Salazarpaulsen4261

Traumatic Brain Injury (TBI) present a significant burden to global health. Close association and mutual regulation exist between the brain and gut microbiota. In addition, metabolites may play an important role as intermediary mediators of the brain and gut microbiota. Consequently, the study sought to investigate the alterations in gut microbiota and metabolites after TBI and conducted a comprehensive analysis of the correlation between gut microbiota and metabolites after TBI in mice.

Changes in intestinal microbiota and metabolites in mice after moderate or severe traumatic brain injury were detected through 16S rDNA sequencing and the non-target LC-MS technology. Additionally, Pearson correlation analysis was used to explore the association between the microbiota and metabolites.

TBI was able to change the composition of intestinal microbiota, resulting to a decrease in microbial diversity in the intestinal tract (sham vs sTBI 8.35±0.12 vs 7.71±0.5, p<0.01; sTBI vs mTBI 7.71±0.5 vs 8.25±0.34, p<0.05). The results also showed that TBI could change the types and abundance of metabolites (723 in mTBI and sham groups; 1221 in sTBI and sham groups; 324 in mTBI and sTBI groups). Moreover, some of the altered gut metabolites were significantly correlated with part of the altered gut microbes after TBI.

TBI significantly changed intestinal microbiota as well as metabolites. Some of the altered microbiota and metabolites had a significant association. The results from this study provide information that paves way for future studies utilizing the brain gut axis theory in the diagnosis and treatment of TBI.

TBI significantly changed intestinal microbiota as well as metabolites. Some of the altered microbiota and metabolites had a significant association. The results from this study provide information that paves way for future studies utilizing the brain gut axis theory in the diagnosis and treatment of TBI.Transforming growth factor beta (TGFβ) and bone morphogenetic protein (BMP) signaling play opposing roles in epithelial-mesenchymal transition (EMT) of lens epithelial cells, a cellular process integral to the pathogenesis of fibrotic cataract. We previously showed that BMP-7-induced Smad1/5 signaling blocks TGFβ-induced Smad2/3-signaling and EMT in rat lens epithelial cell explants. To further explore the antagonistic role of BMPs on TGFβ-signaling, we tested the capability of BMP-4 or newly described BMP agonists, ventromorphins, in blocking TGFβ-induced lens EMT. Primary rat lens epithelial explants were treated with exogenous TGFβ2 alone, or in combination with BMP-4 or ventromorphins. Treatment with TGFβ2 induced lens epithelial cells to undergo EMT and transdifferentiate into myofibroblastic cells with upregulated α-SMA and nuclear translocation of Smad2/3 immunofluorescence. BMP-4 was able to suppress this EMT without blocking TGFβ2-nuclear translocation of Smad2/3. In contrast, the BMP agonists, ventromorphins, were unable to block TGFβ2-induced EMT, despite a transient and early ability to significantly reduce TGFβ2-induced nuclear translocation of Smad2/3. This intriguing disparity highlights new complexities in the responsiveness of the lens to differing BMP-related signaling. Further research is required to better understand the antagonistic relationship between TGFβ and BMPs in lens EMT leading to cataract.Understanding the pathophysiological mechanisms of neuropsychiatric disorders has been a challenging quest for neurobiologists. Recent years have witnessed enormous technological advances in the field of neuroimmunology, blurring boundaries between the central nervous system and the periphery. Consequently, the discipline has expanded to cover interactions between the nervous and immune systems in health and diseases. read more The complex interplay between the peripheral and central immune pathways in neuropsychiatric disorders has recently been documented in various studies, but the genetic determinants remain elusive. Recent transcriptome studies have identified dysregulated genes involved in peripheral immune cell activation, blood-brain barrier integrity, glial cell activation, and synaptic plasticity in major depressive disorder, bipolar disorder, autism spectrum disorder, and schizophrenia. Herein, the key transcriptomic techniques applied in investigating differentially expressed genes and pathways responsible for altered brain-immune interactions in neuropsychiatric disorders are discussed. The application of transcriptomics that can aid in identifying molecular targets in various neuropsychiatric disorders is highlighted.Diabetes mellitus is a metabolic disorder diagnosed by elevated blood glucose levels and a defect in insulin production. Blood glucose, an energy source in the body, is regenerated by two fundamental processes glycolysis and gluconeogenesis. These two processes are the main mechanisms used by humans and many other animals to maintain blood glucose levels, thereby avoiding hypoglycaemia. The released insulin from pancreatic β-cells activates glycolysis. However, the glucagon released from the pancreatic α-cells activates gluconeogenesis in the liver, leading to pyruvate conversion to glucose-6-phosphate by different enzymes such as fructose 1,6-bisphosphatase and glucose 6-phosphatase. These enzymes' expression is controlled by the glucagon/ cyclic adenosine 3',5'-monophosphate (cAMP)/ proteinkinase A (PKA) pathway. This pathway phosphorylates cAMP-response element-binding protein (CREB) in the nucleus to bind it to these enzyme promoters and activate their expression. During fasting, this process is activated to supply the body with glucose; however, it is overactivated in diabetes. Thus, the inhibition of this process by blocking the expression of the enzymes via CREB is an alternative strategy for the treatment of diabetes. This review was designed to investigate the association between CREB activity and the treatment of diabetes and diabetes complications. The phosphorylation of CREB is a crucial step in regulating the gene expression of the enzymes of gluconeogenesis. Many studies have proven that CREB is over-activated by glucagon and many other factors contributing to the elevation of fasting glucose levels in people with diabetes. The physiological function of CREB should be regarded in developing a therapeutic strategy for the treatment of diabetes mellitus and its complications. However, the accessible laboratory findings for CREB activity of the previous research still not strong enough for continuing to the clinical trial yet.