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A study of over 4,000 pregnant New Zealand women suggests the country can improve babies’ health and reduce medical risks for mums by changing how gestational diabetes is diagnosed. The study assessed the value of lowering the blood-sugar threshold for diagnosis.
The University of Auckland researchers, based at the Liggins Institute, tested the blood-sugar level currently used in Aotearoa New Zealand to diagnose diabetes that can develop during pregnancy against a lower level commonly used overseas.
“Treatment for gestational diabetes improves mothers’ and babies’ health but it has been unclear what level of blood sugar should be used to make the diagnosis” says lead investigator, Professor Caroline Crowther.
A total of 4061 women were randomised into the two diagnostic groups.In the group where the lower blood-sugar threshold was used, twice as many women were diagnosed with gestational diabetes and treated — 15.3% of women (310 out of 2022) compared with 6.1% of women (124 of 2039) in the higher blood-sugar threshold group).
Overall, the chance of having a baby born larger than expected for its gestation, which can cause complications during the birth, — the primary outcome of the trial, published in the New England Journal of Medicine on 18 August — was not different between the groups.
Babies born to mothers in the lower blood sugar diagnostic group were more likely to be treated for low blood sugar after birth and the women were more likely to have labour induced, receive pharmaceutical treatment for diabetes, and use more health services compared with women in the higher blood sugar diagnostic group.

Poverty, combined with other types of adversity in early childhood, is associated with greater chances of premature death in adulthood, compared to other adverse childhood experiences, according to a study of more than 46,000 people by researchers at the National Institutes of Health.
Compared to children who did not experience early life adversity, childhood poverty combined with crowded housing was associated with a 41% higher risk for premature death, and early poverty combined with separation from a parent was associated with a 50% increase in premature death. Those who experienced parental harshness and neglect had a 16% higher risk of premature death, and those who experienced family instability had a 28% higher risk for premature death.
The findings build upon earlier studies that linked individual types of adverse childhood experiences to risk of death, as well as other studies that demonstrated that death risk rose as exposure to childhood adversity increased. The current study identifies links between combinations of early childhood adversity and the overall chances of premature death.
“Understanding how patterns of early childhood adversity are associated with shortened life expectancy helps us better understand the toll of early experiences on human health and the extent that this toll carries over from childhood through adulthood,” said the study’s senior author, Stephen E. Gilman, Sc.D., chief of the Social and Behavioral Sciences Branch at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). “In the long run, we hope that results such as ours can inform efforts to develop better interventions that would both reduce exposure to childhood adversity and reduce the health consequences of early adversity among exposed children.”
The study, conducted by investigators Jing Yu, Ph.D., Dr. Gilman and other NICHD colleagues, appears in The Lancet Regional Health — Americas.
The study participants were offspring of mothers who enrolled in the Collaborative Perinatal Project, a study on maternal and child health conducted by NIH. The researchers compared data from death records compiled from 1979 to 2016 to data that assessed the children’s experiences from when they were born, from 1959 to 1966, through age 7. Among the 46,129 study participants in the analysis, 3,344 deaths occurred. Based on questionnaire information and other data collected from the participants’ mothers, the researchers developed five classifications of early childhood adversity: Low adversity: unlikely to have experienced any significant childhood adverse events (48% of participants) Parental harshness and neglect: likely to have experienced such adverse events as parental physical or emotional harshness and physical neglect (4% of participants) Family instability: likely to have experienced two or more changes in their parents’ marital status, parental divorce or separation, frequent changes in residence, a parent’s or sibling’s death, or foster care (9% of participants) Poverty and crowded housing: likely to have experienced poverty and crowded housing conditions (21% of participants) Poverty and parental separation: likely to have experienced poverty, welfare receipt, parental divorce or separation, and marital and residential changes (19% of participants)In addition to the higher death risk of those in the latter four classes, premature death risk increased with the number of adverse childhood experiences. Individuals with two adverse experiences had a 27% higher risk of early death; three adverse experiences, a 29% higher death risk; and four adverse experiences, a 45% higher risk.
