The human body can be genetically inclined to attack its own cells, destroying the beta cells in the pancreas that make insulin, which helps convert sugar into energy. Called Type 1 diabetes, this disorder can occur at any age and can be fatal if not carefully managed with insulin shots or an insulin pump to balance the body’s sugar levels.
But there may be another, personalized option on the horizon, according to Xiaojun “Lance” Lian, associate professor of biomedical engineering and biology at Penn State. For the first time, Lian and his team converted human stem cells into beta cells capable of producing insulin using only small molecules in the laboratory, making the process more efficient and cost-effective.
Stem cells can become other cell types through signals in their environment, and some mature cells can revert to stem cells — induced pluripotency. The researchers found that their approach worked for human embryonic and induced pluripotent stem cells, both derived from federally approved stem cell lines. According to Lian, the effectiveness of their approach could reduce or eliminate the need for human embryonic stem cells in future work.They published their results today (Aug. 26) in Stem Cell Reports.
“Diabetes is a severe disease in the United States and around the world,” Lian said. “The patient’s own immune cells kill their ability to produce insulin and regulate their glucose levels. We thought stem cells could potentially solve the problem and allow a person to regulate their insulin and glucose levels appropriately again.”
Stem cells can become any cell type through environmental conditions or laboratory interference. The trick, Lian said, is figuring out the precise conditions to sway a stem cell to become a functioning version of the desired cell type.
“If we could convert stem cells into pancreatic beta cells and transfer them back to the patient, it might be possible to cure diabetes,” Lian said. “It’s a difficult question. Scientists have been trying to find the solution for more than 20 years. Our lab realized we had to take a different approach.”
In previous attempts, according to Lian, researchers used growth factors, or groups of proteins, to manipulate stem cells into various cell types. Growth factors, however, are expensive and unstable, resulting in a costly and inefficient manufacturing process.

Fine particle pollution may be one reason why Black women have double the risk of developing Alzheimer’s than white women, suggests new research from the Keck School of Medicine of USC.
For decades, research has shown the risk for developing Alzheimer’s disease in the United States is dramatically higher among African American populations than in non-Hispanic white populations. Scientists have suspected a variety of contributing factors, but the underlying reasons have remained unclear.
Now, a new study in The Journals of Gerontology, conducted in collaboration with researchers across the country, points to environmental neurotoxins — specifically, ambient fine particles in the air known as PM2.5 — as possible culprits in the disproportionate number of African American, particularly Black women, affected by dementia.
Zeroing in on fine particle pollution as a factor in racial/ethnic disparities
“Data increasingly show that older people are more likely to develop dementia if they live in locations with high PM2.5, and African American populations are more likely to live in neighborhoods near polluting facilities — like power-generating and petrochemical plants — that emit the particulate matter,” said corresponding author Jiu-Chiuan Chen, MD, associate professor of population and public health sciences at the Keck School of Medicine of USC. “Our study demonstrates that older Black women live in locations with higher levels of PM2.5, and we ask whether their elevated exposure could account for the higher numbers of Alzheimer’s cases. The evidence does reveal a positive association.”
After adjusting for risk factors such as smoking, education, income, diabetes, hypertension and BMI, Black women still had roughly two times greater a risk of developing Alzheimer’s disease than white women, the researchers found.
Chen and his colleagues report two major novel findings in their study, both with important implications. The first is that the increased risk of Alzheimer’s disease in older Black women may be partly explained by their elevated exposure to PM2.5; the second is that older Black women are more susceptible to its adverse effects.
“Our work offers the scientific community an important perspective on the study of dementia; namely, that we must have a greater awareness of environmental racism that can impact brain aging and disproportionately affect people of color,” Chen says. “There is also a key regulatory takeaway, which is that we have to continue enforcing the Clean Air Act, with its mandate to provide a safe margin for air quality that will protect the health of susceptible populations.”
Air pollution and brain health
The study grew out of a long-standing partnership between USC faculty and researchers with the Women’s Health Initiative Memory Study based at Wake Forest University. This research focused on studying Black women compared to non-Hispanic white women, because Black women carry the greatest burden of Alzheimer’s disease and related dementias in the US. As it begins to unravel the complexities of racial disparities in Alzheimer’s disease, the study also elucidates the need for future research.
