Effect of a nursing-based information–motivation–behavioral model on older patients with type 2 diabetes mellitus
Coping under pressure: police-specific stressors and mental health in Catalonia police forces
Iron dyshomeostasis in neuropsychiatric disorders
Exposure to negative physical and social factors accelerates brain aging
Nature Medicine, Published online: 21 April 2026; doi:10.1038/s41591-026-04348-z
In a study that included 18,701 people from 34 countries, 73 aggregated physical and social exposomes exhibited nonlinear, synergistic effects that accelerated brain aging. In some cases, these effects were comparable to or stronger than those of mild cognitive impairment and dementia. Environmental inequities might shape brain aging and demand multisectoral and structural policy responses.
Modifying exposure to plastic-associated chemicals in daily living
Nature Medicine, Published online: 21 April 2026; doi:10.1038/s41591-026-04349-y
A study shows that extensively limiting plastic use in food systems, diet and daily life can reduce exposure to plastic-associated chemicals such as phthalates and bisphenols, indicating that large-scale regulatory actions are needed for true public health impact.
AACR 2026: A Video Update from San Diego
The American Association for Cancer Research (AACR) meeting is off and running in San Diego. Julianna LeMieux, PhD, Deputy Editor in Chief at GEN, and Damian Doherty, Editor in Chief at Inside Precision Medicine, are on the ground—in the talks, expo hall, and press room, covering as much of the news as they can. Here, they take a moment to chat about the first few days at the meeting.
The post AACR 2026: A Video Update from San Diego appeared first on GEN – Genetic Engineering and Biotechnology News.
STAT+: BioAge says experimental pill aimed at reducing heart risks significantly reduced inflammation
BioAge Labs said Tuesday that its investigational pill for cardiovascular risk prevention significantly reduced inflammation in an early study, as more drug companies target inflammation as a way to treat a range of chronic conditions.
In a Phase 1 study of people with obesity and elevated inflammation levels, patients taking a 60-milligram dose of the drug, called BGE-102, experienced an 86% reduction in a measure of inflammation called high-sensitivity C-reactive protein (hs-CRP) after three weeks. That’s a similar level of reduction seen in patients who took a higher 120-mg dose in the study, which the company previously reported.
Additionally, 87% of patients taking the 60-mg dose achieved hs-CRP levels of less than 2 mg/liter, the threshold thought to be associated with a lower risk of cardiovascular complications.
Digging for clues about the North Pole’s past
In the past, even with an icebreaker and during peak melt season, getting to the North Pole wasn’t a sure bet. It took favorable winds to crack the frozen ocean surface, and ships had to fight through ice that had grown many meters thick over several winters. In the summer of 2025, though, Jochen Knies from the Arctic University of Norway, Tromsø, and his team met little resistance on their way to 90 degrees North with the research vessel Kronprins Haakon. The geologist “didn’t hear the usual grinding of ice” against the hull that he remembered from 1996, when he first reached the pole by ship. Instead, thin floes and large stretches of open water made for an easy, quiet passage. To him, it was “a reminder of how quickly the Arctic is changing.”
Since the late 1970s, when satellite observations of the polar seas began, summer ice cover of the Arctic Ocean has declined by more than 40%. In less than half a century, a frozen area the size of the Mediterranean Sea has turned into blue open water with the rapid warming of the high northern latitudes. If this trend continues, there could soon be summers at the North Pole with no sea ice whatsoever. The last time this happened may have been some 120,000 years ago. But no one knows for certain.
That’s why Knies and his colleagues, a team of researchers from Norway and Germany, set out from Svalbard to the central Arctic last August. The aim of their five-week mission was to determine whether this region had been ice-free in recent Earth history—and if so, when. As part of a €12.5 million project financed by the European Union, they also came to answer some questions about the future of the Arctic and beyond: How does the loss of sea ice affect the marine ecosystem? What are the consequences for ocean circulation and global climate?
In search of clues, the expedition collected sediment cores up to 22 meters in length at different locations across the Arctic seafloor. Marine sediments are valuable climate archives that give scientists a window into bygone eras. Like diligent record keepers, they can log past water temperatures, sea-ice coverage, and the strength of ocean currents. These data are encrypted in the chemical and physical properties of the plankton remains and weathered rock deposited on the seabed.



While sediment cores several meters long had been recovered on earlier expeditions in the central Arctic, there is no scientific consensus on how old the deposits actually are or whether sea ice ever completely disappeared in summer.
To decode the Arctic’s climate archive, Knies brought a team of experts from various disciplines onboard the Kronprins Haakon to dig deeper and obtain fresh samples they could subject to the latest analytical techniques.



