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Market Study Report, LLC, adds a thorough analysis of the ' Semiconductor Laser Therapeutic Equipment market', offering a comprehensive report emphasizing every vital aspect of the business vertical. The study has collectively presented refined data characterized by market valuation, SWOT analysis, market participants, regional segmentation, and revenue forecasts, enabling stakeholders to make logical business decisions.

The research report on Semiconductor Laser Therapeutic Equipment market is a comprehensive analysis of this business space and entails all the key aspects of the industry including net revenue estimates, present renumeration, periodic deliverables, segmental share, market size, and market trends.

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A brief assessment of the behavior pattern of the Semiconductor Laser Therapeutic Equipment market over the forecast timeline has been cited in the report. Critical parameters such as growth drivers as well the expected growth rate followed during the study period are also documented in the report. It further elaborates on the potential growth aspects and restraints of this industry.

Main highlights of Semiconductor Laser Therapeutic Equipment market report:

Geographical scrutiny of the Semiconductor Laser Therapeutic Equipment market:

Semiconductor Laser Therapeutic Equipment Market Segmentation:

Key insights presented in the report with respect to the regional outlook:

A thorough analysis of Semiconductor Laser Therapeutic Equipment market with respect to the product landscape and application spectrum:

Product landscape:

Product types: Opthalmology, Dermatology, Gynecology, Dentistry, Urology, Cardiovascular and Others

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Main insights presented in the report:

Application landscape: IIII

Major discoveries of the report:

Other takeaways of Semiconductor Laser Therapeutic Equipment market report:

Additional insight on the competitive outlook of the Semiconductor Laser Therapeutic Equipment market:

Vendor base of the industry: Sirona Dental Systems GmbH, WON TECH, Lumenis Inc., PHYSIOMED ELEKTROMEDIZIN AG, Biolase, Dornier MedTech GmbH, Cutera, IRIDEX Corporation, Quanta System S.p.A, Cynosure, L.H.H. Medical, Shenzhen Tianjiquan, Zhengan Medical, Shandong Shensi, Medicen, Guangdun, Kangjiantong, Wuhan HNC, Helsen, Transverse Industries and Shenzhen GSD

Vital parameters which define the competitive landscape of the Semiconductor Laser Therapeutic Equipment market:

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Semiconductor Laser Therapeutic Equipment Market Detail Analysis focusing on Application, Types and Regional Outlook - AlgosOnline

The 17.5m facility would provide three new theatres two reserved for ophthalmology and a third for other procedures which do not require overnight admission.

An extra outpatients department and day ward also feature in the proposed four-storey building on the Euxton Lane site.

Lancashire Teaching Hospitals NHS Foundation Trust (LTH) is seeking planning permission for the development from Chorley Council and has described the project as exciting.

The Local Democracy Reporting Service understands that the scheme is unrelated to the forthcoming public consultation over the future of the accident and emergency unit at the site, which also has implications for how the rest of the hospital would be used in future.

In January, it emerged that two out of the three options likely to form the basis of that consultation recommended that Chorley Hospital should become a centre of excellence for routine, pre-planned care the like of which could be accommodated by the planned new facility.

However, it is believed that the project will go ahead regardless of the outcome of that exercise, which has itself now been delayed by the coronavirus outbreak.

If permission is granted, the new unit is expected to be open by October 2021 and will bring all opthalmology servies under one roof on the site.

Existing facilities at the Royal Preston would be unaffected by the plans and continue to operate as they do currently.

Dr Geraldine Skailes, medical director at LTH, said: We are really pleased to be able to provide this additional facility which will help us to improve patient experience.

The unit will include a dedicated outpatient and diagnostic space as well as three additional theatres to provide extra capacity for patients requiring a variety of day case procedures.

The new unit will connect to the main hospital on the first and second floors with respective links to the existing outpatients department and theatres.

