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Gut Microbial Metabolite TMAO Enhances Platelet Hyperreactivity and Thrombosis Risk.

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TLDR
Gut microbes, through generation of trimethylamine N-oxide (TMAO), directly contribute to platelet hyperreactivity and enhanced thrombosis potential, revealing a previously unrecognized mechanistic link between specific dietary nutrients, gut microbes, platelet function, and thromBosis risk.
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This article is published in Cell.The article was published on 2016-03-24 and is currently open access. It has received 1219 citations till now. The article focuses on the topics: Platelet activation & Trimethylamine N-oxide.

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New technologies for developing phage-based tools to manipulate the human microbiome.

TL;DR: In this paper, the authors discuss recent advances in cultivation-independent technologies and argue their relevance to different key steps, that is, identifying the modulation targets and developing phage-based tools to precisely modulate gut bacteria and restore a sustainable microbiome in humans.
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Prevention of Vascular Inflammation by Pterostilbene via Trimethylamine-N-Oxide Reduction and Mechanism of Microbiota Regulation.

TL;DR: Data suggest that amelioration of carnitine-induced vascular inflammation after consumption of pterostilbene is partially mediated via modulation of gut microbiota composition and hepatic enzyme FMO3 gene expression.
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Gut Microbiota and Stroke

TL;DR: This review presents the current understanding about the interaction between commensal gut microbiome and brain in determining the course of stroke and examines the role of gut microbiota dysbiosis and various complications and outcomes.
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Gut microbiota-associated trimethylamine N-oxide and increased cardiometabolic risk in adults: a systematic review and dose-response meta-analysis.

TL;DR: Circulating TMAO is positively associated with an increased risk of hypertension and other cardiometabolic disorders in adults and is associated with reduced high-density lipoprotein cholesterol in apparently healthy individuals and reducedHigh- density lipop Protein cholesterol and increased total cholesterol in patients with cardiovascular disease.
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Platelet Abnormalities in CKD and Their Implications for Antiplatelet Therapy

TL;DR: In this article , the authors summarized the knowledge on CKD-induced aberrations in hemostasis, with a special focus on platelet abnormalities, and discussed how prominent alterations in vascular integrity, coagulation, and red blood cell count in CKD may contribute to altered platelet function resulting in either platelet hyper- or hyporeactivity.
References
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Journal ArticleDOI

An obesity-associated gut microbiome with increased capacity for energy harvest

TL;DR: It is demonstrated through metagenomic and biochemical analyses that changes in the relative abundance of the Bacteroidetes and Firmicutes affect the metabolic potential of the mouse gut microbiota and indicates that the obese microbiome has an increased capacity to harvest energy from the diet.
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The gut microbiota as an environmental factor that regulates fat storage

TL;DR: In this article, the authors found that conventionalization of adult germ-free C57BL/6 mice with a normal microbiota harvested from the distal intestine (cecum) of conventionally raised animals produces a 60% increase in body fat content and insulin resistance within 14 days despite reduced food intake.
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Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease

TL;DR: Discovery of a relationship between gut-flora-dependent metabolism of dietary phosphatidylcholine and CVD pathogenesis provides opportunities for the development of new diagnostic tests and therapeutic approaches for atherosclerotic heart disease.
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Intestinal Microbial Metabolism of Phosphatidylcholine and Cardiovascular Risk

TL;DR: The production of TMAO from dietary phosphatidylcholine is dependent on metabolism by the intestinal microbiota and increased levels are associated with an increased risk of incident major adverse cardiovascular events.
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