Culture

In the UK, men from ethnic minorities and women may have experienced worse mental health declines than White British men, according to a study published January 6, 2021 in the open access journal PLOS ONE by Eugenio Proto and Climent Quintana-Domeque of institutions including the University of Glasgow and the University of Exeter, UK.

The COVID-19 pandemic, and the measures enacted to restrict the spread of the virus, have had a major impact on the lives of citizens globally. The authors of the present study examined changes in mental health associated with the pandemic across ethnic groups in the UK.

The researchers used data from the UK Household Longitudinal Study, comparing responses from participants between 2017 and 2019 (i.e.: prior to the pandemic) to responses from the same participants in April 2020 (i.e.: during the pandemic, when severe "lockdown" restrictions were in place in the UK). A total of 14,523 individuals provided responses both before and during the pandemic; 91.5 percent defined their ethnicity as White British and the remaining 8.5 percent as another ethnicity (Black, Asian, and minority ethnic, or BAME). Participants were asked to self-report their health, including their mental wellbeing. These responses were used to measure levels of mental distress, on a scale from 0 to 36.

The authors found that the average mental distress for individuals had increased from 11.28 [95% CI: 11.17, 11.40] in 2017-2019 to 12.51 [95% CI: 12.38, 12.63] in April 2020, a 0.21 standard deviation increase [95% CI: 0.19, 0.23]. Women experienced a greater average increase in mental distress than men, and BAME men also experienced a greater average increase than White British men. While White British men saw an average increase in mental distress of 0.6 units on this scale, White British women experienced an average increase of 1.6 units. BAME men experienced an average increase of 1.5 units, and BAME women of 1.7 units.

While the study conclusions may be limited by the sample size of BAME individuals (only 1,066 of the participants defined themselves as BAME), and by mental distress being measured relatively early on in the pandemic, the research suggests that the pandemic may have particularly affected the mental wellbeing of women and BAME individuals. The authors state that their preliminary findings appear to indicate "the impact of the lockdown and social distancing requirements on mental health being worse among minority ethnic groups."

The authors add: "Women and Black, Asian, and minority ethnic men experienced a higher average increase in mental distress than White British men from 2017-2019 to April 2020."

CAR T cells are a breakthrough class of effective but often toxic cancer therapies

To prevent overactivation, switchable CAR T cells were engineered that can be turned on and off with an approved, widely used cancer drug

BOSTON - Scientists at Dana-Farber Cancer Institute and Mass General Cancer Center have created molecular ON-OFF switches to regulate the activity of CAR T cells, a potent form of cell-based immunotherapy that has had dramatic success in treating some advanced cancers, but which pose a significant risk of toxic side effects.

CAR T cells are immune cells genetically modified to recognize and attack tumors cells. Once given, these "living drugs" proliferate and kill tumor cells over weeks to months, in some cases causing life-threatening inflammatory reactions that are difficult to control. In this way, CAR T cells are unlike more established forms of cancer therapy - chemotherapy or radiotherapy for instance - whose dose can be precisely tuned up or down over time.

The scientists reported in Science Translational Medicine the development of switchable CAR T cells that can be turned on or off by giving a commonly used cancer drug, lenalidomide. In the laboratory, the researchers designed OFF-switch CAR T cells that could be quickly, reversibly turned off by administering the drug, after which the CAR T cells recovered their anti-tumor activity. Separately, the researchers also reported ON-switch CAR T cells that only killed tumor cells during lenalidomide treatment.

In the future, switchable cell therapies might allow patients with their physicians to take a pill - or not - to tune the amount of CAR T cell activity from day to day, hopefully reducing toxic side effects.

"From the start, our goal was to build cancer therapies that are less hard on people. Having built these switches using human genetic sequences and an FDA-approved drug, we are excited for the potential to translate this research to clinical use," said Max Jan, MD, PhD, first author of the report. He is affiliated with the laboratories of Benjamin Ebert, MD, PhD, and Marcela Maus, MD, PhD, the report's senior authors. Other authors include researchers from the Broad Institute of MIT and Harvard, and Harvard Medical School.

CAR T cells are created by harvesting immune T cells from the patient and reprogramming them in the laboratory to produce a finely-tuned receptor molecule, termed a CAR (for chimeric antigen receptor), that recognizes a distinctive protein on the surface of the patient's cancer cells. The CAR T cells, after being engineered in the lab and returned to the patient, circulate through the body and home in on the cancer cells by binding to the distinctive surface protein they have been engineered to recognize. This binding event stimulates an immune attack, destruction of the cancer cells, and proliferation of the CAR T cells.

A drawback, however, is that uncontrolled proliferation of the CAR T cells sometimes triggers cytokine release syndrome (CRS), the release of inflammation-causing signals throughout the body that can cause toxicities ranging from mild fever to life-threatening organ failure. Current management of these toxic reactions relies on intensive care unit support and drugs including immunosuppressive corticosteroids, while many researchers are trying to develop methods of controlling the activity of CAR T cells in order to prevent these toxic side effects.

"CAR T cells can be fantastically effective therapies, but they can also have serious toxicities and can cause significant morbidity and mortality," said Ebert who is Chair of Medical Oncology at Dana-Farber. "They are currently difficult to control once administered to the patient."

