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The Entire Spectrum of Colours and All the Forms, Manners and Expressions of Light are Made Invisible in This White: Or, Rather, Mix All the Colours and You Have This White: Or, Arrange All the Colours and Find an Infinite Rainbow: Or Take the Colours and Light Away and There Resides the Darkness But As Such That in Its Invisible Sphere There Still Remains Another Infinite Rainbow at Various States, That We Can Not See With Our Eyes: Take That All Away and You Have the Utter, Absolute and Primeval Duantum Darkness Within Which Our Matter Universe is Constructed and Does Function: Unless, We Remember This Every Nano-Second of Our Existence We Loose Our Sense and Joy of Eternal Wonder, Awe and Astonishment of This Magnificent Universe, Which is Outside, True, But Which is Nano-Seismically Constructed in the Human Physiology and Psychology: The Study of Medicine Will Always Remain and Fall Short Until It Sees and Learns That It is Dealing with the Universe, When It Goes About Learning and Healing This Human Physiology and Psychology: Alphansum Sovereign Necessarius: Munayem Mayenin: ISBN: 978-0-244-58241-8: April 14: 2020: Imsonium Books

 

WHO Guideline Development Group Advises Against the Use of Remdesivir For COVID-19: Currently No Evidence That It Improves the Survival and Other Important Measures

 

|| Friday: November 20: 2020 || ά. The anti-viral drug Remdesivir is not suggested for patients, admitted to hospital with COVID-19, regardless of how severely ill they are, because there is currently no evidence that it improves survival or the need for ventilation, say a WHO Guideline Development Group:GDG panel of international experts in The BMJ today. The recommendation is part of a living guideline, developed by the World Health Organisation:WHO with the methodological support of MAGIC Evidence Ecosystem Foundation, to provide trustworthy guidance on the management of COVID-19 and help doctors make better decisions with their patients.

Living guidelines are useful in fast moving research areas like COVID-19 because they allow researchers to update previously vetted and peer reviewed evidence summaries as new information becomes available. Remdesivir has received worldwide attention as a potentially effective treatment for severe COVID-19 and is, increasingly, used to treat patients in hospital. But its role in clinical practice has remained uncertain.

Today’s recommendation is based on a new evidence review, comparing the effects of several drug treatments for COVID-19. It includes data from four international randomised trials, involving over 7,000 patients, hospitalised for COVID-19. After thoroughly reviewing this evidence, the WHO’s GDG expert panel, which includes experts from around the world, including, four patients, who have had COVID-19, concluded that Remdesivir has no meaningful effect on mortality or on other important outcomes for patients, such as, the need for mechanical ventilation or time to clinical improvement.

The Panel acknowledged that the certainty of evidence is low and said that the evidence did not prove that Remdesivir has no benefit; rather, there is no evidence, based on currently available data that it does improve important patient outcomes.

But given the remaining possibility of important harm, as well as, the relatively high cost and resource implications, associated with Remdesivir, it must be given intravenously, they judged this to be an appropriate recommendation. They, also, support continued enrolment into trials, evaluating Remdesivir, especially, to provide higher certainty of evidence for specific groups of patients.

In a linked feature article, US journalist Mr Jeremy Hsu asks what now for Remdesivir, given that it is unlikely to be the lifesaving drug for the masses, that many have hoped for?  The full story of Remdesivir will not be known until manufacturer Gilead releases the full clinical Study Reports, writes Mr Hsu but, much will depend on whether future studies are designed to test Remdesivir’s potential effectiveness.

In the meantime, he says that alternative treatments, such as, the well-known, cheap and widely available Corticosteroid Dexamethasone, that has been proved to reduce mortality among severely ill COVID-19 patients, are now impacting discussions about Remdesivir’s cost-effectiveness.

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Higher COVID-19 Virus Level Is Linked to Higher Death Risk: Patients Admitted to Hospital With Higher Levels of the COVID-19 Virus Were More Than Four Times More Likely to Die in the Subsequent 30 Days Than Were Those With Lower Levels of the Virus: The Whole World’s Health Services Must Register and Act Now

 

|| Thursday: November 19: 2020: University of Washington News || ά. Patients, admitted to the hospital with higher levels of the COVID-19 virus, SARS-CoV-2, were more than four times more likely to die in the subsequent 30 days than were those with lower levels of the virus, according to a finding by researchers in laboratory medicine and pathology at the University of Washington School of Medicine. On the other hand, patients, who had generated antibodies against the virus by the time of admission tended to have lower levels of virus.