“Our findings and those of previous studies on childhood adverse experiences highlight the need to reduce children’s exposure to the types of adversities that many face today, including poverty, poor housing conditions and parental separation, said Dr. Yu, a research fellow in the NICHD Social and Behavioral Sciences Branch. “These experiences can affect brain development, social and emotional well-being, behavioral development and, as our results suggest, can reduce life expectancy.

New research from RCSI University of Medicine and Health Sciences has provided greater insight into the causes of Long COVID syndrome.
The findings, which further investigate the link between Long COVID and blood clotting, have been published in the Journal of Thrombosis and Haemostasis.
Long COVID syndrome is a broad collection of symptoms including shortness of breath, fatigue and reduced physical fitness that can continue for many months after initial infection with COVID-19. Understanding is limited about why these symptoms persist in some patients but not others, and the novel syndrome remains a considerable clinical challenge for both doctors and patients alike.
To gain a new understanding of what causes Long COVID, researchers at RCSI studied patients in Ireland with symptoms of Long COVID, and saw that the body’s blood-clotting and immune systems can remain tipped out of balance long after the initial infection.
The team of researchers, led by Professor James O’Donnell at the RCSI School of Pharmacy and Biomolecular Sciences with Dr Helen Fogarty as Clinical Fellow, analysed blood from 50 patients with Long COVID syndrome up to 12 weeks post infection with the COVID-19 virus. They compared the samples to ‘controls’, blood from healthy people who did not have Long COVID syndrome.
The study found that the blood of patients with Long COVID syndrome had higher levels of a blood-clotting booster called von Willebrand Factor (VWF), and lower levels of a protein that normally breaks down VWF, called ADAMTS13. Their analysis also suggests that blood vessels were still being damaged long after the initial infection, and that specific cells of the immune system were at abnormal levels in patients with Long COVID.
“In this study, we examined 50 patients with symptoms of Long COVID syndrome. We saw that, in patients with Long COVID, the normally finely tuned balance of pro- and anti-clotting mechanisms were tipped in favour of blood clotting,” said Dr Helen Fogarty, Health Research Board Irish Clinical Academic Training (ICAT) Programme Fellow and lead author on the paper. “Our analysis also suggests that abnormal clotting and disturbed immunity go hand in hand in Long COVID. Together, these findings may help explain some of the symptoms of Long COVID syndrome.”
Commenting on the study, Professor James O’Donnell said: “Extensive research has been carried on the dangerous clotting observed in patients with acute severe COVID-19 infection, and we now understand a lot more about how and why these deadly clots occur. In this study, we put the focus on Long COVID syndrome, as so much less is known about this persistent illness which is affecting millions of people worldwide.”
The study was carried out by clinical colleagues at St James’s Hospital and researchers at RCSI as part of the Irish COVID-19 Vasculopathy Study (ICVS) collaboration, which includes scientific researchers in RCSI, Trinity College Dublin and University College Dublin as well as clinical partners in St James’s, St Vincent’s and Beaumont Hospitals. The ICVS is supported by a Health Research Board COVID-19 Rapid Response award (COV19-2020-086), and a philanthropic grant from the 3M Foundation to RCSI in support of COVID-19 research.
