Noninvasive serum markers for predicting significant liver histopathology in HBeAg-negative chronic HBV-infected patients with normal alanine aminotransferase.

Unlabelled: This study is to explore the proportion of significant liver histopathology in hepatitis B e antigen (HBeAg)-negative chronic hepatitis B virus (HBV)-infected patients with normal alanine aminotransferase (ALT) and investigate noninvasive indicators for predicting significant liver histopathology. A total of 201 HBeAg-negative chronic HBV-infected patients with normal ALT who underwent liver biopsy were involved in this study. Significant liver histological changes were defined as necroinflammation grade ≥2 (G ≥ 2) and/or fibrosis stage ≥2 (S ≥ 2).

Inhibition of mitochondrial complex I leading to NAD/NADH imbalance in type 2 diabetic patients who developed late stent thrombosis: Evidence from an integrative analysis of platelet bioenergetics and metabolomics.

Type 2 diabetes mellitus (T2DM) is a strong indicator of late stent thrombosis (LST). Platelet bioenergetic dysfunction, although critical to the pathogenesis of diabetic macrovascular complications, remains uncharacterized in T2DM patients who developed LST. Here, we explored the mechanistic link between the alterations in platelet bioenergetics and LST in the setting of T2DM.

A novel 6-metabolite signature for prediction of clinical outcomes in type 2 diabetic patients undergoing percutaneous coronary intervention.

Background: Outcome prediction tools for patients with type 2 diabetes mellitus (T2DM) undergoing percutaneous coronary intervention (PCI) are lacking. Here, we developed a machine learning-based metabolite classifier for predicting 1-year major adverse cardiovascular events (MACEs) after PCI among patients with T2DM.

Methods: Serum metabolomic profiling was performed in a nested case-control study of 108 matched pairs of patients with T2DM occurring and not occurring MACEs at 1 year after PCI, then the matched pairs were 1:1 assigned into the discovery and internal validation sets.

A Descriptive Study of Total Serum Homocysteine Status in Adult Henan Province, China.

Background: Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease. Total serum homocysteine (tHcy) status varies greatly with ethnicity and gender. Here, we studied the tHcy status by investigating concentration of tHcy and calculating prevalence of HHcy according to different age groups and genders.

Poly(ADP-Ribose) Polymerase Activity and Coronary Artery Disease in Type 2 Diabetes Mellitus: An Observational and Bidirectional Mendelian Randomization Study.

Objective: Experimental evidence suggests a close link between PARP (poly[ADP-ribose] polymerase) activation and diabetic endothelial dysfunction. Here, we tested whether PARP activity in circulating leukocytes was associated with coronary artery disease (CAD) among patients with type 2 diabetes mellitus (T2DM). Approach and Results: We performed observational and bidirectional Mendelian randomization studies of 3149 Chinese individuals with T2DM who underwent coronary angiography, with leukocyte PARP activity, 16 tag single-nucleotide polymorphisms in and , and 17 CAD risk single-nucleotide polymorphisms analyzed.

Vitamin D suppress the production of vascular endothelial growth factor in mast cell by inhibiting PI3K/Akt/p38 MAPK/HIF-1α pathway in chronic spontaneous urticaria.

Mast cells play a significant role in urticaria pathogenesis. It's evidenced that vitamin D has positive impact in chronic spontaneous urticaria (CSU) recently, but underlying mechanisms remain unclear. In this study, isobaric tag for relative and absolute quantification-liquid chromatography-mass spectrometer/mass spectrometer was used to detect the expression of proteins in sera of CSU patients and healthy subjects.

Joint effects of mitochondrial DNA deletion and serum folate deficiency on coronary artery disease in type 2 diabetes mellitus.

Background & Aims: The 4977-bp mitochondrial deletion (mtDNA deletion), as a hallmark of mitochondrial oxidative damage, may play an important role in coronary artery disease (CAD), but its interaction with folate deficiency among diabetic patients is largely unknown. We aimed to explore the joint association of leukocyte mtDNA deletion and serum folate status with obstructive CAD in Chinese adults with type 2 diabetes.

