Split views on whether COVID-19's big waves are over

 Opinions are split on whether the waning delta surge will be the last major COVID-19 wave to strike the U.S., as Americans grow eager for the pandemic to end after 19 months. 

The vaccination rate and decreasing cases in most states have provided a ray of hope that the pandemic could be winding down after its final large wave, some experts say. 

But other public health experts caution the unpredictability of the virus suggests another surge could still happen as the country braces for winter — which led to skyrocketing cases, deaths and hospitalizations last year.

Nicholas Reich, a professor of biostatistics at the University of Massachusetts Amherst, said declaring there won’t be another major wave after delta “feels like” a “premature” and “bold” statement.

“Is there a chance? Sure, but I feel like if there's one thing we've learned from this, it's that there's a lot more sort of uncertainty and randomness … in COVID then we've given it credit for so far,” he said.

Some experts, including Reich, pointed out that factors such as the potential development of variants and the unknown endurance of immunity after infection and vaccination could spark larger-scale rises in COVID-19 cases after the country has seen a national decline. 

The downturn in cases comes after the delta strain fueled a spike, reaching a seven-day average of more than 175,000 daily cases in mid-September. But on Thursday, that average dropped below 100,000 for the first time since Aug. 4, according to data from The New York Times. 

Overall, 39 states have seen their seven-day averages of COVID-19 cases fall within the past two weeks. Despite these drops in cases, COVID-19 is not eliminated and “many hundreds of thousands of people are still gonna get infected” as the pandemic continues, Reich said. 

While COVID-19 numbers are moving “in the right direction,” some areas of the country, including Alaska and West Virginia, are still “very much in the midst of the delta wave,” said Leana Wen, an emergency physician and public health professor at George Washington University.

“I'm very concerned about people becoming complacent because they think that the delta wave is passing us,” she said. “We have seen this happen before, where there is a rise in the number of cases, then a decline, and then people let down their guard. And as a result, we plateau at a very high level of cases. That's unacceptable.”

The approaching winter season also makes it difficult to forecast future COVID-19 trends, as coronaviruses can more easily spread in colder weather and in indoor spaces. Last winter, the U.S. saw its highest surge of cases, hospitalizations and deaths amid holiday gatherings held before vaccines became widely available.

Christopher Murray, the director of the Institute for Health Metrics and Evaluation at the University of Washington, said he expects cases to increase in the winter after bottoming out in October, but that it is likely to be lower than the delta surge.  

“I think some people will be surprised that it doesn't just keep going away, and … that doesn't seem very likely,” he said. 

Wen of George Washington University said having just 56.2 percent of the total U.S. population fully vaccinated and fewer restrictions than last year leaves it uncertain that the delta wave could be the U.S.’s final major COVID-19 surge.

“I don't know how we could possibly say that considering we don't know what's going to come our way,” Wen said.

“I'm not sure how we can know for certain that the level of protection we have nailed through vaccination is sufficient,” she said, adding she’s hopeful the end is “on the horizon” with children’s vaccines, oral treatment and more testing. 

Others, including former Food and Drug Administration (FDA) commissioner Scott Gottlieb, took a more optimistic stance, anticipating that cases won’t rise to the summer delta levels again. 

“Barring something unexpected, I’m of the opinion that this is the last major wave of infection,” Gottlieb told The New York Times this week.

Amesh Adalja, a senior scholar at the Johns Hopkins University Center for Health Security, told MSNBC on Friday that any rise in winter cases will likely be “more decoupled from hospitalizations and deaths” due to the increased immunity due to vaccines and infections.

“Many more people have been vaccinated, so many more people have natural immunity from this big delta wave and unfortunately so many people have died that we probably won’t see peaks that are anything like we saw in the past, especially when it comes to what matters which is hospitalization, serious disease and death,” he said.

“I think delta was hopefully the worst that this virus can throw at us,” he added.

David Dowdy, an associate professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health, said he thinks it’s “unlikely” that the U.S. will endure another COVID-19 wave “to the level” of the summer delta and previous winter surges. 

With the vaccination level rising and a “fair amount” of the unvaccinated getting infected, Americans’ immunity is “higher now than it’s ever been,” he said.

The emergence of a new variant could potentially threaten that immunity if the strain evades the vaccines. But Dowdy said he doesn’t expect that in the short-term, as delta has reigned as the dominant variant worldwide for months without another strain usurping it. 