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Published21 minutes agoSharecloseShare pageCopy linkAbout sharingImage source, SPLThe Oxford University team credited with finding effective drugs to treat Covid are trialling an antiviral called tecovirimat to aid monkeypox recovery.More than 3,000 people in the UK have caught the monkeypox virus in recent months, with more cases anticipated.The virus, which is spreading rapidly in other countries as well, has been declared a global health emergency.The infection typically gets better on its own, but recovery can take weeks and there can be serious complications. “The aim is to find a treatment that can help people get better quicker and get out of quarantine,” said Professor Sir Peter Horby, one of the PLATINUM trial researchers at the University of Oxford.Around 500 patients will take part in the trial. Some will be treated twice-daily with tecovirimat tablets while they recuperate from the virus in their own home; others will receive a placebo – or dummy treatment – instead. By comparing the two groups of volunteers, the researchers hope to have the results for the drug trial within months. Tecovirimat prevents the virus from leaving infected cells, stopping its spread within the body. It was licensed earlier this year for monkeypox, based on promising results from initial studies in animals and evidence of safety in healthy human volunteers.What is monkeypox and how do you catch it?Monkeypox and gay men: Separating stigma from health adviceHow to tell if a rash is monkeypoxWhat is monkeypox? It is caused by the monkeypox virus, a member of the same family of viruses as smallpox, although much less severe.Infections are usually mild and the risk to the general population low. However, the UK government has bought stocks of smallpox vaccine to try to halt its spread.The virus can be spread when someone is in close contact with an infected person.It has not previously been described as a sexually-transmitted infection, but it can be passed on by close contact.Anyone with the virus should abstain from sex while they have symptoms.Image source, Harun TulunayHarun Tulunay, 35, from London, was hospitalised with a severe case of monkeypox which included a large lesion on his nose. He was treated with tecovirimat. “When you are really sick and in pain, you are ready to try anything – but you do want to know if it is going to work or not,” he said.”I still wanted to take it. And for the first time, my health improved and I started to feel better. “I don’t want anyone else to become as severely sick as I was.”This study will help patients who are not in hospital to understand how tecovirimat works, what they can expect, and the time frame of the recovery process. “Knowing whether there is an effective treatment may also help to reduce any anxiety around monkeypox,” he added.Minister for Public Health Maggie Throup said: “This government-funded study is an important step to finding a treatment which can help speed up the recovery of those who have monkeypox. She added: ‘Vaccines remain our best defence against the spread of monkeypox – we urge all those eligible to come forward when contacted, and report any symptoms to NHS 111.”More on this storyUK will trial smaller dose of monkeypox vaccine19 hours ago

Anthony Fauci did not set out to become a political lightning rod. But, as Sheryl Gay Stolberg explains, he couldn’t escape becoming a polarizing figure in Donald Trump’s Washington.Blake Hounshell and Dr. Anthony Fauci, the nation’s top infectious disease specialist, told my colleague Sheryl Gay Stolberg on Sunday night that he would soon step down as director of the National Institute of Allergy and Infectious Diseases.Given that he has led the place for nearly four decades, his retirement from government service is huge news in the world of infectious disease — once a relatively sleepy corner of medicine, thrust into the forefront of American politics with the onset of the coronavirus outbreak in January 2020.Since then, more than a million Americans have died from the virus, and nobody has played a more prominent role in handling it — and combating misinformation about it — than Fauci. At the height of the pandemic, when more than 2,000 Americans were dying each day, it was Fauci who went on camera to tell us how to stay safe and when it all might end.In the process, Fauci often had to contradict the advice and mistaken musings of the president himself, Donald Trump. He was vilified on the right, with the Oval Office and those around it calling for him to be fired. And he was lionized on the left, complete with signs in urban neighborhoods saying “Thank you, Dr. Fauci,” takeout cocktails in his name and even bobblehead dolls.Fauci is more than just a pandemic talking head, of course. Over his 38 years in the federal government, he has played a central role in devising strategies to stop other diseases, notably AIDS, and his expertise was essential in speeding the development of the first generation of Covid-19 vaccines.To capture what his legacy means, I exchanged messages today with Sheryl, who knows Fauci as well as any reporter in Washington, as she was catching a flight in Peru. Our conversation, edited lightly for length and clarity:Fauci was a leading figure in not just the fight against the coronavirus but also diseases like Zika and, of course, AIDS. What do you think he’ll be most remembered for — his battles against Donald Trump, or the other stuff?I think Fauci will be remembered for the twin infectious disease outbreaks that have, in a sense, served as bookends to his public-service career: AIDS and the coronavirus pandemic.Both times, he became controversial. But they turned out very differently for him.During the early days of the AIDS epidemic, as so many gay men were dying, they were also protesting Fauci, calling him a murderer and a killer. He brought them into his fold and befriended many of them. He would be the first to tell you that it changed him; it made him more sensitive to the patient’s point of view.Fauci is a master of navigating Washington’s nexus of science and politics. But even he couldn’t escape the polarization of Donald Trump. With Covid, I think he will simply be remembered as a polarizing figure — a hero and a brilliant scientist and public servant to some, but a symbol of bureaucracy run amok to others.Fauci has been criticized as a media hog, to the point where he was spending hours of his day talking to reporters and television hosts about the coronavirus pandemic. Do you think he has mixed feelings about spending so much time talking to the press, as opposed to working in a lab or in more of a backstage role?Mixed feelings? No. Fauci LOVES talking to the press. He considers himself good at it, and, as best I can tell, he never (or at least rarely) turned down a speaking request — except when the Trump White House barred him from accepting them.When President Biden brought Dr. Ashish Jha on as his coronavirus response coordinator, I asked Fauci if he thought he would scale back his speaking requests. He told me in no uncertain terms that he would continue to do as much television as he pleased. Part of this comes from his feeling that he is a good communicator and he has an obligation to get public health messages out. But part of it, I am convinced, is because he enjoys it.The cult of personality around Fauci was really quite something. I remember a bar in Washington selling a drink called a Fauci pouchy during the height of the Covid outbreak. Was that kind of thing ultimately helpful or hurtful to his cause?

