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Immunomodulatory Role of Microbiota in Inflammation and Cancer

Non-small cell lung cancer (NSCLC) is the most prevalent form of lung cancer, accounting for approximately 85% of all cases, and is associated with a poor prognosis. Despite significant advancements in treatment modalities, therapeutic efficacy remains suboptimal, underscoring the urgent need for novel strategies. In recent years, increasing attention has been directed toward the pivotal role of gut microbiota-host interactions in the treatment of NSCLC. This review systematically examines the influence of current NSCLC therapies on gut microbiota and metabolism, explores the relationship between the microbiome and therapeutic response, and highlights the critical functions of probiotics, microbial metabolites, fecal microbiota transplantation (FMT), and dietary interventions in NSCLC management. By elucidating the mechanisms through which gut microbiota and their metabolites modulate treatment efficacy, we investigate the potential of exogenous interventions targeting the gut ecosystem to enhance therapeutic outcomes and mitigate adverse effects. Modulating the intestinal microbiota represents a promising clinical avenue and offers a new frontier for the development of future NSCLC treatment strategies.

The human microbiome comprises a diverse and dynamic community of microorganisms—including bacteria, fungi, viruses—their genetic material, and metabolic byproducts. The resident microbiota is an essential component of host health and homeostasis (1). Most microbiome research to date has focused on bacterial populations, which constitute a major proportion of these resident microbes (2). In the gut, Bacteroidetes, Firmicutes, Proteobacteria, and Actinobacteria dominate the bacterial composition (35). The gut microbiota plays a pivotal role in regulating host immunity and metabolism through the production of numerous metabolites that function as signaling molecules and metabolic substrates, linking dysbiosis with inflammation and tumorigenesis (68).

The cross-link between gut microbiota and lung cancer is a complex multifactorial relationship. Studies have shown that in patients with lung cancer, the abundance of Bacteroidetes, Fusobacteria, Cyanobacteria, and Spirochaetes increases in both pulmonary and intestinal microbiomes, while Firmicutes are significantly reduced (4, 9). Research on both gut and respiratory tract microbiota has revealed notable dysregulation in NSCLC, which is further associated with distant metastasis (DM) (10). The pathogenic contribution of the gut microbiome and its specific metabolites to NSCLC lies in their modulation of chronic inflammation and immune dysregulation (11). A study combining serum metabolomics and fecal microbiome profiling identified potential biomarkers in patients with early-stage NSCLC. The metabolomic analysis revealed elevated levels of sphingolipids (e.g. D-erythrosphingosine 1-phosphate, palmitoylsphingomyelin), fatty acyls (e.g.

Exercise-induced vesicles boost neuron growth when transplanted into sedentary mice

Researchers at the University of Illinois Urbana-Champaign report that extracellular vesicles released into the bloodstream during aerobic exercise can, on their own, drive a robust increase in adult hippocampal neurogenesis when transferred into sedentary mice, even without changes in hippocampal vascular coverage.

Aerobic physical activity preserves cognitive function across the lifespan and repeatedly links to structural and cellular plasticity in the hippocampus. Evidence from plasma transfer experiments indicates that bloodborne factors from exercising animals can transfer pro-neurogenic and pro-cognitive effects to sedentary or aged recipients, partly through reduced inflammation.

Many circulating molecules have been implicated in this exercise–brain connection, including , insulin-like growth factor 1, platelet factor 4, selenoprotein P, irisin, cathepsin B, L-lactate, and interleukin-6. Each contributes to specific aspects of neurogenesis or neuronal survival.

Legend or Truth: Mature CD4+CD8+ Double-Positive T Cells in the Periphery in Health and Disease

The expression of CD4 and CD8 co-receptors defines two distinct T cell populations with specialized functions. While CD4+ T cells support and modulate immune responses through different T-helper (Th) and regulatory subtypes, CD8+ T cells eliminate cells that might threaten the organism, for example, virus-infected or tumor cells. However, a paradoxical population of CD4+CD8+ double-positive (DP) T cells challenging this paradigm has been found in the peripheral blood. This subset has been observed in healthy as well as pathological conditions, suggesting unique and well-defined functions. Furthermore, DP T cells express activation markers and exhibit memory-like features, displaying an effector memory (EM) and central memory (CM) phenotype.

How the human brain anticipates and regulates the body’s needs

They also used a recently validated map of deep brain areas. This in vivo atlas, Brainstem Navigator, maps the regions involved in regulating the autonomic, immune and endocrine systems.

The authors analytic approach was guided by decades of basic research that has identified two main brain pathways in mammals: one set of pathways (allostatic) that sends signals from the brain to control the body’s organs, and the other set (interoceptive) that sends signals from the body to the brain, informing it about what’s happening inside us.

The findings replicated and expanded on their previous 3 Tesla work, confirming nearly all the direct connections identified in non-human mammals: 100% of those between cortical areas and 96% of those linking subcortical areas to both cortical and other subcortical areas. As expected, the authors found two-way connections between the brain areas that help manage the body’s needs (like the anterior cingulate cortex) and the areas that sense what’s happening inside the body (like the posterior insula). This means these regions communicate back and forth, helping the brain predict and regulate what the body needs.

Mounting evidence suggests that one of the brain’s central roles is to anticipate and meet the body’s energy needs. The findings place the monitoring and regulation of the body’s needs at the functional core of the human brain, showing the close connection between mental and physical health.


