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SOX9 knockdown repressed OC development and Wnt/β-catenin pathway. The volume, weight, positive rate of Ki67, CyclinD1, p53 and the degree of tumor necrosis were affected by miR-185 expression. This study demonstrated that DEX could inhibit OC development via upregulating miR-185 expression and inactivating the SOX9/Wnt/β-catenin signaling pathway.The dysregulation of microRNAs (miRNAs) expression is relevant to the progression of many tumors. As reported, the abnormal expression of miR-1269b is pivotal in certain cancers’ progression. This work was designed to study the role and hidden mechanism of miR-1269b in gastric cancer (GC) progression. In this work, we proved that miR-1269b was lowly expressed in GC tissues and cell lines, which was associated with larger tumor size and lymph node metastasis. MiR-1269b overexpression repressed the multiplication, migration and invasion of GC cells while miR-1269b inhibition had the opposite effects. Methyltransferase-like 3 (METTL3) was identified as the direct target of miR-1269b in GC cells, and its overexpression reversed the inhibitory effect of transfection of miR-1269b mimics on GC cell viability, migration and invasion. On all accounts, these data indicated that miR-1269b inhibits GC progression via targeting METTL3.Axis formed by integrin β3 (ITGβ3)-Ras homolog gene family, member A (RhoA), and Yes-associated protein (YAP) plays an important role in atherosclerosis. In addition, ITGβ3 overexpression was noted in high-glucose (HG) exposure podocytes. However, the ITGβ3-RhoA-YAP axis on HG-induced podocyte injury remains unclear. This study aimed to investigate whether ITGβ3 regulates podocyte injury by regulating the RhoA-YAP axis. The function and potential mechanism of ITGβ3 were observed through in vitro wound-healing assays, flow cytometry, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and western blot assay. Results showed that HG treatment increased the ability of wound closure and apoptosis; however, in spite of HG treatment, ITGβ3 inhibition mitigated the ability of wound closure and apoptosis in podocytes. By contrast, overexpression of ITGβ3 increased the wound closure and apoptosis abilities of podocytes. Under HG treatment, ITGβ3 knockdown is associated with upregulation of RhoA, total YAP1, and nucleus YAP1, whereas ITGβ3 overexpression has opposite effect. In addition, RhoA overexpression in podocytes reverses the effect of ITGβ3 overexpression on the wound closure and apoptosis abilities of podocytes, rescue the expression of YAP in ITGβ3 overexpression podocytes. Taken together, ITGβ3 overexpression promotes podocytes injury by inhibiting RhoA-YAP axis. ALKBH5inhibitor2 This will provide a new clue for preventing podocyte from damage.Macrophage activation in the presence of bacterial cells and molecules entails complex programs of gene expression. How such triggers elicit specific gene expression programs is incompletely understood. We previously discovered that TFEB (transcription factor EB) is a key contributor to macrophage activation during bacterial phagocytosis. However, the mechanism linking phagocytosis of bacterial cells to TFEB activation and downstream pro-inflammatory cytokine induction remained unknown. We found that macrophages lacking both TFEB and TFE3 (transcription factor E3) were unable to mount a pro-inflammatory phenotype in response to bacterial infection. The NOX/PHOX (NADPH oxidase)-dependent oxidative burst was required for nuclear translocation of TFEB during phagocytosis of Gram-positive or -negative bacteria, and reactive oxygen species (ROS) were sufficient to trigger TFEB activation in a CD38- and NAADP (nicotinic acid adenine dinucleotide phosphate)-dependent manner. Consistent with the Ca2+-releasing activity of NAADP, intracellular Ca2+ chelation and PPP3/calcineurin inhibition prevented TFEB activation by phagocytosis and ROS (reactive oxygen species), impairing the induction of pro-inflammatory cytokines such as IL6 and TNF/TNFα. Therefore, here we describe a previously unknown pathway that links phagocytosis with macrophage pro-inflammatory polarization via TFEB and related transcription factor TFE3. These findings reveal that activation of TFEB and TFE3 is a key regulatory event for the activation of macrophages, and have important implications for infections, inflammation, cancer, obesity, and atherosclerosis.Diabetic osteoporosis (DOP) is a chronic complication of diabetes in the skeletal system. High level of miR-340-5p may be harmful to the bone formation. In this study, the DOP model of rats was successfully established via streptozotocin (STZ) and ovariectomy (OVX) treatment. It was manifested by reduced body weight, insulin level, alkaline phosphatase (ALP) activity, and osteocalcin (OCN) and collagen-I expressions, as well as increased concentration of fasting blood glucose. Moreover, we found that miR-340-5p expression was increased while runt-related transcription factor-2 (RUNX2) was decreased in femurs. Furthermore, the effects of miR-340-5p on osteogenic differentiation (OD) in high glucose (HG)-treated MC3T3-E1 cells were explored. Exposure to OD and HG contributed to elevated miR-340-5p level. Inhibition of miR-340-5p enhanced ALP level, calcium deposition, and OCN, collagen-I and RUNX2 levels. On the contrary, miR-340-5p overexpression reversed these promotional effects. Luciferase assay indicated that RUNX2 may be a target gene of miR-340-5p. Moreover, RUNX2 deficiency decreased miR-340-5p inhibition-induced ALP activity, calcium accumulation and OCN, collagen-I, RUNX2 levels. In short, the above findings revealed that inhibition of miR-340-5p facilitated osteogenic differentiation through regulating RUNX2 in MC3TC-E1 cells, which provided targeted therapeutic strategies for the treatment of DOP.Purpose To compare on-axis measurements of the axial length (AL) with off-axis measurements in the paracentral horizontal and vertical positions using the Lenstar LS 900 biometer.Methods In this, the samples were selected from patients scheduled for cataract surgery using a systematic randomization method. After applying the exclusion criteria, all subjects underwent optometric examinations and AL measurement using the Lenstar. Five consecutive, non-cycloplegic measurements were done on the right eye centrally, 10° temporally, 10° nasally, 10° superiorly and 10° inferiorly on the retina by the same examiner.Results Two hundred and seven eyes were examined in this study, of which 126 (60%) were for female patients. The mean age of the participants was 64.32 ± 10.77 years (range 34-91 years). The mean central, superior, inferior, temporal, and nasal axial AL was 23.22 ± 1.02, 23.21 ± 1.02, 23.21 ± 1.02, 23.21 ± 1.02, 23.20 ± 1.03, respectively. Comparison of these readings using repeated measures ANOVA showed a statistically significant difference in the AL value among these positions.