Taste matters to fruit flies, just as it does to humans: like people, the flies tend to seek out and consume sweet-tasting foods and reject foods that taste bitter. However, little is known about how sweet and bitter tastes are represented by the brain circuits that link sensation to behavior.
In a new study published in Current Biology, researchers at Brown University described how they developed a new imaging technique and used it to map the neural activity of fruit flies in response to sweet and bitter tastes.
“These results show that the way fly brains encode the taste of food is more complex than we had anticipated,” said study author Nathaniel Snell, who earned his Ph.D. in neuroscience from Brown in 2021 and conducted the research as part of his thesis.
Just as significant as the researchers’ findings is the method they used, said Gilad Barnea, a professor of neuroscience at Brown’s Warren Alpert Medical School and director of the Center for the Neurobiology of Cells and Circuits at the University’s Carney Institute for Brain Science.
To learn more about the brain processes that govern the flies’ reaction to taste sensations, Barnea, Snell and a group of graduate and undergraduate students in Barnea’s lab developed a new imaging technique called “trans-Tango(activity).” This is an adaptation of trans-Tango, a versatile technology invented by the Barnea lab that is used to trace neural circuits in the brain. Barnea said trans-Tango(activity) takes the understanding to a new level by revealing how specific neurons in the circuits respond to stimuli.
The brain response to stimuli is like a relay, Barnea explained: The “stick” passes from one neuron to the next, and then to the next, and so on. Previous techniques could identify a neuron with the stick, but not who gave the stick to that neuron.

By estimating people’s brain age from MRI scans using machine learning, a team led by UCL researchers has identified multiple risk factors for a prematurely ageing brain.
They found that worse cardiovascular health at age 36 predicted a higher brain age later in life, while men also tended to have older brains than women of the same age, as they report in The Lancet Healthy Longevity.
A higher brain age was associated with slightly worse scores on cognitive tests, and also predicted increased brain shrinkage (atrophy) over the following two years, suggesting it could be an important clinical marker for people at risk of cognitive decline or other brain-related ill health.
Lead author Professor Jonathan Schott (UCL Dementia Research Centre, UCL Queen Square Institute of Neurology) said: “We found that despite people in this study all being of very similar real ages, there was a very wide variation in how old the computer model predicted their brains to be. We hope this technique could one day be a useful tool for identifying people at risk of accelerated ageing, so that they may be offered early, targeted prevention strategies to improve their brain health.”
The researchers applied an established MRI based machine learning model to estimate the brain age of members of the Alzheimer’s Research UK-funded Insight 46 study, led by Professor Schott. Insight 46 study members are drawn from the Medical Research Council National Survey of Health and Development (NSHD) 1946 British Birth Cohort. As the participants had been a part of the study throughout their lives, the researchers were able to compare their current brain ages to various factors from across the life course.
The participants were all between 69 and 72 years old, but their estimated brain ages ranged from 46 to 93.
The researchers were able to explain roughly one third of the variability in brain age by reviewing various factors from across the life course.
