Insomnia, disrupted sleep, and daily burnout are linked to a heightened risk of not only becoming infected with coronavirus, but also having more severe disease and a longer recovery period, suggests an international study of healthcare workers, published in the online journal BMJ Nutrition Prevention & Health.
Every 1-hour increase in the amount of time spent asleep at night was associated with 12% lower odds of becoming infected with COVID-19, the findings indicate.
Disrupted/insufficient sleep and work burnout have been linked to a heightened risk of viral and bacterial infections, but it’s not clear if these are also risk factors for COVID-19, say the researchers.
To explore this further, they drew on the responses to an online survey for healthcare workers repeatedly exposed to patients with COVID-19 infection, such as those working in emergency or intensive care, and so at heightened risk of becoming infected themselves.
The survey ran from 17 July to 25 September 2020, and was open to healthcare workers in France, Germany, Italy, Spain, the UK, and the USA.
Respondents provided personal details on lifestyle, health, and use of prescription meds and dietary supplements plus information on the amount of sleep they got at night and in daytime naps over the preceding year; any sleep problems; burnout from work; and workplace exposure to COVID-19 infection.

Infliximab, a powerful biologic that is used to treat inflammatory bowel disease (IBD), blunts the body’s immune response to COVID-19 infection, indicates research published online in the journal Gut.
This impaired response may boost susceptibility to recurrent COVID-19 and help drive the evolution of new variants of SARS-CoV-2, the virus responsible for the infection, warn the researchers.
Careful monitoring of IBD patients treated with infliximab will be needed after vaccination against COVD-19 to ensure they mount a strong enough antibody response to ward off the infection, they advise.
Infliximab belongs to a class of medicines called anti-tumour necrosis factor (anti-TNF) drugs. These drugs suppress the production of an inflammatory protein involved in the development of several conditions, including ulcerative colitis and Crohn’s disease which are types of inflammatory bowel disease.
Around 2 million people worldwide are treated with anti-TNF drugs, which are known to impair protective immunity following vaccination against pneumonia, flu, and viral hepatitis, as well as increasing the risk of serious infection, particularly respiratory infections.
Because of these risks, patients taking these drugs have been advised to shield during the coronavirus pandemic and/or take extra precautions to minimise their risk of catching COVID-19.

Almost 90 percent of infectious travelers could be detected with rapid SARS-CoV-2 tests at the airport, and most imported infections could be prevented with a combination of pre-travel testing and a five-day post-travel quarantine that would only lift with a negative test result, according to a computer simulation by UC San Francisco researchers.
The study offers much-needed data to airlines and states that have struggled through a year of the pandemic with little guidance on how to enable safe travel.
The issue is becoming more pressing as states reopen and travelers return to the skies. Data from the Transportation Security Administration show that air travel has been on the rise since the 2020-2021 holiday season, although it is still only one-third to one-half of what it was before the pandemic.
“This evidence could be useful to standardize testing and quarantine policy for COVID-19 at the airline, city and state level for travelers,” said Nathan Lo, MD, PhD, a resident physician and incoming faculty fellow in infectious diseases at UCSF and senior author of the paper, which was published March 22, 2021, in The Lancet Infectious Diseases. “Nothing will be perfectly safe, and travel will always pose a risk to the individual and for importation to states, but this is a way to substantially minimize the risk.”
The data in the study come from a large-scale computer simulation of how different combinations of testing and quarantine can prevent infectious travelers from spreading COVID-19. The model makes forecasts based on what is already known about how many people are likely to be infected on any given day, how long they are likely to be infectious and how likely different types of tests are to detect infectious people.
The study simulated the probability that 100,000 travelers would be infectious on any given day shortly before, during and after their trips, given a range of different pre-travel testing and post-travel quarantine-plus-testing strategies.