“I think anyone who says that they can predict the future of this pandemic is probably lying to you,” Dowdy said. “But I think we have a lot of reasons to be optimistic that we will not see another massive wave the way that we have seen so far.”

https://thehill.com/policy/healthcare/576030-are-covid-19s-big-waves-over-experts-are-split

Glycerin is safe, effective in psoriasis model

 Patients with psoriasis have reported that glycerin, an inexpensive, harmless, slightly sweet liquid high on the list of ingredients in many skin lotions, is effective at combatting their psoriasis and now scientists have objective evidence to support their reports.

They found that whether applied topically or ingested in drinking water, glycerin, or glycerol, helps calm the classic scaly, red, raised and itchy patches in their psoriasis model, Dr. Wendy Bollag, cell physiologist and skin researcher at the Medical College of Georgia and Charlie Norwood VA Medical Center and her colleagues report in the International Journal of Molecular Sciences.

The studies also provide more evidence of the different ways glycerin enables the healthy maturation of skin cells through four stages that result in a smooth, protective skin layer. Psoriasis is an immune-mediated problem that typically surfaces in young adults in which skin cells instead multiply rapidly, piling up into inflamed patches.

"We have experimental data now to show what these patients with psoriasis are reporting," says Bollag, who nearly 20 years ago first reported in The Journal of Investigative Dermatology that glycerin, a natural alcohol and water attractor known to help the skin look better, also safely helped it function better by helping skin cells mature properly.

Bollag's early report led to many anecdotal reports from individuals and their reports ultimately led to the newly published study.

Topically, glycerin is known to have a soothing, emollient effect. But another key part of its magic, which Dr. Bollag has helped delineate, is its conversion to the lipid, or fat, phosphatidylglycerol, which ultimately regulates the function of keratinocytes, our major skin cell type, and suppresses inflammation in the skin.

Glycerin gets into the skin through avenues like aquaporin-3, a channel expressed in skin cells, and the MCG scientists have shown that once inside, aquaporin 3 funnels glycerin to phospholipase-D-2, an enzyme that converts fats in the external cell membrane into cell signals, ultimately converting glycerin to phosphatidylglycerol.

In 2018, Bollag and team reported that topical application of phosphatidylglycerol reduced inflammation and the characteristic raised skin patches in a mouse model of psoriasis. This time they decided to look at the impact of its widely available precursor glycerin.

For the new studies, they used imiquimod, which is known to produce psoriasis-like plaques on humans using it for problems like genital warts and some skin cancers, to produce an animal model. The mice either drank the sweet natural alcohol or the scientists applied it topically. Either way, glycerin helped reduce development of the characteristic skin lesions, the scientists report, a finding which helps underline that glycerin works in more than one way to improve the skin condition.

Externally, glycerin showed its action as an emollient because even in mice missing phospholipase-D-2, it was beneficial. Additionally, topically it appears to compete with hydrogen peroxide for space inside the aquaporin 3 channel. Hydrogen peroxide is commonly known as a mild antiseptic but we produce it as well and at low levels it's a cell signaling molecule. But at high levels, hydrogen peroxide produces destructive oxidative stress, which can actually cause psoriasis.

The scientists found that topical glycerin reduced the levels of hydrogen peroxide entering skin cells. When they added glycerin and hydrogen peroxide at the same time directly to skin cells, they found that glycerin protected against the oxidative stress from hydrogen peroxide.

"Glycerol is basically outcompeting the hydrogen peroxide in getting in there and preventing it from being able to enter and increase oxidative stress," Bollag says. Oil and water don't mix, so yet another way glycerin may be helpful is by supporting the skin's major role as a water permeability barrier so that, as an extreme, when we sit in a bathtub the bath water doesn't pass through our skin so we blow up like a balloon, she says.

On the other hand, when glycerin was ingested by the mice missing the phospholipase- D-2, which converts fats or lipids in a cell's membrane to signals, it simply did not work, Bollag says, which confirmed their earlier findings that internally anyway, glycerin pairs with the enzyme to produce the signal essential to skin cell maturation.

Some of their other most recent work is detailing more about how phosphatidylglycerol decreases inflammation.

Bollag would like next steps to also include clinical trials with dermatologists and patients and is working to find a formulation scientist who can make what she thinks will be the optimal combination: glycerin and phosphatidylglycerol in the same topical cream.