CAR T cell therapy has had most success in blood cancers. Three CAR T agents have been approved: Kymriah for children and young adults with B-cell precursor acute lymphoblastic leukemia (ALL), both Kymriah and Yescarta for treatment of adults with diffuse large B-cell lymphoma and Tecartus for adults with mantle cell lymphoma. Scientists are investigating an array of different approaches with the aim of extending the reach of CAR T therapies to other blood cancers and to solid tumors, if a number of hurdles can be overcome, including the problem of treatment toxicity.

To create the ON and OFF switch systems for CAR T cells, the scientists used a relatively new technique known as targeted protein degradation. It exploits a mechanism that cells use to dispose of unwanted or abnormal proteins; the proteins are marked for destruction by a structure within cells that acts like a garbage disposal. A small number of drugs, including lenalidomide, act by targeting specific proteins for degradation using this pathway.

The researchers used this technique to engineer small protein tags that are sent to the cellular garbage disposal by lenalidomide. When this degradation tag was affixed to the CAR, it allowed the tagged CAR to be degraded during drug treatment, thereby stopping T cells from recognizing cancer cells. Because CAR proteins are continually manufactured by these engineered T cells, after drug treatment new CAR proteins accumulate and restore the cell's anti-tumor function. The researchers propose that the switch system might in the future allow patients to have their CAR T cell treatment temporarily paused to prevent short-term toxicity and still have long-term therapeutic effects against their cancer.

The scientists also built an ON-switch CAR by further engineering the proteins that physically interact with lenalidomide. This system has the potential to be especially safe, because the T cells only recognize and attack tumor cells during drug treatment. If used to treat cancers such as multiple myeloma that are sensitive to lenalidomide, ON-switch CAR T cells could allow for a coordinated attack by the immune cells and the drug that controls them.

"The long-term goal is to have multiple different drugs that control different on and off switches" so that scientists can develop "ever-more complex cellular therapies," explained Ebert.

Amsterdam, NL, January 6, 2021 - There is growing evidence to support the hypothesis that there is a neurodevelopmental component to the late-onset neurodegeneration occurring in the brain of huntingtin gene (HTT gene) mutation carriers, and that this increased susceptibility to brain cell death begins during childhood. Experts discuss the evidence that the HTT gene mutation affects brain and body growth based on a unique study of children at risk for HD, the Kids-HD study, in a review paper and accompanying research article published in the Journal of Huntington's Disease.

The classic concept is that Huntington's disease is caused by toxic mutant huntingtin (mHTT) acting over time on mature brain cells. However, there is growing evidence for an alternative theory in which mHTT has an effect on brain development and that this altered development plays a vital role in the later degenerative process. This theory is based on the notion that wild-type huntingtin (HTT) function plays a role in normal brain development.

"Although the gene was discovered in 1993, we still don't have a good understanding of what causes HD - how does the mutant gene cause brain cells to become 'sick' then die?" noted lead investigator Peg C. Nopoulos, MD, Department of Psychiatry, Department of Pediatrics, and Department of Neurology, University of Iowa Carver College of Medicine, Iowa City, IA, USA. "The neurodevelopmental hypothesis is a relatively new way of thinking about the disease and can help focus research efforts in a new direction. This review and the accompanying study are important in reshaping our ideas about how we view the nature and timing of preventive treatment for HD and the factors that contribute to disease."

The neurodevelopmental hypothesis of HD posits that the disease-causing gene mutation affects development of a specific region or specific brain circuit. These cells are abnormal in their growth; however, they are compensated for early in life. Therefore, despite abnormal development, there are no overt symptoms. The abnormally developed cells remain in a "mutant steady state." These cells are then vulnerable to dysfunction and degeneration later in life when they are subjected to stresses and strains, either normal (programmed synaptic elimination during puberty or through the aging process) or pathological (toxic effects of mHTT). In the end, the disease pathology results in neural degeneration with its accompanying cognitive and motor deficits.

The two papers focus on the most recent findings from Kids-HD, a unique brain imaging study of children aged six to 18 years old at risk for HD because they have a parent or grandparent with HD. The review discusses the effects of mHTT on brain development and the study evaluates the effect of mHTT on body development.

According to the authors, there is evidence in children as young as 6 who carry a mutation in the HTT gene, that production of mHTT alters the growth and development of the striatum and related circuitry. The gene contains a sequence of three DNA bases - cytosine-adenine-guanine (CAG) - repeated multiple times. The developmental changes appear to be influenced by the CAG repeat length and occur well before onset of symptoms of the disease. Deficits may then be compensated for by increased activity in other brain circuits, particularly those involving the cerebellum, and are manifest only when compensatory systems are no longer working.

The body development analysis used data from the 186 children in the Kids-HD study. Investigators applied simple measures of growth - height, weight, and the combined BMI measure - to compare changes in two groups - those who carried the CAG repeat expansion mutation in the HTT gene and those who did not.

