Association between a single-nucleotide polymorphism of the angiotensin-converting enzyme gene and susceptibility to systemic lupus erythematosus in the Hainanese population of China.

The angiotensin-converting enzyme (ACE) gene plays a significant role in regulating immune responses and inflammatory processes, thus impacting the susceptibility to systemic lupus erythematosus (SLE). Understanding how single-nucleotide polymorphisms (SNPs) within the ACE gene contribute to the genetic susceptibility to SLE is essential for comprehending the disease's aetiology. Therefore, exploring this relationship in the Hainan region of China is crucial for gaining insights into the pathogenesis of SLE.

Exploring the Relationship between ACE Gene Variants and Systemic Lupus Erythematosus Susceptibility in the Hainan Population through Genetic Association Analysis.

Background: The purpose of this study was to determine the association between single nucleotide polymorphisms (SNPs) at the rs4331, rs4341, and rs4351 loci of the angiotensinconverting enzyme (ACE) gene and genetic susceptibility to systemic lupus erythematosus (SLE) in the Hainan population.

Methods: This study involved a total of 428 participants, with 214 individuals diagnosed with SLE and an equal number of healthy controls. The SNaPshot sequencing technique was used to determine the base sequences at the ACE gene rs4331, rs4341, and rs4351 loci in the study subjects.

α-synuclein regulates Cyclin D1 to promote abnormal initiation of the cell cycle and induce apoptosis in dopamine neurons.

The etiology of Parkinson's disease (PD) is characterized by the death of dopamine neurons in the substantia nigra pars compacta, while misfolding and abnormal aggregation of α-synuclein (α-syn) are core pathological features. Previous studies have suggested that damage to dopamine neurons may be related to cell cycle dysregulation, but the specific mechanisms remain unclear. In this study, a PD mouse model was induced by stereotactic injection of α-syn into the nucleus, and treated with the cell cycle inhibitor, roscovitine (Rosc).

Exploring a novel therapeutic strategy: the interplay between gut microbiota and high-fat diet in the pathogenesis of metabolic disorders.

In the past two decades, the rapid increase in the incidence of metabolic diseases, including obesity, diabetes, dyslipidemia, non-alcoholic fatty liver disease, hypertension, and hyperuricemia, has been attributed to high-fat diets (HFD) and decreased physical activity levels. Although the phenotypes and pathologies of these metabolic diseases vary, patients with these diseases exhibit disease-specific alterations in the composition and function of their gut microbiota. Studies in germ-free mice have shown that both HFD and gut microbiota can promote the development of metabolic diseases, and HFD can disrupt the balance of gut microbiota.

Multidirectional associations between the gut microbiota and Parkinson's disease, updated information from the perspectives of humoral pathway, cellular immune pathway and neuronal pathway.

The human gastrointestinal tract is inhabited by a diverse range of microorganisms, collectively known as the gut microbiota, which form a vast and complex ecosystem. It has been reported that the microbiota-gut-brain axis plays a crucial role in regulating host neuroprotective function. Studies have shown that patients with Parkinson's disease (PD) have dysbiosis of the gut microbiota, and experiments involving germ-free mice and fecal microbiota transplantation from PD patients have revealed the pathogenic role of the gut microbiota in PD.

Can kynurenine pathway be considered as a next-generation therapeutic target for Parkinson's disease? An update information.

By far, no revolutionary breakthrough in the treatment of Parkinson's disease (PD) was found. It is indeed a knotty problem to select a satisfactory strategy for treating some patients with advanced stage PD. Development of novel therapeutic targets against PD has been an urgent task faced by global PD researchers.

Sempervirine Mediates Autophagy and Apoptosis the Akt/mTOR Signaling Pathways in Glioma Cells.

The potential antitumor effects of sempervirine (SPV), an alkaloid compound derived from the traditional Chinese medicine Benth., on different malignant tumors were described in detail. The impact of SPV on glioma cells and the basic atomic components remain uncertain.

Impact of Gut Microbiota and Microbiota-Related Metabolites on Hyperlipidemia.

Hyperlipidemia, defined as the presence of excess fat or lipids in the blood, has been considered as a high-risk factor and key indicator of many metabolic diseases. The gut microbiota has been reported playing a vital role in regulating host lipid metabolism. The pathogenic role of gut microbiota in the development of hyperlipidemia has been revealed through fecal microbiota transplantation experiment to germ-free mice.

Alisol B 23-Acetate Ameliorates Azoxymethane/Dextran Sodium Sulfate-Induced Male Murine Colitis-Associated Colorectal Cancer Modulating the Composition of Gut Microbiota and Improving Intestinal Barrier.

Hunting for natural compounds that can modulate the structure of the intestinal flora is a new hotspot for colitis-associated cancer (CAC) prevention or treatment. Alisol B 23-acetate (AB23A) is a natural tetracyclic triterpenoid found in which is well known for dietary herb. is often used clinically to treat gastrointestinal diseases in China.

Alismatis Rhizoma Triterpenes Alleviate High-Fat Diet-Induced Insulin Resistance in Skeletal Muscle of Mice.

Alismatis rhizoma (AR), which is the dried rhizome of (Sam.) Juz. (Alismataceae), is an important component of many famous Chinese formulas for hypoglycemic.

Anti-osteoporotic effects of alisol C 23-acetate via osteoclastogenesis inhibition.

Alismatis rhizoma (AR) is the dried rhizome of Alisma orientale (Sam.) Juz. (Alismataceae).