They, also, had a 30-day risk of death, that was, approximately, half that of patients, who had not generated antibodies; although, this result was not as statistically significant as the association between viral levels and mortality. "Currently, SARS-CoV-2 tests have, generally, only, been authorised to tell, if, the virus is present but not for determining the quantity of virus present.” said Dr Alex Greninger, a Assistant Professor and Assistant Director of the UW Medicine Clinical Virology Laboratory. “Our findings suggest, tests that measuring the amount of virus, the viral load, can help doctors identify those, admitted to the hospital, who are at highest risk of serious disease and need special attention.”

The researchers’ reported findings appear in the journal Open Forum Infectious Disease. In the Study, the researchers identified patients, admitted to UW Medicine's Northwest campus, whose SARS-CoV-2  nasopharyngeal swabs tested positive. The researchers, also, tested serum and blood samples from 245 of these patients for SARS-CoV-2 antibodies and reviewed medical records to determine the date the patients developed symptoms and their subsequent clinical outcomes. The antibody test looked for anti-SARS-CoV-2 nucleocapsid IgG, an antibody, that targets a key viral protein.

The levels of virus were determined by a process, called, qRT-PCR, for quantitative reverse transcription polymerase chain reaction. In this process, a segment of the coronavirus genome, which is made of RNA, is converted into DNA. This process is called reverse transcription. The DNA copies are, then, doubled again and again through repeated cycles of the polymerase chain reaction. This process can generate millions or billions of copies of a single strand of DNA, thereby, enabling the detection of minute amounts of viral RNA in a sample.

The researchers found that patients, who, upon hospital admission, had virus levels high enough that the PCR test turned positive in less than 22 cycles had a four-fold higher risk of dying in the next 30 days than patients whose viral levels required more than 22 cycles to detect the virus.

In the case of antibodies, patients, who had, already, begun making the anti-SARS-CoV-2 nucleocapsid IgG against the virus upon hospital admission tended to have a lower viral load and, also, appeared to do better.  Those patients were about half as likely to die in the next 30 days than those, who did not yet have antibodies.

Because of the relatively small number of patients in the study, the survival benefit seen with the presence of antibodies was not statistically significant, the researchers noted. Not surprisingly, the presence of antibodies was associated with a lower viral load.

“Our findings provide further support for the use of quantitative viral-load assessment and antibody testing in managing patients, especially, on hospital admission.” said Dr Andrew Bryan, Assistant Director of Clinical Microbiology and Medical Director of the Clinical Lboratory at UW Medical Centre, Northwest.  This work was supported by the Department of Laboratory Medicine and Pathology  at the University of Washington School of Medicine.

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Understanding Rare Type of Diabetes Gives Insight Into Critical Mechanisms of Insulin Production

 

|| Sunday: November 15: 2020 || ά. Solving the genetic puzzle of why babies developed a rare type of diabetes has uncovered a new biological pathway, that is fundamental to insulin production and could boost research into new treatments for more common forms of diabetes. Published this week, November 09, in the Journal of Clinical Investigation, the Study used genome sequencing to show that a group of babies with shared clinical features, who developed diabetes soon after birth, all had genetic changes in the YIPF5 gene.

The research combined stem cell research and CRISPR gene editing tools to show that this gene is essential for function of the cells producing insulin. The research team, led by the University of Exeter, the Université Libre de Bruxelles and University of Helsinki, went on to show how these genetic changes result in high levels of stress within the cells, causing cell death. The Study shows, for the first, time that YIPF5 gene function is essential for neurons and insulin-producing beta cells but, appears to be dispensable for the function of other cells.

These results aid understanding on which cellular steps are important for making insulin, which regulated blood sugar levels and maintaining the function of the cells, producing insulin within the pancreas. This insight could help researchers develop better therapies to treat patients with common types of diabetes, which affect 460 million people worldwide.

Dr Elisa De Franco, one of the lead authors of the Study, from the University of Exeter, said, “This Study highlights the importance of gene discovery to further our understanding of fundamental mechanisms in biology. In this case, our research has resulted in the identification of a gene, essential for both insulin-producing cells and neurons, highlighting a biological pathway we previously did not know was so fundamental for insulin-producing cells. This has the potential to open new avenues of research and, ultimately, result in better understanding of how other types of diabetes develop.”