“Our study suggests that PM2.5 may contribute to the difference in Alzheimer’s disease risk based on race, and we also demonstrated that older African American women may be more susceptible to the particulate matter, but we still don’t know why,” Chen says. “Why are these particles more neurotoxic to Black women than to non-Hispanic whites? Going forward, we plan to look for answers by studying the effects of things like nutrition and brain structure.”
When he was first recruited to USC in 2009, Chen set out to develop a new research program to study the health effects of air pollution exposure beyond its well-known impact on airways and lungs. “At the time, I was one of the first faculty members studying environmental influences on brain health,” Chen recalls. “Today, the university has several leading programs, funded by the National Institutes of Health, examining how air pollution exposures affect neurodevelopment and brain aging. An increasing number of USC faculty are trying to better understand whether and why air pollution can cause more damage to the human brains in minority populations or communities with social disadvantages. Our study is just the beginning of vital scientific work that needs to be done.”

COVID-19 vaccines remain effective, but their potency has diminished in recent months, according to a nationwide study at eight sites, including Salt Lake City, Utah.
Scientists calculated vaccine effectiveness to be 80% in a large group of fully vaccinated frontline workers between December 2020 and August 2021, compared to 91% in earlier surveys. The estimates were based on COVID-19 RT-PCR testing and did not measure whether there were changes in efficacy in protecting against severe disease, including hospitalization and death.
The authors say one reason for the change could be waning immunity, a decrease in the strength of the body’s vaccine-activated defenses against the virus. The difference may also reflect the fact that the vaccines are not as effective against the highly contagious Delta variant of the SARS-CoV-2 virus, which since June 2021, has become the most common cause of COVID-19 in the U.S.
“The vaccines are still helping save lives and keep people from getting sick despite a slight diminishing return over many months,” explains Matthew Thiese, Ph.D., associate professor at the University of Utah Rocky Mountain Center for Occupational and Environmental Health (RMCOEH). “These data, combined with other data, demonstrate that vaccinated people are much less likely to get COVID-19 and are much less likely to be hospitalized.” Thiese is co-investigator and RMCOEH assistant professor Sarang Yoon, D.O., is primary investigator of the HEROES-RECOVER (Research on the Epidemiology of SARS-CoV-2 in Essential Response Personnel) study site in Utah.
The study published on August 24 in the Morbidity Mortality Weekly Report (MMWR) from the Centers for Disease Control and Prevention (CDC). Additional study sites in the HEROES-RECOVER network are Phoenix, Tucson, and other areas in Arizona; Miami, Florida; Portland, Oregon; Duluth, Minnesota; and Temple, Texas.
The network followed 4,136 health care personnel, first responders, and essential workers who had not previously had COVID-19. Study participants submitted samples for RT-PCR testing on a weekly basis and 2,976 participants were fully vaccinated within the study period, receiving either the Pfizer-BioNtech (65%), Moderna (33%), or Johnson & Johnson (2%) vaccines. Test results from these groups between December 14, 2020, to August 14, 2021, show that: Among unvaccinated study participants, 194 infections occurred in 181,357 person-days (combined total of number of days of testing for this group). Among fully vaccinated participants, 34 infections occurred in 454,832 person-days.During that time period, the vaccines were 80% effective for all fully vaccinated study participants, but preliminary data indicate that vaccines may wane in intensity over time with lower effectiveness after five or more months following full vaccination. In addition, the vaccines appeared to be less effective during the last 43 days of the study period when Delta became the predominant virus variant. However, because sample sizes were small, these results were not statistically significant. These trends will be investigated further in future studies.
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There’s been a significant rise in the number of people requesting help for Binge Eating Disorder over the past three years, according to the charity Beat.The condition is a serious mental illness, where people eat large quantities of food without feeling like they’re in control of what they’re doing.Beat says calls about binge eating to its helpline more than tripled in the past three years, with much of the increase taking place during the coronavirus lockdown.University student Martha Pierce, 20, told BBC Breakfast about her experience of the disorder, and the struggle to get help.If you or someone you know has been affected by issues in this story, visit the BBC Action Line.

