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Noninvasive Molecular Imaging of the Enhanced Permeability and Retenti | IJN – Dove Medical Press

Posted: November 2, 2020 at 11:52 pm

Betina Brresen,1 Anders Elias Hansen,2,3 Frederikke Petrine Fliedner,2 Jonas Rosager Henriksen,3 Dennis Ringkjbing Elema,3,4 Malene Brandt-Larsen,5 Lotte Kellemann Kristensen,2 6 Annemarie Thuri Kristensen,1 6 Thomas Lars Andresen,3 Andreas Kjr2,5

1Department of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C 1870, Denmark; 2Cluster for Molecular Imaging, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen N 2200, Denmark; 3DTU Health Technology, Center for Nanomedicine and Theranostics, Technical University of Denmark, Lyngby, Kgs 2800, Denmark; 4DTU Health Technology, The Hevesy Laboratory, Center for Nuclear Technologies, Technical University of Denmark, Roskilde, 4000, Denmark; 5Department of Clinical Physiology, Nuclear Medicine and PET, Copenhagen University Hospital, Copenhagen 2100, Denmark; 6Minerva Imaging, Copenhagen N 2200, Denmark

Correspondence: Andreas KjrCluster for Molecular Imaging, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3, Copenhagen N 2200, DenmarkTel +45 35 32 75 04Fax +45 35 32 75 46Email akjaer@sund.ku.dk

Background: The accumulation of liposome encapsulated chemotherapy in solid cancers is dependent on the presence of the enhanced permeability and retention (EPR) effect. Positron emission tomography (PET) imaging with a liposome encapsulated radioisotope, such as liposome encapsulated Cu-64 (64Cu-liposome) may help to identify tumors with high liposome accumulation, and thereby stratify patients based on expected benefit from liposomal chemotherapy. However, intravenous administration of liposomes without a cytotoxic content is complicated by the accelerated blood clearance (ABC) phenomenon for succeeding therapeutic liposome dosing. Alternative markers for assessing the tumors EPR level are therefore warranted.Materials and Methods: To increase our understanding of EPR variations and to ultimately identify an alternative marker for the EPR effect, we investigated the correlation between 64Cu-liposome PET/CT (EPR effect) and 68Ga-RGD PET/CT (neoangiogenesis), 18F-FDG PET/CT (glycolysis), diffusion-weighted MRI (diffusivity) and interstitial fluid pressure in two experimental cancer models (CT26 and COLO 205).Results: 64Cu-liposome and 68Ga-RGD SUVmax displayed a significant moderate correlation, however, none of the other parameters evaluated displayed significant correlations. These results indicate that differences in neoangiogenesis may explain some EPR variability, however, as correlations were only moderate and not observed for SUVmean, 68Ga-RGD is probably insufficient to serve as a stand-alone surrogate marker for quantifying the EPR effect and stratifying patients.

Keywords: EPR effect, liposome, positron emission tomography, neoangiogenesis

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Health Ministry warns simple sneeze can spread billions of virus particles – Colombo Gazette

Posted: November 2, 2020 at 11:52 pm

By Easwaran Rutnam

The Ministry of Health Ministry has warned that the latest variant of the coronavirus is more dangerous than the earlier one.

Health Ministry Secretary Major General Sanjeewa Munasinghe said that the latest variant of the virus has been identified as B142, a subgroup of SARS-CoV-2, the virus that causes COVID-19.

He said that this was confirmed by scientists at the Department of Immunology and Molecular Medicine and Allergy, Immunology and Cell Biology Unit of the University of Sri Jayewardenepura.

In a special statement last evening (Sunday), Major General Sanjeewa Munasinghe said that the latest virus is spreading faster from one person to another.

He noted that the virus load in a person is higher than what it was earlier.

We have identified this virus as being very dangerous, he said.

He also warned that children and senior citizens are at a higher risk of contracting the new virus.

The Health Ministry Secretary said that people suffering from various illnesses, including cancer patients are less immune to the virus.

Major General Sanjeewa Munasinghe said that a simple sneeze can spread billions of virus particles as opposed to 100,000 particles seen earlier.

This shows if there is a patient among the public how far the virus can spread, he said.

As a result, he said it was important for the public to limit their movements, especially out of their home towns as there is a threat of the virus spreading around the country.