According to the planning application, staff facilities will be located on the ground floor, with the remaining space earmarked for future hospital expansion. The fourth floor will house the plant room.

The facility is set to be built on a part of the site currently partially occupied by a storage unit for sterilisation and decontamination, which will be relocated.

The development will see an existing staff car park expanded by 64 spaces to accommodate a total of 174 vehicles.

Highways England have requested that consideration of the application be deferred until the trust has provided further information about expected vehicle trips to the unit, so that their potential impact on junction eight of the M61 motorway can be assessed.

Continued here:
This is the new unit planned for Chorley Hospital and what it will be used for - Chorley Guardian

The massive international effort to map the entire human genome, completed in 2003, opened a new field we now know as personalized medicine.

The breakthrough, which identified the location and function of every human gene, offered the promise of medical care tailored specifically to individual patients, based on their personal genetic makeup.

When researchers identified a gene associated with a 44 per cent risk of breast cancer in women, for example, it seemed that protecting them might be as simple as deactivating that gene.

But the promise of such personalized medicine has not fully materialized, say two McMaster researchers, because the full sophistication of the genetic blueprint has a more complex and far-reaching influence on human health than scientists had first realized.

In the hope of integrating genetics more closely with medical practice, McMaster evolutionary biologists Rama Singh and Bhagwati Gupta have carried out an exhaustive and critical review of decades of research in their field. They lay out their conclusions inan articlepublished today in the Nature Partner JournalGenomic Medicine.

The biochemical pathway that shapes evolution is dense with inherited redundancies, they explain. Genetic information from our ancestors trails along forever in an incremental physical record that interacts significantly with our own most recently evolved and internally complex genetic network, which in turn interacts with the environment, creating almost infinite combinations and potential health outcomes.

Individual genes do not determine sickness or health on their own, the authors say, but act in concert with groups of other genes all in various stages of mutation in ways that are just beginning to be understood.

Our bodies have an immense ability to change and to cope with issues that arise. Context matters in our genome, Gupta says. Even a simple single mutation can have a profound effect on the body, when acting in combination with others.

The scientists conclude that precision medicine is still critical to the future of medicine, but that the same technology that identified the necessary complexity of the genome also needs to be applied to the entire blueprint including the unnecessary elements creating a longer, more complicated road to the same destination.

Any disease we see is a result of the interactions between necessary and unnecessary complexity, says Gupta.

Nature does not go back in time. It goes forward, and as it encounters challenges, it comes up with solutions.

Our genes carry the history of all the changes that have occurred over many generations. It may not be necessary to our function today, but it is embedded in our genes.

Complexity is not a curse. Its a reflection of our evolutionary history, and it needs to be recognized as an important part of the body that medicine is trying to treat, Singh says. Beyond personalized medicine, complexity bears on the evolution of life itself.

Reference:Rama S. Singh, Bhagwati P. Gupta. Genes and genomes and unnecessary complexity in precision medicine. npj Genomic Medicine, 2020; 5 (1) DOI: 10.1038/s41525-020-0128-1.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Personalized Medicine Complicated by Overlapping Versions of Our Genetic History - Technology Networks

As with any medical procedure, to undergo genetic testing, informed consent must be given.According to the National Institutes of Health, informed consent (in the context of genetic testing) is the process of making sure that, wherever possible, a patient fully understands:

With this information, a patient can make an educated, voluntary choice i.e. they are informed to a level such that they can provide consent. This is usually a legal and ethical requirement in medicine.Whilst this might seem like a relatively simple concept, for genetic testing, informed consent suddenly becomes a whole lot more complex. Bioethicists, experts in the ethical practice of biology and medicine, often use case studies to explore these complexities and to discuss potential solutions to the dilemmas arising from them.

Jodie is a 28-year-old woman who is thinking about having children. However, she has a family history of limb-girdle muscular dystrophy and is considering undergoing genetic screening to determine if she is a carrier of any variants (a.k.a. mutations in her genome) associated with the disease.

