Objective: To investigate the expression changes of cyclin-dependent kinase inhibitor 3(CDKN3) indifferent tumors and its effect on tumor staging, prognosis and immunotherapy. Methods: The expression characteristics of CDKN3 in different cancers using data from TCGA, CCLE, ICGC, and GTEx databases were evaluated. The GEPIA2 platform and Kaplan-Meier analysis were utilized to assess the effect of CDKN3 on tumor pathological staging and survival prognosis. The TIMER platform was employed to explore the influence of CDKN3 on the tumor immune microenvironment and immunotherapy. Its effect on immune checkpoint and key immunotherapeutic predictors using bioinformatics methods was explored. The GeneMANIA tool was used to construct the protein-protein interaction(PPI) network of CDKN3. Kyoto Encyclopedia of Genes and Genomes(KEGG) and Gene Onotology(GO) enrichment analyses were conducted to explore the biological processes and signaling pathways associated with CDKN3. The effect of CDKN3 on HepG2 cell proliferation, invasion, migration, and apoptosis was validated through transfection with CDKN3 siRNA. Results: CDKN3 was found to be widely overexpressed in tumors. High expression of CDKN3 was often associated with advanced pathological staging and poor survival prognosis. CDKN3 expression was negatively correlated with most immune checkpoints and positively correlated with tumor mutation burden(TMB), microsatellite instability(MSI), and mismatch repair(MMR) genes. CDKN3 was associated with cell cycle, cellular senescence, and the p53 signaling pathway. Furthermore, EdU staining, JC-1 staining, Transwell, and Wound Healing assays confirmed that CDKN3 promoted HCC cell proliferation, invasion, and migration while inhibiting apoptosis. Conclusion Abnormal expression of CDKN3 is closely related to tumor staging, prognosis, and immune microenvironment characteristics, making it a potential prognostic marker and immunotherapy adjuvant target in cancer.

Objective To investigate the clinical roles of lysine methyltransferase 5A(KMT5A)in human hepatocellular carcinoma(HCC)and its functions in cell migration and invasion. Methods The expression levels of KMT5A of 60 cases were detected by immunohistochemistry(IHC). KMT5A siRNA was used to down-regulate the expression of KMT5A in SMMC-7721 cells. Cell migration and invasion were measured by wound healing assays and transwell assays,respectively. Immunoblotting was used to detect the expression of MMP-2 after siRNA trans-fection. miR-186 mimics were transfected into SMMC-7721 cells and the mRNA levels of KMT5A was detected by qRT-PCR after transfection. Results High expression of KMT5A was associated with large tumor diameter (>5 cm,P=0.047)and advanced TNM stage(Ⅲ+Ⅳ,P=0.035). The expression of KMT5A was knocked down by siRNA in SMMC-7721 cells. Down-regulation of KMT5A suppressed cell migration(P=0.031,P=0.006)and invasion(P=0.010),and impaired MMP-2 expression(P=0.040). Overexpression of miR-186 could significantly inhibit the expression of KMT5A(P = 0.007). Conclusions Over-expression of KMT5A in HCC tissues associ-ates with poor clinical features. KMT5A knockdown inhibits the migration and invasion on HCC cells.

Classic problem-based learning ( PBL ) was applied in a medical microbiology course.The results of questionnaire survey showed most of the students were satisfied with the whole learning program.They thought the case was appropriate,and the discussing could increase their understanding of the knowledge.Based on the problems faced during the application and the students' feedback,the duty of the tutors,summary of the learning topic,arrangement of the course,application of different teaching methods,and selection of the tutors were discussed in detail.

AIM: To investigate the changes in nNOS and iNOS expression of hippocampal CA3 pyramidal neurons and NO - 2/NO - 3 level of hippocampal homogenate of rats induced by stress, and to explore the effect of phenytoin on them. METHODS: Rats were subjected to forced-swimming stress, phenytoin was administered(ip) at 30 min before stress. Using the immunohistochemistry and the computerized image technique, the expression levels of nNOS and iNOS of rat hippocampal CA3 pyramidal neurons were assayed quantitatively, and the NO - 2/NO - 3 level of hippocampal homogenate was also measured using nitric acid deoxidize enzyme method. RESULTS: The nNOS average grey degree of hippocampal CA3 pyramidal neurons was significantly lower in stress group (155 42?3 77)than that in control group(164 54?4 62)and in stress plus phenytoin group(164 27?2 55)( P

In this paper, it was reported that rat thymocytes harbor both high and low affinity ACTHR. The proper number of thymocytes used for deterting ACTHR varies from 1?10~6 /0.2 ml to 2 ?10~6 /ml, the maximum binding of ACTH to ACTHR occurs at 20 minutes. The IC_(50) for ACTH concentration is 800 nM or so. The saturation curves show that thymocyte ACTHRs are saturated at the concentration of 2.5 nM of ~(125)IACTH. There are high affinity ACTHR of 840 sites/cell on thymocyte (KD=0.15nM, Bmax = 2. 8 fmol/2 ? 10~6 cells); whereas low affinity ACTHRs are 12400 sites/cell (KD=4.2 nM, Bmax = 41.5 fmol/2 ? 10~6 cells).Moreover amputation stress can reduce thymocyte ACTHR remarkably.