Major General Sanjeewa Munasinghe said that the public must stay home and go out only if there is an urgent requirement. (Colombo Gazette)

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Trillium Therapeutics Announces Formation of Scientific Advisory Board – GlobeNewswire

Posted: November 2, 2020 at 11:52 pm

CAMBRIDGE, Mass., Nov. 02, 2020 (GLOBE NEWSWIRE) -- Trillium Therapeutics Inc. (Trillium or the Company) (NASDAQ/TSX: TRIL), a clinical stage immuno-oncology company developing innovative therapies for the treatment of cancer, today announced the formation of a Scientific Advisory Board (SAB), including Karen Ferrante, MD, Gordon Freeman, PhD, Tom Reynolds, MD, PhD, Steven Rosen, MD, and Jeff Settleman, PhD.

It is a true privilege to announce this SAB, comprised of leading experts who have had major formative impact on the field of oncology/immuno-oncology over the past 25 years, said Jan Skvarka, Trillium President and Chief Executive Officer. Their combined resume includes several of the most groundbreaking oncology drugs or underlying scientific discoveries, including the PD-1/PD-L1 class, Adcetris, interferon, Iressa, Lemtrada, Velcade, Tarceva, Taxol, and Xalkori, among others. We are looking forward to their guidance as we continue expanding our research and development activities.

Members of the Trilliums SAB include:

Karen J. Ferrante, MD Dr. Ferrante is a hematologist-oncologist with 25 years of experience in oncology drug development. She was the Head of R&D and CMO at Tokai Pharmaceuticals, and Head of the Oncology Therapeutic Area at Takeda and CMO at Millennium Pharmaceuticals, after holding a variety of roles in oncology clinical development at Pfizer and BMS. During her career she was involved in the clinical development of a number of important cancer therapeutics including Taxol, Tarceva and Velcade.

Gordon Freeman, PhD Dr. Freeman is an immunology researcher in the Department of Medical Oncology at Dana-Farber Cancer Institute and a Professor of Medicine at Harvard Medical School. Dr. Freeman is best known for the discovery of the PD-1/PD-L1 pathway, which provided the foundation for developing immune checkpoint blockade immunotherapies. Dr. Freeman is the 2014 recipient of the William B. Coley Award for Distinguished Research in Tumor Immunology, the 2017 recipient of the Warren Alpert Foundation award, and a 2020 co-recipient of the Richard V. Smalley, MD award, the highest award of the Society for Immunotherapy of Cancer.

Tom Reynolds, MD, PhD Dr. Reynolds served as Chief Medical Officer of Seattle Genetics, where he was responsible for building and leading an integrated clinical development, regulatory and medical affairs organization, highlighted by the development and approval of Adcetris. Previously, Dr. Reynolds served at ZymoGenetics (acquired by Bristol-Myers Squibb in 2010), most recently as VP Medical Affairs, where he oversaw the clinical development and regulatory filing of recothrom, and VP Clinical Affairs at Targeted Genetics.

Steven T. Rosen, MD Dr. Rosen is the Provost and Chief Scientific Officer of the City of Hope National Medical Center in Duarte, California. In addition to directing City of Hopes Comprehensive Cancer Center, Dr. Rosen leads the Beckman Research Institute at City of Hope. Previously, Dr. Rosen was the director of the Robert H. Lurie Comprehensive Cancer Center at Northwestern University. In 2015, Dr. Rosen received a lifetime achievement award from the Israel Cancer Research Fund for his work in cancer research. His main areas of research involve the development of new treatments, particularly for hematologic malignancies.

Jeff Settleman, PhD Dr. Settleman is the Chief Scientific Officer for Oncology R&D at Pfizer, where he leads all oncology research from discovery to proof of concept clinical studies. Prior to Pfizer, Dr. Settleman was the Head of Oncology Research at Calico Life Sciences, and the Head of Discovery Oncology at Genentech, following an 18 year career in academia as a Professor at the Harvard School of Medicine, a Director of the Center for Molecular Therapeutics and Scientific Director of the Massachusetts General Hospital Cancer Center, as well as the Head of the Cancer Cell Biology program of the Dana-Farber/Harvard Cancer Center.

