AI algorithm turns mammograms into a ‘two-for-one’ test for women’s heart health

An AI algorithm based only on routine mammogram images plus age can predict a woman’s risk of major cardiovascular disease as well as standard risk assessment methods, finds research published online in the journal Heart.

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Engineered antibodies can direct T-cells to kill cytomegalovirus-infected cells

A UCLA research team has found a new way to prompt the immune system to kill cells infected with cytomegalovirus (CMV), a life-threatening infection that is particularly deadly in immunocompromised people.

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Developing novel drug for acute MI, acute kidney injury, and subsequent chronic organ failure: Study

Acute myocardial infarction and acute kidney injury are life-threatening conditions caused by ischemia, resulting from reduced or blocked blood flow to organs. Although early restoration of blood flow improves survival, many patients still develop chronic heart or kidney failure. The mechanisms driving this transition from acute tissue injury to chronic dysfunction remain poorly understood, and effective treatments are lacking.

In this study, researchers focused on the immune receptor CD300a, which suppresses immune cell activation. Using a mouse model with genetic deficiency of CD300a, they investigated the progression from AMI and AKI to chronic heart and kidney failure. The findings revealed that CD300a deficiency attenuated cardiac dysfunction caused by AMI and reduced subsequent cardiac fibrosis, thereby preserving cardiac function. Similarly, renal dysfunction following AKI was less severe, renal fibrosis in chronic kidney failure was diminished, and renal function was maintained.

The mechanism underlying these protective effects is as follows: in ischemic heart and kidney tissues, CD300a deficiency enhanced macrophage-mediated phagocytosis of dead cells, reducing inflammation. Moreover, in CD300a-deficient mice, SiglecF-/lo neutrophils exhibited increased production of angiogenic and antifibrotic factors, which inhibited progression to chronic organ failure. Importantly, administration of neutralizing antibodies against CD300a in mice produced outcomes comparable to those observed in CD300a-deficient models, suppressing the progression to chronic heart and kidney failure.

The research group now aims to evaluate the efficacy and safety of humanized anti-human CD300a neutralizing antibodies in clinical studies, with the ultimate goal of developing novel therapeutic agents for acute tissue injury and subsequent chronic organ failure in the heart and kidney.

Reference:

Nanako Nishiyama, Hitoshi Koizumi, Chigusa Nakahashi-Oda, Satoshi Fujiyama, Xuewei Ng,Hanbin Lee, Fumie Abe,CD300a immunoreceptor regulates ischemic tissue damage and adverse remodeling in the mouse heart and kidney, Journal of Clinical Investigation, DOI:10.1172/JCI184984 

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Using deep learning for precision cancer therapy

Nearly 50 new cancer therapies are approved every year. This is good news. “But for patients and their treating physicians, it is becoming increasingly difficult to keep track and to select the treatment methods from which the people affected—each with their very individual tumor characteristics—will benefit the most,” says Dr. Altuna Akalin, head of the Bioinformatics and Omics Data Science technology platform at the Berlin Institute for Medical Systems Biology of the Max Delbrück Center (MDC-BIMSB).

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Novel PET tracer detects synaptic changes in spinal cord and brain after spinal cord injury

A new PET tracer can provide insights into how spinal cord injuries affect not only the spinal cord, but also the brain, according to new research published in The Journal of Nuclear Medicine. By identifying synapse loss, the PET approach provides molecularly unique and complementary information to other structural imaging methods, offering a promising objective metric to evaluate novel therapeutics for spinal cord injuries.

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Ebola vaccine reaches epicenter of Congo outbreak as officials race to contain spread

Limited access and required funding are the key challenges facing health officials trying to respond to the latest Ebola outbreak in southern Congo, the World Health Organization said on Friday.

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AOPT-LTL Therapy Improves Melasma via SCF/c-KIT Pathway Inhibition: Study Finds

China: A new study has revealed that AOPT-LTL therapy significantly improves melasma by reducing melanogenesis, inflammation, angiogenesis, mast cell infiltration, and collagen degeneration, likely via inhibition of the SCF/c-KIT signaling pathway.

