Notes

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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. K02288 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 of tumor necrosis factor-α (TNF-α) and nuclear factor-κB (NF-κB) in the brain tissue of the rats, and the mRNA expressions of α subunit of hypoxia-inducible factor 1 (HIF1-α) and vascular endothelial growth factor (VEGF) were detected using RT- PCR.
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