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Stress tested, testing stress: Novel organoid models how the adrenal gland develops

Sitting above each kidney are two small endocrine glands about the size of walnuts. These are the adrenal glands, responsible for producing hormones that help control some of the body’s most critical functions. Among these hormones, cortisol is particularly critical for survival. Often referred to as the “stress hormone,” it helps the body adapt to a wide range of challenges—both emotional and physical, such as trauma or infection—by regulating overall metabolism. Despite its central role in stress and endocrine biology, how the adrenal gland is built and how it functions remains poorly understood.

Now, researchers led by Kotaro Sasaki and Michinori Mayama of the School of Veterinary Medicine have developed a lab-grown organoid system that recapitulates the complex tissue structure, development, and function of the developing human adrenal cortex—the outer layer of the adrenal gland—providing a powerful platform to study its biology. These results, published in Cell Stem Cell, help establish a foundation for regenerative therapies targeting adrenal diseases.

“The adrenal cortex is a major endocrine organ and central to our stress response,” says Sasaki, the Richard King Mellon Associate Professor of Biomedical Sciences. “Despite its importance, adrenal biology has lagged behind that of other organs. Our goal was to create a mini adrenal gland in a dish to better understand how the human adrenal forms and begins to function.”

Goodbye, Prediabetes, Hello, Type 2 Diabetes Stages?

The concept of “prediabetes” may be on its way out. Some experts are proposing a shift to staging type 2 diabetes instead, arguing that the current label can be misleading and may delay more proactive treatment. A stage-based approach could better reflect disease progression and encourage earlier intervention.


Leaders in the diabetes field are proposing eliminating the prediabetes label in favor of type 2 diabetes stages.

New ‘Unifying Theory’ May Explain How Alzheimer’s Emerges in The Brain

The origins of Alzheimer’s remain contentious, but a new study suggests the disease may emerge as two key proteins compete inside brain cells.

Alzheimer’s disease, the most common form of dementia, has long been associated with the build-up of two proteins in the brain: amyloid-beta and tau.

This new study ties those two together, offering a “unifying theory” that, according to the team of chemists proposing it, resolves some conflicting ideas about Alzheimer’s.

Study points toward immune reprogramming to treat candidiasis

Systemic candidiasis is an opportunistic fungal infection that has been difficult to treat effectively. Research published in a paper in the April edition of Cell Host & Microbe suggests that immune metabolic reprogramming could be a new strategy to fight the infection rather than developing another specific antifungal medication.

The fungus Candida albicans causes infections that range from superficial on the skin and nails to invasive into organs and the bloodstream. In recent decades, systemic candidiasis has increased due to more patients with immunosuppression from disease or treatments, prolonged antibiotic exposure, and certain conditions such as kidney disease. Management of systemic candidiasis has become more difficult because of antifungal drug resistance, limited early diagnostic tools, and absence of approved fungal vaccines.

According to Partha Biswas, DVM, Ph.D., lead author of the paper, and a Professor in the Department of Microbiology and Immunology in the Renaissance School of Medicine (RSOM) at Stony Brook University, these challenges have become roadblocks to treating systemic candidiasis and illustrate the need for new and different therapeutic strategies.

Senescence in cancer: Hallmarks, paradoxes, and therapeutic promise

Now online! Cellular senescence, defined by six major hallmarks, is a program that halts cell division while rewiring chromatin, metabolism, microenvironment sensing, and immune interactions to either suppress or promote cancer and is an exciting frontier for precision therapy.

Research moves closer to ‘smart’ sensors in knee replacements

If you have a knee replacement, imagine pointing your phone at your knee and pulling up an app that tells you how much stress the artificial joint is experiencing. Knowing the activities that cause the biggest problems—which can lead to a second replacement surgery—would be invaluable. Research led by Binghamton University is closer to making this technology a reality.

Professor Shahrzad “Sherry” Towfighian—a faculty member from the Thomas J. Watson College of Engineering and Applied Science’s Department of Mechanical Engineering—has worked toward “smart-knee” tech over the past decade.

According to the American College of Rheumatology, nearly 800,000 total knee replacements are done every year in the U.S., and that number is expected to rise sharply by 2030 as the population ages and sports injuries become more common.

Body-wide multi-omic counteraction of aging with GLP-1R agonism

Online now: Body-wide multi-omic counteraction of aging with GLP-1R agonism: (Cell Metabolism 37, 2362–2380.e1–e8; December 2, 2025)


Online now: (Cell Metabolism 37, 2362–2380.e1–e8; December 2, 2025)

Following publication, Steve Horvath and colleagues at the Clock Foundation alerted us to a platemap error in the DNA methylation (DNAm) data. Our investigation pinpointed the potential source of this error. We provided samples on 96-well plates in a row-wise orientation instead of the column-wise orientation specified in the Clock Foundation’s protocol. Subsequently, incorrect assignment of metadata for 36 samples (out of 459) that contributed data to the paper likely occurred during the transposition and rearrangement of a subset of samples on two incompletely filled plates prior to the assay. Working with Clock Foundation colleagues, we have corrected the metadata for 33 samples and discarded 3 samples for which we could not retrieve the metadata with total certainty.

This error impacted DNAm data for the following tissues:

High-throughput platform helps engineer fast-acting covalent protein drugs

A team led by principal investigators Bobo Dang and Ting Zhou at Westlake University/Westlake Laboratory have developed a high-throughput platform for engineering fast-acting covalent protein therapeutics. Their study, titled “A high-throughput selection system for fast-acting covalent protein drugs” published in Science, opens new avenues for next-generation biologics.

Covalent small-molecule drugs have shown great success in cancer therapy by forming irreversible bonds with their targets. This has inspired efforts to extend covalent strategies to protein therapeutics, especially engineered miniproteins. However, their development is limited by a kinetic mismatch: Miniproteins are rapidly cleared in vivo, whereas covalent bond formation is typically slow. In addition, high-throughput platforms for systematically optimizing covalent protein reactivity have been lacking.

To address this challenge, the researchers proposed that precise spatial positioning of chemical warheads within protein scaffolds could enable molecular preorganization, thereby accelerating covalent bond formation without increasing intrinsic reactivity.

Abstract: Genetic analysis of neurodegenerative diseases:

As part of the JCI’s Review Series on Neurodegeneration, Sonja W. Scholz and colleagues highlight key genomic technologies advancing diagnosis and research in neurodegeneration.


1Neurodegenerative Diseases Research Section, National Institute of Neurological Disorders and Stroke;

2Neurogenetics Branch, National Institute of Neurological Disorders and Stroke; and.

3Neuromuscular Diseases Research Section, National Institute on Aging, National Institutes of Health (NIH), Bethesda, Maryland, USA.

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