Goodwinandersson1197

This review aims to summarize the current knowledge on the cardiac signaling pathways modulated by these two antineoplastic drugs highly used in the management of breast cancer, not only focusing on cardiomyocytes but also to broaden the knowledge of the potential impact on other cells found in the heart.

Myocardial ischemia-reperfusion (I/R) injury is considered as a major obstacle of myocardial perfusion to save acute myocardial infarction, and causes a serious threat to human health. An extensive body of evidence has unveiled that mesenchymal stem cells (MSCs) as adult stem cells play a vital role in the field of damaged myocardial regeneration and repair. However, the biological role of MSCs derived-exosomes in the protection of myocardial I/R injury has not been elucidated.

In this study, we isolated and characterized MSCs from the bone marrow of rats femur and tibia. H9c2 cells were administrated to established the cellular hypoxia-reoxygenation (H/R) model, and co-cultured with MSCs and MSCs-derived exosomes.

Functional experiments revealed that MSCs and MSCs-derived exosomes inhibited H/R-induced cell apoptosis and cell autophagy. Interestingly, rapamycin as an activator of autophagy reversed the positive effects of MSCs-derived exosomes, while 3-methyladenine (3-MA) as autophagy inhibitor further promoted the effects of MSCs-derived exosomes, indicating MSCs exerted its function on H/R injury by mediating autophagy. Subsequently, we found that CHK2-Beclin2 pathway participated in H/R-induced autophagy. Mechanistically, miR-143-3p directly targeted CHK2 and negatively regulated CHK2 expression. Moreover, repression of exosomal miR-143-3p promoted H/R-induced autophagy via CHK2-Beclin2 pathway. Consistent with the results of in vitro experiments, in vivo experiments confirmed that exosomal miR-143-3p effectively reduced cell apoptosis by regulating autophagy via CHK2-Beclin2 pathway.

Collectively, our results indicated that MSCs-derived exosomal miR-143-3p might represent a promising option for the treatment of I/R injury.

Collectively, our results indicated that MSCs-derived exosomal miR-143-3p might represent a promising option for the treatment of I/R injury.

Saxagliptin, a selective/potent dipeptidyl peptidase-4 inhibitor, has revealed remarkable anti-inflammatory features in murine models of nephrotoxicity, hepatic injury, and neuroinflammation. However, its potential effect on ethanol-induced gastric mucosal injury has not been examined. Hence, the present work investigated the prospect of saxagliptin to attenuate ethanol-evoked gastric injury, with emphasis on the AMPK/mTOR-driven autophagy and NLRP3/ASC/caspase-1 pathway.

In ethanol-induced gastropathy, the gastric tissues were examined by immunohistochemistry, immunoblotting, histopathology, and ELISA.

The results demonstrated that saxagliptin (10mg/kg; by gavage) suppressed the gastric pathological signs (area of gastric ulcer and ulcer index scores), histopathologic aberrations/damage scores, without provoking hypoglycemia in rats. These protective features were attributed to the enhancement of gastric mucosal autophagy flux, as proven with increased expression of LC3-II and Beclin 1, decreased accumriven autophagy and inhibiting NLRP3 inflammasome.Sea turtles complete migrations across vast distances, covering entire ocean basins. To track these migrations, satellite tracking tags are attached to their shells. The impact of these tags must be considered to ensure that turtles' natural behavior is not artificially and adversely impacted through tag-related drag, and that the data collected by a small sample of sea turtles accurately represents the larger population. Additionally, it can be difficult to study animal energetics in the field over large migration distances. In this work, we modify a computational behavior model to study how satellite tracking tags affect turtle migration behavior. Our agent based model contains synthetic magnetic field environments that are used for navigation cues, an ocean current, resource distributions that represent locations of food, and an agent that attempts to migrate to several different goals. The agent loses energy as it progresses, and searches for the resource distributions to replenish itself. Our novel simulation framework demonstrates the relationship between an agent's available energy capacity, its energy consumption based on mechanical power expended, and its ability to navigate to all migratory goal points. This study can be utilized to (1) probe the impacts of an animal's energy capacity and foraging behavior on its resulting navigation and ecology, (2) guide future satellite tag designs, and (3) develop usage recommendations for a suitable tracking tag based on the type of experiment being conducted. Our model can be expanded beyond sea turtles to study other marine species (e.g., sharks, whales). Additionally, this model could be expanded to other domains within the marine environment. For example, it could be modified to examine design trade-offs in remotely operated vehicles (ROVs), which share many of the same operational constraints as sea turtles and other migratory species.Various human tissues and cells express phospholipase A1 member A (PLA1A), including the liver, lung, prostate gland, and immune cells. The enzyme belongs to the pancreatic lipase family. PLA1A specifically hydrolyzes sn-1 fatty acid of phosphatidylserine (PS) or 1-acyl-lysophosphatidylserine (1-acyl-lysoPS). PS externalized by activated cells or apoptotic cells or extracellular vesicles is a potential source of substrate for the production of unsaturated lysoPS species by PLA1A. Maturation and functions of many immune cells, such as T cells, dendritic cells, macrophages, and mast cells, can be regulated by PLA1A and lysoPS. Several lysoPS receptors, including GPR34, GPR174 and P2Y10, have been identified. High serum levels and high PLA1A expression are associated with autoimmune disorders such as Graves' disease and systemic lupus erythematosus. Increased expression of PLA1A is associated with metastatic melanomas. C1632 PLA1A may contribute to cardiometabolic disorders through mediating cholesterol transportation and producing lysoPS.