The study, led by Bingrong Zhou and colleagues from the Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, China, was published in the Journal of Cosmetic Dermatology. The research assessed both the effectiveness and the biological mechanisms of advanced optimal pulse technology intense pulsed light in low-energy triple-pulse long-width mode (AOPT-LTL) for treating melasma.
To explore this, the investigators first developed an animal model of melasma using guinea pigs exposed to progesterone injections and ultraviolet B radiation. Animals were then treated with three sessions of AOPT-LTL therapy administered weekly. Alongside this preclinical work, 20 patients with melasma underwent three monthly sessions of the same treatment. Their progress was evaluated using the Modified Melasma Area and Severity Index (mMASI) and the Erythema Index (EI).
The study led to the following findings:
  • In the animal model, AOPT-LTL treatment significantly reduced pigmentation and suppressed genes associated with melanin production.
  • The therapy decreased mast cell infiltration and lowered the expression of inflammatory and angiogenic factors.
  • By inhibiting angiogenesis and reducing collagen breakdown, the treatment improved skin quality and alleviated signs of photoaging.
  • AOPT-LTL also blocked the SCF/c-KIT signaling pathway, which regulates mast cell activity and proliferation, suggesting a key molecular mechanism behind its effects.
  • Clinical results were consistent with the experimental findings, showing clear therapeutic benefits in patients.
  • After three sessions, patients experienced reduced melanin levels and erythema, along with improved mMASI and EI scores.
  • The improvements demonstrated both lightening of pigmentation and reduced redness, supporting its effectiveness in enhancing skin tone and texture in melasma.
The authors emphasized that AOPT-LTL therapy offers multiple benefits beyond pigment reduction, targeting inflammation, angiogenesis, and structural degeneration, which are all key processes involved in melasma pathology. By acting on several pathways simultaneously, it may provide a more comprehensive approach compared to conventional treatment modalities.
However, the researchers also acknowledged certain limitations. The study lacked direct head-to-head comparisons with conventional IPL methods, making it difficult to quantify its relative advantages. The sample size of patients was small, and the follow-up period was short, meaning long-term recurrence rates could not be fully assessed. Further laboratory studies are also required to confirm the precise mechanisms of mast cell inhibition observed in vivo.
“The study demonstrated that AOPT-LTL therapy can effectively treat melasma through its broad-spectrum action on melanogenesis, inflammation, vascular changes, and collagen degradation. With its ability to target multiple biological pathways, it shows promise as a novel therapeutic option for patients with melasma, although larger and longer clinical trials are needed to validate its long-term efficacy and safety,” the authors concluded.
Reference:
Wang, J., Wang, X., Gu, L., Shi, Z., Xu, Z., Shen, S., Gu, L., Chen, L., Ju, L., Jin, C., Zhou, B., & Hua, H. (2025). Efficacy of Intense Pulsed Light AOPT-LTL Technique in the Treatment of Melasma: An In Vivo and Clinical Study. Journal of Cosmetic Dermatology, 24(9), e70443. https://doi.org/10.1111/jocd.70443

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Psoriatic Arthritis Patients Face Higher Burden of Metabolic Syndrome, Meta-Analysis Shows

Sweden: A new meta-analysis published in Clinical Rheumatology highlights that individuals with psoriatic arthritis (PsA) face a significantly greater burden of metabolic syndrome (MetS) compared with the general population and patients with other inflammatory arthropathies such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS).