Around puberty the study began to show an altered trajectory of growth in HTT gene mutation carriers. The pace at which their BMI increased slowed over time so that at by about 17 years old, that group had substantially lower BMI than the group without the gene mutation. Boys with the gene mutation tended to be taller than the control group, but with lower weight; girls with the gene mutation tended to be around the same height, but lower in weight.

Importantly, although the gene mutation carriers were roughly 30 years from the expected time of onset of the disease, the mutant HTT gene had already affected their growth and development. This work is important because it suggests that the mutation is altering the body even before the onset of neurological disease in midlife.

Gene therapy trials are currently underway to evaluate the effectiveness of drugs to slow disease progression in affected individuals, and future trials will ultimately aim to prevent disease onset by delivery of gene therapy to gene mutation carriers - those with mHTT, but no symptoms.

"Gene therapy trials are finally here. However, interfering with a gene responsible for brain development early in life must be done with an abundance of caution," commented Dr. Nopoulos. "Understanding how mHTT affects brain development is vital in the context of planning disease prevention therapies."

HD is a fatal genetic neurodegenerative disease that causes the progressive breakdown of nerve cells in the brain. An estimated 250,000 people in the United States are either diagnosed with, or at risk for, the disease. Symptoms include personality changes, mood swings and depression, forgetfulness and impaired judgment, unsteady gait, and involuntary movements (chorea). Every child of an HD parent has a 50% chance of inheriting the gene. Patients usually survive 10 - 20 years after diagnosis.

A survey of approximately 5,000 Americans suggests that 31.1 percent of the U.S. public does not intend to get the COVID-19 vaccine once it becomes available to them - and the likelihood of vaccine refusal is highest among Black Americans, women and conservatives.

Timothy Callaghan, assistant professor at the Texas A&M University School of Public Health, led the study with the aim of better understanding the intentions of the American public regarding vaccines. The results were recently published in Social Science and Medicine.

According to the study, survey respondents answered a series of questions about their behaviors and attitudes about COVID-19, including why or why not they intend to pursue vaccination. Women are 71 percent more likely to not to pursue vaccination, researchers found, followed by Blacks at 41 percent.

Survey results also showed that politics play a role: each one-point increase in conservatism increases the odds of vaccine refusal by 18 percent. Those who said they intended to vote for President Donald Trump in the presidential election - the survey was conducted in mid-2020 - were 29 percent more likely to refuse vaccination.

The study revealed two top reasons for vaccine refusal: concerns about safety and effectiveness. However, reasons for vaccine reluctance varied across sub-populations.

For instance, women who were surveyed said they are hesitant based on safety concerns and effectiveness, while surveyed Black Americans said their hesitancy stems from similar concerns plus a lack of financial resources or health insurance.

For conservatives, Callaghan points to previous studies that have shown these people are generally less trusting of vaccines, as well as medical and scientific professionals.

The finding that most surprised Callaghan is that Black individuals, who are being infected with COVID-19 and dying at higher rates, are less likely to vaccinate because of a combination of concerns, including those related to safety and affordability.

"This points to the need for the medical community and policymakers to find ways to both build trust in the vaccine in the African American community and to ensure that it is delivered affordably," Callaghan said.

The authors of the study also state that anti-vaccine advocacy groups "have made a concerted effort" to target Black Americans, writing that if they are successful in framing COVID-19 vaccination in terms of past medical abuses against minority groups, it could decrease the likelihood that racial minorities will pursue COVID-19 vaccination, particularly in light of recent findings emphasizing the implications of peripheral trauma."

Now that COVID-19 vaccine-hesitant populations have been identified, Callaghan plans to explore what kind of health interventions and health promotion efforts are most effective in promoting the vaccine to these populations. Additionally, he said it is important to explore the similarities and differences between populations that are generally vaccine hesitant and populations that are hesitant specifically toward the COVID-19 vaccine.

Philadelphia, January 6, 2021 - A multidisciplinary team of researchers led by Children's Hospital of Philadelphia (CHOP) has discovered several genetic markers associated with bone mineral accrual, which could ultimately help identify causes of eventual osteoporosis earlier in life through genetic testing. The findings, which were made possible by following a group of children over several years, were published online by the journal Genome Biology.

Osteoporosis is widely considered a disease of old age. However, the accrual of bone density early in life is critical for achieving optimal bone mass in adulthood and influences bone health throughout a person's life. While studies have looked at genetic markers associated with bone health in adulthood, very few have been performed in children during the most critical period of bone growth.

Additionally, genome-wide association studies (GWAS) have attempted to pinpoint genetic markers associated with bone growth, but an improved understanding of the spatial organization of the human genome can reveal underlying causal genes that may have otherwise been missed.

"We wanted to do a GWAS study that measured bone mineral accrual at multiple time points to provide us with proper longitudinal data at ages when the skeleton is growing and developing," said Struan F.A. Grant, PhD, Director of the Center for Spatial and Functional Genomics and the Daniel B. Burke Endowed Chair for Diabetes Research at CHOP and lead author of the study. "By doing a longitudinal study, we had much greater power in a relatively small cohort of patients."