About Trillium Therapeutics

Trillium is an immuno-oncology company developing innovative therapies for the treatment of cancer. The companys two clinical programs, TTI-621 and TTI-622,target CD47, a dont eat me signal that cancer cells frequently use to evade the immune system.

For more information visit: http://www.trilliumtherapeutics.com

Caution Regarding Forward-Looking Information

This press release contains forward-looking statements within the meaning of applicable United States securities laws and forward-looking information within the meaning of Canadian securities laws (collectively, "forward-looking statements"). Forward-looking statements in this press release include statements about, without limitation, the membership and our plans for our scientific advisory board. With respect to the forward-looking statements contained in this press release, Trillium has made numerous assumptions regarding, among other things: the impact of the COVID-19 pandemic on its operations, the effectiveness and timeliness of preclinical and clinical trials; and the completeness, accuracy and usefulness of the data. While Trillium considers these assumptions to be reasonable, these assumptions are inherently subject to significant scientific, business, economic, competitive, market and social uncertainties and contingencies. Additionally, there are known and unknown risk factors that could cause Trillium's actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements contained in this press release. A discussion of risks and uncertainties facing Trillium appears in Trillium's Annual Information Form for the year ended December 31, 2019 filed with Canadian securities authorities and on Form 40-F with the U.S. Securities Exchange Commission, each as updated by Trillium's continuous disclosure filings, which are available at http://www.sedar.comand at http://www.sec.gov. All forward-looking statements herein are qualified in their entirety by this cautionary statement, and Trillium disclaims any obligation to revise or update any such forward-looking statements or to publicly announce the result of any revisions to any of the forward-looking statements contained herein to reflect future results, events or developments, except as required by law.

Investor Relations:James ParsonsChief Financial OfficerTrillium Therapeutics Inc. 416-595-0627 x232james@trilliumtherapeutics.com http://www.trilliumtherapeutics.com

Media Relations:Mike BeyerSam Brown Inc.312-961-2502mikebeyer@sambrown.com

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Re-emergence of Covid-19 | Probe continues to identify strain – nation.lk – The Nation Newspaper

Posted: November 2, 2020 at 11:52 pm

Current strain a mutation of Covid-19 virusYet to pinpoint virus country of origin

Health authorities are proceeding with investigations to identify the exact strain of the Covid-19 virus that hit the country last month, after identifying that the current virus spreading in the country was a different strain from the one witnessed earlier this year.

When contacted by The Morning, Ministry of Health Chief Epidemiologist Dr. Sudath Samaraweera said the virus was mutating and the current strain was also a mutation of the Covid-19 virus.

When asked from which country the virus had come to Sri Lanka, he said that answer could only be given by a microbiologist or virologist. Meanwhile, the Health Ministry has warned that the latest variant of the coronavirus is more dangerous than the earlier one.

Health Ministry Secretary Maj. Gen. Dr. Sanjeewa Munasinghe said that the latest variant of the virus has been identified as B142, a subgroup of SARS (severe acute respiratory syndrome).

He said that this was confirmed by scientists at the Department of Immunology and Molecular Medicine and the Allergy, Immunology, and Cell Biology Unit of the University of Sri Jayewardenepura.

Dr. Munasinghe noted that the viral load in a person is higher than what it was earlier.

When contacted, Government Medical Officers Association (GMOA) Secretary Dr. Senal Fernando told The Morning that they suspected the virus could be a different strain as the asymptomatic patients have also been identified as spreading the virus, contrary to the previous strain in the country.

The universitys efforts should be appreciated even though the exact strain has not been identified. With the limited resources they have, it has been identified that the virus strain is similar to that of the one in Europe, he added.

At present, 6,134 active cases continue to receive treatment at selected hospitals across the country.

Meanwhile, the total of Sri Lankas Covid-19 recoveries reached 4,905 yesterday (2) after 506 patients were discharged from hospitals as they had returned to health.

The country has also witnessed 22 Covid-19-positive deaths.

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Race, genetics, and their impact on health – Mumbai Mirror

Posted: November 2, 2020 at 11:50 pm

Amongst the various forms of discriminations the world has seen, Apartheid, a system of institutionalised racial segregation practised in South Africa, was one of the worst. I went to medical school with several South African students and the stories of discrimination they told me about were horrifying. Thankfully Apartheid, which was based on white supremacy and lasted more than 40 years, ended in the early 1990s.