The study, conducted by Sara Andreasson and Anna Södergren from the Department of Public Health and Clinical Medicine, Umeå University, Sweden, highlights the need for proactive screening and preventive strategies in PsA care.
The researchers systematically reviewed evidence from major databases, including Ovid Medline, Web of Science, and Scopus, up to February 2024. Out of 1,526 screened publications, 20 relevant studies were included in the final analysis. A random-effects model was used to assess prevalence, and funnel plots were used to evaluate potential bias.
The study revealed the following findings:
  • PsA patients had higher odds of developing metabolic syndrome compared to the general population (LogOR 0.93).
  • The risk of metabolic syndrome was greater in PsA patients than in those with rheumatoid arthritis (LogOR 0.63).
  • PsA patients also had a higher prevalence of metabolic syndrome than ankylosing spondylitis patients (LogOR 1.04).
  • The prevalence of metabolic syndrome in PsA was similar to that seen in cutaneous psoriasis (LogOR 0.15).
  • PsA patients showed increased risks of central obesity, hypertriglyceridemia, impaired glucose tolerance, and diabetes mellitus compared with rheumatoid arthritis patients.
The study emphasizes that MetS—a cluster of conditions including abdominal obesity, dyslipidemia, hypertension, and glucose intolerance—significantly contributes to cardiovascular morbidity. The overlap between psoriatic disease pathways, obesity, and endothelial dysfunction may partly explain why PsA patients are particularly vulnerable.
While the findings strongly support intensified monitoring of metabolic health in PsA patients, the authors acknowledged several limitations. Few studies matched participants for age and sex, sample sizes varied widely, and outcome measures were inconsistent. High heterogeneity was observed in some analyses, and a potential publication bias was suggested, particularly in comparisons between PsA and PsO. Moreover, limited data prevented detailed evaluation of MetS components in PsA versus PsO, AS, and general population groups.
Despite these challenges, the meta-analysis reinforces the importance of incorporating cardiovascular risk assessment into routine PsA management. According to the authors, understanding how disease activity, systemic inflammation, and antirheumatic treatments influence MetS development remains an area requiring further research.
“PsA was consistently associated with a higher prevalence of metabolic syndrome compared to the general population, RA, and AS. This highlights the need for systematic screening and early intervention to reduce long-term cardiovascular risks in these patients,” the study noted.
“The results add to growing evidence that comprehensive PsA care should extend beyond joint and skin manifestations to address broader metabolic and cardiovascular health. Proactive measures, including lifestyle modification, treatment of metabolic risk factors, and achieving minimal disease activity, could play a key role in reducing complications for this vulnerable patient population,” the authors concluded.
Reference:
Andreasson, S., Södergren, A. Prevalence of metabolic syndrome and its components in psoriatic arthritis compared with general population, cutaneous psoriasis, and other inflammatory arthropathies: a meta-analysis. Clin Rheumatol (2025). https://doi.org/10.1007/s10067-025-07637-z

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Excessive screen time among youth may pose heart health risks: Study

Children and young adults who spend excessive hours glued to screens and electronic devices may have higher risks for cardiometabolic diseases, such as high blood pressure, high cholesterol and insulin resistance, according to new research published today in the Journal of the American Heart Association, an open-access, peer-reviewed journal of the American Heart Association.

A 2023 scientific statement from the American Heart Association noted that “cardiometabolic risk is accruing at younger and younger ages,” and only 29% of American youth, ages 2 to 19 years, had favorable cardiometabolic health based on 2013-2018 data from the National Health and Nutrition Examination Survey.

This analysis of more than 1,000 participants in two studies in Denmark found that increased recreational screen time was significantly associated with higher cardiovascular risks and cardiometabolic risks among children and adolescents.

“Limiting discretionary screen time in childhood and adolescence may protect long-term heart and metabolic health,” said study lead author David Horner, M.D., PhD., a researcher at the Copenhagen Prospective Studies on Asthma in Childhood (COPSAC) at the University of Copenhagen in Denmark. “Our study provides evidence that this connection starts early and highlights the importance of having balanced daily routines.”

Using data from a group of 10-year-olds studied in 2010 and a group of 18-year-olds in 2000 that were part of the Copenhagen Prospective Studies on Asthma in Childhood cohorts, researchers examined the relationship between screen time and cardiometabolic risk factors. Screen time included time spent watching TV, movies, gaming or using phones, tablets or computers for leisure.