The study team, which included experts in genetics as well as bone biology, compiled data from approximately 11,000 bone density measurements that were conducted as part of the Bone Mineral Density in Childhood Study (BMDCS), a project headed by Babette S. Zemel, PhD, Associate Program Director of the Clinical and Translational Research Center, Director of the Bionutrition Core Laboratory at CHOP and first author of the study. Once the genetic markers were identified, the researchers used a variant-to-gene mapping method to look for both underlying causal variants as well as corresponding effector genes. They further investigated specific genetic markers, or loci, to characterize their impact on osteoblast function.

Using this method, the researchers identified 40 distinct loci - including 35 that had not been previously reported - associated with bone accrual. Several of these loci are associated with fracture risk later in life. Additionally, the researchers identified two novel effector genes that are potentially causative. Finally, they also identified multiple genetic pathways involved in variation in bone accrual that have important roles in determining whether cells eventually become osteoblasts (bone cells) or adipocytes (fat cells).

"This study is one of many that demonstrates how these loci are manifesting themselves earlier in life than we had previously thought," said Zemel. "In this case, our findings may help us better tailor lifestyle interventions, such as exercise and dietary changes, that will help patients later in life, and they may also lead to novel therapeutic interventions."

All athletes want to be at the top of their game when they compete, but some resort to nefarious approaches to achieve peak muscle growth, speed and agility. Recent developments in gene editing technology could tempt athletes to change their DNA to get an edge. Now, researchers reporting in ACS' Analytical Chemistry demonstrate first steps toward detecting this type of doping both in human plasma and in live mice.

The gene editing method called CRISPR/Cas is a popular way for scientists to precisely change the DNA in many organisms, and it recently gained even more attention when key developers of the method were awarded the 2020 Nobel Prize in Chemistry. With this method, researchers add an RNA molecule and a protein into cells. The RNA molecule guides the protein to the appropriate DNA sequence, and then the protein cuts DNA, like a pair of scissors, to allow alterations. Despite the ethical concerns that have been raised about the method's potential application in humans, some athletes could ignore the risks and misuse it to alter their genes. Because CRISPR/Cas changes DNA, it is considered "gene doping" and is banned by the World Anti-Doping Agency, an independent international organization. A sufficient method to detect CRISPR/Cas gene editing needs to be developed, however. So, Mario Thevis and colleagues wanted to see whether they could identify the protein most likely to be used in this type of doping, Cas9 from the bacteria Streptococcus pyogenes (SpCas9), in human plasma samples and in mouse models.

The team spiked the SpCas9 protein into human plasma, then isolated the protein and cut it into pieces. When the pieces were analyzed by mass spectrometry, the researchers found that they could successfully identify unique components of the SpCas9 protein from the complex plasma matrix. In another experiment, inactivated SpCas9, which can regulate gene expression without altering DNA, was spiked into human plasma samples. With a slight modification, the method allowed the team to purify and detect the inactive form. Finally, the team injected mice with SpCas9 and showed that their concentrations peaked in circulating blood after 2 hours and could be detected up to 8 hours after administration into muscle tissue. The researchers say that although much work still needs to be done, this is an initial step toward a test to pinpoint athletes trying to gain an unfair advantage.

Conductive ink is a great tool for printing flexible electronic circuits on surfaces. But these inks can be costly, they do not work on some materials, and devices to apply them can plug up. Now, scientists report in ACS Applied Electronic Materials that they have developed inexpensive conductive inks for clog-free ballpoint pens that can allow users to "write" circuits almost anywhere -- even on human skin.

Flexible electronics are widely used in applications such as biosensors, electronic skin and energy storage. Recent advances to produce such devices include pens that can draw circuits on surfaces, without the need for a printer. These pens can write on a variety of textures, and some can even draw on rough or irregular surfaces unsuitable for printing. However, it's difficult to make ballpoint pens that maintain good circuit-writing performance because the tips can clog. Another challenge is that the metal inks typically used in these systems are expensive to make. And it's unclear how stable these pens and inks are over time. So Yu Liao, Jun Qian and colleagues set out to design a cheap and effective pen-and-ink system.

Building on prior work, the scientists developed a water-based ink containing conductive carbon particles composed of graphene nanosheets, multiwalled carbon nanotubes and carbon black. Maleic anhydride modified rosin resin was added as a binder to reduce the ink's solid content and viscosity, and xanthan gum was added to stabilize the dispersion so the carbon wouldn't settle out of the ink. The researchers optimized viscosity and the size of the conductive particles relative to the pen tip to create a system that provided stable and smooth writing performance on both flat and irregular surfaces -- even a loofah. Circuits drawn on paper with the pen withstood multiple cycles of folding without deterioration. The ink remained stable after sitting for 12 hours, released no harmful gases during use and cost much less than others reported in the literature, the researchers note. The pens could be used to draw flexible, wearable electronic devices on soft substrates or human skin.

Using copper foil, glass containers and a conventional household microwave oven, University of Wyoming researchers have demonstrated that pulverized coal powder can be converted into higher-value nano-graphite.

The discovery is another step forward in the effort to find alternative uses for Wyoming's Powder River Basin coal, at a time when demand for coal to generate electricity is declining due to concerns about climate change.