Some babies develop diabetes before they are six months old. In more than 85% of cases, this is due to a spelling mistake in their DNA, often, called, a genetic mutation. Some of these children, also, have additional health issues, which can involve their brain.

To learn more about which genes in the DNA are important for insulin-producing cells, researchers from the University of Exeter studied the genetics of, almost, 190 patients from all over the world, who developed diabetes soon after birth. Using the latest genetic technologies, they found that six babies with extremely similar clinical features, including, epilepsy and an extremely small head, known as, microcephaly, had genetic mutations in the YIPF5 gene.

Researchers at the Université Libre de Bruxelles and University of Helsinki, then, used advanced techniques in insulin-producing cells and in stem cells to try and understand how YIPF5 works in the insulin-producing cells. Their results showed that when YIPF5 is absent or has the genetic change found in patients, insulin-producing cells can not produce insulin as they normally do. In an attempt to cope with this malfunction, the cells activate stress mechanisms, which, ultimately, result in cell death.

Professor Miriam Cnop, one of the senior authors of the Study, from the Université Libre de Bruxelles, said, “The possibility to generate insulin-producing cells from stem cells has given us the possibility to study what goes wrong in beta cells from patients with this rare form and, also, other types of diabetes. It is an extraordinary disease-in-a-dish model to study mechanisms of disease and test treatments.”

Professor Timo Otonkoski, one of the senior authors, from the University of Helsinki, said, “Using the CRISPR ‘gene scissor’ DNA-editing technology, that just received the Nobel Prize, we could correct the patient mutation in stem cells in order to fully understand its effects. The combination of gene editing with stem cells provides powerful new tools for the study of disease mechanisms.“

Professor Andrew Hattersley, one of the senior authors of the Study, from the University of Exeter, said, “We are very grateful to the patients, their families and their doctors for their participation in the Study. Without them, we could not have accomplished this. It is our wish that further research will benefit the patients, to facilitate diagnosis and treatment of their diabetes.”

The Paper: YIPF5 mutations cause neonatal diabetes and microcephaly through endoplasmic reticulum stress. The Journal of Clinical Investigation, 2020: E. De Franco, M. Lytrivi, H. Ibrahim, H. Montaser, M. N. Wakeling, F. Fantuzzi, K. Patel, C. Demarez, Y. Cai, M. Igoillo-Esteve, C. Cosentino, V. Lithovius, H. Vihinen, E. Jokitalo, T. W. Laver, M. B. Johnson, T. Sawatani, H. Shakeri, N. Pachera, B. Haliloglu, M. Nuri Ozbek, E. Unal, R. Yıldırım, T. Godbole, M. Yildiz, B. Aydin, A. Bilheu, I. Suzuki, S. E. Flanagan, P. Vanderhaeghen, V. Senée, C. Julier, P. Marchetti, D. L. Eizirik, S. Ellard, J. Saarimäki-Vire, T. Otonkoski, M. Cnop, A. T. Hattersley https://www.jci.org/articles/view/141455

Caption: On green insulin-producing sells that are generated from stem cells. The sells suffer from stress due to the YIPF5 gene mutation: Image: Hazem Ibrahim

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Tokyo Medical and Dental University and Kyocera Begin Joint Research on Vitals Measurement Headset to Support the Recovery of COVID-19 Patients

 

|| Wednesday: July 01: 2020 || ά. Kyocera Corporation and Tokyo Medical and Dental University:TMDU have announced a joint research project to develop a wireless headset, that can remotely monitor high accuracy patient biometrics, such as, blood oxygen saturation. The Department of Cardiovascular Medicine of TMDU Medical Hospital began preparing for clinical research of the wearable headset system in May 2020.

The Rehabilitation Centre at TMDU Medical Hospital has introduced rehabilitation therapy for severely ill COVID-19 patients and remote rehabilitation for moderately ill patients, who have recovered enough to walk independently. Aimed at helping patients recover faster, this will, also, help contribute to limiting infection risk for rehabilitation staff and preserving vital medical PPE for other uses. Dr Tomoko Sakai, the Director of the Rehabilitation Centre, says, “The role of the Rehabilitation Centre is important for recovering COVID-19 patients because of their tendency to develop thrombosis, blood clots and cerebral infarctions, strokes.”