Previous studies in both animal models and humans have pointed to the existence of a distributed system in the brain that helps it anticipate and prepare for the body’s energy needs — a process called allostasis — as well as monitor the sensory conditions inside the body, known as interoception.

In an earlier study using 3 Tesla fMRI, the team mapped a network supporting allostasis and interoception in the human brain, but the comparatively limited spatial resolution and sensitivity of the 3 Tesla technology made it difficult to fully capture the system’s smaller structures in the brainstem, which are known to play a key role in these processes.

Family history key to predicting antidepressant response

A new study from Queen Mary University of London shows that a family’s experience with certain medicines could help doctors predict how future generations will respond to the same drugs.

The researchers found that people were almost five times more likely to have a affecting how they process antidepressants if both they and a parent had stopped taking the same medication early.

Published in Communications Medicine, the study looked at 600 British, Bangladeshi and Pakistani families from the Genes and Health Project—one of the world’s largest community genetics studies.

Dr. Julia Moore Vogel — Scripps Research — Visionary, Patient-Centric Health Research For All

Visionary, patient-centric health research for all — dr. julia moore vogel, phd — scripps research / long covid treatment trial.


Dr. Julia Moore Vogel, PhD, MBA is Assistant Professor and Senior Program Director at The Scripps Research Institute (https://www.scripps.edu/science-and-me… where she is responsible for managing a broad portfolio of patient-centric health research studies, including The Long COVID Treatment Trial (https://longcovid.scripps.edu/locitt-t/), a fully remote, randomized, placebo-controlled clinical trial targeting individuals with long COVID, testing whether the drug Tirzepatide can reduce or alleviate symptoms of long COVID.

Prior to this current role, Dr. Vogel managed The Participant Center (TPC) for the NIH All of Us Research Program (https://www.scripps.edu/science-and-me… which was charged with recruiting and retaining 350,000 individuals that represent the diversity of the United States. TPC aims to make it possible for interested individuals anywhere in the US to become active participants, for example by collaborating with numerous outreach partners to raise awareness, collecting biosamples nationwide, returning participants’ results and developing self-guided workflows that enable participants to join whenever is convenient for them.

Prior to joining the Scripps Research Translational Institute, Dr. Vogel created, proposed, fundraised for, and implemented research and clinical genomics initiatives at the New York Genome Center and The Rockefeller University. She oversaw the proposal and execution of grants, including a $44M NIH Center for Common Disease Genomics in collaboration with over 20 scientific contributors across seven institutions. She also managed corporate partnerships, including one with IBM that assessed the relative value of several genomic assays for cancer patients.

Dr. Vogel has a BS in Mathematics from Rensselaer Polytechnic Institute, a PhD in Computational Biology and Medicine from Cornell and an MBA from Cornell.

Experimental drug protects mitochondria and prevents kidney injury in mice

Serious damage to short-term kidney function—known as acute kidney injury, or AKI—can be fatal and also increase the risk of irreversible chronic kidney disease. It can be triggered by stressors ranging from sepsis to heart surgery, and it affects more than half of ICU patients. There are currently no drugs to treat AKI.

Now, researchers at University of Utah Health (U of U Health) have found that AKI is triggered by fatty molecules called ceramides, which cause serious injury by damaging kidney mitochondria. Using a backup drug candidate that changes metabolism, the team was able to preserve mitochondrial integrity and prevent kidney injury in .

“We completely reversed the pathology of by inactivating ceramides,” says Scott Summers, Ph.D., distinguished professor and Chair of the Department of Nutrition and Integrative Physiology in the University of Utah College of Health and senior author on a paper describing the results.

Shared gut microbe imbalances found across autism, ADHD, and anorexia nervosa

A new study has identified distinct patterns in the gut bacteria of children and adolescents with autism spectrum disorder, attention-deficit/hyperactivity disorder, and anorexia nervosa. Published in the journal Neuroscience, the research also reveals altered levels of hormones that regulate appetite, suggesting a complex interplay between gut microbes, eating behaviors, and brain health in these conditions.

The human digestive tract is home to a bustling community of trillions of microorganisms, collectively known as the gut microbiota. This internal ecosystem communicates with the brain through a complex network of signals, often called the gut-brain axis. Researchers are increasingly recognizing that an imbalance in this microbial community, sometimes referred to as dysbiosis, may be associated with a range of health conditions, including those affecting the brain.

Neurodevelopmental disorders like autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), along with the psychiatric disorder anorexia nervosa (AN), are frequently accompanied by gastrointestinal issues and atypical eating patterns.

Functional Connectivity Changes in Traumatic Brain InjuryA Systematic Review and Coordinate-Based Meta-Analysis of fMRI Studies

Importance There lacks data clarifying the meningioma risk conferred by depot medroxyprogesterone acetate in the US.

Objective To examine the relative risk of meningioma diagnosis in women using depot medroxyprogesterone acetate and other related progestins.

Design, Setting, and Participants This retrospective population-based cohort study used data from TriNetX, a US national database of 68 health care organizations. Data were analyzed from December 2004 to December 2024. The incidence of meningioma diagnosis was compared between treatment groups through propensity-score matched analyses. Participants included a sample of females with use of only 1 of the following progestins/contraceptives: depot medroxyprogesterone acetate, oral medroxyprogesterone acetate, combined oral contraceptives, intrauterine devices, progestin only pills, or subdermal implantable contraceptive. The control group included females without use of these hormonal treatments. Of the 118 289 082 total patients in TriNetX at the time of analysis, 61 588 239 patients were female and eligible.

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