In a paper published in the journal Nano-Structures & Nano-Objects, the UW researchers report that they created an environment in a microwave oven to successfully convert raw coal powder into nano-graphite, which is used as a lubricant and in items ranging from fire extinguishers to lithium ion batteries. This "one-step method with metal-assisted microwave treatment" is a new approach that could represent a simple and relatively inexpensive coal-conversion technology.

"This method provides a new route to convert abundant carbon sources to high-value materials with ecological and economic benefits," wrote the research team, led by Associate Professor TeYu Chien, in UW's Department of Physics and Astronomy.

Others involved in the project were Professor Jinke Tang, in the Department of Physics and Astronomy; Associate Professor Brian Leonard, in the Department of Chemistry; Professor Maohong Fan, in the Department of Petroleum Engineering and the School of Energy Resources; graduate students Rabindra Dulal, of Nepal, Joann Hilman, of Laramie, Wyo., Chris Masi, of Syracuse, N.Y., and Teneil Schumacher, of Buffalo, Wyo.; and postdoctoral researchers Gaurab Rimal, of Nepal, and Bang Xu, of China.

While previous research has shown that microwaves can be used to reduce the moisture content of coal and remove sulfur and other minerals, most such methods require specific chemical pretreatment of the coal. In their experiment, the UW researchers simply ground raw Powder River Basin coal into powder.

That powder was then placed on copper foil and sealed in glass containers with a gas mixture of argon and hydrogen, before being placed in a microwave oven. A conventional microwave oven was chosen because of convenience and because it provided the desired levels of radiation.

"By cutting the copper foil into a fork shape, the sparks were induced by the microwave radiation, generating an extremely high temperature of more than 1,800 degrees Fahrenheit within a few seconds," says Masi, lead author of the paper. "This is why you shouldn't place a metal fork inside a microwave oven."

The sparks caused by the microwaves generated the high temperatures necessary to transform the coal powder into polycrystalline graphite, with the copper foil and hydrogen gas also contributing to the process.

While the experiment included microwave durations ranging from 3 to 45 minutes, the optimal duration was found to be 15 minutes.

The researchers say this new method of coal conversion could be refined and performed at a larger scale to yield both a higher quality and quantity of nano-graphite materials.

"Finite graphite reserves and environmental concerns for the graphite extraction procedures make this method of converting coal to graphite a great alternative source of graphite production," the scientists wrote.

Hoppy beers such as pale ales are becoming increasingly popular. One reason is their pleasant fruity aroma that partially stems from compounds called thiols. Brewers have been looking for an accurate way to track thiols in beer, but current methods typically are not sensitive enough or require use of potentially harmful substances. Now, researchers in ACS' Journal of Agricultural and Food Chemistry present an automated, solvent-less process to assess thiols at very low concentrations.

Thiols, along with other compounds such as terpenes and esters, contribute to the enjoyable odors in "hop-forward" beer styles. Although very small amounts of thiols are present in beer, a little bit of these compounds goes a long way toward achieving a hoppy flavor and fruity aroma. Brewers would like more information about these volatile substances, but it's challenging to accurately detect such small quantities. Previous studies have reported complex, multi-step methods for thiol analysis in beer, but the approaches could not measure all of the thiols brewers want to know about, and some processes used harmful mercury-containing compounds. Thiols also contribute to wine aromas, and researchers have used coated polymers that they can put into the air above the beverage to convert aerosolized wine thiols to more easily measureable compounds. The downside is that this method is not sensitive enough to measure the trace concentrations in beer. To develop a more robust analysis, Nils Rettberg and colleagues wanted to modify previous methods and come up with a safer, faster and more sensitive approach.

In initial experiments to develop the new process, the team modified the sample preparation method used in wine analyses to convert aerosolized thiols to compounds with higher analytical sensitivity. Then, they tweaked and applied a tandem mass spectrometry approach to maximally detect and measure the resulting compounds. Finally, the team tested their new method on 13 commercially available beers from multiple countries made with hop varieties expected to have high thiol content. The distribution of thiols within the selected beers was consistent with prior studies. Surprisingly, the team could only detect one of the three expected thiols in a beer with real grapefruit added, suggesting that the fruit itself likely contributed scent compounds other than thiols. The researchers say the method meets the requirements to detect thiols in beer, while also processing samples in a safer, simpler and quicker manner.

ITHACA, N.Y. - For more than seven years, a mysterious wasting disease has nearly killed off sea star populations around the world. Some of these species stand at the brink of extinction.

New Cornell University-led research suggests that starfish, victims of sea star wasting disease (SSWD), may actually be in respiratory distress - literally "drowning" in their own environment - as elevated microbial activity derived from nearby organic matter and warm ocean temperatures rob the creatures of their ability to breathe.

"As humans, we breathe, we ventilate, we bring air into our lungs and we exhale," said Ian Hewson, professor of microbiology at Cornell University. "Sea stars diffuse oxygen over their outer surface through little structures called papulae, or skin gills. If there is not enough oxygen surrounding the papulae, the starfish can't breathe."

The research, "Evidence That Microorganisms at the Animal-Water Interface Drive Sea Star Wasting Disease," was published in the journal Frontiers in Microbiology.