This rehabilitation programme has been well received by many patients as a way to help improve muscle strength, relieve stress and facilitate psychological care. In order to perform this kind of rehabilitation treatment, the Department of Cardiovascular Medicine of TMDU Medical Hospital proposed to incorporate the wearable headset system in joint research with Kyocera. The project is aimed at bringing remote telemedicine to rehabilitation for patients with COVID-19 and has started preparation for clinical research on the wearable headset system.

A prototype in development can allow healthcare providers to check patient biometrics, such as, blood oxygen saturation:SpO2 during rehabilitation in real time while communicating over standard wireless phone networks. It, also, allows medical professionals a more thorough evaluation and shortening the time of medical care.

The new headset system incorporates bone-conduction audio technology instead of a traditional microphone and loudspeaker. This technology helps cancel unwanted ambient noise while letting patients move their limbs freely during exercise. Future development goals include miniaturising the headset to allow convenient, real-time biometric monitoring of patients during at-home recuperation.

Kyocera Corporation and TMDU will continue the trial operation in Japan to verify the effectiveness of remote medical care and rehabilitation for patients and examine the system’s potential for treating other ailments.

About Tokyo Medical and Dental University:TMDU: TMDU is located in the Yushima:Shoheizaka area, which is considered the sacred birthplace of scholarship and learning in Japan. As a comprehensive medical university, TMDU cultivates professionals with knowledge and humanity, who embark on a lifetime of service, advancing the health and social welfare of people in the local community and spreading their wings to do the same in other communities across the globe.

About Kyocera: Headquartered in Kyoto, Japan, Kyocera Corporation is one of the world's leading manufacturers of fine ceramic components for the technology industry. The strategically important divisions in the Kyocera Group, which is comprised of 298 subsidiaries, are information and communications technologies, products, which increase quality of life and environmentally friendly products. The technology group is, also, one of the most experienced producers of smart energy systems worldwide, with more than 40 years of know-how in the industry.

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Antiviral Drug Lopinavir:Ritonavir Does Not Reduce Death in Hospitalised Patients With COVID-19: Preliminary Trial Results Find

 

|| Tuesday: July 01: 2020 || ά. The ‘RECOVERY’ trial has released preliminary results, showing Lopinavir:Ritonavir, an antiviral drug, commonly used to treat HIV, had no significant mortality benefit in hospitalised COVID-19 patients. Randomised Evaluation of COVid-19 thERapY oe The RECOVERY trial, was funded by UKRI as part of the UKRI:DHSC:NIHR COVID-19 rapid research response. To provide real-time information in the pandemic, the results have been announced as quickly as possible, so it should be noted that the findings have not yet been peer-reviewed and accepted in a journal.

A range of potential treatments have been suggested for COVID-19 but nobody knows, if, any of them will turn out to be more effective in improving survival than the usual standard of hospital care, which all patients will receive. The RECOVERY trial has, also, recently announced preliminary results showing: low-cost Dexamethasone reduced death by up to one third in hospitalised patients with severe respiratory complications of COVID-19 and no effect on mortality from the use of Hydroxychloroquine in patients admitted to hospital with COVID-19.

Lopinavir is an HIV protease inhibitor, which is combined with Ritonavir to increase Lopinavir’s plasma half-life. Lopinavir:Ritonavir had shown promising activity against SARS and MERS corona viruses. Professor Peter Horby, University of Oxford and the Chief Investigator for the trial, said, “Today we release the third set of results from the RECOVERY trial. These preliminary results show that for patients hospitalised with COVID-19 and not on a ventilator, Lopinavir-Ritonavir is not an effective treatment.

In 100 days, the RECOVERY trial has provided results, enabling change in global practice three times. This extraordinary national effort has shown that two drugs used to treat hospitalised COVID patients throughout the world, Hydroxychloroquine and Lopinavir-Ritonavir, do not improve survival, whilst one drug, that was not recommended, Dexamethasone, saves lives.”