SharecloseShare pageCopy linkAbout sharingimage sourceGetty ImagesA Florida doctor has been removed from his hospital job amid reports that he offered parents medical letters to circumvent school mask requirements.Local school rules require masking unless a medical reason is given. Tallahassee physician Brian Warden was reportedly advertising such medical exemption letters for $50 (£36.46) on a Facebook group for anti-mask parents.The issue of mask mandates in schools has sparked debates nationwide as the new academic year begins.Dr Warden’s employer, the Capitol Regional Medical Center in Tallahassee, told the BBC that it began the process of removing him from providing services to their patients “immediately” upon learning of his actions. Dr Warden was reportedly offering the letters on the Parents Against Masks group, according to local media. He said he was not signing letters affiliated with a hospital or medical group.In one post, the Tallahassee Democrat newspaper reported, Dr Warden advertised that he could provide a letter on signed stationary. Dr Warden said he was not able to provide comment to the paper.Florida has been in the national spotlight over the ongoing mask row between school officials, parents and the government.On Friday, a judge is expected to rule on a lawsuit challenging Governor Ron DeSantis’s ban on mask mandates in schools. Mr DeSantis has said he believes that parents, rather than schools, should decide whether students wear masks. At least eight school districts across the state have defied the governor’s order, including its largest school district, Miami-Dade County, and Leon County, where Dr Warden was employed.Covid-19 cases have surged in Florida due to the contagious Delta variant, with more people admitted to hospital and dying of the virus than at any other point during the pandemic. Funeral homes have said that they are unable to keep up. News Channel 8 reported one home as saying bodies awaiting cremation were “stacked to the ceiling”. Hospitals have also been stretched thin. The crisis has prompted Orlando’s mayor to ask residents to conserve water to preserve liquid oxygen, which is being used to treat coronavirus patients. The state now accounts for 20% of all paediatric Covid-19 cases. Though the Delta variant is affecting more younger people, fewer than 2% of children’s cases require hospital care, and no more than 0.03% have resulted in death, according to the American Academy of Pediatrics.

COVID-19 survivors report significantly higher symptoms of post-traumatic stress, and these symptoms are associated with changes to the brain’s connectivity, according to a study coauthored by Vince Calhoun, Distinguished Professor of Psychology at Georgia State University and director of the Center for Translational Research in Neuroimaging and Data Science (TReNDS).
Although COVID-19 is primarily considered a respiratory disease, experts recognize it also affects the nervous system, sometimes causing severe neurological symptoms. Some COVID-19 survivors also experience long-term mental health problems, including anxiety, depression and post-traumatic stress disorder.
Few studies have examined functional abnormalities in the brain, which might reveal the physiological processes that underlie prolonged mental health symptoms in COVID-19 survivors.
In this paper, published in Neurobiology of Stress, the researchers set out to determine whether survivors experience functional disruption of large-scale brain networks, collections of discrete and widespread regions of the brain that work together to perform complex cognitive tasks. They collected functional MRI (fMRI) data and self-reported post-traumatic stress symptoms from 50 COVID-19 survivors, along with matched control subjects. The COVID-19 survivors were discharged between February and March 2020 from hospitals in Wuhan, China, and were tested about six months after their discharge.
The findings showed COVID-19 survivors self-reported significantly more symptoms of post-traumatic stress than the controls. The study also revealed COVID-19 survivors exhibited abnormal patterns of brain connectivity over time, which were significantly associated with greater post-traumatic stress symptoms.
“Until recently,” said Calhoun, a Georgia Research Alliance Eminent Scholar, “analysis approaches used for fMRI data assumed that the brain’s functional connectivity was static. But we now have approaches that can capture dynamic functional brain connectivity, showing the way brain patterns change over time in fundamental and reoccurring ways.”
The researchers identified three distinct, reoccurring states of functional connectivity in the subjects’ brains. The COVID-19 survivors showed an increased occurrence of a particular state marked by patterns of connections between brain networks involving sensorimotor functions and visual networks.
“When we looked within the COVID-19 survivor group, we also found a significant relationship between the severity of their post-traumatic stress symptoms and how often their brain patterns are in that state,” said Calhoun. “If they spend more time in that state, they tend to have higher values on those symptom scales.”