The addition of phosphatidylglyerol itself, rather than just the glycerin that makes it, is essentially a backup since there is some evidence that in psoriasis the essential conversion of glycerin to phosphatidylglycerol is not optimal. Bollag's lab and others have shown reduced levels of aquaporin 3 in psoriasis, which likely means less phosphatidylgycerol, so making more glycerin available may help, albeit not as efficiently, raise the availability of this lipid essential to normal skin cell proliferation.

Moving quickly into clinical trials should be comparatively easy since, as with glycerin, there already is experience with the use of phosphatidylglycerol in humans. For example, it's a component of some high-end cosmetics, Bollag says.

She suspects that this sort of two-punch combination, could help keep early signs of psoriasis at bay and, with more advanced disease, use existing psoriasis treatments to get the skin condition under control then start applying glycerin to help keep it that way.

Bollag and her colleagues reported in 2018 in the Journal of Investigative Dermatology that in a mouse model of psoriasis, phosphtidylglycerol reduced inflammation and the characteristic raised skin lesions of psoriasis.

While its exact cause is unclear, psoriasis is an immune-mediated condition and patients have higher levels of inflammation, as well as too many skin cells being produced then maturing abnormally. The heightened inflammation also puts them at increased risk for problems like heart disease.

Biologics used to treat psoriasis work different ways to stem this overactive immune response but in addition to their high cost, can put the patient at risk for problems like serious infections and cancer. The only side effect she has seen in about 20 years of working with glycerin and the clinical and cosmetic use already out there, is it can leave the skin feeling slightly sticky.

Our bodies can make glycerol from the carbohydrates, proteins and fats that we eat or already have in our body.

The research was funded in part by the Veterans Administration.

Story Source:

Materials provided by Medical College of Georgia at Augusta University. Original written by Toni Baker. Note: Content may be edited for style and length.

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Journal Reference:

1. Vivek Choudhary, Ismail Kaddour-Djebbar, Victoria E. Custer, Rawipan Uaratanawong, Xunsheng Chen, Elyssa Cohen, Rong Yang, Etsubdenk Ajebo, Sarah Hossack, Wendy B. Bollag. Glycerol Improves Skin Lesion Development in the Imiquimod Mouse Model of Psoriasis: Experimental Confirmation of Anecdotal Reports from Patients with Psoriasis. International Journal of Molecular Sciences, 2021; 22 (16): 8749 DOI: 10.3390/ijms22168749

https://www.sciencedaily.com/releases/2021/10/211004104229.htm

Super-enhancers: The villain fueling certain cancers

 In a recent study published in Cancer Research, a team led by researchers at Tokyo Medical and Dental University (TMDU) identified a specific small RNA molecule, called a microRNA (miRNA or miR), that has the potential to be used as an anti-cancer therapeutic. The new research indicates that the molecule, called miR-766-5p, can significantly reduce levels of the oncogene MYC -- a specific gene that is expressed at high levels in tumor cells and helps fuel cancer growth and progression.

At its most basic level, cancer is driven by abnormal and uncontrolled gene expression. Numerous different molecular mechanisms contribute to the activation and overexpression of oncogenes in cancer. MiRNAs work as negative regulators of gene expression. This means that they can directly bind and interact with certain gene messages and block them from being translated into a protein. Therefore, any molecular pathway controlled by that specific protein is also affected by this miRNA-mediated regulation. In a previous study, the TMDU group used cell culture experiments to demonstrate that treating cancer cells with miR-766-5p resulted in lower MYC expression and inhibited cancer cell growth rates. Following these intriguing findings, the group aimed to determine the specific mechanism behind these results.

"MYC is a critical oncogene in many tumor types," says lead author of the study Yasuyuki Gen. "It can promote cancer cell proliferation, can suppress the body's immune response to fighting the cancer, and can generally be the main driver of tumor progression in many patients."

The researchers found that miR-766-5p could directly target and reduce expression of two proteins called CBP and BRD4. CBP can induce a molecular change called acetylation that causes DNA to become more "open," which allows genes present in that area to be more easily expressed. BRD4 can then be recruited to these sites and help promote transcription of these gene messages.

"Areas of DNA with high activity of proteins like CBP and BRD4 are known as super-enhancers," explains Johji Inazawa, senior author. "Many cancer cells develop super-enhancers near oncogenes, like MYC, that drive increased oncogene expression and therefore promote cancer."