I am often asked by my Caucasian friends if I felt discriminated against in the UK because of my brownness. I reply that it may have been true in early 1970s. I remember waiting in line to be served a pint of beer, only to be ignored by the proprietor of the pub. When I had the good fortune of going with a white girl, there was never a problem getting served.

Of course things have changed in the UK, which is today a proudly multicultural country. Overt discrimination of the kind that existed earlier is no longer tolerated. Asian communities especially are a thriving group, eagerly courted by political parties. Today when I go to a pub in London, I find the barmaid waiving me in.

This brings us to the topic of todays column: the role of race in health outcomes. Differences in health status, life expectancy and other indicators in different racial and ethnic groups are well documented. But before we get to that, let me get a somewhat controversial subject out of the way: the dominance of black athletes.

Black athletes enjoy a huge over-representation at the highest level of many sports - from the 100 metres sprint through to the marathon, every single record is currently held by athletes of African origin.

Sir Roger Bannister, who ran the first sub-4-minute mile, said in a speech to the British Association of Advancement of Science in 1995 that heel-bone length, subcutaneous fat and differences in the length of the Achilles tendon may explain the advantage that Africans may have in running sports. A study published in the Journal of Applied Physiology reported that Africans display an enhanced resistance to fatigue while running on a treadmill. There are tens of such studies - many of them controversial - which are beyond the scope of one column.

Coming back to race and health outcomes: Diabetes, for example, is 60 per cent more common among African Americans than white Americans. Black Americans are 2.5 times more likely to suffer limb amputations and 5.5 times likely to suffer from kidney disease because of diabetes.

Blacks in America are more likely to die of asthma than whites and, despite lower tobacco exposure, Blacks are 50 per cent more likely to get lung cancer.

Black Americans suffer twice the risk of stroke than Whites; strokes kill four times more 35- to 54-year-old Blacks than white. Black men have a 40 per cent high cancer death rate, and women 20 per cent higher death rate, than their white counterparts.

The stats for the other major minority group in America - the hispanics - are similarly depressing.

Around 15 years ago, the US FDA controversially approved a drug called BiDil for a single racial-ethnic group - African Americans - for treatment of congestive heart failure. The scientific research leading to BiDils approval tested the drug only in African American populations.

Craig Venter, the famous American biotechnologist who produced the map of the human genome, said it was disturbing to see things categorised in terms of race.

Is race really a surrogate marker for describing human genetic variation? In India genetics and race are certainly considered interchangeable. People still prefer getting married to someone of their own community. One of the major consequence of endogamy - the practice of marrying within the same community - is genetic diseases arising out of a limited gene pool. We would certainly be better off if we looked to widen our gene pool.

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Race, genetics, and their impact on health - Mumbai Mirror

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Your Dog Could Have the Same Genetic Makeup as Canines Living During the Ice Age – Yahoo Lifestyle

Posted: November 2, 2020 at 11:50 pm

Your Dog Could Have the Same Genetic Makeup as Canines Living During the Ice Age

There are at least five types of dogs that have DNA tying to breeds from 11,000 years ago, according to a new study.

Is your dog your very best companion? We understand. There's a good reason that canines are said to be a man'sor woman'sbest friend. But just how long exactly have dogs been around? A group of researchersconsisting of scientists from the Francis Crick Institute, the University of Oxford, the University of Vienna, and archaeologists from over 10 countriespublished a study in the journal Science that just gave their answer. According to the article, titled "Origins and Genetic Legacy of Prehistoric Dogs," the team dug deep to discover that the genetic makeup of the modern dog traces back to the end of the Ice Agewhich means your dogs are actually connected to some of the most ancient pet species, CNN reports.

Hillary Kladke / Getty Images

To come to their findings, the scientists studied the DNA from ancient dog bones. From there, they found that there were five types of dogs with specific genetics that came out of the Ice Age. These dogs have "mixed and combined" lineages that are still found in the everyday dog today. The researchers uncovered that Rhodesian ridgebacks have ties to DNA from an ancient Middle Eastern or African lineage, Siberian huskies have genetic makeup from an ancient Siberian lineage, and dogs like chihuahuas and Mexican hairless dogs have some pre-Columbian DNA.