Scientists from the Department of Physiology of the University of Granada (UGR) have shown that caffeine (about 3 mg/kg, the equivalent of a strong coffee) ingested half an hour before aerobic exercise significantly increases the rate of fat-burning. They also found that if the exercise is performed in the afternoon, the effects of the caffeine are more marked than in the morning.
In their study, published in the Journal of the International Society of Sports Nutrition, the researchers aimed to determine whether caffeine — one of the most commonly-consumed ergogenic substances in the world to improve sports performance — actually does increase oxidation or “burning” of fat during exercise. Despite the fact that its consumption in the form of supplements is very common, the scientific evidence for its beneficial claims is scarce.
“The recommendation to exercise on an empty stomach in the morning to increase fat oxidation is commonplace. However, this recommendation may be lacking a scientific basis, as it is unknown whether this increase is due to exercising in the morning or due to going without food for a longer period of time,” explains the lead author of this research, Francisco José Amaro-Gahete of the UGR’s Department of Physiology.
A total of 15 men (mean age, 32) participated in the research, completing an exercise test four times at seven-day intervals. Subjects ingested 3 mg/kg of caffeine or a placebo at 8am and 5pm (each subject completed the tests in all four conditions in a random order). The conditions prior to each exercise test (hours elapsed since last meal, physical exercise, or consumption of stimulant substances) were strictly standardized, and fat oxidation during exercise was calculated accordingly.
Maximum fat oxidation
“The results of our study showed that acute caffeine ingestion 30 minutes before performing an aerobic exercise test increased maximum fat oxidation during exercise regardless of the time of day,” explains Francisco J. Amaro. The existence of a diurnal variation in fat oxidation during exercise was confirmed, the values being higher in the afternoon than in the morning for equal hours of fasting.
These results also show that caffeine increases fat oxidation during morning exercise in a similar way to that observed without caffeine intake in the afternoon.
In summary, the findings of this study suggest that the combination of acute caffeine intake and aerobic exercise performed at moderate intensity in the afternoon provides the optimal scenario for people seeking to increase fat-burning during physical exercise.
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Materials provided by University of Granada. Note: Content may be edited for style and length.

Scientists at Sanford Burnham Prebys Medical Discovery Institute have identified a drug candidate that blocks the uptake of glutamine, a key food source for many tumors, and slows the growth of melanoma. The drug is a small molecule that targets a glutamine transporter, SLC1A5, which pumps the nutrient into cancer cells — offering a promising new approach for treating melanoma and other cancers. The study was published in the journal Molecular Cancer Therapeutics.
“While great strides have been made recently in the treatment of melanoma, many patients’ tumors become resistant to therapy, and this has become a major obstacle in the successful treatment of the disease,” says Ze’ev Ronai, Ph.D., director of the National Cancer Institute (NCI)-designated Cancer Center at Sanford Burnham Prebys and senior author of the study. “This study describes a promising compound that selectively targets the uptake of glutamine, an amino acid nutrient that tumors rely on for survival. We are hopeful this drug will fill an unmet medical need for people living with this deadly cancer.”
More than 7,000 people die from melanoma each year in the U.S., according to the American Cancer Society, and cases continue to increase annually. In the past decade, immunotherapy and personalized treatments have extended survival times for many patients. However, because of the high incidence of cancer recurrence, scientists are increasingly focused on therapeutic strategies to prevent relapse and increase overall survival.
“This is a very important study because many targeted drugs for melanoma treatment have been significantly hindered by the rapid development of treatment resistance, sometimes as quickly as within several months. While immunotherapy approaches are promising, they are only effective in a subset of patients, and treatment resistance can also develop in this setting as well,” says M. Celeste Simon, Ph.D., Arthur H. Rubenstein, MBBCh Professor in the department of Cell and Developmental Biology and scientific director of the Abramson Family Cancer Research Institute at the Perelman School of Medicine at the University of Pennsylvania. “The drug candidate identified in Dr. Ronai’s study offers an exciting new therapeutic approach for treating tumors addicted to glutamine, which includes a long list of human cancers, and will hopefully lengthen the amount of time that people with melanoma respond to available treatments.”
Blocking the tumor’s food supply
Researchers know that rapidly growing tumors are able to reprogram their metabolism to generate extra energy to survive and grow. Tumors often achieve this by pumping increasing levels of the amino acid glutamine into their cells, primarily through a pump called SLC1A5. As a result, cancer researchers are working to find drugs that block SLC1A5 and reduce glutamine levels.
In the study, Ronai and his team set out to identify drug(s) that can inhibit glutamine uptake. Working in collaboration with researchers at the Institute’s Conrad Prebys Center for Chemical Genomics, the scientists screened 7,000 diverse compounds for their ability to interfere with SLC1A5. This work identified about 20 hits, or promising options, and one was selected based on its superior ability to prevent SLC1A5 from reaching the cell membrane. This drug candidate, IMD-0354, inhibited tumor growth in both cell culture and in mice with melanoma.
“Our study shows that targeting SLC1A5, which stops glutamine from ever entering the cell in the first place, is an effective way to slow cancer cell growth,” says Yongmei Feng, Ph.D., staff scientist in the Ronai lab at Sanford Burnham Prebys and first author of the study. “Because many tumor types are dependent upon glutamine for survival, this drug may be able to treat many different types of cancers.”
As a next step, Ronai and his team will further refine IMD-0354, with a focus on improving biophysical properties that will help accelerate preclinical evaluation of the drug candidate.