According to Hewson, ocean conditions lead to the production of unusual amounts of organic material, which he said prompts bacteria to thrive. As bacteria consume the organic matter, they deplete the oxygen in the water - creating a low-oxygen micro-environment that surrounds starfish and leads to deflation, discoloration, puffiness, and limb twisting or curling.

"It's a cascade of problems that starts with changes in the environment," Hewson said, explaining that most of the organic matter comes from microscopic algae exudation (a discharge), zooplankton excretion and egestion, and from decaying animal carcasses. This stimulates a group of bacteria called copiotrophs, which survive on carbon and rapidly consume organic matter, he said.

The copiotrophs respire, he said, so while absorbing the organic matter, they deplete oxygen in the sea star's watery space.

"It's organic matter concentrations in the water," he said. "If you have a dead and rotting starfish next to starfish that are healthy, all of that dead one's organic matter drifts and fuels the bacteria, creating a hypoxic environment. It looks like disease is being transmitted."

Hewson said that while more scientific work must be done, "This reframes the discussion about marine disease ecology, which has focused on pathogenic disease," he said. "We should now include microorganisms that don't directly cause the pathology, since they may hold a key to affecting sea star health."

Young adults ages 18-24 years old in the U.S. say that porn is their most helpful source of information about how to have sex, according to a new study led by a Boston University School of Public Health (BUSPH) researcher published in the journal Archives of Sexual Behavior.

In the nationally representative survey, a quarter of young adults said porn was their most helpful source of information about how to have sex. Slightly less than a quarter said sexual partners were the most helpful source, and fewer pointed to friends, parents, media, or healthcare professionals. However, female respondents were much more likely than male respondents to report that their partners were the most helpful source of information about how to have sex. Heterosexual men were most likely to say that porn was their most helpful source of information about how to have sex.

"The evidence suggests that young adults, and in particular heterosexual men, undervalue talking to their partners about what is pleasurable--too many of them may believe that it's possible to be 'good at sex' independent of any feedback from a particular sex partner, which is a belief they may be getting from pornography," says study lead author Dr. Emily Rothman, professor of community health sciences at BUSPH.

Rothman and colleagues at Indiana University School of Public Health-Bloomington used data from the Indiana University-based 2015 National Survey of Sexual Health and Behavior, and analyzed responses from 357 young adults (18-24 years old) and 324 adolescents (14-17 years old) who said that they had gotten helpful information about how to have sex. (Nearly as many young adults and adolescents in the survey reported that they hadn't gotten any helpful information.)

Among 14-17-year-old adolescents, parents were the leading source of information, followed by friends. Only 8% of the adolescents said porn was the most helpful source of information. However, among adolescents who had never had a helpful conversation with parents about sex, media (23.4%) and sexual partners (12.8%) were their primary sources of information. Like their older peers, boys were also more likely than girls to report that porn was their most helpful source of information about how to have sex.

"The good news is that, when parents have conversations with their teenage children about sex, we think that their children are listening and are less likely to see porn as a good source of information," Rothman says.

"The bad news is that young adults are misunderstanding what porn is there for. Most free, online pornography is there for entertainment and to make money for the creators. It isn't there to teach you what you are supposed to do when you are having sex."

From a public health perspective, Rothman says it is worrisome that a sizable percentage of young adults consider porn a helpful source of information about how to have sex. "Comprehensive sex education that teaches what I think of as 'sexual social skills,' or interpersonal communication about sex, is needed and important, and research that helps us determine how to teach young people how to have fulfilling, safer, consensual sex is crucial."

New Rochelle, NY, January 6, 2021--Women physicians feel pressured to spend more time in work-related citizenship tasks, based largely on their age and race. Nearly half of women perceived that they spent more time on citizenship tasks than their male colleagues, according to a study in Journal of Women's Health. Click here to read the article now.

"When compared to their younger counterpart, women physicians older than 49 years stated to feel obligated to volunteer for these tasks because of their age," state Priscila Armijo, MD, University of Nebraska Medical Center, and coauthors. "We also found that a higher proportion of women of color physicians perceived race as a factor in feeling obligated to volunteer for work-related citizenship tasks, when compared to white women physicians."

In the accompanying editorial entitled, "Abolish the Minority Woman Tax!" José Rodríguez, MD, University of Utah Health, Family and Preventive Medicine, and coauthors write: "The specific obstacles faced by underrepresented minority (URM) faculty in academic medicine are best described as a system of disparities or taxes. URM faculty take on additional work, including diversity efforts land clinical responsibilities, while experiencing the challenges of racism, isolation, disparate compensation, and a lack of mentorship. This minority women tax is an additional injustice that must be named, acknowledged, and eliminated."

They are as thin as a hair, only a hundred thousand times thinner--so-called two-dimensional materials, consisting of a single layer of atoms, have been booming in research for years. They became known to a wider audience when two Russian-British scientists were awarded the Nobel Prize in Physics in 2010 for the discovery of graphene, a building block of graphite. The special feature of such materials is that they possess novel properties that can only be explained with the help of the laws of quantum mechanics and that may be relevant for enhanced technologies. Researchers at the University of Bonn (Germany) have now used ultracold atoms to gain new insights into previously unknown quantum phenomena. They found out that the magnetic orders between two coupled thin films of atoms compete with each other. The study has been published in the journal Nature.