Related: The Most Low-Energy, Non-Shedding Dog Breeds

Anders Bergstrom, the lead author and post-doctoral researcher in the Ancient Genomics Laboratory at London's Francis Crick Institute, also shared that canines have been housebroken and found worldwide for some time now. "Already by 11,000 years agobefore agriculture, and before any other animal had been domesticateddogs had not only been domesticated, but they had already diversified genetically and likely spread across large parts of the world."

Bergstrom added, though, that the mixing of DNA is common in dogs. "All dog breeds from Europe share a common history that started with an ancient mixture, many thousands of years ago, between two very distinct dog lineagesone related to dogs in the Near East, and the other related to dogs in Siberia. This ancient mixing event between these two lineages gave rise to the European dog gene pool which later would give rise to all present-day European dog breeds," he said. "We find that when we compare the history of dogs to the history of humans, to a quite large degree they mirror each other, suggesting that in many cases, the history of dogs has been shaped by humans. In many cases humans would simply bring their dogs with them as they migrated and moved across the world."

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How Long Does It Take to Grow a Beard? Tips, Genetics, and More – Healthline

Posted: November 2, 2020 at 11:50 pm

Facial hair, like scalp hair, grows in stages and understanding it may help you maximize your beard-growing potential.

A full beard can take 2 to 4 months to grow, as facial hair tends to grow between 0.3 and 0.5 millimeters (mm) every 24 hours. This works out to between one third and one half an inch per month.

Many factors can affect the growth of your beard, but there are some lifestyle strategies you can try to enhance your beard growth. Read on to learn more about what influences beard growth and if it can be influenced.

Once you stop shaving, you can expect facial hair to grow in stages. Hair may grow fuller and faster in certain areas, especially at first. Be patient, though, as this is a normal growth pattern for most guys.

Your ethnicity, age, genetics, and hormones not to mention various medical conditions can all affect whether your beard comes in faster or slower, or in all the places you desire.

If your beard seems to be taking a long time to grow in, one of the following factors may be at play.

You may remember guys in high school who seemed to have a full beard before they got their drivers license. Theyre the exception, not the rule.

Typically, full beard growth is possible starting at around age 18, but for many men, that time may not arrive until theyre 30. So, if youre not getting the beard growth you want, it may be because its not your time.

Certain ethnic groups tend to be more hirsute than others. Chinese men, for example, generally have less facial hair than white men, and men of Mediterranean descent generally have thicker beards.

Beyond your ethnic origins, your direct family traits have much to do with whether you can grow a full beard. Likewise, your genetics also determine the texture of your hair, your likelihood of going bald, and so forth.

For clues about your beards future, look to your male relatives. While theres no guarantee that a dad with a full beard will have a son who can pull off the same thing, hair patterns do tend to be hereditary.

Low levels of testosterone can make it more difficult to grow a beard. Talk with your doctor about taking supplements or trying testosterone therapy to help combat low testosterone.

If you want to grow your beard faster, there are a few strategies worth trying. Understand, however, that these tips may not work for everyone.

For general health, its recommended you have a balanced diet that includes fruits, vegetables, whole grains, and lean proteins, while avoiding processed food and added sugars.

For healthy hair growth, some key nutrients should have a place in your diet, including:

Too much stress and too little sleep can cause countless health problems, not to mention affect your beard growth.

Aim for 7 to 8 hours of sleep each night, and try strategies such as meditation or deep-breathing techniques to help de-stress.

Its not uncommon for guys to have thicker hair around their mouths and parts of their sideburns but a little less on their cheeks.

One way to help mask thinner (or zero) growth in those spots is to let the hair around them grow longer. You can hide those sparse spots a little with longer beard hair nearby.

Hair growth, whether its on your scalp or your face, is subject to many changes in your health.

Underlying medical conditions such as alopecia barbae or alopecia areata can cause hair loss from your beard or make it harder to grow a beard that isnt patchy or thin in places.

Alopecia areata is the more common condition. It occurs when the bodys immune system mistakenly attacks healthy hair follicles. When beard alopecia areata develops, men are usually middle-aged and hair loss is typically along the jawline.

Unusual conditions, such as prolactinoma a noncancerous tumor of the pituitary gland can also result in thin or missing facial hair.

Conversely, a noncancerous birthmark called Beckers nevus can sometimes cause excessive, coarse hair to form at the site of the birthmark.