Genetic Counselor Margarita Raygada, Ph.D., explains the role of a genetic counselor in cancer care and shares the benefits and implications of genetic testing for patients and their families.Genetic counselors are individuals educated in both medical genetics and counseling. This gives them the expertise to provide patients with the knowledge required to give consent, but also to offer guidance and support. As such, they are most likely the person who will be responsible for gaining informed consent from the patient.

Laura Hercher, Director of Research in Human Genetics at Sarah Lawrence College, has almost 20 years experience working as a genetic counselor. She emphasizes that the role of counseling goes far beyond testing alone:

Genetic counseling is about more than genetic testing. It can obviously be about that, and a genetic counselor would be a good person to discuss genetic testing with, but we meet with people where genetic testing isn't on the table at all.

I think that there is an element of education in many genetic counseling sessions or interpretation but also in many circumstances, theres what we call establishing a therapeutic relationship, where you do the counseling side of it.

Continuing on this theme, Hercher points out a key aspect of genetic counseling and something which is crucial to the consent process but often forgotten amongst the hype surrounding genetic testing.

We [genetic counselors] don't take for granted that somebody will want genetic testing. They have the right to say no these are shared norms in genetics in the UK and the US.

However, in Jodies case, she has expressed interest in genetic testing. How does a genetic counselor go about establishing informed consent for this?

You have to consider both of these two very basic things, Hercher begins. Make sure the person has an understanding of what genetic testing may tell them and also have an understanding of what genetic testing may not tell them.

These are very important to understand because, number one, you don't want someone to walk away from the experience saying, "Okay, great, I've been tested. I don't have a disease, if that isn't comprehensive.

Number two, we want to talk about what the test will show the patient, both in terms of setting up correct expectations that's consent but also by identifying additional things they might find out that are not necessarily the goals of testing.

The blood sample provided by Jodie undergoes whole exome sequencing. Upon sequence analysis, its found that Jodie does not have any of the variants currently associated with limb-girdle muscular dystrophy. However, the person analyzing the data also checks for other common disease-associated variants. They discover that Jodie has a mutation in BRCA2 that puts her at a higher risk of developing breast and/or ovarian cancer.

The discovery described above is known as a secondary finding, meaning that whilst its identification may not have been the main goal of the test, its presence was actively sought. This is different to an incidental finding, although the terms are often used interchangeably.The potential for secondary findings demonstrates how consent in genetic testing isnt as simple as a single yes or no answer. The decision to actively look for other variants and have them reported back provides an additional layer of consideration to the consent process.

In 2013, the American College of Medical Genetics and Genomics (AMCG) published recommendations for the responsible handling of incidental findings emerging from clinical exome or genome sequencing. This includes clinicians being responsible for alerting patients to the possibility that sequencing could result in incidental findings, and that these may warrant further investigation.1A proper informed consent for genetic testing would give the person a notion of what they might encounter as a part of testing, and what choices they have, about what [testing or results] they can get and what not to get, if there are choices available in the setting in which you're operating.

Jodie doesnt just have a decision to make about whether or not she wants the test, she also has to consider what results she would want reported back to her. The availability of choice is an important one because of the potential implications, both physically and mentally, of being given information you werent expecting or didnt want to receive.

Jodies results show that she, and potentially her first-degree relatives, are at a high risk of developing breast and/or ovarian cancer. Although it isnt a guarantee that she would develop those diseases, this knowledge could impact upon decisions she makes about her healthcare. For people carrying a disease-associated BRCA mutation, preventative, albeit drastic, surgical measures may be available, including mastectomies and oophorectomies.

Preventative surgery, or even just knowing that you may develop a disease can also take an emotional toll. In addition, a patient could find out that they have variation that means they will develop a condition at some point in their lifetime, such as Huntingtons disease. This may have an impact on mental health if there are currently very limited or no treatment options for the condition diagnosed, although further and continual research needs to be conducted to assess the extent of such an impact.