The team then experimentally treated cells with a synthetic version of miR-766-5p, finding that the resulting suppression of CBP and BRD4 caused decreased MYC levels in cancer cells, but not in normal cells. Additionally, tumors that were engrafted in lab mice showed significantly suppressed growth when treated with miR-766-5p compared with a control miRNA.

"Our findings suggest that miR-766-5p-mediated control of CBP and BRD4 blocks formation of the super-enhancers that contribute to MYC overexpression in cancer cells," explains Gen.

In recent years, efforts have been made to develop specific miRNAs into targeted therapies for various cancers. This study provides considerable evidence that miR-766-5p could be used to fight MYC-driven cancers by targeting super-enhancers.

Story Source:

Materials provided by Tokyo Medical and Dental University. Note: Content may be edited for style and length.

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Journal Reference:

1. Yasuyuki Gen, Tomoki Muramatsu, Jun Inoue, Johji Inazawa. miR-766-5p targets super-enhancers by downregulating CBP and BRD4. Cancer Research, 2021; canres.0649.2021 DOI: 10.1158/0008-5472.CAN-21-0649

https://www.sciencedaily.com/releases/2021/10/211005124701.htm

'Cousin' of Viagra reduces obesity by stimulating cells to burn fat

 Researchers at Johns Hopkins Medicine have found that a drug first developed to treat Alzheimer's disease, schizophrenia and sickle cell disease reduces obesity and fatty liver in mice and improves their heart function -- without changes in food intake or daily activity.

These findings, published online Oct. 7 in the Journal of Clinical Investigation, reveal that a chemical inhibitor of the enzyme PDE9 stimulates cells to burn more fat. This occurred in male mice and in female mice whose sex hormones were reduced by removing their ovaries, thus mimicking menopause. Postmenopausal women are well known to be at increased risk for obesity around their waist as well as at risk for cardiovascular and metabolic disease.

Inhibiting PDE9 did not cause these changes in female mice that had their ovaries, so female sex hormone status was important in the study.

"Currently, there isn't a pill that has been proven effective for treating severe obesity, yet such obesity is a global health problem that increases the risk of many other diseases," says senior investigator David Kass, M.D., Abraham and Virginia Weiss Professor of Cardiology at the Johns Hopkins University School of Medicine. "What makes our findings exciting is that we found an oral medication that activates fat-burning in mice to reduce obesity and fat buildup in organs like the liver and heart that contribute to disease; this is new."

This study follows work reported by the same laboratory in 2015 that first showed the PDE9 enzyme is present in the heart and contributes to heart disease triggered by high blood pressure. Blocking PDE9 increases the amount of a small molecule known as cyclic GMP, which in turn controls many aspects of cell function throughout the body. PDE9 is the enzyme cousin of another protein called PDE5, which also controls cyclic GMP and is blocked by drugs such as Viagra. Inhibitors of PDE9 are experimental, so there is no drug name yet.

Based on these results, the investigators suspected PDE9 inhibition might improve cardiometabolic syndrome (CMS), a constellation of common conditions including high blood pressure; high blood sugar, cholesterol and triglycerides; and excess body fat, particularly around the waist. CMS is considered a pandemic by medical experts and a major risk factor for heart disease, stroke, type 2 diabetes, cancers and COVID-19.

While PDE9 inhibitors remain experimental, they have been developed by several pharmaceutical companies and tested in humans for diseases such as Alzheimer's and sickle cell. The current mouse study used a PDE9 inhibitor made by Pfizer Inc. (PF-04447943) that was first tested for Alzheimer's disease, though eventually abandoned for this use. Between the two reported clinical trials, over 100 subjects received this drug, and it was found to be well tolerated with no serious adverse side effects. A different PDE9 inhibitor is now being tested for human heart failure.

To test the effects of a PDE9 inhibitor on obesity and cardiometabolic syndrome, the researchers put mice on a high-fat diet that led to doubling their body weight, high blood lipids and diabetes after four months. A group of female mice had their ovaries surgically removed, and most of the mice also had a pressure stress applied to the heart to better mimic cardiometabolic syndrome. The mice were then assigned to receive either the PDE9 inhibitor or a placebo by mouth over the next six to eight weeks.

