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How intermittent fasting may shield the brain from chronic stress

Chronic stress, the prolonged exposure to psychological and/or physical strain, is known to be a risk factor for depression, anxiety and some other psychiatric disorders. Past studies suggest that chronic stress disrupts the integrity of myelin, a fatty insulating layer that surrounds nerve fibers and helps electrical signals travel efficiently between brain cells.

Identifying lifestyle changes that can reverse or diminish the adverse effects of chronic stress on the brain could be advantageous, as they could potentially help prevent or delay the onset of various psychiatric conditions. Recently, some researchers have been exploring the potential brain benefits of intermittent fasting (IF), a dietary pattern that entails alternating between set periods of eating and fasting.

Past findings suggest that IF can improve people’s metabolism and help reduce inflammation, the body’s natural response to disease or injury. Yet its effects on people’s mental health and well-being have not yet been clearly determined.

‘Pink noise’ can help make anesthesia work better during surgery

In the brain, specific electrical waves are associated with different states of consciousness. For instance, delta waves—also known as slow waves—are especially prevalent during deep sleep, as well as during states of unconsciousness induced by coma and general anesthesia. They are considered a “signature” of these altered states of consciousness.

Over a decade ago, research showed that it is possible to amplify these delta waves through highly precise auditory stimulation, a technique initially studied in the context of sleep.

Now researchers at Université de Montréal are bringing this technique into the operating room to help optimize general anesthesia, which also induces a state characterized by abundant delta waves.

Biomarkers could help identify ICU patients at risk of chronic critical illness

New research, published in The Journal of Immunology, identifies biomarkers of a distinct immune profile that could be used to identify patients at risk for chronic critical illness (CCI) on admission to the intensive care unit (ICU) after traumatic injury. Identifying which patients are at increased risk for CCI could allow doctors to intervene earlier, leading to shorter ICU stays and improved patient outcomes.

“Our findings are highly novel, challenging what scientists have long thought about the immune changes that cause organ dysfunction and mortality in severely injured trauma patients. Rather than the immune system being exhausted, our data show overactivity and dysfunction,” said Dr. Scott Brakenridge, professor of surgery at the University of Washington and senior author of the study.

Severe traumatic injury, such as from a car crash or fall, causes changes to the immune system that can lead to immune and organ dysfunction, as well as recurrent infections. Researchers have long thought this was due to a deficiency in an immune signal, or cytokine, called interferon-gamma (IFN which regulates immune responses.

Misinformation exploits outrage to spread online

We tested a hypothesis that misinformation exploits outrage to spread online, examining generalizability across multiple platforms, time periods, and classifications of misinformation. Outrage is highly engaging and need not be accurate to achieve its communicative goals, making it an attractive signal to embed in misinformation. In eight studies that used US data from Facebook (1,063,298 links) and Twitter (44,529 tweets, 24,007 users) and two behavioral experiments (1475 participants), we show that (i) misinformation sources evoke more outrage than do trustworthy sources; (ii) outrage facilitates the sharing of misinformation at least as strongly as sharing of trustworthy news; and (iii) users are more willing to share outrage-evoking misinformation without reading it first.

AARS1 promotes tumor progression and immune evasion via ATF6 lactylation-mediated tryptophan metabolism in hepatocellular carcinoma

Wang et al. identify a metabolic-immune feedback circuit in hepatocellular carcinoma, in which tumor cell-intrinsic AARS1-mediated ATF6 lactylation activates the TDO2-kynurenine axis to promote Treg differentiation and immunosuppression, while Treg-derived eNAMPT enhances tumor glycolysis and lactate production, revealing a therapeutic vulnerability to AARS1 inhibition combined with PD-1/PD-L1 blockade.

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