Secondary findings can also emerge with advances in research; a variant that may not have been considered a pathogenic variant before could be considered so in the future, or vice versa. Patients like Jodie would need to think about whether they would want to be re-contacted with new or updated information.

Thats a lot of factors for someone to consider before consenting. How can we simplify consent to account for all of those decisions and outcomes, if its even possible?

This requires time something which the healthcare system doesnt always have enough of. How do we create a process that works for both clinicians and patients?

The answers people are coming up with tend to be that we need better tools, Hercher tells me. And that includes online or digital tools that would allow people to interact with the information. You know, if you sit somebody down and spout off 15 minutes worth of information, dense information, you're not doing anything for them.

So, what's needed to improve the situation is new tools that allow people to tackle it over time, at their own pace, exploring what they want to and when. That would optimize the situation for both the caregiver and the patient. And allow them to go back to it [the information] to refresh their memory and so on. The optimal consent process is not "let's decide everything we can fit into this space of time consent, optimally, is an ongoing process.

Research conducted in the UK seems to agree. A recent report from the Joint Committee on Genomics in Medicine sums it up nicely:Consent may be more appropriately seen as an ongoing conversation that needs updating and clarifying where necessary, rather than as a single historical event that needs to be revisited.Reference

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Exploring the Ethics of Genetic Testing: What Does Consent Mean? - Technology Networks

Glaucoma is an eye disease affecting almost 80 million people and is the second leading cause of blindness worldwide.

Glaucoma results in progressive damage to the optic nerve head, which leads to a corresponding visual field loss and when severe, blindness. The pressure within the eye (intraocular pressure) is the only modifiable risk factor for glaucoma.

Glaucoma has a clear genetic component and tens of common genetic variants affecting intraocular pressure and/or glaucoma risk have been identified. The clinical impact of these results has, however, thus far been negligible.

In this study, published in the journal PLOS Genetics, researchers searched for less common genetic variants which might lower intraocular pressure and protect from glaucoma and focused on those with a clear effect on the function of the corresponding protein product. Such variants have particularly high therapeutic potential since they would highlight a specific gene and a genetic modification that protects from disease.

The results of the study are based on two big European cohorts with large-scale genome and health information data available. Altogether more than 514,000 individuals from the UK Biobank and the FinnishFinnGenstudies were examined. Both cohorts include thousands of individuals with a glaucoma diagnosis. Furthermore, over 120 000 UK Biobank participants have participated in the intraocular pressure measurement tests.

Both study cohorts provided independent, complementary and convincing evidence for the role of theANGPTL7gene in glaucoma. UK Biobank participants carried several rare genetic changes that were shown to reduce intraocular pressure, while FinnGen study provided very strong evidence of another variant specific to the Finnish population which significantly decreased glaucoma risk.

The variant we identified is more than 50 times more common in the Finnish population than elsewhere in the world. In fact, more than 8% of Finns carry it and have a substantially reduced risk of glaucoma. This again demonstrates how the population history of the Finns makes it much easier to identify clinically important genetic variants, said ProfessorMark Dalyfrom the Institute for Molecular Medicine Finland (FIMM), University of Helsinki who co-led the study.

With clinic-based recruitment focused on several areas including ophthalmology, and with more than 30 % of the participants being above age 70, FinnGen is particularly well-powered for aging-associated endpoints.

We often think of the body as a machine whereby taking a single bolt out of that machine and something could go wrong. In this study that hypothetical bolt made the machine work even better by protecting human individuals from glaucoma. Our results highlight the benefits of multi-cohort analysis for the discovery of rare protein-altering variants in common diseases, and ANGPTL7 provides the best therapeutic hypothesis out there for glaucoma, saidManuel Rivas,assistant professor of biomedical data science, Stanford Universitys School of Medicine, who co-led the study.