A new research study at the University of Chicago Medicine has found that when it comes to COVID-19, having vitamin D levels above those traditionally considered sufficient may lower the risk of infection, especially for Black people.
The study, published March 19 in JAMA Open Network, retrospectively examined the relationship between vitamin D levels and likelihood of testing positive for COVID-19. While levels of 30 ng/ml or more are usually considered “sufficient,” the authors found that Black individuals who had levels of 30 to 40 ng/ml had a 2.64 times higher risk of testing positive for COVID-19 than people with levels of 40 ng/ml or greater. Statistically significant associations of vitamin D levels with COVID-19 risk were not found in white people. The study looked at data from over 3,000 patients at UChicago Medicine who had had their vitamin D levels tested within 14 days before a COVID-19 test.
The research team is now recruiting participants for two separate clinical trials testing the efficacy of vitamin D supplements for preventing COVID-19.
This research is an expansion of an earlier study showing that a vitamin D deficiency (less than 20 ng/ml) may raise the risk of testing positive for COVID-19. In the current study, those results were further supported, finding that individuals with a vitamin D deficiency had a 7.2% chance of testing positive for the virus. A separate study recently found that over 80% of patients diagnosed with COVID-19 were vitamin D deficient.
“These new results tell us that having vitamin D levels above those normally considered sufficient is associated with decreased risk of testing positive for COVID-19, at least in Black individuals,” said David Meltzer, MD, PhD, Chief of Hospital Medicine at UChicago Medicine and lead author of the study. “This supports arguments for designing clinical trials that can test whether or not vitamin D may be a viable intervention to lower the risk of the disease, especially in persons of color.”
Meltzer was inspired to investigate this topic after seeing an article in early 2020 that found people with vitamin D deficiency who had randomly been assigned to receive vitamin D supplementation had much lower rates of viral respiratory infections compared to those who did not receive supplementation. He decided to examine data being collected at UChicago Medicine on COVID-19 to determine the role that vitamin D levels might be playing.
“There’s a lot of literature on vitamin D. Most of it has been focused on bone health, which is where the current standards for sufficient vitamin D levels come from,” Meltzer explained. “But there’s also some evidence that vitamin D might improve immune function and decrease inflammation. So far, the data has been relatively inconclusive. Based on these results, we think that earlier studies may have given doses that were too low to have much of an effect on the immune system, even if they were sufficient for bone health. It may be that different levels of vitamin D are adequate for different functions.”
Vitamin D can be obtained through diet or supplements, or produced by the body in response to exposure of the skin to sunlight. Meltzer noted that most individuals, especially people with darker skin, have lower levels of vitamin D; roughly half of the world’s population has levels below 30ng/ml. “Lifeguards, surfers, those are the kinds of folks who tend to have more than sufficient vitamin D levels,” he said. “Most folks living in Chicago in the winter are going to have levels that are well below that.”
While vitamin D supplements are relatively safe to take, excessive consumption of vitamin D supplements is associated with hypercalcemia, a condition in which calcium builds up in the blood stream and causes nausea, vomiting, weakness, and frequent urination. If left unchecked, it can further lead to bone pain and kidney stones.
“Currently, the adult recommended dietary allowance for vitamin D is 600 to 800 international units (IUs) per day,” said Meltzer. “The National Academy of Medicine has said that taking up to 4,000 IUs per day is safe for the vast majority of people, and risk of hypercalcemia increases at levels over 10,000 IUs per day.”
One of the challenges of this study is that it is currently difficult to determine exactly how vitamin D may be supporting immune function. “This is an observational study,” said Meltzer. “We can see that there’s an association between vitamin D levels and likelihood of a COVID-19 diagnosis, but we don’t know exactly why that is, or whether these results are due to the vitamin D directly or other related biological factors.”
Prompted by the evidence that people with vitamin D deficiency are more likely to test positive for COVID-19 and experience significant symptoms, a team at the University of Chicago and Rush University is conducting two studies to learn whether taking a daily vitamin D supplement can help prevent COVID-19 or decrease the severity of its symptoms.