Professor Fiona Watt, the Executive Chair of the Medical Research Council, which helped fund the trial, said, ‘’It is very important that we test potential therapies in randomised clinical trials so that we can find out whether re-purposed drugs work or not. The UK’s RECOVERY trial is the world’s largest randomised trial of potential COVID-19 treatments and has worked with unprecedented speed to start delivering the answers we need. Whilst it is disappointing that Lopinavir:Ritonavir, like Hydroxychloroquine, has been found to be ineffective, the earlier findings with Dexamethasone were positive. Researchers and health professionals are now focusing their efforts and patient care, on other promising drugs.’’

On the latest findings for Lopinavir:Ritonavir, Professor Peter Horby and Professor Martin Landray, the Chief Investigators of the trial, said in a statement: ‘In March 2020, the RECOVERY trial was established as a randomised clinical trial to test a range of potential treatments for COVID-19, including, Lopinavir-Ritonavir, an antiviral treatment, commonly used to treat HIV. Over 11,800 patients have been enrolled from 176 NHS hospitals in the UK.

‘’On Thursday, June 25, the independent Data Monitoring Committee conducted a routine review of the emerging data and recommended that the chief investigators be unblinded to the results for the Lopinavir-Ritonavir arm. ‘’A total of 1,596 patients were randomised to Lopinavir-Ritonavir and compared with 3376 patients randomised to usual care alone. Of these patients, 04% required invasive mechanical ventilation when they entered the trial, 70% required oxygen alone and 26% did not require any respiratory intervention.

There was no significant difference in the primary endpoint of 28-day mortality, 22.1% Lopinavir-Ritonavir vs. 21.3% usual care; relative risk 1.04, 95% confidence interval 0.91-1.18; p=0.58 and the results were consistent in different sub-groups of patients. There was, also, no evidence of beneficial effects on the risk of progression to mechanical ventilation or length of hospital stay.

‘These data convincingly rule out any meaningful mortality benefit of Lopinavir-Ritonavir in the hospitalised COVID-19 patients we studied. We were unable to study a large number of patients on invasive mechanical ventilation because of difficulty administering the drug to patients on ventilators. As such, we can not make conclusions about the effectiveness in mechanically ventilated patients. Full results will be made available as soon as possible.’’

Professor Martin Landray, University of Oxford, and the Deputy Chief Investigator, said, “These are clear results and once again emphasise the value of large randomised clinical trials in differentiating drugs we hope work from treatments we know do work. In many countries, current guidelines recommend lopinavir-ritonavir as a treatment for COVID-19. The results from this trial, together with those from other large randomised trials, should inform revisions to those guidelines and changes to the way individual patients are treated.

These results have been made possible by the huge efforts of the many doctors, nurses and other healthcare staff that are contributing to RECOVERY and, above all, the patients, whose participation is driving forward our knowledge of how best to treat COVID-19.”

RECOVERY continues to enrol patients to allow the study of Azithromycin, Tocilizumab and convalescent plasma. It is anticipated that other treatments will be included for study in the future.

The RECOVERY Trial is conducted by the registered clinical trials units with the Nuffield Department of Population Health in partnership with the Nuffield Department of Medicine. The trial is supported by a grant to the University of Oxford fromUK Research and Innovation:National Institute for Health Research:NIHR and by core funding provided byNIHR Oxford Biomedical Research Centre, Wellcome,theBill and Melinda Gates Foundation,theDepartment for International Development,Health Data Research UK, theMedical Research Council Population Health Research Unit, andNIHR Clinical Trials Unit Support Funding.

The RECOVERY trial involves many thousands of doctors, nurses, pharmacists and research administrators at 176 hospitals across the whole of the UK, supported by staff at the NIHR Clinical Research Network, NHS DigiTrials, Public Health England, Department of Health & Social Care, the Intensive Care National Audit and Research Centre, Public Health Scotland, the Secure Anonymised Information Linkage at University of Swansea, and the NHS in England, Scotland, Wales and Northern Ireland.

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Preliminary Breakthrough Trial Results Find: Dexamethasone Reduces the Risk of Death Among Patients With Severe Respiratory Complications in COVID-19

 

 

|| Tuesday: June 16: 2020 || ά. The ‘RECOVERY’ trial has released preliminary results, showing low-cost Dexamethasone reduces death by up to one third in hospitalised patients with severe respiratory complications of COVID-19.  The RECOVERY or ‘Randomised Evaluation of COVid-19 thERapY’, was funded by UK Research and Innovation:UKRI as part of the UKRI:DHSC:NIHR COVID-19 rapid research response. To provide real-time information in the pandemic, the results have been announced as quickly as possible, so it should be noted that the findings have not yet been peer-reviewed and accepted in a journal.