Quantum systems realize very unique states of matter originating from the world of nanostructures. They facilitate a wide variety of new technological applications, e.g. contributing to secure data encryption, introducing ever smaller and faster technical devices and even enabling the development of a quantum computer. In the future, such a computer could solve problems which conventional computers cannot solve at all or only over a long period of time.

How unusual quantum phenomena arise is still far from being fully understood. To shed light on this, a team of physicists led by Prof. Michael Köhl at the Matter and Light for Quantum Computing Cluster of Excellence at the University of Bonn are using so-called quantum simulators, which mimic the interaction of several quantum particles--something that cannot be done with conventional methods. Even state-of-the-art computer models cannot calculate complex processes such as magnetism and electricity down to the last detail.

Ultracold atoms simulate solids

The simulator used by the scientists consists of ultracold atoms--ultracold because their temperature is only a millionth of a degree above absolute zero. The atoms are cooled down using lasers and magnetic fields. The atoms are located in optical lattices, i.e. standing waves formed by superimposing laser beams. This way, the atoms simulate the behavior of electrons in a solid state. The experimental setup allows the scientists to perform a wide variety of experiments without external modifications.

Within the quantum simulator, the scientists have, for the first time, succeeded in measuring the magnetic correlations of exactly two coupled layers of a crystal lattice. "Via the strength of this coupling, we were able to rotate the direction in which magnetism forms by 90 degrees--without changing the material in any other way," first authors Nicola Wurz and Marcell Gall, doctoral students in Michael Köhl's research group, explain.

To study the distribution of atoms in the optical lattice, the physicists used a high-resolution microscope with which they were able to measure magnetic correlations between the individual lattice layers. In this way, they investigated the magnetic order, i.e. the mutual alignment of the atomic magnetic moments in the simulated solid state. They observed that the magnetic order between layers competed with the original order within a single layer, concluding that the more strongly layers were coupled, the more strongly correlations formed between the layers. At the same time, correlations within individual layers were reduced.

The new results make it possible to better understand the magnetism propagating in the coupled layer systems at the microscopic level. In the future, the findings are to help make predictions about material properties and achieve new functionalities of solids, among other things. Since, for example, high-temperature superconductivity is closely linked to magnetic couplings, the new findings could, in the long run, contribute to the development of new technologies based on such superconductors.

The Matter and Light for Quantum Computing (ML4Q) Cluster of Excellence

The Matter and Light for Quantum Computing (ML4Q) Cluster of Excellence is a research cooperation by the universities of Cologne, Aachen and Bonn, as well as the Forschungszentrum Jülich. It is funded as part of the Excellence Strategy of the German federal and state governments. The aim of ML4Q is to develop new computing and networking architectures using the principles of quantum mechanics. ML4Q builds on and extends the complementary expertise in the three key research fields: solid-state physics, quantum optics, and quantum information science.

The Cluster of Excellence is embedded in the Transdisciplinary Research Area "Building Blocks of Matter and Fundamental Interactions" at the University of Bonn. In six different TRAs, scientists from a wide range of faculties and disciplines come together to work on future-relevant research topics.

LA JOLLA--New data suggest that nearly all COVID-19 survivors have the immune cells necessary to fight re-infection.

The findings, based on analyses of blood samples from 188 COVID-19 patients, suggest that responses to the novel coronavirus, SARS-CoV-2, from all major players in the "adaptive" immune system, which learns to fight specific pathogens, can last for at least eight months after the onset of symptoms from the initial infection.

"Our data suggest that the immune response is there--and it stays," LJI Professor Alessandro Sette, Dr. Biol. Sci., who co-led the study with LJI Professor Shane Crotty, Ph.D., and LJI Research Assistant Professor Daniela Weiskopf, Ph.D.

"We measured antibodies, memory B cells, helper T cells and killer T cells all at the same time," says Crotty. "As far as we know, this is the largest study ever, for any acute infection, that has measured all four of those components of immune memory."

The findings, published in the January 6, 2021, online edition of Science, could mean that COVID-19 survivors have protective immunity against serious disease from the SARS-CoV-2 virus for months, perhaps years after infection.

The new study helps clarify some concerning COVID-19 data from other labs, which showed a dramatic drop-off of COVID-fighting antibodies in the months following infection. Some feared that this decline in antibodies meant that the body wouldn't be equipped to defend itself against reinfection.

Sette explains that a decline in antibodies is very normal. "Of course, the immune response decreases over time to a certain extent, but that's normal. That's what immune responses do. They have a first phase of ramping up, and after that fantastic expansion, eventually the immune response contracts somewhat and gets to a steady state," Sette says.

The researchers found that virus-specific antibodies do persist in the bloodstream months after infection. Importantly the body also has immune cells called memory B cells at the ready. If a person encounters SARS-CoV-2 again, these memory B cells could reactivate and produce SARS-CoV-2 antibodies to fight re-infection.

The SARS-CoV-2 virus uses its "spike" protein to initiate infection of human cells, so the researchers looked for memory B cells specific for the SARS-CoV-2 spike. They found that spike-specific memory B cells actually increased in the blood six months after infection.

