trimethylamine/otok

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Metabolomic analysis of the plasma of patients with high-altitude pulmonary edema (HAPE) using 1H NMR.

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Upon rapid ascent to a high altitude, non-acclimatized individuals, although healthy, are highly prone to contracting high-altitude pulmonary edema (HAPE). Early diagnosis is difficult and there is no reliable biomarker available. We used proton ((1)H) NMR metabolomics to profile the altered

The Presence of High Levels of Circulating Trimethylamine N-Oxide Exacerbates Central and Peripheral Inflammation and Inflammatory Hyperalgesia in Rats Following Carrageenan Injection.

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Gut microbiota-derived metabolite trimethylamine N-oxide (TMAO) has recently been shown to promote inflammation in peripheral tissues and the central nervous system (CNS), contributing to the pathogenesis of various human diseases. Here, we examined whether the presence of high levels of circulating

Choline Diet and Its Gut Microbe-Derived Metabolite, Trimethylamine N-Oxide, Exacerbate Pressure Overload-Induced Heart Failure.

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BACKGROUND Trimethylamine N-oxide (TMAO), a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients, is both elevated in the circulation of patients having heart failure and heralds worse overall prognosis. In animal studies, dietary choline or TMAO

[Nephrotoxicity study of Aristolochia fangchi in rats by metabonomics].

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OBJECTIVE To study the changes of metabolites in rat urine after treatment of Aristolochia fangchi decoction by metabonomic method. METHODS Sixty-four male SD rats were divided into Aristolochia fangchi group and normal control group. Rats in the Aristolochia fangchi group were orally administered

Follow-up by one- and two-dimensional NMR of plasma from pigs with ischemia-induced acute liver failure treated with a bioartificial liver.

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Hepatic encephalopathy may occur following acute hepatic failure (AHF), which results in the release of toxic compounds from the injured liver. These compounds, which induce cerebral edema, are not well characterized, yet. The aim of this study was to evaluate the potential interest of NMR

Dissociation between maternal and fetal toxicity of methyl isocyanate in mice and rats.

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The contribution of maternal hormonal changes and pulmonary damage on the fetal toxicity of methyl isocyanate (MIC) was studied in mice and rats. Exposure to MIC decreased maternal plasma progesterone levels in mice that lost but not in mice that retained pregnancy. Fetal toxicity of MIC was not

1H NMR-based metabolomics study on repeat dose toxicity of fine particulate matter in rats after intratracheal instillation.

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Systemic metabolic effects and toxicity mechanisms of ambient fine particulate matter (PM2.5) remain uncertain. In order to investigate the mechanisms in PM2.5 toxicity, we explored the endogenous metabolic changes and possible influenced metabolic pathways in rats after intratracheal instillation

[Osmotic cerebral oedema: the role of plasma osmolarity and blood brain barrier].

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There are five types of oedema: vasogenic, cytotoxic, interstitial, hyperemic and osmotic. The differences lie on the type and localization of the oedema, the state of the blood-brain barrier (BBB) and the pathological context. Under physiological conditions, the osmolarity of extra cellular fluids

TMAO: How gut microbiota contributes to heart failure

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An increasing amount of evidence reveals that the gut microbiota is involved in the pathogenesis and progression of various cardiovascular diseases. In patients with heart failure (HF), splanchnic hypoperfusion causes ischemia and intestinal edema, allowing bacterial translocation and bacterial

Gut Microbiota in Cardiovascular Health and Disease.

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Significant interest in recent years has focused on gut microbiota-host interaction because accumulating evidence has revealed that intestinal microbiota play an important role in human health and disease, including cardiovascular diseases. Changes in the composition of gut microbiota associated

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