A range of potential treatments has been suggested for COVID-19 but nobody knows, if, any of them will turn out to be more effective in improving survival than the usual standard of hospital care, which all patients will receive. Professor Peter Horby and Professor Martin Landray, the Chief Investigators of the trial, said in a statement, ‘’In March of this year, RECOVERY was established as a randomised clinical trial to test a range of potential treatments for COVID-19, including, low-dose Dexamethasone, a steroid treatment. Over 11,500 patients have been enrolled from over 175 NHS hospitals in the UK.’’

On June 08, recruitment to the Dexamethasone arm was halted since, in the view of the trial Steering Committee, sufficient patients had been enrolled to establish whether or not the drug had a meaningful benefit. A total of 2104 patients were randomised to receive Dexamethasone 6mg once per day, either by mouth or by intravenous injection, for ten days and were compared with 4321 patients randomised to usual care alone.

Among the patients, who received usual care alone, 28-day mortality was highest in those, who required ventilation, 41%, intermediate in those patients, who required oxygen only, 25% and lowest among those, who did not require any respiratory intervention, 13%. Dexamethasone reduced deaths by one-third in ventilated patients, rate ratio 0.65: 95% confidence interval 0.48 to 0.88; p=0.0003 and by one fifth in other patients, receiving oxygen only, 0.80: 0.67 to 0.96; p=0.0021. There was no benefit among those patients, who did not require respiratory support, 1.22: 0.86 to 1.75; p=0.14.

‘’Based on these results, one death would be prevented by treatment of around eight ventilated patients or around 25 patients requiring oxygen alone. Given the public health importance of these results, we are now working to publish the full details as soon as possible.’’

Overall dexamethasone reduced the 28-day mortality rate by 17%, 0.83: 0.74 to 0.92; P=0.0007, with a highly significant trend, showing greatest benefit among those patients, requiring ventilation: test for trend p<0.001. ‘’But it is important to recognise that we found no evidence of benefit for patients, who did not require oxygen and we did not study patients outside the hospital setting. Follow-up is complete for over 94% of participants.’’ The Chief Investigators said.

Professor Peter Horby, of Emerging Infectious Diseases in the Nuffield Department of Medicine, University of Oxford and one of the Chief Investigators for the trial, said, “Dexamethasone is the first drug to be shown to improve survival in COVID-19. This is an extremely welcome result. The survival benefit is clear and large in those patients, who are sick enough to require oxygen treatment, so Dexamethasone should now become standard of care in these patients. Dexamethasone is inexpensive, on the shelf and can be used immediately to save lives worldwide.”

Professor Martin Landray, of Medicine and Epidemiology at the Nuffield Department of Population Health, University of Oxford, one of the Chief Investigators, said, “Since the appearance of COVID-19 six months ago, the search has been on for treatments, that can improve survival, particularly, in the sickest patients. These preliminary results from the RECOVERY trial are very clear: Dexamethasone reduces the risk of death among patients with severe respiratory complications. COVID-19 is a global disease; it is fantastic that the first treatment demonstrated to reduce mortality is one, that is instantly available and affordable worldwide.”

The RECOVERY trial is conducted by the registered clinical trials units with the Nuffield Department of Population Health in partnership with the Nuffield Department of Medicine. The trial is supported by a grant to the University of Oxford fromUK Research and Innovation:National Institute for Health Research:NIHR and by core funding provided byNIHR Oxford Biomedical Research Centre, Wellcome, theBill and Melinda Gates Foundation,theDepartment for International Development,Health Data Research UK, theMedical Research Council Population Health Research Unit andNIHR Clinical Trials Unit Support Funding.

The RECOVERY trial involves many thousands of doctors, nurses, pharmacists and research administrators at over 175 hospitals across the whole of the UK, supported by staff at the NIHR Clinical Research Network, NHS DigiTrials, Public Health England, Public Health Scotland, Department of Health and Social Care and the NHS in England, Scotland, Wales and Northern Ireland.

The RECOVERY trial, also, recently announced preliminary results showing no effect on mortality from the use of hydroxychloroquine in patients admitted to hospital with COVID-19.

