he weighed a healthy 3.9 kg.Mutugi was as precocious a toddler as can be, and all was fine in the Njuguna household until the boy developed a peculiar walking style.He would push his left foot ahead while walking and he didnt seem to quite stand up straight, Muthamia says.We thought it was a unique walking style he had developed, and let him be. And weirdly, when wearing a pair of shorts or trousers, he would pull them up with his arms while walking and many assumed we were buying him over-sized clothes, she says.Later, Ferdinand began falling while walking. He also started having a hard time standing up from a sitting position. Climbing stairs became a hardship and he couldnt run as fast as he used to.He would get tired very fast and even started walking on his toes. We took him to various hospitals and eventually ended up at Kenyatta National Hospital where he was diagnosed with Duchenne muscular dystrophy,she says.

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The disease that wastes away boys' muscles - The Standard

Poor patient-reported outcomes insurvivors of childhood hematologic malignancies are associated with thepresence of chronic health conditions, regardless of whether patients had receivedhematopoietic stem cell transplantation (HSCT) or conventional therapy,according to a study published in Blood.

Investigators compared symptomprevalence, health-related quality of life (HRQoL), and risk factors in adultsurvivors. In multivariate logistic regression analyses, these patient-reportedoutcomes were compared with results of surveys and medical assessments given tomembers of a noncancer control group (242 patients). Survivors of hematologicmalignancies were organized by treatment type to either HSCT group (112patients) or conventional treatment group (1106 patients).

Compared with individuals in the noncancer group, survivors who had received HSCT reported substantially higher rates of symptom prevalence across memory (adjusted odds ratio [aOR], 4.8), sensation (aOR, 4.7), pulmonary (aOR, 4.6), and motor/movement domains (aOR, 4.3). Physical HRQoL was also significantly worse for survivors who received HSCT, compared with patients who did not have cancer (aOR, 6.9).

The investigators found nosignificant difference between survivors from each treatment group in terms ofHRQoL and symptom prevalence by domain. Organ-specific chronic healthconditions were a greater indicator of the prevalence of most symptom domainsthan treatment type.

Some ocular symptoms showed higher cumulative prevalence among those who received HSCT compared with conventional treatment. These related to eye dryness (P <.0001), difficulty seeing while aided by glasses (P <.0001), and double vision (P =.04).

The goal of cancersurvivorship care is not merely to identify and manage medical complications,but also to improve daily functional status and HRQOL, the investigators wrote.

The researchers also indicatedthat clinicians should consider proactively screening survivors of pediatrichematologic malignancies, particularly those treated with HSCT who have chronichealth conditions, for symptoms phenotypes to aid in the early identificationof adverse events.

Reference

Yen HJ, Eissa H, Bhatt NS, et al. Patient-reported outcomes in survivors of childhood hematologic malignancies with hematopoietic stem cell transplant [published online April 2, 2020]. Blood. doi: 10.1182/blood.2019003858

This article originally appeared on Hematology Advisor

Original post:
Chronic Health Conditions, Not Transplant Receipt, Linked to Symptom Prevalence in Survivors of Childhood Hematologic Malignancies - Clinical Advisor

A POPULAR driving instructor who taught hundreds of Warrington students has sadly died following a year-long illness.

Sara Ashbrook, from Latchford was diagnosed with Acute Lymphoblastic Leukaemia in February last year.

After needing a stem cell transplant, Sara matched with a 21-year-old donor in the Netherlands and underwent the operation in September.

The 48-year-old mum got through the most important 100 days after the transplant, meaning it was a success.

Unfortunately, one of the drugs that Sara took to help the transplant caused her cholesterol to sky-rocket and she developed pancreatitis in January.

Sara and her husband Ste

Sara was admitted to the intensive care unit at the The Royal Liverpool University Hospital and further complications meant she was placed in a coma.

Her daughter Zoe, said: "My mum was a big music fan, she always had the radio on no matter where she was.

"She had Radio 1 with Chris Moyles on in the kitchen every morning and then in the car she would have it so loud.

"She would sing to her favourites from 80s Bananarama to the Arctic Monkeys.

"Mum and her friend would dance like maniacs in the living room to Scooter's Jumping All Over the World or with me to Rihanna's Pon de Replay.

"Mum was a kind-hearted, generous and thoughtful person.

"She encouraged us three children to think of others and was a great role model; giving blood on a regular basis, raising money for cancer research and other charities or simply donating to charity shops.

"Even when she was suffering in pain she would sit down and talk to the nurses about their day and let them vent.

"She would take them sweets, chocolate and cakes to cheer them up.

"Not long after she came out of her coma she asked me to buy some sweets for the nurses."

Sara slowly started to get better and signs of her 'amazing' personality started to show.