Some of this work was done while the researchers were still at sea. Now, at their home laboratories, they are finalizing their analysis of the seafloor samples. One important task is dating the sediments, which may be up to 2 million years old. The team uses a combination of methods to do this, including measuring magnetization, the decay of radioactive elements, and the exposure of mineral grains to sunlight before sinking to the depths. Once they can place them on a timeline, the materials in the cores will help researchers paint a picture of what the Arctic Ocean looked like in times that were warmer than today. For example, the presence or absence of the molecule IP25, which is produced exclusively by ice algae, could tell them how far the sea ice receded at a given time.

At the end of the study, the team hopes to have data that could improve climate projections for a future ice-free “blue Arctic,” helping us understand how it could affect marine life and carbon storage, Atlantic Ocean circulation, or extreme weather events in Europe and North America.
Tim Kalvelage is a freelance science reporter based in Bremen, Germany, who focuses on climate, ocean, and polar research. He has been to the North Pole twice.
CRISPR Screens Map Human T‑Cell Genes That Promote or Block HIV Infection
How does HIV, armed with only nine genes, manage to hijack the immune system so effectively? For decades, researchers have known that the virus depends on human proteins to enter, replicate, and persist—yet the full roster of those host factors has remained elusive. One major reason: most HIV studies have relied on immortalized cell lines rather than the primary CD4+ T cells the virus actually infects in the body. As a result, scientists have lacked a comprehensive picture of how real human T cells respond when HIV attacks.
A new study from Gladstone Institutes and the University of California, San Francisco (UCSF), changes that. In the study, titled “Systematic Discovery of Pro- and Anti-HIV Host Factors in Primary Human CD4+ T Cells” and published in Cell, researchers report the first genome‑wide map of human genes that either promote or restrict HIV infection in primary human CD4+ T cells, offering a long‑sought blueprint of the host–virus interface.
“HIV has been a global crisis for over 40 years,” said Alex Marson, MD, PhD, director of the Gladstone‑UCSF Institute of Genomic Immunology and senior author of the study. “By studying human T cells, which are the primary target of the virus, we’ve finally mapped the genes—many of which were previously unknown—that influence whether or not they can be infected by HIV.”

Achieving this required overcoming a fundamental technical barrier. “One challenge of using real human T cells for research is they’re very difficult to infect with HIV; out of a whole dish of cells, typically only one or two percent would get infected,” said first author Ujjwal Rathore, PhD. After years of optimization, the team pushed infection rates to roughly 70%, enabling genome‑scale CRISPR perturbations in primary cells for the first time.
With that platform in hand, the researchers performed orthogonal genome‑wide CRISPR activation (CRISPRa) and CRISPR knockout (CRISPRn) screens in CD4+ T cells, systematically testing nearly every human gene. Disrupting genes revealed those HIV depends on, while overactivating genes exposed natural antiviral defenses that HIV normally suppresses. “Over‑activating the genes gave us a wealth of information,” said co–first author Eli Dugan, a PhD candidate in Marson’s lab. “We discovered natural antiviral proteins that were previously invisible because the virus could effectively silence them.”
Across both screens, the team identified hundreds of host factors that shape HIV infection. Among the most striking were two previously unrecognized antiviral proteins: PI16 and PPID (Cyp40). “PI16 interacts with host factors involved in HIV fusion and inhibits viral entry, whereas PPID, a paralog of the proviral cyclophilin CypA, binds capsid and reduces nuclear import of the HIV core,” wrote the authors. Targeted mutagenesis, along with structural modeling and evolutionary analyses, pinpointed residues essential for PPID’s restriction activity, and engineered variants were up to tenfold more potent, according to Dugan.
To test whether these defenses could counter real‑world viral strains, the team collaborated with HIV pioneer Jay Levy, MD, who provided isolates from the early AIDS epidemic. Elevated levels of PI16 or PPID restricted even these aggressive HIV strains.
“This was the first genome‑wide effort to show how human genes affect HIV infection in cells taken directly from human blood samples,” said Nevan Krogan, PhD, director of the HIV Accessory and Regulatory Complexes (HARC) Center. “Our findings could eventually lead to new treatments that help the body’s immune system resist the virus.”
Beyond identifying antiviral factors, the study offers the potential for a powerful new platform for probing HIV latency—the persistent reservoir that evades antiretroviral therapy. “Now, we have the platform to ask the biggest questions in the field,” Rathore said, “and hopefully learn how to eliminate hidden HIV that current drugs can’t reach.”
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