In female mice without their ovaries (a model of postmenopause), the difference in median percent weight change between the drug and placebo groups was -27.5%, and in males it was -19.5%. Lean body mass was not altered in either group, nor was daily food consumption or physical activity. The PDE9 inhibitor lowered blood cholesterol and triglycerides, and reduced fat in the liver to levels found in mice fed a normal diet. The heart also improved with PDE9 inhibition, with ejection fraction (which measures the percentage of blood leaving the heart each time it contracts) relatively higher by 7%-15% and heart mass (hypertrophy) rising 70% less compared with the placebo. An increase in heart mass is evidence of abnormal heart stress. However, having this lowered by the inhibitor indicates stress on the heart was reduced.

The investigators found PDE9 inhibition produces these effects by activating a master regulator of fat metabolism known as PPARa. By stimulating PPARa, levels of genes for proteins that control fat uptake into cells and their use as fuel are broadly increased. When PPARa was blocked in cells or the whole animal, the effects from PDE9 inhibition on obesity and fat-burning were also lost. They found estrogen normally plays this role of PPARa on fat regulation in females, but when its levels fall like they do after menopause, PPARa becomes more important to regulate fat and so PDE9 inhibition has a greater effect.

"The finding that the experimental drug did not benefit female mice that had their ovaries shows that these sex hormones, particularly estrogen, had already achieved what inhibiting PDE9 does to stimulate fat-burning," notes Sumita Mishra, the research associate who performed much of the work. "Menopause reduces sex hormone levels, and their control over fat metabolism then shifts to the protein regulated by PDE9, so the drug treatment is now effective."

According to the U.S. Centers for Disease Control and Prevention, more than 40% of people living in the U.S. are obese; and 43% of American women over the age of 60 -- long past menopause -- are considered obese.

Kass notes that if his lab's findings in mice apply to people, someone weighing 250 pounds could lose about 50 pounds with an oral PDE9 inhibitor without changing eating or exercise habits.

"I'm not suggesting to be a couch potato and take a pill, but I suspect that combined with diet and exercise, the effects from PDE9 inhibition may be even greater," says Kass. The next step would be testing in humans to see if PDE9 inhibitors produce similar effects in men and postmenopausal women.

"PDE9 inhibitors are already being studied in humans, so a clinical obesity study should not be that far away," Kass says.

Funding for this study was supported by NIH R35-HL135827, RO1-HL-119012, P01HL10715, and AHA 16SFRN28620000 (DAK), NIH DK084171 (GWW), NIH-RO1-HL134821 (BOR), NIH T32-HL007227 (VSH), 16SFRN27870000 (KS), DK116625, AHA 16SFRN28620000 (SC), 16SFRN28420002 (DDS), F32 DK-116520 (RPC), and OE 688/1-1 (CUO). PF-04447943 was provided by Pfizer Inc. under a material transfer agreement.

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Story Source:

Materials provided by Johns Hopkins Medicine. Note: Content may be edited for style and length.

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Journal Reference:

1. Sumita Mishra, Nandhini Sadagopan, Brittany Dunkerly-Eyring, Susana Rodriguez, Dylan C. Sarver, Ryan P. Ceddia, Sean A. Murphy, Hildur Knutsdottir, Vivek P. Jani, Deepthi Ashok, Christian U. Oeing, Brian O'Rourke, Jon A. Gangoiti, Dorothy D. Sears, G. William Wong, Sheila Collins, David Kass. Inhibition of phosphodiesterase type 9 reduces obesity and cardiometabolic syndrome in mice. Journal of Clinical Investigation, 2021; DOI: 10.1172/JCI148798

https://www.sciencedaily.com/releases/2021/10/211007122238.htm

Common gut bacteria can fuel the growth of prostate cancers

 Scientists revealed how gut bacteria contribute to the progression of advanced prostate cancers and their resistance to hormone therapy -- by providing an alternative source of growth-promoting androgens, or male hormones.

Hormone therapy is the standard of care for advanced prostate cancer and works by lowering levels of androgens. But researchers found that low androgen levels in patients can drive the expansion of gut bacteria, which can become hormone factories to sustain prostate cancer growth.

Bacterial 'fingerprints' identified by scientists may help pick out patients at high risk of developing resistance to treatment who could benefit from strategies to manipulate their 'microbiome'. For example, men could undergo a faecal transplant or take a yoghurt drink enriched with favourable bacteria.

A team of scientists from The Institute of Cancer Research, London, the Institute of Oncology Research in Bellinzona, Switzerland and the Swiss Federal Institute of Technology used mice and patient samples to investigate the role of gut bacteria in prostate cancer growth and progression.