Importantly, cohorts such as FinnGen and UK Biobank make it possible for the researchers to assess whether the identified protective variants increase the risk of some other condition.

Using the comprehensive health information in the two population cohorts, we assessed the potential impacts of rare genetic variants inANGPTL7on a spectrum of human disorders. We did not find any severe medical consequences that would be of obvious concern in developing a therapeutic to mimic the effect of these alleles, saidYosuke Tanigawa,doctoral student, Stanford Universitys School of Medicine, the first author of the study.

Better understanding of the genetic and pathological mechanism behind intraocular pressure can open up new ways of preventing or treating glaucoma. In this case, the genetic findings support inhibition or lowering the amount of ANGPTL7 as a potentially safe and effective therapeutic strategy for glaucoma.

Our results position angiopoietin like 7 as an appealing and safe target for glaucoma therapies. If a drug can be developed that mimics the protective effect of these mutations, intraocular pressure in at-risk individuals could be lowered, saidMark Daly.

Reference:Tanigawa et al. (2020).Rare protein-altering variants in ANGPTL7 lower intraocular pressure and protect against glaucoma. PLOS Genetics. DOI: https://doi.org/10.1371/journal.pgen.1008682.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Gene Variants That Protect Against Glaucoma Discovered - Technology Networks

- 70 sepsis risk genes identified from UK Biobank, 61% of which are present specifically in severe COVID-19 patients ('COVID risk genes')

- 13 'COVID risk genes' identified as known druggable targets

- 59 compounds and drugs identified with potential for accelerated drug discovery ('repurposing')

- Study also offers potential for identifying COVID-19 high risk biomarkers

OXFORD, England, May 6, 2020 /PRNewswire/ -- Data scientists from UK-headquartered AI precision medicine company, PrecisionLife, have used the Company's proprietary AI enabled precision medicine platform to identify 59 repurposing drug candidates that could be used to develop new therapeutic strategies to increase the survival rate of patients who develop sepsis while suffering from severe COVID-19.

Disease architecture of the sepsis cohort generated by the PrecisionLife platform. Each circle represents a disease associated SNP genotype, edges represent co-association in patients, and colors represent distinct patient sub-populations or communities'.

The new study, released today on Biorxiv sought to identify genetic risk factors for sepsis especially in the context of COVID-19, and to use these insights to identify existing drugs that might be used to treat life-threatening late-stage disease.

"Ours is the first study looking at host genomics and opportunities to treat later stage severe disease where host immune processes take over,"said Dr Steve Gardner CEO of PrecisionLife.

Like the initial genomic studies on COVID-19 patients, previous analyses of sepsis patients have failed to identify more than a handful of genetic variants that predispose individuals to developing the disease. By providing deeper insights, this study identifies novel approaches and hope for new therapies.

PrecisionLife analyzed patient datasets compiled by UK Biobank to identify genes associated with sepsis, which are also found in severe COVID-19 patients. Sepsis is observed in 60% of severe COVID-19 patients and is a life-threatening condition with a mortality rate of approximately 20%.

The team identified mutations in 70 sepsis risk genes, 61% of which were also present specifically in severe COVID-19 patients. Several of the disease associated genetic signatures found in both sepsis and severe COVID-19 patients have previously been linked to cancer, immune response, endothelial and vascular inflammation and neuronal signalling.

13 of the sepsis risk genes, which the study shows are also COVID risk genes, are known to be druggable i.e. targeted by active chemical compounds used to treat these other diseases and therefore represent potential drug repurposing opportunities. The study went on to identify 59 compounds and drugs that are known to be active against these 13 targets. These could form the basis for future drug trials and repurposing projects. They could also offer potential as COVID-19 high risk biomarkers.

"Our high-resolution genomic analysis tools have allowed us to develop new insights into two serious and complex diseases for which new therapeutic options are urgently required. We hope that these will lead to better understanding of what drives sepsis in COVID-19 patients and result in new ways to treat seriously ill patients," said Dr Gardner.