The time it takes to grow a beard not to mention the look of the final product varies from person to person.

If youre trying to grow a full beard, plan on waiting a couple of months before you reach your goal. That means being patient and watching for signs of medical conditions that may affect your beard growth.

If youre concerned about a lack of beard growth, talk with your doctor or a dermatologist.

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Yale New Haven Health Docs: Interpreting the Uptick in Covid-19 Cases – Greenwich Free Press

Posted: October 31, 2020 at 11:56 pm

At a press conference this week, doctors from Yale New Haven Health System gave a snapshot of the Covid-19 uptick in Connecticut.

On Tuesday the System had 90 inpatients, more than 3-1/2 times the number at the end of September.

In the past two weeks the System had seen a 50% increase from 64 on Oct 13th to 92 cases on Monday.

A month ago there were only two Covid patients in the Systems ICUs. On Tuesday there were 22 with eight on ventilators. That was after many days with no ventilated Covid-positive patients.

While the numbers represent an uptick, they are still well below the peak of 800 cases last spring.

But it doesnt feel very good, said CEO Marna Borgstron. People are tired. Tired of the pandemic. Tired of social distancing. Tired of wearing masks.

As of Tuesday, the 90 Covid-19 cases across the System were as follows:

51 at Yale New Haven Hospital 16 at Bridgeport Hospital 11 at Lawrence and Memorial Hospital in New London 5 at Greenwich Hospital 6 at Westerly Hospital.

Dr. Tom Balcezak, Chief Medical Officer for the System, and Yale New Haven Hospital Infectious Disease Specialist Dr. Onyema Ogbuagu, who is working on the Pfizer trial for a vaccination and is deeply involved in care for Covid-19 patients, talked about the recent uptick.

We didnt know that (mask wearing) worked in the first part of this pandemic, Balcezak said. There is now scientific certainty that mask wearing and social distancing does work.

How Bad Will It Get?

Balcezak said it was impossible to forecast numbers or predict when a peak might come.

He said a wastewater sampling model showed the Greenwich area was seeing some slow growth, and the hot spot area to watch was eastern Connecticut.

As for Thanksgiving and Halloween, Balcezak said, We all have families and desire to reconnect with out families and friends, but this is not the time to be doing that.

Implications for Flu Season

Balcezak said with the arrival of fall, there was the potential for a flu pandemic in addition to Covid-19. He urged residents to get flu shots to avoid a twindemic of flu and Covid-19.

Dr. Ogbuagu said there was concern about how the flu would mimic Covid-19.

Balcezak agreed, adding the challenge wold be to sort out flu patients from Covid patients, who need different therapies and cohorting.

Balcezak said the southern hemisphere foreshadows what might be in store for Connecticut.

It appears the southern hemisphere had a very light flu season this year, he said. But we need to do everything we can to lock that in. That means getting your flu shot this year. We dont need our emergency departments and doctors offices clogged with folks that have respiratory illness.

Vaccine Trial at Yale New Haven Hospital with Pfizer

Dr. Ogbuagu said there are 300 people in the trial in New Haven. The target number is 44,000, which they are approaching, as the trial is multinational.

Enrollment is going well. Up to 70% of participants have already received the second of two vaccines. (The second vaccine comes three weeks after the first.)

I think the earliest a vaccine would receive approval would be end of December or January 2021, at best, Dr. Ogbuagu said.

Its been incredible to watch the speed with which our science has moved with this pandemic, Balcezak said. Were already talking about novel therapeutics and hopefully will have a vaccine approved in the next couple of months.

Balcezak added that when the first vaccine becomes available, it might not be the best vaccine, and wont prevent the virus.

He explained when the Covid-19 virus enters the body through the respiratory system, the immunity will stop it replicating, but the vaccine will not prevent infection. It will prevent symptoms but vaccinated people could still be contagious.

We may have to wait for a vaccine that prevents infection, he said. Even if you have got the vaccine, you will still be infectious. Therefore, mask wearing will still be the standard.

Dr. Ogbuagu said the Pfizer trial has already gone through phases 1 and 2, and the phase 3 trials are advanced. The trials are randomized. Half the people receive the vaccine and the others receive a placebo.