The first year of the COVID-19 pandemic has taken the lives of millions of people around the world but has also left hundreds with lingering symptoms or completely new symptoms weeks after recovery.
Much is unknown about what causes these symptoms and how long they last. But with nearly 740,000 cases of COVID reported in New York City since last March — and 28 million in the United States — physicians are increasingly seeing these “long-haulers” in their practices.
“Over the course of the summer, we started getting a sense of what issues these people were having,” says Ani Nalbandian, MD, a cardiology fellow at Columbia University Vagelos College of Physicians and Surgeons and first author of a new review of post-acute COVID-19.
“We felt that a review of all these possible issues would be important not only for health care providers but also for patients. It’s important for patients to know that what they’re experiencing may be a consequence of COVID-19 infection and that they are not alone in experiencing lingering effects of COVID-19 infection.”
Nalbandian, along with co-first author Kartik Sehgal, MD, medical oncologist at Harvard Medical School and Dana Farber Cancer Institute, spearheaded the review effort, bringing together more than 30 experts from Columbia and other medical centers hit by the initial wave. The review summarizes what the physicians were seeing in their own patients and what others had reported in the literature. The experts represented a wide range of fields, including neurology, cardiology, and nephrology.
Nalbandian and Elaine Y. Wan, MD, the Esther Aboodi Assistant Professor of Medicine in Cardiology and Cardiac Electrophysiology at Columbia University, the review’s senior author, discuss the symptoms that patients and providers should know about COVID-19 long haulers.

An unfortunate biological “feed-forward” loop drives cartilage cells in an arthritic joint to actually contribute to progression of the disease, say researchers at Duke University and Washington University in Saint Louis.
Pain researcher and mechanobiologist Wolfgang Liedtke, a professor of neurology at Duke, partnered with former Duke colleague and cartilage expert Farshid Guilak, now at the Washington University School of Medicine, to examine the activity of pressure-sensitive ion channels in cartilage. Their study appears the week of March 22 in the Proceedings of the National Academy of Sciences.
Cartilage is the highly lubricated, low-friction, elastic tissue that lines joint surfaces, cushioning movements and absorbing millions of cycles of mechanical compression. As cartilage breaks down in painful osteoarthritis, the ends of bones can come together bone-on-bone, increasing pain even more.
The cells that build and maintain cartilage are called chondrocytes, and on their surface can be found ion channels that are sensitive to force, called Piezo1 and Piezo2. In response to mechanical loads on the joint, Piezo channels send signals into the cell that can change gene activity in that cell.
Normally, chondrocytes produce extracellular matrix, the structural proteins and other biomolecules that give cartilage its mechanical stiffness, elasticity and low friction. But in osteoarthritis, degeneration and malfunction of these cells — which are incapable of repair by cell division — contribute to the progressive breakdown of cartilage.
One of the other hallmarks of osteoarthritis is chronic, low-grade inflammation, driven by a signaling molecule called interleukin-1 alpha. Using cartilage cells from pigs and from human joints removed for replacement surgeries, the researchers wanted to see how inflammation affects chondrocytes.

A University of New Mexico research team conducted a data analysis that has found that as a larger portion of the population gets vaccinated against COVID-19, it becomes economically advantageous to start relaxing social distancing measures and open businesses.
Francesco Sorrentino, associate professor of mechanical engineering, is lead author of “Data-driven Optimized Control of the COVID-19 Epidemics,” published March 22 in Scientific Reports.
Co-authors of the study are Afroza Shirin of the Department of Mechanical Engineering and the Department of Electrical and Computer Engineering, and Yen Ting Lin, a staff scientist of the Information Science Group in the Computer, Computational and Statistical Sciences Division at Los Alamos National Laboratory.
The study looked at data from four metropolitan statistical areas (MSAs) within the United States: Seattle, New York City, Los Angeles and Houston from January 21 to July 8, 2020. The four cities were chosen because they have had divergent trends with the virus (Seattle and New York City were early hotspots, while Los Angeles and Houston peaked in the summer).
Sorrentino said that while the findings perhaps may seem obvious, they are significant because the model is inferred and parametrized by regional new case reports and could potentially help guide policy decisions as more businesses, schools and other organizations ponder when and how to reopen during the pandemic.
“Our work is quantitative, so it can hopefully offer some evidence that shows the vaccines are going to allow us to loosen social distancing measures, including opening businesses,” he said. “It provides a measure of hope as we go forward and increase the percentage of citizens who are vaccinated.”
He points out that the study was looking at just the numbers, what he calls an “optimization problem,” to determine the economic cost of keeping many businesses closed or at reduced capacity. Sorrentino said the study defined economic impact by the extent that a city’s economy was closed — businesses like restaurants, gyms, salons and airports that would lose business without people’s physical presence. The study took into account both the costs associated with quarantining (which requires supervision costs as well as costs due to lowered productivity) as well as social distancing (which incurs costs only due to productivity).

