This study offers insightful outlooks on the scalable fabrication of a porous few-layered structure with a promoted photocatalytic performance. Mitochondria are indispensable organelles that perform critical cellular functions, including energy metabolism, neurotransmission, and synaptic maintenance. Mitochondrial dysfunction and impairment in the organellar homeostasis are key hallmarks implicated in the progression of neurodegenerative disorders. The members of DJ-1/ThiJ/PfpI family are highly conserved, and loss of DJ-1 (PARK7) function in humans results in the impairment of mitochondrial homeostasis, which is one of the key cellular etiology implicated in the progression of Parkinson’s Disease. However, the underlying molecular mechanism involved in mitochondrial maintenance and other cellular processes by DJ-1 paralogs is poorly understood. By utilizing genetic approaches from S. cerevisiae, we uncovered intricate mechanisms associated with the mitochondrial phenotypic variations regulated by DJ-1 paralogs. The deletion of DJ-1 paralogs led to respiratory incompetence and the accumulation of enhanced functional mitochondrial mass. The lack of DJ-1 paralogs also displayed enriched mitochondrial interconnectivity due to upregulation in the fusion-mediating proteins, facilitated by the elevation in the basal cellular ROS and oxidized glutathione levels. Intriguingly, these mitochondrial phenotypes variations cause cell size abnormalities, partially suppressed by reestablishing redox balance and upregulation of fission protein levels. Besides, in the absence of DJ-1 paralogs, cells exhibited a significant delay in the cell-cycle progression in the G2/M phase, attributed to mitochondrial hyperfusion and partial DNA damage. Additionally, the aberrations in mitochondrial dynamics and cell-cycle induce cell death mediated by apoptosis. Taken together, our findings first-time provide evidence to show how DJ-1 family members regulate mitochondrial homeostasis and other intricate cellular processes, including cell cycle and apoptosis. In Experiment 1, the effects of glucose concentration in extender (0 mM, 67 mM, 147 mM, 270 mM; G0, G67, G147, and G270, respectively) and storage temperature of extended semen (5, 10, 15 and 20 °C) were evaluated after storage for up to 5 days (T0h to T120h). For all time points tested, mean total (TMOT) and progressive (PMOT) sperm motility were lower in G0 than all other treatment groups (P  0.05). In conclusion, the absence of added glucose in extender reduced the motion characteristics of stallion sperm during long-term storage (5 days), but VAI was not affected. The use of temperatures between 5 and 15 °C for long-term storage (5 days) best maintained sperm motility and VAI. The threshold concentration of added glucose in extender required to optimize sperm motion characteristics was 40 mM. Published by Elsevier Inc.B lymphocyte-induced maturation protein-1 (Blimp1) is a key regulator that promotes the terminal differentiation of mature B lymphocytes into plasma cells, and is essential for the survival of Multiple myeloma (MM)cells. However, the expression of Blimp1 in MM and its effect on the signaling pathway remain unknown. Studies have found that during long-term endoplasmic reticulum (ER) stress, activated ATF4 may also stimulate the CCAAT-enhancer-binding protein homologous protein (CHOP) gene, triggering the unfolded protein response (UPR) terminal apoptotic pathway in plasma cells. Moreover Aspirin can induce MM cell apoptosis through mitochondria and death receptor pathway. Therefore, we aim to explore whether Aspirin could induce AFT4/CHOP apoptosis pathway in MM by inhibiting Blimp1 expression, thereby promoting MM cell apoptosis and exerting anti-tumor effects. Dexmedetomidine (Dex) has been reported to be cardioprotective. Differential expression of miR-208b-3p is associated with myocardial injury. But it is unknown that aberrant expression of miR-208b-3p is implicated in myocardial protection of Dex. Hypoxia/reoxygenation (HR) model was established in H9C2 cells. qRT-PCR was performed to detect expression levels of miR-208b-3p in H9C2 undergoing HR, Dex preconditioning, overexpression of miR-208b-3p or inhibition, and to assess expression of Med13 in H9C2 following knockdown of Med13 mRNA. CCK8 and, flow cytometry and Western blot were conducted respectively to examine viability, apoptosis rate and protein expressions of H9C2 subjected to a variety of treatments. read more Dex preconditioning reduced expression of miR-208b-3p and apoptosis of H9C2 cells caused by HR, while Dex preconditioning increased viability of H9C2. Dex preconditioning increased expression of Med13, which was reduced after knockdown of Med13 mRNA in H9C2. Overexpression of miR-208b-3p attenuated Dex exerted protective effects of myocardial cells, which was reversed by inhibition of miR-208b-3p. Increased expression of Med13 or/and decreased expression of miR-208b-3p decreased expression levels of Wnt/β-catenin signaling pathway-related proteins (Wnt3a, Wnt5a and β-catenin), while knockdown of Med13 mRNA or increased expression of miR-208b-3p increased the expression levels of those proteins. Dex protects H9C2 cells against HR injury through miR-208b-3p/Med13/Wnt/β-catenin signaling pathway axis. Members of ADP-ribosylation factor (ARF)/ARF-like protein (ARL) family regulate malignant phenotype of cancer cells. The present study aims to investigate the clinical relevance of ARF/ARL family members in endometrial cancer. We report that several ARF/ARL family genes serve as prognostic biomarkers for endometrial cancer. Through a combination of TCGA database and immunohistochemistry analysis, we revealed that ARL4C, a member of ARL family, was overexpressed in endometrial cancer and might function as an oncogene in endometrial carcinogenesis. Gene set enrichment analysis (GSEA) and functional studies demonstrated that cell cycle and cell adhesion pathways were the potential mechanism of ARL4C in promoting endometrial cancer cell proliferation, migration and invasion. Moreover, we also observed the involvement of ARL4C in metformin-inhibited cellular proliferation of endometrial cancer. Collectively, knowledge of the expression and function of ARF/ARL family genes could provide a potential therapeutic strategy for endometrial cancer.