Dr. Ogbuagu said the study has a diverse enrollment, and not only enrolls adults and elderly individuals, but also enrolls pediatric age participants from age 12 +, and immune-compromised patients including HIV patients. Over half the people enrolled in the trial identify as racial minorities.

Asked about the use of embryonic stem cells in some vaccine trials, Dr. Ogbuagu said that scenario was not unique to Covid vaccines.

There were vaccines long before Covid, like Rubella, which is German measles, and shingles vaccines, which have utilized human embryonic cells to advance development, he said.

Dr. Balcezak said it was important to note that these are tissues have been grown over many years.

They are involved in early development, he said. But for large scale mass production of these vaccines, theyre going to use traditional manufacturing methodologies that dont involve stem cells.

Why are Covid-19 Illnesses Less Severe than in the Spring?

Dr. Balcezak said much had been learned about treating Covid-19 patients.

Were more liberal with the use of steroids than we were early on, he said. And we have figured out what medications do not work.

Theres been a lot of negative studies whether it be Hydroxychloroquine, or Azithromycin weve stopped the utilization of those drugs, Balcezak said.

We continue to use Rendesivir, which seems to have a small benefit, at least in terms of length of hospitalization.

He said theyd also learned more about non therapeutic therapies.

Its putting patients on their bellies, or proning them. Its how you manage the ventilator and how you use oxygen and high flow oxygen, he said. Weve seen mortality rates fall substantially.

Balcezak cautioned, Doing better was far from perfect, and while the System is seeing a small number of deaths compared to the spring, theyd like to see the number fall to zero.

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Molecular Architecture of Early Dissemination and Massive Second Wave of the SARS-CoV-2 Virus in a Major Metropolitan Area – DocWire News

Posted: October 31, 2020 at 11:55 pm

This article was originally published here

mBio. 2020 Oct 30;11(6):e02707-20. doi: 10.1128/mBio.02707-20.

ABSTRACT

We sequenced the genomes of 5,085 severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains causing two coronavirus disease 2019 (COVID-19) disease waves in metropolitan Houston, TX, an ethnically diverse region with 7 million residents. The genomes were from viruses recovered in the earliest recognized phase of the pandemic in Houston and from viruses recovered in an ongoing massive second wave of infections. The virus was originally introduced into Houston many times independently. Virtually all strains in the second wave have a Gly614 amino acid replacement in the spike protein, a polymorphism that has been linked to increased transmission and infectivity. Patients infected with the Gly614 variant strains had significantly higher virus loads in the nasopharynx on initial diagnosis. We found little evidence of a significant relationship between virus genotype and altered virulence, stressing the linkage between disease severity, underlying medical conditions, and host genetics. Some regions of the spike protein-the primary target of global vaccine efforts-are replete with amino acid replacements, perhaps indicating the action of selection. We exploited the genomic data to generate defined single amino acid replacements in the receptor binding domain of spike protein that, importantly, produced decreased recognition by the neutralizing monoclonal antibody CR3022. Our report represents the first analysis of the molecular architecture of SARS-CoV-2 in two infection waves in a major metropolitan region. The findings will help us to understand the origin, composition, and trajectory of future infection waves and the potential effect of the host immune response and therapeutic maneuvers on SARS-CoV-2 evolution.IMPORTANCE There is concern about second and subsequent waves of COVID-19 caused by the SARS-CoV-2 coronavirus occurring in communities globally that had an initial disease wave. Metropolitan Houston, TX, with a population of 7 million, is experiencing a massive second disease wave that began in late May 2020. To understand SARS-CoV-2 molecular population genomic architecture and evolution and the relationship between virus genotypes and patient features, we sequenced the genomes of 5,085 SARS-CoV-2 strains from these two waves. Our report provides the first molecular characterization of SARS-CoV-2 strains causing two distinct COVID-19 disease waves.

PMID:33127862 | DOI:10.1128/mBio.02707-20

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Autism, intellectual disability linked to levels of fragile X protein – Spectrum

Posted: October 31, 2020 at 11:55 pm

Mixed results: Cheek swabs and blood samples from people with fragile X show that key protein levels can vary from cell to cell and influence trait severity.

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People with particularly low levels of FMRP, the protein lacking in those with fragile X syndrome, are more likely to also have autism and severe intellectual disability, according to a new study1. The lower the level of FMRP, the more severe a persons traits.