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Researchers Now Understand Better As to How Sex Bias Works in Increasing or Reducing Vulnerability

 

 

|| Monday: May 11: 2020: Harvard Medical School News: Stephanie Dutchen Writing || ά. Some diseases exhibit a clear sex bias, occurring more often, hitting harder or eliciting different symptoms in men or women. For instance, the autoimmune conditions Lupus and Sjögren's Syndrome affect nine times more women than men, while Schizophrenia affects more men and tends to cause more severe symptoms than in women.

Likewise, early reports suggest that despite similar rates of infection, men are dying from COVID-19 more often than women, as happened during previous outbreaks of the related diseases SARS and MERS. For decades, scientists have tried to pinpoint why some diseases have an unexpected sex bias. Behaviour can play a role but, that explains only a piece of the puzzle. Hormones are commonly invoked but, how exactly they contribute to the disparity is unclear. As for genes, few, if, any, answers have been found on the X and Y sex chromosomes for most diseases.

Now, work led by researchers in the Blavatnik Institute at Harvard Medical School and at the Broad Institute of MIT and Harvard provides a clear genetic explanation behind the sex bias observed in some of these diseases. The research team's findings, reported on May 11 in Nature, suggest that greater abundance of an immune-related protein in men protects against Lupus and Sjögren's but heightens vulnerability to Schizophrenia.

The protein, called, complement component 4:C4 and produced by the C4 gene, tags cellular debris for prompt removal by immune cells.

The key findings:

::: People with the most C4 genes were seven times less likely to develop systemic Lupus Erythematosus, an autoimmune condition, that can range from mild to life-threatening and 16 times less likely to develop primary Sjögren's Syndrome, a systemic autoimmune syndrome, characterized by dry eyes and dry mouth, than those with the fewest C4 genes. Conversely, those with the most C4 genes were 01.6 times more likely to develop the neuropsychiatric condition Schizophrenia.

::: Even, in people with similar complement gene profiles, the genes produce more protein in men than in women, further skewing disease susceptibility and protection.

"Sex acts as a lens, that magnifies the effects of genetic variation." said the Study's First Author, Mr Nolan Kamitaki, Research Associate in Genetics in the Steven McCarroll Lab at HMS and the Broad.

"We all know about illnesses, that either women or men get a lot more but, we've had no idea why." said Professor Steven McCarroll, the Dorothy and Milton Flier Professor of Biomedical Science and Genetics at HMS and the Director of Genomic Neuro-biology at the Stanley Centre for Psychiatric Research at the Broad. "This work is exciting because it gives us one of our first handles on the biology."

Professor McCarroll is Co-senior Author of the Study with Mr Timothy Vyse of King's College London. Although, C4 variation appears to contribute powerfully to disease risk, it is only one among many genetic and environmental factors, that influence disease development.

According to the authors the Study's results are informing the on-going development of drugs, that modulate the complement system. "For example, researchers will need to make sure that drugs, that tone down the complement system do not unintentionally increase risk for autoimmune disease." said Professor McCarroll. "Scientists will, also, need to consider the possibility that such drugs, may be, differentially helpful in male and female patients."

On a broader level, the work offers a more solid foundation for understanding sex variation in disease than has been available before. "It's helpful to be able to think about sex-biased disease biology in terms of specific molecules, beyond vague references to 'hormones.'" Professor McCarroll said. "We now realise that the complement system shapes vulnerability for a wide variety of illnesses."

In 2016, researchers led by Mr Aswin Sekar, a former McCarroll lab member, who is a Co-author of the new Study, made international headlines when they showed that specific C4 gene variants underlay the largest common genetic risk factor for developing Schizophrenia.

The new work suggests that C4 genes confer both an advantage and disadvantage to carriers, much as the gene variant, that causes Sickle Cell Disease, also, protects people against Malaria. "C4 gene variants come with this yin and yang of heightened and reduced vulnerability in different organ systems." said Professor McCarroll.

The findings, when combined with insights from earlier work, offer insights into what may be happening at the molecular level. When cells are injured, whether from a sunburn or infection, they leak their contents into the surrounding tissue. Cells from the adaptive immune system, which specialise in recognising unfamiliar molecules around distressed cells, spot debris from the cell nuclei. If, these immune cells mistake the flotsam for an invading pathogen, they may instigate an attack against material, that isn’t foreign at all, the essence of autoimmunity.