Researchers developed a composite score based on a cluster of metabolic syndrome components — waist size, blood pressure, high-density lipoprotein or HDL “good” cholesterol, triglycerides and blood sugar levels – and adjusted for sex and age. The cardiometabolic score reflected a participant’s overall risk relative to the study group average (measured in standard deviations): 0 means average risk, and 1 means one standard deviation above average.

The analysis found that each extra hour of screen time increased the cardiometabolic score by about 0.08 standard deviations in the 10-year-olds and 0.13 standard deviations in the 18-year-olds. “This means a child with three extra hours of screen time a day would have roughly a quarter to half a standard-deviation higher risk than their peers,” Horner said.

“It’s a small change per hour, but when screen time accumulates to three, five or even six hours a day, as we saw in many adolescents, that adds up,” he said. “Multiply that across a whole population of children, and you’re looking at a meaningful shift in early cardiometabolic risk that could carry into adulthood.”

The analysis also found that both sleep duration and sleep timing affected the relationship between screen time and cardiometabolic risk. Both shorter sleep duration and going to sleep later intensified the relationship between screen time and cardiometabolic risk. Children and adolescents who had less sleep showed significantly higher risk associated with the same amount of screen time.

“In childhood, sleep duration not only moderated this relationship but also partially explained it: about 12% of the association between screen time and cardiometabolic risk was mediated through shorter sleep duration,” Horner said. “These findings suggest that insufficient sleep may not only magnify the impact of screen time but could be a key pathway linking screen habits to early metabolic changes.”

In addition, a machine learning analysis identified a unique metabolic signature in the blood that appeared to be associated with screen time.

“We were able to detect a set of blood-metabolite changes, a ‘screen-time fingerprint,’ validating the potential biological impact of the screen time behavior,” he said. “Using the same metabolomics data, we also assessed whether screen time was linked to predicted cardiovascular risk in adulthood, finding a positive trend in childhood and a significant association in adolescence. This suggests that screen-related metabolic changes may carry early signals of long-term heart health risk.

“Recognizing and discussing screen habits during pediatric appointments could become part of broader lifestyle counseling, much like diet or physical activity,” he said. “These results also open the door to using metabolomic signatures as early objective markers of lifestyle risk.”

Amanda Marma Perak, M.D., M.S.CI., FAHA, chair of the American Heart Association’s Young Hearts Cardiovascular Disease Prevention Committee, who was not involved in this research, said focusing on sleep is a great starting point to change screen time patterns.

“If cutting back on screen time feels difficult, start by moving screentime earlier and focusing on getting into bed earlier and for longer,” said Perak, an assistant professor of pediatrics and preventive medicine at Northwestern University Feinberg School of Medicine in Chicago.

Adults can also set an example, she said. “All of us use screens, so it’s important to guide kids, teens and young adults to healthy screen use in a way that grows with them. As a parent, you can model healthy screen use – when to put it away, how to use it, how to avoid multitasking. And as kids get a little older, be more explicit, narrating why you put away your devices during dinner or other times together.

“Make sure they know how to entertain and soothe themselves without a screen and can handle being bored! Boredom breeds brilliance and creativity, so don’t be bothered when your kids complain they’re bored. Loneliness and discomfort will happen throughout life, so those are opportunities to support and mentor your kids in healthy ways to respond that don’t involve scrolling.”

As an observational study using prospectively collected data, the findings reflect associations rather than proving cause and effect. Moreover, parents of the 10-year-olds and the 18-year-olds reported screen time through questionnaires, which may not accurately reflect the actual time youth spent on screens.

Horner suggested that future research could explore whether limiting screen use in the hours before sleep, when light from screen exposure may disrupt circadian rhythms and disrupt sleep onset, may be an avenue to help reduce cardiometabolic risk.

