Evaluation of the protective bioactivity and molecular mechanism verification of lactoferrin in an Alzheimer's mouse model with ulcerative enteritis.

The development of new drug therapies for Alzheimer's disease (AD) is an important research topic today, but the pathogenesis of AD has not been thoroughly studied, and there are still several shortcomings in existing drug therapies. Therefore, this study aimed to explore the molecular mechanism of lactoferrin (LF) in the treatments of AD and ulcerative colitis (UC) that is susceptible to AD, starting from the principle of one drug, two diseases, and the same treatment. This study used pathological staining and specific indicator staining to preliminarily evaluate the interventions of LF on UC injury and AD progression.

TET2 regulation of alcoholic fatty liver via mRNA in paraspeckles.

Epigenetic modifications have emerged as key regulators of metabolism-related complex diseases including the alcoholic fatty liver disease (AFLD) prevalent chronic liver disorder with significant economic implications. Building upon previous research that emphasizes ten-eleven translocation (TET) proteins' involvement in adipocyte insulin sensitization and fatty acid oxidation, we explored the role of TET2 protein in AFLD pathogenesis which catalyzes 5-methylcytosine into 5-hydroxymethylcytosine in DNA/RNA. Our findings revealed that TET2 deficiency exacerbates AFLD progression.

Adipose improves muscular atrophy caused by Sirtuin1 deficiency by promoting mitochondria synthesis.

Muscular dysplasia is a common muscle disease, but its pathological mechanism is still unclear. Adipose is originally identified as a highly conservative and widely expressed anti-obesity gene, and our previous study has reported that Adipose is also a positive regulator of myogenesis. Considering the vital role of during muscle development, this study was to demonstrate a potential relationship between Sirtuin1 and Adipose and clarified the mechanism by which Adipose regulated muscle development.

sSTEAP4 regulates cellular homeostasis and improves high-fat-diet-caused oxidative stress in hepatocytes.

Aim: Nonalcoholic fatty liver disease (NAFLD) has become a global epidemic, but its pathogenesis is unclear. STEAP4, a member of six transmembrane protein family, integrates inflammatory and metabolic responses. Our present aim is to explore the roles of STEAP4 in maintaining cellular homeostasis and improving high-fat-diet (HFD)-caused oxidative stress in hepatocytes.

Sirt1 Promotes the Restoration of Hepatic Progenitor Cell (HPC)-Mediated Liver Fatty Injury in NAFLD Through Activating the Wnt/β-Catenin Signal Pathway.

Non-alcoholic fatty liver disease (NAFLD) has developed into the world's largest chronic epidemic. In NAFLD, hepatic steatosis causes hepatocytes dysfunction and even apoptosis. The liver has a strong restoration or regeneration ability after an injury, however, it is unclear through which pattern fatty liver injury in NAFLD is repaired and what the repair mechanism is.

PPARγ enhanced Adiponectin polymerization and trafficking by promoting RUVBL2 expression during adipogenic differentiation.

Adipocyte differentiation is an essential part of adipose tissue development, and is closely related to obesity and obesity-related diseases. In this study, we found that the expression of PPARγ, RUVBL2 and Adiponectin were concurrently obviously increased in the 5th-7th day of 3T3-L1 cell differentiation. PPARγ overexpression or the PPARγ activator facilitated Adiponectin trafficking and secretion and upregulated RUVBL2 expression as well as AS160 phosphorylation during adipogenic differentiation of 3T3-L1 cells.

KLF15-activating Twist2 ameliorated hepatic steatosis by inhibiting inflammation and improving mitochondrial dysfunction NF-κB-FGF21 or SREBP1c-FGF21 pathway.

Twist-related protein 2 (TWIST2) is identified as a basic helix-loop-helix (b-HLH) transcription repressor by dimerizing with other b-HLH proteins. The significance of TWIST2 has been emphasized in various tumors; however, few studies report its functions in metabolism and metabolic diseases. Here we aimed to explore the novel role and regulation mechanism of TWIST2 in hepatic steatosis.

Methamidophos Influences Midgut Proteinase Activity and Subcellular Structures in the Wolf Spider Pardosa pseudoamulata (Araneae: Lycosidae).

A piezoelectric quartz crystal impedance (PQCI) sensor was used to investigate influences of the insecticide methamidophos on proteinase activity in midguts of the wolf spider, Pardosa pseudoamulata (Araneae: Lycosidae). Results from PQCI indicated that low-concentration dose methamidophos (0.008%) can activate the proteinase but high-concentration dose methamidophos (0.

Biotoxicity of Cry1Ab protein on wolf spider Pardosa pseudoannulata.

In this research, we carried out a tritrophic bioassay to assess the potential effect of Cry1Ab-expressing rice on the foraging behavior of the common wolf spider Pardosa pseudoannulata and its underlying molecular mechanism. Results indicated the Bt-containing spiders expressed a higher foraging range when compared to controls. The high throughput de novo transcriptome sequencing was further carried out for central nervous system (CNS) of P.