The findings could help researchers identify who would benefit most from certain treatments, says co-investigator Dejan Budimirovic, assistant professor of psychiatry and behavioral sciences at Johns Hopkins University in Baltimore, Maryland. They could also be used to design better outcome measures for pharmaceutical trials for the condition.

This really helped us to work on closing a gap in the field between a persons traits and those traits molecular origins, Budimirovic says. You really need to pair that with the clinical outcomes that can be translated to the bedside that the clinicians and patients and families can see, What does it mean to me?

Fragile X syndrome occurs when a section of the FMR1 gene, which codes for FMRP, contains more DNA letter repeats than usual. The repeats silence the gene by driving DNA methylation: Molecules called methyl groups attach to a region of the gene where it can be switched on, blocking production of FMRP, a protein necessary for communication among neurons. Most people with the syndrome have intellectual disability (ID), and many also have autism.

The extent to which the methyl groups attach to the gene can vary among people with fragile X and from cell to cell, leading to different levels of FMRP in people with the same underlying genetics2. The new work confirms the relationship between the number of repeats and an individuals traits with greater precision than before: More repeats lead to more methylation, causing lower protein levels and more severe traits.

The findings confirm the chain of events that connect expanded repeats to the severity of traits seen in fragile X,and future treatments could potentially intervene anywhere along the chain, says David Amor, professor of clinical genetics at the Murdoch Childrens Research Institute in Victoria, Australia, who was not involved in the work. Amor worked on a separate October study that found that boys with fragile X with higher levels of methylation have lower cognitive abilities and more severe autism traits3.

The new work also demonstrates the complexity of fragile X syndrome, Amor says: Each affected individual probably has a unique molecular variant of the condition.

The researchers analyzed blood samples and cheek swabs from 42 people with FMR1 mutations, nine of them female. Two male and three female participants have 55 to 200 DNA letter repeats, something known as a premutation.

They were able to analyze FMRP levels in 31 individuals who have full mutations more than 200 repeats. The boys and men have lower FMRP levels than the girls and women. Because FMR1 is located on the X chromosome, girls and women who have two X chromosomes are less likely to be severely affected.

Among the 26 boys and men with full mutations, those who show mosaicism, or different levels of methylation or gene expression in different cells, have twice as much FMRP overall as those without mosaicism. (There were too few girls and women in the study for this analysis.) Individuals with full mutations have higher methylation levels and lower FMRP levels than do those with premutations.

The researchers evaluated the participants with full mutations for autism, anxiety, practical life skills, difficult behaviors and ID, as measured by intelligence quotient (IQ). Nearly all have some level of ID, and almost half also have autism.

Those with fragile X and autism have half as much FMRP as those without autism, the team found. Among boys and men with fragile X, those with severe ID have even lower levels of the protein than boys and men with mild or moderate disability, regardless of whether they are autistic.

The findings were published in Brain Science in September.

The FMRP results are remarkable, says Randi Hagerman, medical director of the University of California, Davis MIND Institute, who was not involved in the work. It shows the importance of really drilling down in the molecular variables.

Not all people in the study fit the trend: Three male participants with low FMRP levels and some mosaicism have only mild or moderate ID. Another has high FMRP and moderate disability, but no detectable mosaicism.

These exceptions suggest that interactions between genetics, epigenetics and proteins provide a more complete picture of the condition than any single measure, says co-investigator Gary Latham, senior vice president of research and development at the molecular diagnostic company Asuragen in Austin, Texas.

Its not any one shot, he says. Its a whole shooting match.

The findings could be important for identifying who can benefit from drugs that increase FMRP levels, Hagerman says. The epilepsy and bipolar disorder drug divalproex sodium (marketed as Depakote), for example, may be able to boost FMRP levels but hasnt yet been shown to be effective in people with fragile X, she says4.

Amors study, which analyzed methylation markers in dried blood spots collected at birth, demonstrates that methylation levels could potentially be used to screen for fragile X in newborns and predict the type or severity of traits an individual might show. But much more work would be needed for that to be realistic, Latham says.

Budimirovic and Latham say they hope to see their technique used in larger cohorts to better assess the nuances of the relationships between protein levels and individuals traits.

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Autism, intellectual disability linked to levels of fragile X protein - Spectrum

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