COVID-19 survivors also had an army of T cells ready to fight reinfection. Memory CD4+ "helper" T cells lingered, ready to trigger an immune response if they saw SARS-CoV-2 again. Many memory CB8+ "killer" T cells also remained, ready to destroy infected cells and halt a reinfection.

The different parts of the adaptive immune system work together, so seeing COVID-fighting antibodies, memory B cells, memory CD4+ T cells and memory CD8+ T cells in the blood more than eight months following infection is a good sign.

"This implies that there's a good chance people would have protective immunity, at least against serious disease, for that period of time, and probably well beyond that," says Crotty.

The team cautions that protective immunity does vary dramatically from person to person. In fact, the researchers saw a 100-fold range in the magnitude of immune memory. People with a weak immune memory may be vulnerable to a case of recurrent COVID-19 in the future, or they may be more likely to infect others.

"There are some people that are way down at the bottom of how much immune memory they have, and maybe those people are a lot more susceptible to reinfection," says Crotty.

"It looks like people who have been infected are going to have some degree of protective immunity against re-infection," adds Weiskopf. "How much protection remains to be established."

The fact that immune memory against SARS-CoV-2 is possible is also a good sign for vaccine developers. Weiskopf emphasizes that the study tracked responses to natural SARS-CoV-2 infection, not immune memory after vaccination.

"It is possible that immune memory will be similarly long lasting similar following vaccination, but we will have to wait until the data come in to be able to tell for sure," says Weiskopf. "Several months ago, our studies showed that natural infection induced a strong response, and this study now shows that the responses lasts. The vaccine studies are at the initial stages, and so far have been associated with strong protection. We are hopeful that a similar pattern of responses lasting over time will also emerge for the vaccine-induced responses."

The researchers will continue to analyze samples from COVID-19 patients in the coming months and hope to track their responses 12 to 18 months after the onset of symptoms.

"We are also doing very detailed analyses at a much, much higher granularity on what pieces of the virus are recognized," says Sette. "And we plan to evaluate the immune response not only following natural infection but following vaccination."

The team is also working to understand how immune memory differs across people of different ages and how that may influence COVID-19 case severity.

E. coli food poisoning is one of the worst food poisonings, causing bloody diarrhea and kidney damage. But all the carnage might be just an unintended side effect, researchers from UConn Health report in the 27 November issue of Science Immunology. Their findings might lead to more effective treatments for this potentially deadly disease.

Escherichia coli are a diverse group of bacteria that often live in animal guts. Many types of E. coli never make us sick; other varieties can cause traveler's diarrhea. But swallowing even a few cells of the type of E. coli that makes Shiga toxin can make us very, very ill. Shiga toxin damages blood vessels in the intestines, causing bloody diarrhea. If Shiga toxin gets into the bloodstream it can cause kidney failure.

"This is especially common in children; about 15% of kids with Shiga toxin-producing E. coli infections get kidney disease, and some can suffer long term kidney damage," says UConn Health immunologist Sivapriya Vanaja.

A group of Shiga toxin-producing E. coli called enterohemorrhagic E. coli, or EHEC, are especially common in the United States. When you hear that a batch of romaine lettuce is being recalled because of a dangerous outbreak of food poisoning, it's almost certainly due to EHEC.

EHEC normally live in cattle without making them sick. It used to be relatively common to have EHEC outbreaks coming from unhygienically prepared ground meat, but stringent regulations on slaughterhouses have made this less common. Now it's more likely for EHEC to appear on vegetables grown in fields adjacent to cattle or manure runoff.

But no matter where it comes from, once EHEC bacteria get inside a human, the infection is hard to treat. Antibiotics tend to make it worse--when the bacteria feel themselves dying, they make more Shiga toxin. And EHEC are very good at inhibiting the part of the immune system that normally responds early to this kind of infection, allowing them to grow unchecked in the human gut.

In a study led by Morena Havira, a postdoctoral fellow in Vanaja's lab, the team wanted to know how EHEC suppresses the immune system. The body normally responds to early stages of E. coli infections by activating an enzyme that kicks off an alarm inside cells. The cell bursts open to release a cloud of warning molecules that call other parts of the immune system to come and fight the bacteria.

But EHEC squashes that early response. To figure out how it does that, Vanaja and her colleagues decided to see which individual gene in EHEC was responsible. They took many different varieties of EHEC from a bacterial mutant library, and infected immune cells with them.

The team found that cells infected with EHEC that was missing the gene for Shiga toxin mustered a higher immune response compared to normal EHEC.

"It was surprising. Shiga toxin is very well-studied for its toxic activity; it wasn't known that it had another function," Dr. Vanaja says. So Shiga toxin's stealthy suppression of the immune system may have a link to all the bloody drama that ensues. Spurred on by this exciting observation, they conducted a series of detailed molecular studies, which revealed that Shiga toxin blocks a protein from bursting open the infected cell and alerting the body of infection.

Now that Vanaja and her colleagues know the specific molecular step Shiga toxin interferes with inside the immune cells, they are trying to figure out how, exactly, it blocks it. Once they know that, they may be able to find medicines that prevent toxin from interfering with immune responses.