The findings, once further validated in the clinic, could provide new opportunities for the treatment of prostate cancer through manipulation of the microbiome.

The study, published in the journal Science, was funded by the Prostate Cancer Foundation, Movember, Prostate Cancer UK, Cancer Research UK and The John Black Charitable Foundation.

Gut bacteria are part of our microbiome and are usually valuable to humans. However, cancer and other diseases can ruin this mutually beneficial balance -- for example by promoting the expansion of gut bacteria and encouraging them to release toxins or other molecules that affect cancer cells.

Given the role these 'gut bugs' can play in cancer, researchers looked at whether the gut bacteria from men with prostate cancer could also alter patients' hormone metabolism, and so affect cancer growth.

Scientists found that getting rid of all gut bacteria in mice with prostate cancer slowed tumour growth and delayed the emergence of hormone resistance.

They also found that transplanting faeces from mice with hormone-resistant prostate cancer into mice with low androgen levels that had not yet developed resistance encouraged tumour growth.

The researchers demonstrated in mice that gut bacteria were able to make androgen hormones from precursor molecules.

To translate the findings into humans, researchers analysed the gut bacteria from patients who were being treated at The Royal Marsden NHS Foundation Trust. They looked at two different groups of patients -- 19 men whose prostate cancers were still responding to hormone therapy and 55 men with advanced hormone-resistant prostate cancer.

Transplanting stool from prostate cancer patients with hormone-resistant prostate cancer into mice whose cancers were not resistant promoted tumour growth and hormone resistance.

Scientists also analysed microbial genetic material from the stool of men with prostate cancer and identified a specific bacterium -- Ruminococcus - that may play a major role in the development of resistance. In contrast, the bacterium Prevotella stercorea was associated with favourable clinical outcomes.

Researchers incubated mini-tumours called organoids derived from prostate cancer patients with different gut bacteria and attempted to treat them in the lab. This helped them identify favourable and unfavourable bacterial 'fingerprints' linked to prostate cancer outcome, which could help identify men who could benefit from strategies to manipulate the microbiome.

Study author Professor Johann de Bono, Professor of Experimental Cancer Medicine at The Institute of Cancer Research, London, and Consultant Medical Oncologist at The Royal Marsden NHS Foundation Trust, said:

"Our findings reveal that the initiation of hormone therapy for prostate cancer can trigger 'gut bugs' to start producing androgen hormones. These androgens can then sustain prostate cancer's growth and drive resistance to hormone therapy -- worsening men's survival outcomes.

"Excitingly, our research has identified particular signatures among gut bacteria which could indicate that some men with prostate cancer who have these gut bugs are more likely to develop resistance to hormone therapy. The next step will be to further explore how we apply these signatures in patients, with the aim of devising tests to pick out men who would benefit from faecal transplants, antibiotic therapy and other strategies to manipulate the microbiome. In the long-term, our aim would be to produce a 'yoghurt' enriched with favourable bacteria to prevent resistance to treatment."

Professor Kristian Helin, Chief Executive of The Institute of Cancer Research, London, said:

"The influence of the gut microbiome on cancer is a fascinating new area of science that we are just beginning to understand. These exciting findings are the first to unveil a mechanism through which the gut microbiome can drive prostate cancer growth and resistance to hormone therapy.

"Understanding how common, 'good' bacteria in the gut -- which play a vital role in keeping us healthy -- can interfere with hormone metabolism in men with prostate cancer could help us devise new treatment strategies. I look forward to this research moving forward into the clinic and hope that strategies to manipulate the microbiome could make a real difference for patients."

Professor Andrea Alimonti, Head of Molecular Oncology at the Institute of Oncology Research (IOR), Professor at Università della Svizzera italiana (USI), at the University of Padova and at the Swiss Federal Institute of Technology (ETH), said:

"Our discoveries pave the way to adjuvant therapeutic strategies that, through microbiota manipulations, counteract the expansion of androgen-producing bacterial species."

Story Source:

Materials provided by Institute of Cancer Research. Note: Content may be edited for style and length.

