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Our results indicate that UGT84B1 plays an important role in IAA and PAA homeostasis in Arabidopsis.Presbycusis is a form of age-related hearing loss (AHL). Many studies have shown that the degeneration of various structures in the cochlea of the inner ear is related to AHL, and DNA damage is an important factor leading to the above process. As an E2 ubiquitin-conjugated enzyme, RAD6B plays an important role in DNA damage repair (DDR) through histone ubiquitination. However, the molecular mechanism is still unclear. In this study, we investigated the role of RAD6B in the morphological changes and DDR mechanisms in aging-related degeneration of the cochlea of mice. We observed that the hair cells, stria vascularis and spiral ganglion in the cochlea of the RAD6B knockout mice showed significant degenerative changes and abnormal expression of proteins associated with DDR mechanisms compared with those of the littermate wild-type mice. In conclusion, our results suggest that the deletion of RAD6B may lead to abnormalities in DDR, thereby accelerating the degeneration of various structures in the cochlea and senescence and apoptosis of cochlea cells.Since the first discovery of phenolic acid decarboxylase transcriptional regulator (PadR), its homologs have been identified mostly in bacterial species and constitute the PadR family. PadR family members commonly contain a winged helix-turn-helix (wHTH) motif and function as a transcription factor. However, the PadR family members are varied in terms of molecular size and structure. As a result, they are divided into PadR subfamily-1 and PadR subfamily-2. PadR subfamily-2 proteins have been reported in some pathogenic bacteria, including Listeria monocytogenes and Streptococcus pneumoniae, and implicated in drug resistance processes. Despite the growing numbers of known PadR family proteins and their critical functions in bacteria survival, biochemical and biophysical studies of the PadR subfamily-2 are limited. Here, we report the crystal structure of a PadR subfamily-2 member from Streptococcus pneumoniae (SpPadR) at a 2.40 Å resolution. SpPadR forms a dimer using its N-terminal and C-terminal helices. The two wHTH motifs of a SpPadR dimer expose their positively charged residues presumably to interact with DNA. Our structure-based mutational and biochemical study indicates that SpPadR specifically recognizes a palindromic nucleotide sequence upstream of its encoding region as a transcriptional regulator. Furthermore, comparative structural analysis of diverse PadR family members combined with a modeling study highlights the structural and regulatory features of SpPadR that are canonical to the PadR family or specific to the PadR subfamily-2.
This study aimed to investigate the involvement of lncRNA CTBP1-AS2 in the progression of diabetic nephropathy (DN) by affecting high glucose (HG)-induced human glomerular mesangial cells (HGMCs).

HGMCs were selected for the establishment of cell injury induced by HG. The expression of CTBP1-AS2, miR-155-5p and FOXO1 was detected by real-time PCR and western blotting. The target association between miR-155-5p and CTBP1-AS2 or FOXO1 was confirmed by dual-luciferase reporter assays. Cell proliferation and oxidative stress were revealed by CCK-8 colorimetry, and the measurement of reactive oxygen species (ROS) and the activities of antioxidant enzymes. Extracellular matrix (ECM) protein accumulation and the production of inflammatory cytokines were investigated by western blotting and ELISA.

The expression of CTBP1-AS2 was downregulated, and miR-155-5p was highly expressed in peripheral blood of DN patients and HG-treated HGMCs. Further investigation revealed that CTBP1-AS2 overexpression inhibited proliferation, oxidative stress, ECM accumulation and inflammatory response in HG-induced HGMCs. Mechanical analysis revealed that CTBP1-AS2 regulated FOXO1 expression via sponging miR-155-5p. Rescue experiments demonstrated that miR-155-5p overexpression or FOXO1 inhibition reversed the effects of CTBP1-AS2 in HG-stimulated HGMCs.