PrecisionLife is disclosing its new insights and will be working with international collaborators to investigate therapeutic strategies that may help to reduce the high mortality rates in patients who develop sepsis with or without the context of COVID-19.

Story continues

As more COVID-19 patient data become available in UK Biobank and other patient data sources, PrecisionLife will be able to analyze the clinical impact of these disease signatures in a larger group of patients.

For more information, please see http://www.precisionlife.com, or email covid-19@precisionlife.com.

Follow us on Twitter @precisionlifeAI and on LinkedIn http://www.linkedin.com/company/precisionlifeai

About PrecisionLife

PrecisionLife Ltd started in 2015, built on a shared vision to bring a new level of analytical capability to computational biology, genomic medicine and healthcare. Its powerful data analytics platform is built on a unique mathematical framework and over 30 years' experience in delivering new technologies and products to enable the discovery of richer and more useful links between patients, disease, targets and drugs.

Headquartered in the UK, PrecisionLife also has operations in the US, Denmark and Poland.

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AI Precision Medicine Company, PrecisionLife, Have Identified 59 Repurposing Drug Candidates That Could Be Used to Increase the Survival Rate of...

Higher alcohol consumption was shown to be associated with an increased risk of having a stroke or developing peripheral artery disease, according to new research published in Circulation: Genomic and Precision Medicine.While observational studies have consistently shown that heavy alcohol consumption is associated with an increased risk of certain cardiovascular diseases, they often use self-reported data and are unable to determine cause. Researchers in this study used a different technique called Mendelian randomization that identifies genetic variants with a known association to potential risk factors to determine the potential degree of disease risk.

Since genetic variants are determined at conception and cannot be affected by subsequent environmental factors, this technique allows us to better determine whether a risk factor in this case, heavy alcohol consumption is the cause of a disease, or if it is simply associated, said Susanna Larsson, Ph.D., senior researcher and associate professor of cardiovascular and nutritional epidemiology at Karolinska Institutet in Stockholm, Sweden. To our knowledge, this is the first Mendelian randomization study on alcohol consumption and several cardiovascular diseases.

Researchers analyzed the genetic data from several large-scale consortia and the UK Biobank, which follows the health and well-being of 500,000 United Kingdom residents. Results indicate that with higher alcohol consumption:

Higher alcohol consumption is a known cause of death and disability, yet it was previously unclear if alcohol consumption is also a cause of cardiovascular disease. Considering that many people consume alcohol regularly, it is important to disentangle any risks or benefits, Larsson said.Researchers noted that this study suggested the mechanism by which higher consumption was associated with the risk of stroke and PAD may be blood pressure.

According to a statement on dietary health, the American Heart Association believes that alcohol intake can be a component of a healthy diet if consumed in moderation (no more than one alcoholic drink per day for women and 2 alcohol drinks per day for men) and only by nonpregnant women and adults when there is no risk to existing health conditions, medication-alcohol interaction, or personal safety and work situations. One drink is equivalent to 12 ounces of beer (5% alcohol); 5 ounces of wine (12% alcohol); or 1.5 ounces of 80-proof distilled spirits (40% alcohol).

The study has some limitations. According to Dr. Larsson, the prevalence of heavy drinking in the UK Biobank was low, and it is unlikely that the burden of increased risk of cardiovascular disease is restricted to heavy drinkers alone. Also, the exact amount and frequency of alcohol consumed could not be quantified for this study. The researchers said the causal role of alcohol consumption on cardiovascular diseases other than stroke and peripheral artery disease requires further research.ReferenceLarsson et al. (2020). Alcohol Consumption and Cardiovascular Disease: A Mendelian Randomization Study. Circulation: Genomic and Precision Medicine. DOI: https://doi.org/10.1161/CIRCGEN.119.002814

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Genetic Study Links Higher Alcohol Consumption to Increased Stroke and PAD Risk - Technology Networks

New research suggests the prevalence of infection has links to the development of some types of cancer.

