Regeneration of Non-Alcoholic Fatty Liver Cells Using Chimeric FGF21/HGFR: A Novel Therapeutic Approach.

Non-alcoholic fatty liver disease (NAFLD) has emerged as a significant liver ailment attributed to factors like obesity and diabetes. While ongoing research explores treatments for NAFLD, further investigation is imperative to address this escalating health concern. NAFLD manifests as hepatic steatosis, precipitating insulin resistance and metabolic syndrome. This study aims to validate the regenerative potential of chimeric fibroblast growth factor 21 (FGF21) and Hepatocyte Growth Factor Receptor (HGFR) in NAFLD-afflicted liver cells. AML12, a murine hepatocyte cell line, was utilized to gauge the regenerative effects of chimeric FGF21/HGFR expression. Polysaccharide accumulation was affirmed through Periodic acid-Schiff (PAS) staining, while LDL uptake was microscopically observed with labeled LDL. The expression of FGF21/HGFR and NAFLD markers was analyzed by mRNA analysis with RT-PCR, which showed a decreased expression in acetyl-CoA carboxylase 1 (ACC1) and sterol regulatory element binding protein (SREBP) cleavage-activating protein (SCAP) with increased expression of hepatocellular growth factor (HGF), hepatocellular nuclear factor 4 alpha (HNF4A), and albumin (ALB). These findings affirm the hepato-regenerative properties of chimeric FGF21/HGFR within AML12 cells, opening novel avenues for therapeutic exploration in NAFLD.

Case series of branch retinal vein occlusion secondary to rhegmatogenous retinal detachment and its surgical management.

BACKGROUND: To review cases of branch retinal vein occlusion (BRVO) secondary to rhegmatogenous retinal detachment (RRD) and its surgical management and presume their mechanism. METHODS: Medical records of patients who underwent surgery for RRD between 2015 and 2019 at a single tertiary care center were retrospectively reviewed. New BRVO secondary to RRD or its surgical procedure was diagnosed based on the fundus examination and its clinical course. RESULTS: A total of 734 RRD surgeries were performed for five years, and six cases of new BRVOs were noticed in the first year after surgery (incidence was 0.68%: six cases of BRVO / 734 cases of surgical RRD); five cases occurred after vitrectomy, and one occurred after scleral buckling. In three cases, retinal veins were presumed to already be partially occluded related due to a kink of the retinal vein seen before surgery. In the other three cases, the retinal veins were presumed to have incurred damage during vitrectomy. CONCLUSION: In the present cohort, RRD or its related procedures caused BRVO within a year of surgery at an incidence of 0.68%. The proposed mechanisms are kinks of the retinal vein on the detached retina and damage to the retinal vein during vitrectomy.

Adiponectin prevents skin inflammation in rosacea by suppressing S6 phosphorylation in keratinocytes.

Numerous recent evidence highlights epidemiological connections between rosacea and metabolic disorders. However, the precise path through which metabolic factors impact rosacea risk is still unclear. Therefore, this study aims to investigate the role of adiponectin, a crucial adipokine that regulates metabolic homeostasis, in the pathogenesis of rosacea. We elucidated a detrimental feedback loop between rosacea-like skin inflammation and decreased levels of skin adiponectin. To elaborate, rosacea lesional skin exhibits diminished adiponectin expression compared to non-lesional areas in the same patients. Induction of rosacea-like inflammation reduced adiponectin levels in the skin by generating inflammatory cytokines that suppress adiponectin production from subcutaneous adipocytes. Conversely, complete depletion of adiponectin exacerbated rosacea-like features in the mouse model. Mechanistically, adiponectin deficiency led to heightened S6 phosphorylation, a marker of the mTORC1 signaling pathway, in the epidermis. Adiponectin significantly inhibited S6 phosphorylation in cultured keratinocytes. Notably, replenishing adiponectin whole protein or topically applying an agonist for adiponectin receptor 1 successfully improved rosacea-like features in mice. This study contributes to understanding the role of adiponectin in skin inflammation associated with rosacea pathophysiology, suggesting that restoring adiponectin function in the skin could be a potential therapeutic strategy.