Taken together, this study revealed CTBP1-AS2 attenuated HG-induced HGMC proliferation, oxidative stress, ECM accumulation, and inflammation through miR-155-5p/FOXO1 signaling.
Taken together, this study revealed CTBP1-AS2 attenuated HG-induced HGMC proliferation, oxidative stress, ECM accumulation, and inflammation through miR-155-5p/FOXO1 signaling.Phosphatidylcholine-specific phospholipase Cγ1 (PLCγ1) is involved in regulating cell metabolism. However, little is known how PLCγ1 directs BMSC differentiation. Here, we investigated the role of PLCγ1 in rat BMSC differentiation into osteoblasts and chondrocytes. The results of Alizarin red and Alcian blue staining showed that PLCγ1 inhibitor U73122 significantly enhanced the mineralization capacity and proteoglycan deposition of BMSCs. The results of qPCR technique and Western blot analysis showed that long-term treatment of U73122 enhanced COL1A1 and OPG mRNA levels and Collagen 1A1, BMP2, and p-Smad1/5/9 protein levels and that short-term treatment of U73122 enhanced COL2A1 and SOX9 mRNA levels and Collagen 2, SOX9, Aggrecan, TGF-β3, and p-Smad2/3 protein levels. Decreased p-mTOR and p-P38 contributed to enhanced osteogenic potentials of BMSCs and increased p-P38 contributed to enhanced chondrogenic potentials of BMSCs. The scaffold transplantation with U73122+BMSC was more efficacious than BMSC alone for osteochondral defect repair in a rat model. Therefore, suppressing PLCγ1 could improve the capacity to effectively use BMSCs for cell therapy of osteochondral defect.Critical limb ischemia (CLI) is the leading cause of lower limb amputation. Traditional treatments for CLI have limitations. Studies have shown that thrombospondin-4 (TSP4) can promote the growth of neovascularization. In this study, we observed the angiogenesis efficiency of TSP4-overexpressing BMSC transplantation in CLI treatment. The recombinant FT106-tsp4-gfp lentiviral vector plasmid was constructed and transfected into 293FT cells. Primary BMSCs were successfully infected with the tsp4 virus, and TSP4 overexpression was confirmed before TSP4-BMSCs infusion. learn more A rat CLI model was established, and 60 CLI rats were randomly divided into the CLI, BMSC + CLI and TSP4-BMSC + CLI groups. The effect of TSP4-BMSC on angiogenesis was detected by the motor function, immunohistochemistry and immunofluorescence staining assays. Neovascular density was detected by digital subtraction angiography (DSA). Our results demonstrated that TSP4-BMSCs improved the motor function score of the CLI rats and increased MMP2, MMP9, Ang-1, VEGF and vWF protein expression in tissue of the ischaemic area. Meanwhile, new blood vessels can be observed around the ischemic area after TSP4-BMSCs treatment. link2 Our data illustrate that TSP4-BMSCs can promote the recovery of motor function in diabetic hind limb ischaemic rats. TSP4-BMSCs have better therapeutic effects than BMSCs.Defective pluripotent cells are removed from embryos prior to differentiation, presumably due to upregulation of the p53 pathway. However, the mechanism underlying p53 protein activation is still unknown. Embryonic stem cells (ESCs), corresponding to cells of the preimplantation blastocyst, likely have similar mechanisms for abnormal cell elimination. Using a mouse ESC cell line with inducible ulk1 gene expression, we showed that Ulk1 upregulation is accompanied by p53 phosphorylation on Ser15. ESCs tolerated the activated p53 and did not undergo apoptosis or cell cycle blockade upon Ulk1 overexpression. However, massive cell death was observed after retinoic acid treatment, suggesting a role of Ulk1-induced p53 activation in the elimination of defective pluripotent cells prior to differentiation.Pleotropic growth factor, transforming growth factor (TGF)-β drives the modification and elongation of glycosaminoglycan (GAG) chains on proteoglycans. Hyperelongated GAG chains bind and trap lipoproteins in the intima leading to the formation of atherosclerotic plaques. We have identified that phosphorylation of Smad2 linker region drives GAG chain modification. link3 The identification of an inhibitor of Smad2 linker region phosphorylation and GAG chain modification signifies a potential therapeutic for cardiovascular diseases. Artemisinin renowned for its potent anti-malarial effects possesses a broad range of biological effects. Our aim was to characterise the anti-atherogenic role of artemisinin in vascular smooth muscle cells (VSMCs). We demonstrate that TGF-β mediated Smad2 linker region phosphorylation and GAG chain elongation was attenuated by artemisinin; however, we observed no effect on VSMC proliferation. Our data demonstrates the potential for artemisinin to be developed as a therapy to inhibit the development of atherosclerosis by prevention of lipid deposition in the vessel wall without affecting the proliferation of VSMCs.
In this study, we aimed to describe the relationship between the localization of rarely seen upper extremity war injuries and their complications in the subacute period, and define our preferences for surgery and antibiotic use.

Patients with an upper extremity war injury who presented to our institution between 2015 and 2018 were retrospectively evaluated. Data regarding demographics, time between injury and presentation, location of injury, type of damage, complications, treatment methods, infection rates and antibiotic use were recorded. Tissue defects, fracture fixation, neurovascular damage, infection development and treatment approaches were analyzed.

Sixty-two male patients with isolated upper extremity injuries (mean age 31.66±8.28 years) were included in the study. The average time between trauma and hospitalization was 14 days. The mean hematocrit (Hct) level at presentation was 36.3±6.8%. Patients had been followed up for an average period of 95.6±32.1 days. Twenty-nine patients (46.8%) had ne risks.
Compared with term neonates, preterm babies are more likely to die from sepsis. However, the combined effects of sepsis and prematurity on neonatal postoperative mortality are largely unknown. Our objective was to quantify the proportion of neonatal postoperative mortality that is attributable to the synergistic effects of preoperative sepsis and prematurity.

We performed a multicentre, propensity-score-weighted, retrospective, cohort study of neonates who underwent inpatient surgery across hospitals participating in the United States National Surgical Quality Improvement Program-Pediatric (2012-2017). We assessed the proportion of the observed hazard ratio of mortality and complications that is attributable to the synergistic effect of prematurity and sepsis by estimating the attributable proportion (AP) and its 95% confidence interval (CI).

We identified 19 312 neonates who realised a total of 321 321 person-days of postsurgical observations, during which 683 died (mortality rate 2.1 per 1000 person-days). The proportion of mortality risk that is attributable to the synergistic effect of prematurity and sepsis was 50.5% (AP=50.5%; 95% CI, 28.8-72.3%; P < 0.001). About half of mortality events among preterm neonates with sepsis occurred within 24 h after surgery. Just over 45% of postoperative complications were attributable to the synergistic effect of prematurity and sepsis when both conditions were present (AP=45.8; 95% CI, 13.4-78.1%; P<0.001).

Approximately half of postsurgical mortality and complications were attributable to the combined effect of sepsis and prematurity among neonates with both exposures. These neonates typically died within a few days after surgery, indicating a very narrow window of opportunity to predict and prevent mortality.

Not applicable.
Not applicable.
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