She was slowly weaned off the ventilator and spent time on a voice box.

Sara eventually came off ventilation but at this stage, her body started fighting numerous infections, including sepsis, which put more strain on her breathing.

This meant Sara had to be put back on ventilation and became very unwell.

Sara sadly passed away on Saturday, April 11 at 3.40pm surrounded by her family.

She is survived by her husband Ste, three children Zoe, Declan and Connor, two stepchildren, four grandchildren, her siblings and parents.

Zoe added: "Mum seemed to rise above her pain and suffering and was always putting others before her no matter what she was going through.

"She touched so many lives over the years. Everyone thought so much more of her, she became a friend to everyone she met.

"She always has been and always will be my number one inspiration."

Her family is now fundraising to help towards the fight against Leukaemia and contribute towards the University of Liverpool's Pancreatic Cancer Fund.

You can donate here http://www.justgiving.com/crowdfunding/remembersara

Here is the original post:
Tributes paid as much-loved and inspirational driving instructor dies - Warrington Guardian

Patients who are most at risk of severe complications from COVID-19 have been asked to 'shield' themselves. This means that they should stay at home and avoid face-to-face contact with anyone from outside of their household. Members of their household are advised to stringently follow social distancing rules.

The following patients were on the CMO's original list of high-risk patients:

The following groups have since been added to the list:

* During a webinar on Thursday 23 April, NHS England primary care medical director Dr Nikki Kanani said that patients who have had a splenectomy had also been added to the list and had been sent letters. However, this has not been updated on official guidance. She also asked practices to check to make sure that these patients had been added to the list.

**An RCGP learning module on shielded patients has also been updated to advise the patients with interstitial lung disease, some with bronchiectasis and those with pulmonary hypertension should also be included in the group. It adds: 'These patients will be identified and contacted by secondary care, but you may receive queries from them in primary care.'

#A primary care bulletin on 27 April confirmed that renal dialysis patients have been added to the shielded list. Renal units will contact patients and send them a letter.

Around 900,000 patients were identified via hospital data at the end of March and received a letter advising them to shield. Flags should have been added to GP systems to identify these people. A second phase identified a further 400,000 patients using primary care data and letters and texts started being sent to this group on 7 April.

Practices should have received advice on how to run a system search for a report containing this list of patients from their system suppliers. Current search guidance for each system provider can be found in the annex to this letter to practices.

If GPs considered there were patients on the register who should not be included, they were advised to code them low/medium risk vulnerability system suppliers should have advised the practice of which code to use. The original code will remain in the record, but any reports run will use the most-recently added code.

If these patients were on the initial central list they may have already received a letter advising them to 'shield'. Therefore practices may need to contact these patients to discuss their circumstances.

There has been some confusion about adding further patients to this list because practices were initially asked to identify additional people using guidance produced by NHS England, the BMA and the RCGP, which suggested the patient groups this could cover. NHS England later told practices to distragard this.

GPs and consultants will also be able to add additional patients to the shielding group throughout the pandemic by using appropriate codes. Any patient identified by the practice should have been sent a letter (template letters are here). Patients identified in secondary care should receive a letter from their hospital doctor, who should also inform the practice that they have identified this patient.

If GPs don't agree that a patient identified as 'high risk' by the hospital falls into this category they should discuss it with the trust. If different opinions still exist the patient should remain in the highest risk category.

Patients have also been asked to self-identify via the government website and practices should receive a list of these patients from their system supplier between 17 and 24 April. The guidance says the list of patients who will need adding to the high-risk list is likely to be very small given the review practices will have already completed.

Practices should review this new list by 28 April and determine which patients should be flagged as high, medium or low risk. For those flagged as high risk the practice will need to send them a shielding letter.

If patients not included on the register want to follow shielding advice that is there own choice. However the latest guidance says that those not on the register, but in the broader group of patients at risk (which is effectively the groups entitled to a free flu jab), should be advised to follow social distancing.

NHS Digital will pull details of the patient records that are flagged every week. This means that these people will be able to access the government's shielding support for food and medicines delivery although support is initially focused on people who have no other means of getting food and medicine. The guidance says that there may be a lag in processing this information and, if so, patients requiring urgent help should contact their local authority.

Patients are also required to register for this support here: https://www.gov.uk/coronavirus-extremely-vulnerable If someone does not have access to the internet, refer them to the phone line in the letter.

The NHS is also providing further support to patients at risk via the Goodsam App and NHS Volunteer Responders. Any health professional or local authority can refer people who require assistance. Referrals can be made via the NHS Volunteer Responders portal here https://goodsamapp.org/NHSreferral or by calling 0808 196 3382. This support is available to anyone in need and not just the highest-risk group.

