Kejserfournier5063

spase-1-mediated pyroptosis through the lysosome pathway to improve kidney damages in rat models of DN.

To investigate the status of anxiety and depression in patients requiring emergency treatment during the epidemic of COVID-19 to identify the patients with acute psychological stress disorder.

During the COVID-19 epidemic, the medical staff divided the patients visiting the emergency department into suspected group, fever group and control group through interview of the patients at triage. Self-rating anxiety scale (SAS) and self-rating depression scale (SDS) were distributed to each patient, and a trained medical staff was responsible for assisting the patient to complete the scales.

A total of 557 sets of scales were distributed, including 211 in suspected COVID-19 case group, 167 in fever group and 179 in the control group. A total of 516 scales were retrieved, including 197 in suspected case group, 151 in fever group and 168 in control group. In the 3 groups, the incidence rates of anxiety and depression were 57.87% and 58.88%, 48.34% and 43.71%, and 18.31% and 18.99%, respectively, and the rates were significantly higher in suspected group and fever group than in the control group (

< 0.01), and significantly higher in suspected group than in fever group (

< 0.05). The standardized anxiety and depression scale scores in suspected case group, fever group and control group were 57.38±16.25 and 42.58±14.27, 51.23±15.29 and 38.32±15.39, and 32.58±17.8 and 12.25±12.94, respectively. Compared with the control group, both suspected case group and fever group had significantly higher standard scores for anxiety and depression (

< 0.01), and suspected case group had significantly higher standardized scores than fever group (

< 0.01).

Among the patients visiting the emergency treatment, the patients with suspected COVID-19 and common fever are more likely to develop anxiety and depressive symptoms.

Among the patients visiting the emergency treatment, the patients with suspected COVID-19 and common fever are more likely to develop anxiety and depressive symptoms.

To investigate the pattern of shikonin-induced cell death in testicular cancer cell I-10 and seminoma TCAM-2 cells and explore the possible mechanism in light of mitochondrial function and glycolysis.

I-10 cells treated with 0, 1.2, 1.4 and 1.6 μmol/L shikonin and TCAM-2 cells treated with 0, 0.5, 1 and 1.5 μmol/L shikonin were examined for mitochondrial membrane potential and production of reactive oxygen species (ROS) using JC-1 kit and ROS kit, respectively. The levels of intracellular lactic acid in the cells were detected using a lactic acid kit. The inhibitory effect of shikonin on the proliferation of the cells was assessed with MTT assay. The death patterns of the cells were observed by transmission electron microscopy, and annexin V-FITC/PI double staining was used to detect cell apoptosis. Western blotting was used to detect the relative expression levels of the apoptotic proteins Bax, Bcl-2, and cleaved caspase-3, the autophagy- related protein LC3B and glycolysis- related proteins PKM2, GLUT1 cells probably by affecting energy metabolism of the cells.

Shikonin can inhibit the proliferation, induce apoptosis and increase autophagy in both I-10 and TCAM-2 cells probably by affecting energy metabolism of the cells.

To investigate whether DNMT1 protein induces retinoblastoma proliferation by silencing MEG3 gene.

Two retinoblastoma cell lines (HXO-RB44 and SO-RB50) and a normal human retinal pigment epithelial (RPE) cell line were transfected with the plasmid pcDNA-DNMT1 or si-DNMT1 for up-regulating or interference of DNMT1 expression, and with pcDNA-MEG3 or si-MEG3 for up-regulating or interference of MEG3 expression. Western blotting was used to detect the changes in the expression of DNMT1 protein in the transfected cells, and CCK-8 and EdU assays were used to detect the changes in cell proliferation. Real-time quantitative PCR (qRT-PCR) was performed to detect MEG3 expression in SO-RB50 and HXO-RB44 cells after transfection, and the methylation level of MEG3 gene promoter after interference of DNMT1 expression was detected using methylation-specific PCR.

SO-RB50 and HXO-RB44 cells showed significantly increased expression of DNMT1 protein as compared with normal RPE cells (

< 0.05). In HXO-RB44 cells, transfection with pcDNADNMT1 resulted in significantly increased expression of DNMT1 protein, enhanced cell proliferation ability, and significantly reduced expression of MEG3 (

< 0.05). In SO-RB50 cells, transfection with si-DNMT1 significantly reduced the expression of DNMT1 protein, suppressed the cell proliferation, and increased MEG3 expression (

< 0.05). Interference of DNMT1 significantly reduced the methylation level of MEG3 gene promoter. After reversing the regulatory effect of DNMT1 on MEG3 gene, DNMT1 protein showed significantly weakened ability to regulate retinoblastoma cell proliferation (

< 0.05).

In retinoblastoma cells, the up-regulation of DNMT1 protein induces promoter methylation and inactivation of MEG3 gene and eventually leads to abnormal cell proliferation.

In retinoblastoma cells, the up-regulation of DNMT1 protein induces promoter methylation and inactivation of MEG3 gene and eventually leads to abnormal cell proliferation.

To study the effect of rapamycin on scar formation in rabbit eyes following filtering operation and explore the possible mechanism.

Ninety-six healthy adult rabbits were subjected to trabeculectomy of the left eye and subsequently randomly divided into 4 groups (

=24) for treatment with castor oil (control) or rapamycin (1%, 3%, or 5%) eye drops of the operated eyes 4 times a day. The morphology and function of the filtering blebs of the rabbits were compared at 7, 14, 21 and 28 days after the operation; at each of the time points, 6 rabbits from each group were euthanized for detection of expressions of proliferating cell nuclear antigen (PCNA) and α-smooth muscle actin (α-SMA) in the tissues in the surgical area using immunohistochemistry. Cultured rabbit subconjunctival fibroblasts (RTFSs) were treated with different concentrations of rapamycin (0.06, 0.25, 1, and 4 mg/L) and the cell apoptosis was detected using flow cytometry.

