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Infections of the nervous system, such as acute bacterial meningitis, pose serious health problems that require immediate intervention. In experimental animals, exposure to lipopolysaccharide (LPS) is used to induce meningitis. Aside from drug intervention to reduce inflammation in meningitis, aerobic exercise helps to maintain the regulatory mechanisms of brain homeostasis through anti-inflammatory mechanisms.

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Lipid A, a well-known saccharolipid, acts as the inner lipid-glycan anchor of lipopolysaccharides in Gram-negative bacterial cell membranes and functions as an endotoxin. Its structure is composed of two glucosamines with β(1 → 6) linkages and various fatty acyl and phosphate groups. The lipid A structure can be used for the identification of bacterial species, but its complexity poses significant structural characterization challenges.

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Understanding the neurobiological mechanisms of LPS‑induced memory impairment.

Acta Neurobiol Exp (Wars)

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Department of Physiology, School of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran; Bio Environmental Health Hazards Research Center, Jiroft University of Medical Sciences, Jiroft, Iran.

In recent years, growing evidence suggests that lipopolysaccharide (LPS), a bacterial endotoxin found in the outer membrane of gram‑negative bacteria, can influence cognitive functions, particularly memory formation and retrieval. However, the underlying mechanisms through which LPS exerts its effects on memory remain incompletely understood. This review used various electronic databases, including PubMed, Scopus, and Web of Science, to identify relevant studies published between 2000 and 2024.

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Diagnostic Accuracy of Microbiome-Derived Biomarkers in Periodontitis: Systematic Review and Meta-Analysis.

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Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, UK.

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Gut microbiome dysbiosis is not associated with portal vein thrombosis in patients with end-stage liver disease: a cross-sectional study.

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University of Groningen, Department of Surgery, Section of Hepatobiliary Surgery and Liver Transplantation, University Medical Center Groningen, Groningen, the Netherlands. Electronic address:

Background: Portal vein thrombosis (PVT) is a common complication in patients with end-stage liver disease (ESLD). The portal vein in ESLD patients is proposedly an inflammatory vascular bed due to translocation of endotoxins and cytokines from the gut. We hypothesized that a pro-inflammatory gut microbiome and elevated trimethylamine N-oxide (TMAO), a driver of thrombosis, may contribute to PVT development.

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