Development and external validation of a risk prediction model for depression in patients with coronary heart disease.

Background: Depression is an independent risk factor for adverse outcomes of coronary heart disease (CHD). This study aimed to develop a depression risk prediction model for CHD patients.

Methods: This study utilized data from the National Health and Nutrition Examination Survey (NHANES).

Effect of different hypoglycemic drugs and insulin on the risk of new-onset atrial fibrillation in people with diabetes: a network meta-analysis.

Objective: Diabetes is considered a significant risk factor for the development of atrial fibrillation/flutter (AF/AFL). However, there is still insufficient evidence to determine the varying effects of different hypoglycemic drugs (HDs) on the incidence of new-onset AF/AFL in diabetic patients. To address this gap, we conducted a network meta-analysis to investigate whether various HDs have different effects on the risk of new-onset AF/AFL compared with insulin.

Long-term effects of different hypoglycemic drugs on carotid intima-media thickness progression: a systematic review and network meta-analysis.

Objective: The progression of carotid intima-media thickness (cIMT) can partially predict the occurrence of future cardiovascular events. This network meta-analysis compared the effects of 14 antidiabetic drugs (acarbose, alogliptin, exenatide, glibenclamide, glimepiride, ipragliflozin, metformin, nateglinide, pioglitazone, rosiglitazone, sitagliptin, tofoglifozin, troglitazone, voglibose) on the progression of cIMT.

Method: PubMed, EMBASE, Cochrane Library, and Web of Science were searched to screen all clinical trials of treatment of cIMT with hypoglycemic agents before March 1, 2024.

Efficacy of physical exercise on the physical ability, cardiac function and cardiopulmonary fitness of patients with atrial fibrillation: a systematic review and meta-analysis.

Objective: It is advised that patients engage in physical activity to enhance their quality of life and achieve better results. The purpose of the current study was to measure the efficacy of exercise on the physical ability, cardiac function and cardiopulmonary fitness of patients with AF.

Method: A comprehensive systematic literature search was performed in PubMed, Embase, and Web of Science from 1991 to 2023 for RCTs comparing physical exercise combined with AF routine treatments to routine treatments alone.

Association of sleep characteristics with cardiovascular disease risk in adults over 40 years of age: a cross-sectional survey.

Background: The relationship between sleep characteristics and cardiovascular disease (CVD) risk has yet to reach a consistent conclusion, and more research needs to be carried out. This study aimed to explore the relationship between snoring, daytime sleepiness, bedtime, sleep duration, and high-risk sleep patterns with CVD risk.

Methods: Data from the National Health and Nutrition Examination Survey (NHANES) 2015-2018 were collected and analyzed.

Simulated and Verification of Mass and Heat Transfer Coupled Model of Jujube Slices Dried by Hot Air Combined with Radio Frequency Heat Treatment at Different Drying Stages.

This study investigates the impact of radio frequency (RF) heat treatment on heat and mass transfer during the hot air drying of jujube slices. Experiments were conducted at different drying stages, comparing single-hot air drying with hot air combined with RF treatment. Numerical models using COMSOL Multiphysics were developed to simulate the process, and the results were compared to validate the models.

Intestinal Epithelial STAT6 Activation Rescues the Defective Anti-Helminth Responses Caused by Deletion.

Dynamic regulation of intestinal epithelial cell (IEC) proliferation and differentiation is crucial for maintaining mucosa homeostasis and the response to helminth infection. O-GlcNAc transferase (OGT), an enzyme catalyzing the transfer of GlcNAc from the donor substrate UDP-GlcNAc onto acceptor proteins, has been proposed to promote intestinal epithelial remodeling for helminth expulsion by modifying and activating epithelial STAT6, but whether the IEC intrinsic OGT-STAT6 axis is involved in anti-helminth responses has not been tested in vivo. Here, we show that the inducible deletion of in IECs of adult mice leads to reduced tuft and goblet cell differentiation, increased crypt cell proliferation, and aberrant Paneth cell localization.

Sirtuin 6 maintains epithelial STAT6 activity to support intestinal tuft cell development and type 2 immunity.

Dynamic regulation of intestinal epithelial cell (IEC) differentiation is crucial for both homeostasis and the response to helminth infection. SIRT6 belongs to the NAD-dependent deacetylases and has established diverse roles in aging, metabolism and disease. Here, we report that IEC Sirt6 deletion leads to impaired tuft cell development and type 2 immunity in response to helminth infection, thereby resulting in compromised worm expulsion.

Epithelial STAT6 O-GlcNAcylation drives a concerted anti-helminth alarmin response dependent on tuft cell hyperplasia and Gasdermin C.

The epithelium is an integral component of mucosal barrier and host immunity. Following helminth infection, the intestinal epithelial cells secrete "alarmin" cytokines, such as interleukin-25 (IL-25) and IL-33, to initiate the type 2 immune responses for helminth expulsion and tolerance. However, it is unknown how helminth infection and the resulting cytokine milieu drive epithelial remodeling and orchestrate alarmin secretion.

NAMPT-mediated NAD biosynthesis suppresses activation of hepatic stellate cells and protects against CCl-induced liver fibrosis in mice.

Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the salvage pathway of mammalian nicotinamide adenine dinucleotide (NAD) biosynthesis. Through its NAD-biosynthetic activity, NAMPT is able to regulate the development of hepatic steatosis and inflammation induced by diet or alcohol. However, the roles NAMPT plays in the development of liver fibrosis remain obscure.

Persistent mTORC1 activation via Depdc5 deletion results in spontaneous hepatocellular carcinoma but does not exacerbate carcinogen- and high-fat diet-induced hepatic carcinogenesis in mice.

The mechanistic target of rapamycin complex 1 (mTORC1) acts as a central regulator of metabolic pathways that drive cellular growth. Abnormal activation of mTORC1 occurs at high frequency in human and mouse hepatocellular carcinoma (HCC). DEP domain-containing protein 5 (DEPDC5), a component of GATOR1 complex, is a repressor of amino acid-sensing branch of the mTORC1 pathway.

Depdc5 deficiency exacerbates alcohol-induced hepatic steatosis via suppression of PPARα pathway.

Alcohol-related liver disease (ALD), a condition caused by alcohol overconsumption, occurs in three stages of liver injury including steatosis, hepatitis, and cirrhosis. DEP domain-containing protein 5 (DEPDC5), a component of GAP activities towards Rags 1 (GATOR1) complex, is a repressor of amino acid-sensing branch of the mammalian target of rapamycin complex 1 (mTORC1) pathway. In the current study, we found that aberrant activation of mTORC1 was likely attributed to the reduction of DEPDC5 in the livers of ethanol-fed mice or ALD patients.

Adipocyte-specific deletion of Depdc5 exacerbates insulin resistance and adipose tissue inflammation in mice.

The mammalian target of rapamycin complex 1 (mTORC1) is a crucial regulator of adipogenesis and systemic energy metabolism. Its dysregulation leads to a diversity of metabolic diseases, including obesity and type 2 diabetes. DEP-domain containing 5 (DEPDC5) is a critical component of GATOR1 complex that functions as a key inhibitor of mTORC1.

Sirtuin 6 ameliorates alcohol-induced liver injury by reducing endoplasmic reticulum stress in mice.

Alcoholic liver disease (ALD) occurs as a result of chronic and excessive alcohol consumption. It encompasses a wide spectrum of chronic liver abnormalities that range from steatosis to alcoholic hepatitis, progressive fibrosis and cirrhosis. Endoplasmic reticulum (ER) stress induced by ethanol metabolism in hepatocytes has been established as an important contributor to the pathogenesis of ALD.