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Journal Reference:

1. Nicolò Pernigoni et al. Commensal bacteria promote endocrine resistance in prostate cancer through androgen biosynthesis. Science, 2021 DOI: 10.1126/science.abf8403

https://www.sciencedaily.com/releases/2021/10/211007145906.htm

Russian-speaking hacking group scaling up ransomware attacks on hospitals

 A Russian-speaking cyber criminal group is disproportionately using ransomware attacks to target hospitals and health care groups across North America as the COVID-19 pandemic continues, according to new research released Thursday. 

Cybersecurity organization Mandiant labeled the group “FIN12” as part of a report detailing the group’s activities, with Mandiant noting that it has been in existence since at least 2018, but was increasingly hitting organizations in North America with annual revenues of more than $300 million with ransomware attacks. Many of these companies made even more, with the average annual revenue of North American groups targeted at just under $6 billion. 

According to Mandiant, one in five of FIN12’s victims were health care groups, many of which operate hospitals, while other victims have included groups in business services, education, finance, government, manufacturing, retail and technology.

While the majority of victims have been located in North America, other victims are located in Europe and Asian Pacific nations. FIN12 has made a massive profit in targeting these companies, with Mandiant noting that most ransom demands were likely between $5 million and $50 million. 

Kimberly Goody, director of Financial Crime Analysis at Mandiant, described FIN12 Thursday as “one of the most aggressive ransomware threat actors tracked by Mandiant.”

“Unlike other actors who are branching out into other forms of extortion, this group remains focused purely on ransomware, moving faster than its peers and hitting big targets,” Goody said in a statement. ”They are behind several attacks on the healthcare system and they focus heavily on high-revenue victims.”

Mandiant noted that the group was the same organization that led a coalition of U.S. federal agencies to issue a report last year warning that hospitals and health care providers were being increasingly targeted. FIN12 often uses the Ryuk ransomware virus, which was linked last year to the attack on Pennsylvania-headquartered hospital chain Universal Health Services, which operates about 250 U.S. health care facilities.

At the time, Mandiant, which was previously FireEye, labeled the group “UNC1878,” warning in a report that “the operators conducting these campaigns have actively targeted hospitals, retirement communities and medical centers, even in the midst of a global health crisis, demonstrating a clear disregard for human life.”

FIN12 is fairly unique in its increased targeting of health care groups, with the Mandiant report noting that while “it may also be easier or cheaper to obtain access to healthcare organizations,” FIN12 would like “face increased scrutiny from law enforcement agencies.”

Mandiant noted in the report that FIN12 intrusions had made up around 20 percent of the ransomware attack engagements the company had over the past year.

Ransomware attacks have become an increasing threat to hospitals, schools, and other critical organizations during the COVID-19 pandemic, which saw more of everyday life move online and often on to aging, vulnerable systems. Ransomware attacks against major groups have also endangered key supply chains, including the attacks in May on Colonial Pipeline and meat producer JBS USA. 

https://thehill.com/policy/cybersecurity/575787-russian-speaking-hacking-group-scaling-up-ransomware-attacks-on

UK to offer new vaccine shots to Novavax trial volunteers

 Britain announced Friday that it will offer new vaccinations to thousands of people who volunteered for trials of the Novavax coronavirus vaccine, which hasn't yet been approved for use in any country.

Around 15,000 people in the U.K. got Novavax shots as part of a clinical trial. While the U.K. recognizes them as vaccinated, most countries don’t, meaning they can’t travel.

Britain’s health department said more than 15,000 participants will be given two doses of the Pfizer/BioNTech vaccine. The government says it plans to expand the offer to about 6,000 U.K. participants in trials of other vaccines that also haven't been approved for use.

Britain has appealed to other members of the Group of 20 nations to classify clinical trial volunteers as vaccinated, but most haven't done so.

England’s deputy chief medical officer, Jonathan Van-Tam, noted that “if more countries around the world had reciprocated by allowing U.K. volunteers to enjoy fully vaccinated status for overseas travel, these measures would not have been necessary.”

In June, Novavax announced that its vaccine had proved about 90% effective against symptomatic COVID-19 in a study of nearly 30,000 people in the U.S. and Mexico.

U.S.-based Novavax has asked the World Health Organization to approve its COVID-19 vaccine for emergency use so it can be part of the COVAX global vaccine program. But it has delayed seeking approval in Europe or the United States.

The Novavax shots are easier to store and transport than some other options, and have long been expected to play an important role in increasing supplies in poor countries desperate for more vaccine doses.

https://abcnews.go.com/Health/wireStory/uk-offer-vaccine-shots-novavax-trial-volunteers-80475143