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Category: biotech/medical

Invisible threads: How our environment quietly shapes disease

From the air we breathe to the food we eat, we are constantly exposed to thousands of chemicals—yet how these exposures affect our health has remained surprisingly difficult to understand. A new study led by researchers at the CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences and the Ludwig Boltzmann Institute for Network Medicine at the University of Vienna, published in Nature Communications, offers a unifying view: Diverse substances can disrupt the same biological systems and thereby contribute to disease risk in predictable ways.

Environmental pollution is estimated to contribute to around one in six deaths worldwide, but scientists have long struggled to connect specific exposures to specific diseases. One reason is the sheer complexity of the “exposome” —the totality of all environmental influences a person encounters over a lifetime. Traditionally, chemicals have been grouped by their structure or origin, but this says little about what they actually do inside the body. Two nearly identical molecules can have completely different effects, while entirely unrelated substances may trigger the same illness. This has made it difficult to move from observation to understanding.

A new study, led by Jörg Menche, CeMM adjunct PI and director of the Ludwig Boltzmann Institute for Network Medicine, and first authored by former Ph.D. student at CeMM and LBI NetMed (now a postdoc at Harvard Medical School) Salvo Danilo Lombardo, takes a different route: Instead of asking what chemicals look like, the researchers asked what they do. They compiled nearly 10,000 environmental exposures, ranging from pollutants and food components to medications, and mapped how each affects human genes. The result is a large-scale network that links exposures based on shared biological effects.

Mayo Clinic study identifies new brain targets for individualized epilepsy treatment

ROCHESTER, Minn. — Mayo Clinic researchers have created a detailed map of the pulvinar, a deep brain region that could help doctors more precisely target brain stimulation therapies for people with drug-resistant epilepsy. The findings, published in the Journal of Neuroscience, reveal that brain regions separated by only a few millimeters connect to entirely different

Abstract: 1 Department of Cardiovascular Medicine, Osaka Metropolitan University Graduate School of Medicine, Osaka, Japan

1 Department of Cardiovascular Medicine, Osaka Metropolitan University Graduate School of Medicine, Osaka, Japan.

2Division of Cardiovascular and Genetic Research, Center for Molecular Medicine, and.

3Department of Cardiovascular Medicine, Jichi Medical University, Tochigi, Japan.

Are lung cancer tumors hijacking the nervous system?

According to the Cleveland Clinic, a quarter of cancer deaths can be attributed to one source: cachexia. Cachexia is a syndrome that accompanies underlying chronic illness and causes unwanted muscle and fat loss, reducing quality of life and sometimes even limiting treatment options.

A new study led by Thales Papagiannakopoulos, Ph.D., an incoming Salk professor, published in Science, points to a potential new target for preventing cachexia.

The researchers found that a common genetic subset of lung cancer is more prone to cachexia and that tumors from this subtype talk to the brain through sensory neurons in the lung. Silencing these sensory nerves to disrupt the tumor-to-brain connection reduced cachexia, as did blocking the production of the lipid signaling molecule prostaglandin E2 (PGE2) through dietary changes.

Why Living Past 115 Is Almost Impossible | The Limit

Today, more people are living past 100 than ever before — even though the maximum human lifespan hasn’t moved past 115 years. But is that about to change?

The Limit host Daniel T. Allen spent months talking to medical researchers, biohackers, and centenarians. He also went through a battery of tests worth over $12,000 at a longevity clinic to find out how long he might live.

In this episode, Business Insider looked into what could radically extend human lifespan, including FDA-approved drugs, cellular reprogramming, and Bryan Johnson’s $2 million \.

New Insights into HIV Life Cycle, Th1/Th2 Shift during HIV Infection and Preferential Virus Infection of Th2 Cells: Implications of Early HIV Treatment Initiation and Care

The theory of immune regulation involves a homeostatic balance between T-helper 1 (Th1) and T-helper 2 (Th2) responses. The Th1 and Th2 theories were introduced in 1986 as a result of studies in mice, whereby T-helper cell subsets were found to direct different immune response pathways. Subsequently, this hypothesis was extended to human immunity, with Th1 cells mediating cellular immunity to fight intracellular pathogens, while Th2 cells mediated humoral immunity to fight extracellular pathogens. Several disease conditions were later found to tilt the balance between Th1 and Th2 immune response pathways, including HIV infection, but the exact mechanism for the shift from Th1 to Th2 cells was poorly understood. This review provides new insights into the molecular biology of HIV, wherein the HIV life cycle is discussed in detail.

Scientists Turned Human Cells into Tiny Biological Computers

The researchers also built in a warning signal. When the cell received a confusing instruction—the biological equivalent of two commands arriving at once—it produced a separate alert instead of continuing as if nothing had happened.

To show how the system might one day be used in medicine, the team programmed cells to secrete IL-15, an immune protein that can help activate cancer-fighting immune cells.

The experiments relied on engineered circuits delivered into cells under controlled lab conditions. The authors note several challenges ahead, including avoiding unwanted RNA interactions, limiting leaky genetic switches, and finding reliable ways to insert larger circuits into cell genomes.

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