People with worse cardiovascular health at age 36 or 69 had worse brain health, as did those with increased cerebrovascular disease on MRI (relating to blood flow and blood vessels in the brain). This aligns with a previous study led by Professor Schott finding that high blood pressure at age 36 predicted poorer brain health late in life.
The study did not identify any associations between childhood cognitive function, education level or socioeconomic status, and a prematurely ageing brain.
The researchers also found that higher brain age was associated with higher concentration of neurofilament light protein (NfL) in the blood. NfL elevation is thought to arise due to nerve cell damage and is increasingly being recognised as a useful marker of neurodegeneration.
Dr Sara Imarisio, Head of Research at Alzheimer’s Research UK, said: “The Insight 46 study is helping reveal more about the complex relationship between the different factors influencing people’s brain health throughout their life. Using machine learning, researchers in this study have uncovered yet more evidence that poorer heart health in midlife is linked to greater brain shrinkage in later life. We’re incredibly grateful to the dedicated group of individuals who have contributed to research their entire lives making this work possible.”
The study was supported by Alzheimer’s Research UK, the Medical Research Council Dementia Platforms UK, Selfridges Group Foundation, the Wolfson Foundation, Wellcome, Brain Research UK, and the Alzheimer’s Association.
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Rice University and Baylor College of Medicine researchers have shown they can eradicate advanced-stage mesothelioma tumors in mice in just a few days with a treatment combining Rice’s cytokine “drug factory” implants and a checkpoint inhibitor drug.
The researchers administered the drug-producing beads, which are no larger than the head of a pin, next to tumors where they could produce continuous, high doses of interleukin-2 (IL-2), a natural compound that activates white blood cells to fight cancer.
The study, published online today in Clinical Cancer Research, is the latest in a string of successes for the drug-factory technology invented in the lab of Rice bioengineer Omid Veiseh, including Food and Drug Administration (FDA) approval to begin clinical trials of the technology this fall in ovarian cancer patients.
“From the beginning, our objective was to develop a platform therapy that can be used for multiple different types of immune system disorders or different types of cancers,” said Rice graduate student Amanda Nash, who spent several years developing the implant technology with study co-lead author Samira Aghlara-Fotovat, a fellow student in Veiseh’s lab.
The cytokine factories consist of alginate beads loaded with tens of thousands of cells that are genetically engineered to produce natural IL-2, one of two cytokines the FDA has approved for treatment of cancer. The factories are just 1.5 millimeters wide and can be implanted with minimally invasive surgery to deliver high doses of IL-2 directly to tumors. In the mesothelioma study, the beads were placed beside tumors and inside the thin layer of tissue known as the pleura, which covers the lungs and lines the interior wall of the chest.
“I take care of patients who have malignant pleural mesothelioma,” said Dr. Bryan Burt, professor and chief of Baylor’s Division of Thoracic Surgery in the Michael E. DeBakey Department of Surgery. “This is a very aggressive malignancy of the lining of the lungs. And it’s very hard to treat completely by surgical resection. In other words, there is often residual disease that is left behind. The treatment of this residual disease with local immunotherapy — the local delivery of relatively high doses of immunotherapy to that pleural space — is a very attractive way to treat this disease.”
Veiseh said the mesothelioma study began when Burt and Baylor surgeon and associate professor Dr. Ravi Ghanta heard about the early results of ovarian cancer animal tests Veiseh’s team was conducting with collaborators at the University of Texas MD Anderson Cancer Center. In March, Veiseh and MD Anderson collaborators published a study showing IL-2-producing beads could eradicate advanced-stage ovarian and colorectal tumors in mice in less than a week.

Adults aged 60 and older who sit for long periods watching TV or other such passive, sedentary behaviors may be at increased risk of developing dementia, according to a new study by USC and University of Arizona researchers.
Their study also showed that the risk is lower for those who are active while sitting, such as when they read or use computers.
The study was published today in the journal Proceedings of the National Academy of Sciences. It also revealed that the link between sedentary behavior and dementia risk persisted even among participants who were physically active.
“It isn’t the time spent sitting, per se, but the type of sedentary activity performed during leisure time that impacts dementia risk,” said study author David Raichlen, professor of biological sciences and anthropology at the USC Dornsife College of Letters, Arts and Sciences.