Researchers believe that complement proteins help tag these leaked molecules as trash so they're quickly removed by other cells, before the adaptive immune system pays too much attention to them. In people with lower levels of complement proteins, however, the uncollected debris lingers longer and adaptive immune cells may become confused into acting, as, if, the debris is itself the cause of problem.

As part of the new Study, Mr Kamitaki and his colleagues measured complement protein levels in the cerebrospinal fluid of 589 people and blood plasma of 1,844 people. They found that samples from women, aged, 20 through 50, had significantly fewer complement proteins, including, not only C4 but, also, C3, which activates C4, than samples from men of the same age.

‘’That's the same age range in which Lupus, Sjögren's and Schizophrenia vulnerabilities differ by sex.’’ Mr Kamitaki said. The results align with previous observations by other groups that severe early-onset Lupus is sometimes associated with a complete lack of complement proteins, that lupus flare-ups can be linked to drops in complement protein levels and that a common gene variant associated with Lupus affects the C3 receptor.

"There were all these medical hints." said Professor McCarroll. "Human genetics helps put those hints together." The bulk of the findings arose from analyses of whole genomes from 1,265 people along with single nucleotide polymorphism:SNP data from 6,700 people with lupus and 11,500 controls.

C4 genes and proteins come in two types, C4A and C4B. The researchers found that having more copies of the C4A gene and higher levels of C4A proteins was associated with greater protection against Lupus and Sjögren's, while C4B genes had a significant but more modest effect. On the other hand, C4A was linked with increased risk of Schizophrenia, while C4B had no effect on that illness.

In men, common combinations of C4A and C4B produced a 14-fold range of risk for Lupus and 31-fold range of risk for Sjögren’s, compared to only 6-fold and 15-fold ranges in women, respectively. The researchers didn't expect the genes' effects to be so strong.

"Large genetic effects tend to come from rare variants, while common gene variants generally have small effects." said Professor McCarroll. "The C4 gene variants are common, yet, they are very impactful in Lupus and Sjögren’s." Still, complement genes don't tell the full story of Lupus, Sjögren's or Schizophrenia risk, none of which are caused entirely by genetics.

"The complement system contributes to the sex bias but, it's only one of probably many genetic and environmental contributors." said Mr Kamitaki. Complement genes and another family of immune-related genes, called, human leukocyte antigen or HLA genes, are interspersed throughout the same complex stretch of the human genome. HLA variants have been shown to raise risk of developing other autoimmune diseases, including, Type One Diabetes, Celiac Disease and Rheumatoid Arthritis and researchers had long believed that something similar was happening with Lupus and Sjögren's.

The culprit, however, remained stubbornly hard to pin down, because specific variants in HLA genes and C4 genes always seemed to appear together in the same people. Mr Kamitaki and his colleagues overcame this hurdle by analysing DNA from a cohort of several thousand African American research participants. The participants' DNA contained many more re-combinations between complement and HLA genes, allowing the researchers to, finally, tease apart the genes' contributions.

"It became quite clear which gene was responsible." said Professor McCarroll. ‘’That that was a real gift to science from African American research participants. The authors assert that the discovery provides further proof that the field of genetics would benefit from diversifying the populations it studies.’’ the authors said. "It will really help for genetics to expand more strongly beyond European ancestries and learn from genetic variation and ancestries all over the world." said Professor McCarroll.

"Our paper shows the real value in being inclusive in large-scale genetic studies." agreed Mr Vyse. "The paper solves a 40-year controversy in systemic Lupus Erythematosus genetics and shows clearly that too little C4 and too much HLA promote systemic autoimmunity."

According to the authors, C4 variation could contribute to sex-based vulnerabilities in other diseases not yet analysed. It's not yet clear whether C4 pertains to the sex bias seen in COVID-19. "We don't know the mechanism yet for why men seem to get sicker from COVID-19." said Professor McCarroll. "Complement molecules are potentially important in any immune or inflammatory condition and in COVID-19, it seems the immune response can be part of a downward spiral in some patients. But we don’t know the key details yet."

It, also, remains to be seen, how the differing effects of complement genes apply to people with intersex traits, also, known as disorders or differences of sex development, who don't always fit textbook genetic or biological definitions of male and female.

The Study included the participation of the Schizophrenia Working Group of the Psychiatric Genomics Consortium.

 

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