Methods: We cross-sectionally analyzed the angiographic data of 2017 diabetic patients without B-vitamin supplementation.

Mitochondrial 8-hydroxy-2'-deoxyguanosine and coronary artery disease in patients with type 2 diabetes mellitus.

Background: Little is known about whether mitochondria 8-hydroxy-2'-deoxyguanosine (8-OHdG), a biomarker of mitochondrial DNA (mtDNA) oxidative damage, contributes to the development of coronary artery disease (CAD) in diabetic patients. Here, we explored the associations of mtDNA 8-OHdG in leukocytes with obstructive CAD, coronary stenosis severity, cardiovascular biomarkers, and 1-year adverse outcomes after coronary revascularization in patients with type 2 diabetes mellitus (T2DM).

Methods: In a total of 1920 consecutive patients with T2DM who underwent coronary angiography due to symptoms of angina or angina equivalents, the presence of obstructive CAD, the number of diseased vessels with ≥ 50% stenosis, and modified Gensini score were cross-sectionally evaluated; the level of mtDNA 8-OHdG was quantified by quantitative PCR.

Identification of a blood-based 12-gene signature that predicts the severity of coronary artery stenosis: An integrative approach based on gene network construction, Support Vector Machine algorithm, and multi-cohort validation.

Background And Aims: We aimed to identify a blood-based gene expression score (GES) to predict the severity of coronary artery stenosis in patients with known or suspected coronary artery disease (CAD) by integrative use of gene network construction, Support Vector Machine (SVM) algorithm, and multi-cohort validation.

Methods: In the discovery phase, a public blood-based microarray dataset of 110 patients with known CAD was analyzed by weighted gene coexpression network analysis and protein-protein interaction network analysis to identify candidate hub genes. In the training set with 151 CAD patients, bioinformatically identified hub genes were experimentally verified by real-time polymerase chain reaction, and statistically filtered with the SVM algorithm to develop a GES.

LRRK2 is involved in the pathogenesis of system lupus erythematosus through promoting pathogenic antibody production.

Background: Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by the presence of pathogenic autoantibodies associated with polyclonal B cell hyperreactivity. Previous study reported that autophagy-related gene Leucine-rich repeat kinase 2 (LRRK2) was likely a susceptible gene for SLE. However, the pathogenic function of LRRK2 in SLE is undefined.

Identification of Promoter Hypermethylation as a Biomarker for Intra-Epithelial Lesion and Cervical Cancer: A Meta-Analysis of Published Studies, TCGA, and GEO Datasets.

Promoter hypermethylation in death-associated protein kinase 1 () gene has been long linked to cervical neoplasia, but the established results remained controversial. Here, we performed a meta-analysis to assess the associations of promoter hypermethylation with low-grade intra-epithelial lesion (HSIL), high-grade intra-epithelial lesion (HSIL), cervical cancer (CC), and clinicopathological features of CC. Published studies with qualitative methylation data were initially searched from PubMed, Web of Science, EMBASE, and China National Knowledge Infrastructure databases (up to March 2018).

Intestinal Epithelial Cell-Derived LKB1 Suppresses Colitogenic Microbiota.

Dysregulation of the immune barrier function of the intestinal epithelium can often result in dysbiosis. In this study we report a novel role of intestinal epithelial cell (IEC)-derived liver kinase B1 (LKB1) in suppressing colitogenic microbiota. IEC-specific deletion of LKB1 (LKB1) resulted in an increased susceptibility to dextran sodium sulfate (DSS)-induced colitis and a definitive shift in the composition of the microbial population in the mouse intestine.

LRRK2 promotes the activation of NLRC4 inflammasome during Typhimurium infection.

Although genetic polymorphisms in the gene are associated with a variety of diseases, the physiological function of LRRK2 remains poorly understood. In this study, we report a crucial role for LRRK2 in the activation of the NLRC4 inflammasome during host defense against serovar Typhimurium infection. deficiency reduced caspase-1 activation and IL-1β secretion in response to NLRC4 inflammasome activators in macrophages.