“Our findings provide evidence that COVID might affect transient brain dynamics rather than its ongoing activity,” said Zening Fu, the study’s first author and a research scientist at TReNDS.
The results highlight the importance of evaluating transient, time-varying functional network changes among COVID-19 survivors, although Calhoun notes there are still many unanswered questions, including why this one brain state is linked to post-traumatic stress. The research team is also interested in replicating the study using other data and looking at changes within subjects before and after contracting COVID-19.
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Neuroinflammation is the key driver of the spread of pathologically misfolded proteins in the brain and causes cognitive impairment in patients with Alzheimer’s disease, researchers from the University of Pittsburgh School of Medicine reveal in a paper published today in Nature Medicine.
For the first time ever, the researchers showed in living patients that neuroinflammation — or activation of the brain’s resident immune cells, called microglial cells — is not merely a consequence of disease progression; rather, it is a key upstream mechanism that is indispensable for disease development.
“As a young resident neurologist in my home country of Brazil, I noticed that many patients with Alzheimer’s disease are left neglected and without access to appropriate care,” said lead author Tharick Pascoal, M.D., Ph.D., assistant professor of psychiatry and neurology at Pitt. “Our research suggests that combination therapy aimed to reduce amyloid plaque formation and limit neuroinflammation might be more effective than addressing each pathology individually.”
Alzheimer’s disease is characterized by the accumulation of amyloid plaques — protein aggregates lodged between nerve cells of the brain — and clumps of disordered protein fibers, called tau tangles, forming inside the nerve cells. Although studies in cultured cells and lab animals amassed ample evidence that microglial activation drives the spread of tau fibers in Alzheimer’s disease, this process has never been proven in humans.
The study findings suggest that targeting neuroinflammation might be beneficial for people with early-stage Alzheimer’s disease and that it might help reverse or at least slow down the accumulation of pathologic tau protein in the brain and stave off dementia.
To determine the mechanism by which disordered tangles of tau protein fibers and amyloid plaques spread across the brain and lead to dementia, the researchers used live imaging to look deep into the brains of people with various stages of Alzheimer’s disease and healthy aging individuals.
The researchers found that neuroinflammation was more prevalent in older people and that it was even more pronounced in patients with mild cognitive impairments and those with Alzheimer’s disease-associated dementia. Bioinformatics analysis confirmed that tau propagation depended on microglial activation — it is a key element that links the effects of amyloid plaque aggregation to tau spread and, ultimately, cognitive impairment and dementia.
“Many elderly people have amyloid plaques in their brains but never progress to developing Alzheimer’s disease,” said Pascoal. “We know that amyloid accumulation on its own is not enough to cause dementia — our results suggest that it is the interaction between neuroinflammation and amyloid pathology that unleashes tau propagation and eventually leads to wide-spread brain damage and cognitive impairment.”
Pedro Rosa-Neto, M.D., Ph.D., of McGill University, is senior and co-corresponding author of this paper. Other authors are from McGill University; University of Gothenburg, Sweden; University of Antwerp, Belgium; University of Toronto, Canada; Imperial College London, UK; Sahlgrenska University Hospital, Mölndal, Sweden; and Cornell University.
This research was supported by the Alzheimer’s Association (# AACSF-20-648075, NIRG-12-92090 and NIRP-12-259245), Weston Brain Institute and the Canadian Institutes of Health Research (no. MOP-11-51-31).
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A new study published in the journal Nature estimates that 103 million Americans, or 31 percent of the U.S. population, had been infected with SARS-CoV-2 by the end of 2020. Columbia University Mailman School of Public Health researchers modeled the spread of the coronavirus, finding that fewer than one-quarter of infections (22%) were accounted for in cases confirmed through public health reports based on testing.
The study is the first to comprehensively quantify the overall burden and characteristics of COVID-19 in the U.S. during 2020. The researchers simulated the transmission of SARS-CoV-2 within and between all 3,142 U.S. counties using population, mobility, and confirmed case data.