In the first, second and third weeks after the operation, the rate of functional follicle formation was significantly higher in the 3 rapamycin groups than in the control group (

< 0.05), and the number of α- SMA-positive fibroblasts decreased over time in the 3 rapamycin groups. In cultured RTFSs, treatment with rapamycin at different concentrations resulted in increased apoptosis of the cells, and rapamycin above 0.25 mg/L significantly increased the cell apoptosis in a dose-dependent manner.

Rapamycin can inhibit hyperplasia of the filtering passage tissue, helps to preserve the functional filtering blebs and prolong their life span, and induces apoptosis of RTFS.

Rapamycin can inhibit hyperplasia of the filtering passage tissue, helps to preserve the functional filtering blebs and prolong their life span, and induces apoptosis of RTFS.

To explore the effect of mild hypothermia on inflammatory response and angiogenesis in brain tissues of rats with intracerebral hemorrhage (ICH) and its possible mechanism for improving behavioral deficits of the rats After ICH.

A total of 120 healthy male SD rats were randomly divided into sham operation group, ICH group and mild hypothermia group. Rat models of ICH were established in the latter two groups by stereotactic injection of autogenous blood in the brain, and the rats in the sham operation group received injection of normal saline in the same manner. At 15 min after modeling, the rats in hypothermia group were subjected to mild hypothermia (30-32 ℃) for 8 h followed by rewarming (37-38 ℃); the body temperature was maintained at 37-38 ℃ in the other two groups. At 2, 4, 7, 14 and 21 days after the treatment, Longa scoring, balance beam scoring and Berderson scoring were used to evaluate the behavioral deficits of the rats. Immunohistochemical staining was used to detect the protein expressions sibly by antagonizing brain inflammation and promoting angiogenesis.

Mild hypothermia can improve behavioral deficits in rats with ICH possibly by antagonizing brain inflammation and promoting angiogenesis.

To construct and validate an individualized nomogram to predict the probability of occurrence of portal vein thrombosis (PVT) after splenectomy in patients with hepatitis B cirrhosis.

We retrospectively collected the clinical data from 180 patients with hepatitis B cirrhosis undergoing splenectomy with postoperative anticoagulation therapy during the period from January, 2014 to January, 2020 in our hospital. EHT 1864 chemical structure The patients were randomized into modeling group (

= 120) and validation group (

=60), and the former group was further divided into PVT group (

=49) and non-PVT group (

=71) according to the occurrence of PVT occurred within 1 month after splenectomy. The independent risk factors of PVT after splenectomy were screened in the modeling group using univariate and multivariate binary logistic regression analyses and were used for construction of the nomogram prediction model. link2 The area under the receiver-operating characteristic (AUROC) curve (C-index), GiViTI calibration belt and Hosmer-Lemeshow tes, respectively, suggesting a high reliability of the predicted probability by the model. DCA curve analysis showed a threshold probability of 30.5%, with a net benefit of 30% in the modeling group and 34% in the validation group, indicating a good clinical efficiency of the model.

The model for predicting the risk of PVT after splenectomy in patients with hepatitis B cirrhosis can help in early identification of patients having high risks of PVT.

The model for predicting the risk of PVT after splenectomy in patients with hepatitis B cirrhosis can help in early identification of patients having high risks of PVT.

To investigate the effect of Aurora kinase B (AURKB) silencing-induced autophagy on apoptosis of osteosarcoma 143B cells and the underlying molecular mechanisms.

Human osteosarcoma 143B cells were transfected with Lv/shAURKB or the negative control vector Lv/shScrambled followed by treatment with chloroquine (CQ) for 24 h. Western blotting was performed to detect the protein expression levels of AURKB, P62, LC3, cleaved caspase-3, Bcl-2, and P-ULK1

. Transmission electron microscopy and LC3 dual-label fluorescence method were used to trace the autophagosomes in 143B cells to assess cell autophagy, and the cell apoptosis was detected using flow cytometry and TUNEL assay. link3 Co-immunoprecipitation assay was used to detect the interaction between AURKB and ULK1.

The ratio of autophagy-related proteins LC3 II/I and the number of autophagosomes were significantly increased in 143B cells after transfection with Lv/shAURKB (

< 0.05), which significantly increased the expression of cleaved caspase-3 and reduced the expression of Bcl-2 (

< 0.05). Combined treatment of the cells with Lv/shAURKB and the autophagy inhibitor chloroquine obviously restored the expressions of caspase-3 and Bcl-2 (

< 0.05). Transfection with Lv/shAURKB significantly increased the apoptosis rate of 143B cells (

< 0.05), and this effect was significantly antagonized by combined treatment with chloroquine (

< 0.05). AURKB silencing strongly activated the phosphorylation of the autophagy-initiating protein ULK1

in 143B cells (

< 0.05). The results of co-immunoprecipitation assay confirmed when AURKB was immunoprecipitated, ULK1 also precipitated.

Silencing AURKB can induce autophagy by activating ULK1

phosphorylation to promote apoptosis in 143B cells.

Silencing AURKB can induce autophagy by activating ULK1Ser555 phosphorylation to promote apoptosis in 143B cells.