Study details, background and design:

  • The two prospective research groups at COPSAC in Denmark consisted of mother-child pairs, with analysis of data collected at planned clinical visits and study assessments from the birth of the children through age 10 in the 2010 study group and age 18 in the 2000 study group.
  • Through questionnaires, parents of children in the 10-year-old group and 18-year-olds detailed the number of hours the young participants spent watching TV or movies, gaming on a console/TV and using phones, tablets or computers for leisure.
  • For the 2010 group, the number of hours of screen time was available for 657 children at age 6 and 630 children at age 10. Average screen time was two hours per day at age 6, and 3.2 hours per day at age 10, representing a significant increase over time.
  • For the 2000 group of 18-year-olds, screen time was available for 364 individuals. Screen time at 18 years was significantly higher at an average of 6.1 hours per day.
  • Sleep was measured by sensors over a 14-day period.

Reference:

David Horner, Marie Jahn, Screen Time Is Associated With Cardiometabolic and Cardiovascular Disease Risk in Childhood and Adolescence, Journal of the American Heart Association, DOI: 10.1161/JAHA.125.041486 

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Exposure to air pollution worsens Alzheimer’s disease, Penn research finds

Exposure to high concentrations of air pollution may worsen Alzheimer’s disease (AD) by accelerating the buildup of toxic proteins in the brain and speeding up cognitive decline. For the first time, post-mortem tissue from people with AD revealed that those who lived in areas with higher concentrations of fine particulate matter in the air even just one year had more severe accumulation of amyloid plaques and tau tangles-hallmarks of Alzheimer’s pathology-compared to those with less exposure. These individuals also experienced faster cognitive and functional decline, including memory loss, impaired judgment, and difficulty with personal care, according to research published today in JAMA Neurology from the Perelman School of Medicine at the University of Pennsylvania.

“This study shows that air pollution doesn’t just increase the risk of dementia-it actually makes Alzheimer’s disease worse,” said Edward Lee, MD, PhD, co-director of Penn’s Institute on Aging. “As researchers continue to search for new treatments, it’s important to uncover all of the factors that contribute to the disease, including the influence of the environment in which they live.”

Health risks from tiny air particles

Air pollution is made up of fine particulate matter, or the tiny, inhalable particles, ranging from 10 micrometers to less than 2.5 micrometers wide, about half the width of a single strand of spider web. It can come from wildfire smoke, car exhaust, construction site debris, or combustion from factories. Particulate matter 2.5 micrometers and smaller (PM2.5) is so small that when inhaled, the particles can be absorbed into the blood stream and cause health concerns. Previous research has linked air pollution containing PM2.5 with dementia, loss of cognitive function, and accelerated cognitive decline.

The researchers examined brain samples from over 600 autopsies from the Penn Medicine Brain Bank. Using data from satellites and local air quality monitors, the researchers modeled the amount of PM2.5 in the air based on where each person lived. They found that for every increase of 1 microgram per cubic meter of PM2.5, the risk for worse Alzheimer’s disease amyloid and tau buildup increased by 19 percent.

Further, when they examined the clinical records of these individuals, researchers found that those who lived in areas with high concentrations of PM2.5 with advanced pathology also had greater cognitive impairment and more rapid onset of symptoms, including memory loss, difficulty with speech, and diminished judgement, compared to people who lived in areas with lower concentrations of air pollution.

While this study focused on exposures to PM2.5 based on geographic location, researchers acknowledge that they could not account for individual-specific exposures to air pollution, such as exposure to second-hand smoke in the home, or working with potentially dangerous chemicals.

“In the United States, air pollution is at the lowest levels in decades, but even just a year living in an area with high levels of pollution can have a big impact on a person’s risk for developing Alzheimer’s disease,” said Lee. “It underscores the value of environmental justice efforts that focus on reducing air pollution to improve public health.”

Reference:

Kim B, Blam K, Elser H, et al. Ambient Air Pollution and the Severity of Alzheimer Disease Neuropathology. JAMA Neurol. Published online September 08, 2025. doi:10.1001/jamaneurol.2025.3316

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