Infections were more widespread in some areas of the country
In areas of the upper Midwest and Mississippi valley, including the Dakotas, Minnesota, Wisconsin and Iowa, more than 60 percent of the population is estimated to have been infected by the end of 2020. In five metropolitan areas the researchers examined, 48 percent of residents of Chicago, 52 percent of Los Angeles, 42 percent of Miami, 44 percent of New York City, and 27 percent of people in Phoenix, had been infected in the same timeframe.
Testing picked up on a growing number of infections but offered an incomplete picture
The portion of confirmed cases reflected in the study’s estimates, i.e. the ascertainment rate, rose from 11 percent in March to 25 percent in December, reflecting improved testing capacity, a relaxation of initial restrictions on test usage, and increasing recognition, concern, and care-seeking among the public. However, the ascertainment rate remained well below 100 percent, as individuals with mild or asymptomatic infections, who could still spread the virus, were less likely to be tested.

An analysis of data from 1.5 million people has identified 579 locations in the genome associated with a predisposition to different behaviors and disorders related to self-regulation, including addiction and child behavioral problems.
With these findings, researchers have constructed a genetic risk score — a number reflecting a person’s overall genetic propensity based on how many risk variants they carry — that predicts a range of behavioral, medical and social outcomes, including education levels, obesity, opioid use disorder, suicide, HIV infections, criminal convictions and unemployment.
“[This study] illustrates that genes don’t code for a particular disorder or outcome; there are no genes ‘for’ substance use disorder, or ‘for’ behavior problems,” said joint senior author Danielle Dick, Ph.D., Commonwealth Professor of Psychology and Human and Molecular Genetics at Virginia Commonwealth University. “Instead, genes influence the way our brains are wired, which can make us more at risk for certain outcomes. In this case, we find that there are genes that broadly influence self-control or impulsivity, and that this predisposition then confers risk for a variety of life outcomes.”
The study, “Multivariate analysis of 1.5 million people identifies genetic associations with traits related to self-regulation and addiction,” was published today in the journal Nature Neuroscience and was conducted by a consortium of 26 researchers at 17 institutions in the United States and the Netherlands.
It was led by Dick; Philipp Koellinger, Ph.D., professor of social science genetics at the University of Wisconsin Madison and Vrije Universiteit Amsterdam; Kathryn Paige Harden, Ph.D., professor of psychology at the University of Texas at Austin; and Abraham A. Palmer, Ph.D., professor of psychiatry at the University of California, San Diego.
The study is one of the largest genome-wide association studies ever conducted, pooling data from an effective sample size of 1.5 million people of European descent. The researchers’ genetic risk score has one of the largest effect sizes — a measurement of the prediction power — of any genetic risk score for a behavioral outcome to date.

Turbulence is everywhere — in the movement of the wind, the ocean waves and even magnetic fields in space. It can also be seen in more transient phenomena, like smoke billowing from a chimney, or a cough.
Understanding this latter type of turbulence — called puff turbulence — is important not only for the advancement of fundamental science, but also for practical health and environmental measures, like calculating how far cough droplets will travel, or how pollutants released from a chimney or cigarette might disperse into the surroundings. But creating a complete model of how turbulent puffs of gases and liquids behave has so far proven elusive.
“The very nature of turbulence is chaotic, so it’s hard to predict,” said Professor Marco Edoardo Rosti, who leads the Complex Fluids and Flows Unit at Okinawa Institute of Science and Technology Graduate University (OIST). “Puff turbulence, which occurs when the ejection of a gas or liquid into the environment is disrupted, rather than continuous, has more complicated characteristics, so it’s even more challenging to study. But it’s of vital importance — especially right now for understanding airborne transmission of viruses like SARS-CoV-2.”
Until now, the most recent theory was developed in the 1970s, and focused on the dynamics of a puff only at the scale of the puff itself, like how fast it moved and how wide it spread.
The new model, developed in a collaboration between Prof. Rosti from OIST, Japan and Prof. Andrea Mazzino from the University of Genova in Italy, builds on this theory to include how minute fluctuations within the puff behave, and how both large-scale and small-scale dynamics are impacted by changes in temperature and humidity. Their findings were published in Physical Review Letters on August 25th 2021.
Interestingly, the scientists found that at cooler temperatures (15°C or lower), their model deviated from the classical model for turbulence.