“We know from past studies that watching TV involves low levels of muscle activity and energy use compared with using a computer or reading,” he said. “And while research has shown that uninterrupted sitting for long periods is linked with reduced blood flow in the brain, the relatively greater intellectual stimulation that occurs during computer use may counteract the negative effects of sitting.”
Researchers used self-reported data from the U.K. Biobank, a large-scale biomedical database of more than 500,000 participants across the United Kingdom, to investigate possible correlations between sedentary leisure activity and dementia in older adults.

A modified tuberculosis (TB) vaccine developed at Texas Biomed could help treat a form of bladder cancer, called non-muscle invasive bladder cancer, without strong side effects. Results in mouse models and human cells show promising results and pave the way for human clinical trials. The research, conducted in close collaboration with UT Health San Antonio, was published online in June in the journal Cancer Immunology, Immunotherapy.
“I’m hopeful that with grant or industry support, we can move this right along to clinical trials and explore this treatment for patients who don’t have options other than bladder removal,” says Robert S. Svatek, MD, a urologic oncologist who treats bladder cancer patients at the Mays Cancer Center at UT Health San Antonio and is co-senior author of the research paper.
Each year in the United States, about 61,700 men and 19,480 women get bladder cancer, and about 17,100 deaths due to the disease occur (12,120 men and 4,980 women), according to the American Cancer Society. Bladder cancer is the fourth most common type of cancer in men. About 75% of bladder cancer cases are classified as non-muscle invasive, which means the cancer affects the tissue lining the inner surface of the bladder, but not the bladder muscle.
The Mycobacterium bovis bacille Calmette-Guérin (BCG) vaccine was developed for tuberculosis in the 1920s, and has also been used to treat non-muscle invasive bladder cancer since the late 1970s by stimulating an immune response at the cancer site. It was one of the first cancer immunotherapies and is more effective than chemotherapy for this type of cancer — but up to 84% of patients cannot tolerate the strong side effects and don’t complete the three years of BCG treatment. When treatments fail, the last option is to remove the bladder, which leads to reduced quality of life.
“Imagine that there’s this great drug that works really well, but you’re not able to tolerate it,” Dr. Svatek says. “We’re talking about a very select group of patients, but for whom this really, really matters.”
Texas Biomed Professor Jordi B. Torrelles, PhD, specializes in tuberculosis, and has been working on a modified BCG vaccine for the past six years to improve TB treatment in the lungs. Specifically, Dr. Torrelles and his team remove certain lipids from the cell envelopes of the bacteria in the BCG vaccine. This “delipidated” vaccine still triggers the body to produce well-regulated immune responses, but reduces overzealous inflammation that causes severe tissue damage.
“It is more targeted and allows for a longer, slower response, which makes it more effective,” Dr. Torrelles says.
Thanks to a San Antonio Medical Foundation grant, Dr. Torrelles was able to team up with Dr. Svatek and Hong Dixon, PhD, a research scientist specializing in drug development at Southwest Research Institute (SwRI), to test the modified vaccine for bladder cancer as well.
Dr. Torrelles and his lab made two versions of the delipidated vaccine based on different TB bacteria strains: one known as sub-strain TICE, which is developed in the U.S., and one known as sub-strain Tokyo, which is developed in Japan.
Dr. Svatek’s lab conducted the tests in a mouse model of bladder cancer and in cells collected from human cancer patients. They tested both delipidated BCG versions, and found that both were equally effective compared with the original BCG vaccine at killing the cancer, but that the modified Tokyo version performed better than the TICE version, with far less inflammation and minimal side effects.
“We were not expecting such a clear difference between the strains,” says Dr. Torrelles, who has patented the modified vaccine for bladder cancer. Now, the collaborators plan to seek funding for a phase 1 clinical trial in human patients. SwRI is assessing manufacturing the modified vaccine for the clinical trial.
“We are excited to see this move forward and since it is based on an already U.S. FDA-approved treatment, we are hopeful it can proceed in a timely way,” Dr. Torrelles says.