A new study has suggested that before developing some forms of cancer, people experienced increased rates of infectious diseases, such as influenza and pneumonia.

The study, published in the journal Cancer Immunology Research, might help develop diagnostic methods for detecting cancers.

Previous research has indicated that there is a link between immunity, inflammation, and cancer.

Inflammation can promote the development of cancers. This can compromise a persons immune system, which can, in turn, increase inflammation.

Dr. Shinako Inaida, a visiting researcher at the Graduate School of Medicine at Kyoto University in Japan and the corresponding author of the study, explains. Cancer can develop in an inflammatory environment caused by infections, immunity disruption, exposure to chemical carcinogens, or chronic or genetic conditions.

An individuals immunity is thought to be a factor in the development of cancer, but additional research is needed to understand the relationship [between] precancerous immunity, infections, and cancer development. This information may contribute to efforts to prevent or detect cancer.

Consequently, it may be valuable to investigate the relationship between immunity, inflammation, and cancers.

The researchers wanted to understand the relationship between the prevalence of specific infectious diseases that could cause inflammation and cancer development.

To investigate, the authors took their information from a 7-year Japanese social health insurance system database.

The researchers looked at data from 50,749 participants. All the participants were over the age of 30 and did not have any detected immunodeficiency.

The case group comprised 2,354 participants who had developed a form of cancer in the 7th year of the study. The control group consisted of 48,395 people who had no cancer diagnosis during the 7 years of the study, plus an additional final year.

The authors then calculated the prevalence of influenza, gastroenteritis, hepatitis, and pneumonia infections for the two groups.

The authors found a clear link between the prevalence of the four illnesses and the later development of cancer.

The case group experienced significantly higher infection rates than the control group in the 6 years before cancer diagnosis.

Members of the case group experienced higher rates of infection in the year before their cancer diagnosis than those in the control group. During this year, the case group experienced an 18% greater infection of influenza, 46.1% of gastroenteritis, 232.1% of hepatitis, and 135.9% for pneumonia than the control group.

The authors also noted that there was a relationship between different infections and different cancers.

For example, people who developed male germ cell cancers were more likely to have experienced influenza. People who developed stomach cancer were more likely to have had pneumonia, and people who developed blood or bone cancers were more likely to have had hepatitis.

However, as Dr. Inaida points out, [i]nterestingly, we found that infection afflicting a specific organ did not necessarily correlate with increased risk of cancer in the same organ.

The authors point out that the study had some limitations. For example, the data provided limited information on underlying genetic and medical conditions, as well as environmental exposures and different lifestyles. These may have affected the chances of infection and developing cancer.

Nonetheless, by making clear an association between infections, inflammation, immunity, and the development of cancers, future research can look in more detail at the precise mechanisms that govern these relationships.

This may then open the door to better diagnostic methods.

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Infection rates may have links to cancer - Medical News Today

DetailsCategory: More NewsPublished on Monday, 04 May 2020 11:30Hits: 525

SAN RAFAEL, CA, USA I May 3, 2020 I BioMarin Pharmaceutical Inc. (Nasdaq: BMRN) today announced that the company has entered into a preclinical collaboration and license agreement with DiNAQOR AG (DiNAQOR), a gene therapy platform company, to develop novel gene therapies to treat rare genetic cardiomyopathies. DiNAQOR will receive an undisclosed upfront payment and is eligible to receive development, regulatory and commercial milestones on product sales in addition to tiered royalties on worldwide sales. The company did not disclose financial terms. BioMarin management reiterated its 2020 GAAP net income guidance of $20 to $80 million, inclusive of this collaboration.

