&lt;p&gt;Microbial Modulation of Coagulation Disorders in Venous Thromboembolism&lt;/p&gt;

Xie

et al. 2021

JIR

Background Although many works have been conducted to explore the biomarkers for diagnosing major depressive disorder (MDD), the widely accepted biomarkers are still not identified. Thus, the combined application of serum metabolomics and fecal microbial communities was used to identify gut microbiota-derived inflammation-related serum metabolites as potential biomarkers for MDD. Methods MDD patients and healthy controls (HCs) were included in this study. Both serum samples and fecal samples were collected. The liquid chromatography mass spectrometry (LC-MS) was used to detect the metabolites in serum samples, and the 16S rRNA gene sequencing was used to analyze the gut microbiota compositions in fecal samples. Results Totally, 60 MDD patients and 60 HCs were recruited. The 24 differential serum metabolites were identified, and 10 of these were inflammation-related metabolites. Three significantly affected inflammation-related pathways were identified using differential metabolites. The 17 differential genera were identified, and 14 of these genera belonged to phyla Firmicutes. Four significantly affected inflammation-related pathways were identified using differential genera. Five inflammation-related metabolites (LysoPC(16:0), deoxycholic acid, docosahexaenoic acid, taurocholic acid and LysoPC(20:0)) were identified as potential biomarkers. These potential biomarkers had significant correlations with genera belonged to phyla Firmicutes. The panel consisting of these biomarkers could effectively distinguish MDD patients from HCs with an area under the curve (AUC) of 0.95 in training set and 0.92 in testing set. Conclusion These findings suggested that the disturbance of phyla Firmicutes might be involved in the onset of depression by regulating host’s inflammatory response, and these potential biomarkers could be useful for future investigating the objective methods for diagnosing MDD.

Section: Introductionmentioning

confidence: 99%

Gut Microbiota-Derived Inflammation-Related Serum Metabolites as Potential Biomarkers for Major Depressive Disorder

Xie

et al. 2021

JIR

“…Studies have already observed that gut microbiota alter the risk of cardiovascular disease (Witkowski et al, 2020;Jin et al, 2021). Gut microbiota-derived metabolites may increase the risk of venous thromboembolisms (Zhu et al, 2016;Hasan et al, 2020;Lichota et al, 2020). However, the influence of gut microbiota-derived metabolites has not been evaluated in the context of HIT or HITT.…”

Section: Metagenomicsmentioning

confidence: 99%

Elucidation of Cellular Contributions to Heparin-Induced Thrombocytopenia Using Omic Approaches

et al. 2022

Heparin-induced thrombocytopenia (HIT) is an unpredictable, complex, immune-mediated adverse drug reaction associated with a high mortality. Despite decades of research into HIT, fundamental knowledge gaps persist regarding HIT likely due to the complex and unusual nature of the HIT immune response. Such knowledge gaps include the identity of a HIT immunogen, the intrinsic roles of various cell types and their interactions, and the molecular basis that distinguishes pathogenic and non-pathogenic PF4/heparin antibodies. While a key feature of HIT, thrombocytopenia, implicates platelets as a seminal cell fragment in HIT pathogenesis, strong evidence exists for critical roles of multiple cell types. The rise in omic technologies over the last decade has resulted in a number of agnostic, whole system approaches for biological research that may be especially informative for complex phenotypes. Applying multi-omics techniques to HIT has the potential to bring new insights into HIT pathophysiology and identify biomarkers with clinical utility. In this review, we review the clinical, immunological, and molecular features of HIT with emphasis on key cell types and their roles. We then address the applicability of several omic techniques underutilized in HIT, which have the potential to fill knowledge gaps related to HIT biology.

“…Trimethylamine produced by bacteria is oxidized to trimethylamine-N-oxide (TMAO) by flavin-containing monooxygenase [6]. This enzyme is expressed in the liver and oxidizes xenobiotics containing amines or sulfides [105]. A significantly higher level of this compound was observed in the plasma of CKD patients (30.33 µmol/L) in comparison to the level in healthy subjects (2.08 µmol/L) [106].…”

Section: Other Compoundsmentioning

confidence: 99%

“…Bacterial infections are the leading cause of hospitalization of CKD patients and are related to vascular access, which is the most common source of bacteremia in hemodialyzed patients. Sepsis is associated with an increased risk of thrombosis, myocardial infarction, congestive heart failure, stroke, and peripheral arterial disease [105,141].…”

Section: Implications Of Uremic Toxins and Oxidative Stress In Cardiovascular Diseasementioning

confidence: 99%

Uremic Toxins and Their Relation with Oxidative Stress Induced in Patients with CKD

Pieniążek

Bernasińska-Słomczewska

Gwoździński

2021

IJMS

The presence of toxins is believed to be a major factor in the development of uremia in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). Uremic toxins have been divided into 3 groups: small substances dissolved in water, medium molecules: peptides and low molecular weight proteins, and protein-bound toxins. One of the earliest known toxins is urea, the concentration of which was considered negligible in CKD patients. However, subsequent studies have shown that it can lead to increased production of reactive oxygen species (ROS), and induce insulin resistance in vitro and in vivo, as well as cause carbamylation of proteins, peptides, and amino acids. Other uremic toxins and their participation in the damage caused by oxidative stress to biological material are also presented. Macromolecules and molecules modified as a result of carbamylation, oxidative stress, and their adducts with uremic toxins, may lead to cardiovascular diseases, and increased risk of mortality in patients with CKD.