SharecloseShare pageCopy linkAbout sharingimage copyrightReutersThe European Union has warned it could ban exports of vaccines produced there, as it struggles to speed up its vaccination rollout.European Commission President Ursula von der Leyen told AstraZeneca: “You fulfil your part of the deal towards Europe, before you start to deliver to other countries.”Why is the EU having vaccine problems?Where is the AstraZeneca vaccine made?The Oxford-AstraZeneca vaccine is made in the UK at two sites: in Oxford and Keele. A third plant in Wrexham puts the vaccine into vials and packages it up for distribution. The UK has ordered 100 million doses. Almost all will come from within the UK, but 10 million doses are being made by the Serum Institute in India.Half of these have already been received, with half held up by delays.Why is India struggling to meet global vaccine demand?The EU has ordered 400 million doses of the Oxford-AstraZeneca vaccine. The company says supplies are coming mainly from the US and a site in Seneffe in Belgium. AstraZeneca is working with suppliers in 15 countries to make the vaccine.A site in Leiden in the Netherlands is also producing some vaccine, although the pharmaceutical company said it was not significant. AstraZeneca confirmed that the UK has not received any vaccines or components from the EU – apart from one “tiny” batch from the Leiden plant.Who funded the AstraZeneca vaccine? The Oxford-AstraZeneca vaccine was, as the name implies, chiefly funded by the university and the pharmaceutical company. The research also received £65.5m in funding from the UK government.There was some other investment, but a University of Oxford spokesperson said it was difficult to untangle, because of the way research is funded. Why is the EU unhappy with AstraZeneca? In January, AstraZeneca said it would have to cut the number of doses it could deliver to the EU. It blamed production delays in Belgium and the Netherlands. This prompted criticism from the EU. AstraZeneca said its agreement with the EU allowed the option of supplying Europe from UK sites, but only once the UK had sufficient supplies.image copyrightReutersThe full details of the company’s deals with the UK and the EU have not been made public. But analysis by the Politico website points to a clause in the UK’s contract which says the government “may terminate the deal and invoke what appear to be punishment clauses” if there is a delay in supply. According to Politico, the EU waived its right to sue the company in the event of delivery delays. The European Commission says it is now involved in a “dispute mechanism” with the company.Is the EU running out of AstraZeneca doses?No – in fact, EU countries have been reporting hundreds of thousands of unused doses because of a drop in public confidence in the jab. Fact-checking President Macron’s vaccine claimWhy is the EU warning the UK over vaccines?France and Germany have used only about half of the AstraZeneca jabs they have received, according to the European Centre for Disease Prevention and Control (ECDC). As of 22 March, France has distributed 1.4 million out of 2.7 million doses available, while Germany received 3.4 million but has used only 1.8 million. The Netherlands has used only 38% of its supply. In most other EU countries, the proportion of the unused AstraZeneca vaccines is much higher than the proportion of unused Pfizer jabs. What about other vaccines?The Pfizer jab is mostly made in Puurs in Belgium, and a manufacturing site has also been set up in the German town of Marburg.The UK has ordered 40 million doses. The company says these deliveries are on track, but did not comment on whether they could be affected by an EU export ban. In Europe, the Moderna vaccine is produced in Switzerland and put into vials in Spain – the UK has ordered 17 million doses. The Janssen jab is made in the Netherlands – the UK has ordered 30 million doses.Vaccines may be produced in one place but “filled and finished” – put into vials and prepared for export – in another. And some components used in making the vaccine may be made at yet another location. For example, a UK company called Croda is supplying a component to Pfizer to make its vaccine. The lipid components – fat molecules used to encase the virus’s fragile genetic material and transport it into the body – are in relatively short supply, according to science data company Airfinity.Can the EU ban vaccine exports? The EU imposed export controls on coronavirus vaccines at the end of January. The measures will be in place until the end of June. They were used for the first time in March, to stop a shipment of 250,000 doses of AstraZeneca vaccine, from Italy to Australia.Ms von der Leyen has pointed out that more than 10 million doses of vaccine (Pfizer) produced in the EU have been exported to the UK. The UK government has not been able to confirm whether any vaccines have gone the other way but insists a ban is not in place.Prime Minister Boris Johnson has said: “I am reassured by talking to EU partners over the last few months that they don’t want to see blockades.”