The license initially covers DiNAQOR's lead program, DiNA-001 for MYBPC3 hypertrophic cardiomyopathy (HCM). Additionally, the companies will collaborate on several of DiNAQOR's other pipeline programs, and BioMarin has the option to extend the license to include these additional programs on similar terms. Reflecting the long-term commitment to the collaboration, BioMarin is simultaneously investing in DiNAQOR.

"With this agreement, BioMarin is continuing to apply its gene therapy know-how and manufacturing expertise in new areas like cardiology," said Jean-Jacques Bienaim, Chairman and Chief Executive Officer at BioMarin. "This collaboration extends our global leadership position in gene therapy and boosts our potential to transform the lives of patients worldwide with rare genetic cardiomyopathies."

"We are thrilled to collaborate with the researchers at DiNAQOR to conduct this pioneering work on the development of gene therapies for inherited cardiomyophathies," said Lon Cardon, Chief Scientific Strategy Officer and Senior Vice President at BioMarin. "We believe there is tremendous potential in combining our experience in gene therapy research and development with DiNAQOR's in-depth knowledge of genetic heart diseases."

DiNAQOR was founded and is led by several leading pharmaceutical and biotechnology executives and academics with deep cardiology and gene therapy expertise. The company's holistic approach to gene therapy is focused on gene therapies for the heart that deliver a medical solution that can safely deliver gene therapies to the heart muscle, ensure transduction of the cardiac cells, and limit the exposure of the therapy to other organs.

"BioMarin is a global leader in rare disease research, development and commercialization, and their commitment to DiNA-001 is a powerful validation of DiNAQOR's gene therapy platform," said Dr. Johannes Holzmeister, Co-Founder, Chairman and CEO at DiNAQOR. "We believe our platform has many potential applications and this milestone agreement will enable us to invest in expanding our genetic medicine pipeline."

"Momentum for gene therapies continues to build, and BioMarin has demonstrated tremendous scientific, clinical, and manufacturing leadership and expertise in the space," said Thomas Voit, M.D., Ph.D., Co-Founder and Chief Scientific Officer at DiNAQOR and Director of the Biomedical Research Centre at the Great Ormond Street Hospital and the UCL Institute of Child Health, University College London. "We are looking forward to combining our strengths to expand the promise of gene therapy treatments by targeting the heart muscle to treat rare genetic cardiomyopathies."

About HCM and MYBPC3

Hypertrophic cardiomyopathy (HCM) is one of the most common genetic heart diseases, with about 500,000 patients diagnosed with HCM worldwide.Up to 60% of HCM cases have a genetic origin, and it is estimated that 40% of those have mutations in MYBPC3, the gene that encodes cardiac myosin-binding protein C (MyBP-C).

HCMaffects the heart muscle, causing the muscle to enlarge. HCM patients have an increased risk of developing heart failure and life-threatening arrhythmias. There are no approved pharmacological treatment options available that address the underlying disease biology of HCM and invasive surgery or heart transplantation may be the only options available for patients with advanced disease.

About BioMarin

BioMarin is a global biotechnology company that develops and commercializes innovative therapies for serious and life-threatening rare genetic diseases. The Company's portfolio consists of six commercialized products and multiple clinical and pre-clinical product candidates. For additional information, please visitwww.biomarin.com. Information on BioMarin's website is not incorporated by reference into this press release.

About DiNAQOR

Founded in 2019, DiNAQOR AG is a global gene therapy platform company focused on advancing novel solutions for patients suffering from heart disease. The company's lead preclinical program, DiNA-001 is focused on the treatment of MYBPC3-linked cardiomyopathy. DiNAQOR is headquartered in Pfffikon, Switzerland, with additional presence in London, England and Boston, Massachusetts (US). For more information visit http://www.dinaqor.com.

SOURCE: BioMarin Pharmaceutical

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BioMarin Extends Gene Therapy Leadership with DiNAQOR in a Preclinical Collaboration and License Agreement to Develop Gene Therapies for Rare Genetic...

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.

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Working to Improve COVID-19 Testing - UVM News