A letter from NHS chief executive Sir Simon Stevens set out the steps practices should take in the second phase of the pandemic. Practices were told that patients who are shielding should be proactively contacted to'ensure they know how toaccess care, are receiving their medications', and practices should provide home visitingwhere clinically necessary.

During a webinar on 23 April, Dr Nikki Kanani said that practices should be contacting these patients to check that they understand what is happening. A presentation during the webinar suggested that these conversations should:

NHS England is setting up an expert group that will be chaired by deputry primary care medical director Dr Raj Patel, and involve input from the RCGP, to consider what healthcare support should be provided to patients who are shielding in the coming months.

According to the latest standard operating procedure (dated 6 April), practices should:

The standard operating procedure advises that these patients should be dealt with remotely wherever possible. However, if they need to be seen face-to-face they should have a home visit.

It also recommends that local areas set up separate home visiting services for these patients for when they do need a face-to-face appointment. They shouldn't attend the surgery. Strict infection control processes should be employed when visiting these patients.

Continued here:
How GP practices should support shielded patients during the COVID-19 outbreak - GP online

One of the few bright spots in the Covid-19 pandemic has been the perception that children are mostly spared from its worst effects. But what about kids already at risk of contracting serious infections due to a compromised immune system? Do they have the same protection?

"One group we always worry about when it comes to viral illnesses is immunocompromised children," said Dr Reggie Duerst, director of the stem cell transplant programme at Children's Hospital of Chicago. These kids are typically more at risk of known viral illnesses, such as chickenpox, common cold viruses and flu.

But, he said, because there's so little information available on Covid-19 infections, it's hard to know how much higher the risk might be for children with compromised immune systems.

So far, he said, the incidence of Covid-19 infections in his hospital is very low.

Dr Basim Asmar, chief of infectious disease at Children's Hospital of Michigan, said it's just not clear yet whether or not children with compromised immune systems are more likely to get Covid-19 infections. It's also unclear if they would have more severe complications if they got an infection.

"We're not really sure right now. We're still learning, and every day we're learning something new. But with other viral infections, immunocompromised children tend to have a more prolonged course," Asmar said.

Dr Mehreen Arshad, a member of the Infectious Diseases Society of America and an assistant professor of paediatrics at Northwestern University in Chicago, agreed that there's just not a lot of data on children and Covid-19 yet, especially kids with compromised immune systems. She said that immunocompromised children likely have less risk from Covid-19 than older adults do, but they may have more risk than children with healthy immune systems. She added it's important to "take all precautions" to lessen the risk of infection for these children.

Which kids have a compromised immune system?

Duerst said many children who are being treated for cancer and those receiving stem cell transplants or organ transplants tend to have compromised immune systems. There are also inherited immune deficiency conditions. Children who have certain autoimmune diseases, such as rheumatoid arthritis or lupus, may take medications that dampen their immune system's response.

Other children who might be at a higher risk include those with cystic fibrosis and other lung diseases because their lung capacity is already compromised.

Among children who've received a stem cell transplant, the immune systems of those who get their own cells back (autologous transplant) are close to normal after a year or two, Duerst said. In kids who get stem cells from a donor (allogeneic transplant), "they are on ongoing immune suppression for three to six months, and often longer. If they have a smooth course, by two years they begin to return to normal," he said.

Kids who've had an organ transplant may remain on immune-suppressing drugs for a long time, often for life.

So, what steps do parents need to take to keep these youngsters safe?

Arshad said, "I would be a little more stringent for children with compromised immunity. Stay inside as much as possible. Don't have contact with anyone at higher risk, like grandparents, or anyone with symptoms. Don't go to stores. Avoid crowds."

She noted that "these families are used to taking precautions already. They may be more aware of the potential dangers."

Asmar agreed that it's important to follow common-sense infection prevention. And, he added, "If someone is ill within the family, even the mother or father, they should try to avoid coming in contact with the child, and should stay in a separate room."

In addition, Asmar said that children with compromised immune systems should be as up-to-date on immunisations as possible.

If your child has a compromised immune system and gets sick, Duerst said to call the physician treating the immune-compromising condition to get instructions. "There are multiple reasons you do not want to enter just any emergency room entrance," he said. But with a number of precautions and screening in place, hospitals are "still a relatively safe place to be," he added.

Arshad said that for more routine visits, kids can often be seen via telehealth. And if there's something a doctor needs to see your child for, the doctor might have your child stay in the car and come out to you.

"While we're not seeing immune-compromised children get an overwhelming number of infections, there's no reason to be complacent," she noted.

READ | Coronavirus hitting younger children harder than we thought

READ | Keep TB vaccine for babies, implore experts

READ | Up 50 000 US kids may be hospitalised with Covid-19 by year's end

See the article here:
Are immune-compromised kids at greater risk from Covid-19? - Health24