Retinitis pigmentosa (RP) is a common sight-threatening eye disease.RP is characterized by highly genetical and phenotypical heterogeneity.Identification of the causative genes of RP is the first step toward the understand of the molecular basis of RP and,subsequently,toward the prevention and treatment of RP.In recent years,there have been new progress in the study on RP.This review mainly focuses on recent advances in the gene-related studies of autosomal dominant RP (adRP) and autosomal recessive RP (arRP) with emphasis on the roles of common genes,as well as their possible mechanisms in RP in order to provide the essential reference for the genetics research of RP.

Objective To study the liver X receptor(LXR)and the gene expression of cholesterol ester transfer protein(CETP),cyclooxygenase-2(COX2)in obstructive sleep apnea hypopnea syndrome(OSAHS)patients.Methods Macrophages were separated from the blood drawn in 30 cases of OSAHS patients and 30 healthy control subjects in the morning,RT-PCR gel eletrophoresis was used to determine the patterns of gene expression.Results OSAHS patients had higher LXR,COX2,CETP expression(P

Objective To evaluate the role of modified Buyanghuanwu decoction in the treatment of vascular dementia. Methods Adopting international standards for the diagnosis,30 cases with mild to moderate vascular dementia were treated by modified Buyanghuanwu decoction,six months as a course of treatment. 30 patients of the control group were treated by Yinxingye Tablets. Results After using modified Buyanghuanwu decoction,MMSE scores were increased (P

This article analyzed the current problems existing in the public health master cur-ricula system, such as educational ideas being backward, tralning objectives not explicit, curricula teaching unsatisfactory and effects of practical curriculum needing to be improved. Based on the pro-fessional competencies, we discussed the ideas and principles of the new curricula system of master of public health, and proposed making sure of a refined professional competencies, making strict traln-ing standards, confirming tralning objectives, embodying advantages, setting up reasonable curricula, fostering practical abilities, strengthening cooperation and carrying on professional identification.

OBJECTIVE:To study the inhibitory effects of ampelopsin sodium (AMP-Na) combined with carboplatin on the proliferation of Lewis cell of lung cancer. METHODS:6.25,12.5,25,50 and 100 μg/ml AMP-Na and 3.125,6.25,12.5,25 and 50 μg/ml carboplatin were used to culture the cells for 4 h,and the cell viability was determined and the inhibition rate and half in-hibition concentration(IC50)were calculated. 12.5,25,50 and 100 μg/ml AMP-Na and 12.5 μg/ml carboplatin were used to culture the cells for 12 h,and the flow cytometry was used to determine the expression of Caspase-3. RESULTS:AMP-Na with serial con-centrations combined with carboplatin with serial concentrations had obvious inhibitory effects on the cell proliferation. With the in-crease of mass concentration,the IC50 of carboplatin on the Lewis cells was gradually decreased;when the AMP-Na of 6.25-50μg/ml was combined with carboplatin of 3.125-25 μg/ml,it showed the strongest inhibitory effects on the Lewis cell proliferation. When cells were cultured with AMP-Na and carboplatin for 24 h,the expression of Caspase-3 increased significantly. CONCLU-SIONS:AMP-Na combined with carboplatin has synergistic inhibitory effect on the Lewis cell proliferation by a mechanism that may be related to the apoptosis induced by Caspase-3 activated by AMP-Na.

Background Chronic low-level exposure to lead can damage the central nervous system and cause anxiety-like behavior. However, whether changes of blood metabolites occur in this process and its relationship with lead-induced neurobehavioral disorder remain unclear. Objective To explore the effects of chronic lead acetate (PbAc) exposure at different concentrations on anxiety-like behavior and serum metabolites and their relationships in mice, as well as the mechanism of lead exposure on neurobehavioral injury in mice from the perspective of metabolomics. Methods A total of 64 healthy 4-week-old C57BL/6J mice, half male and half female, were randomly divided into four groups: control group (normal drinking water), 20 mg·L⁻¹ PbAc group, 100 mg·L⁻¹ PbAc group, and 500 mg·L⁻¹ PbAc group. After 10 weeks of free drinking of water containing designed concentrations of PbAc, the mice were tested for anxiety-like behavioral changes by open field experiment. After the mice were anesthetized, blood was collected from the eyes, the serum was separated, and the effects of designed doses of lead exposure on metabolites in the serum of mice were compared by liquid chromatography with tandem mass spectrometry combined with principal component analysis and partial least squares discrimination analysis. Results The results of the open field experiment showed that the reductions in movement time spent in central area in the 100 mg·L⁻¹ and 500 mg·L⁻¹ PbAc groups compared with the control group were of statistical significance (P<0.05); the reduction in crossing times of central region in the 500 mg·L⁻¹ PbAc group was statistically significant compared with the control group (P<0.05); the increases in defecation frequency in the 100 mg·L⁻¹ and 500 mg·L⁻¹ PbAc groups were statistically significant compared to the control group (P<0.05). In both positive and negative ion modes, compared with the control group, 157 differential metabolites were screened out in the 20 mg·L⁻¹ PbAc group, of which 80 were up-regulated and 77 were down-regulated; 172 differential metabolites were screened out in the 100 mg·L⁻¹ PbAc group, of which 57 were up-regulated and 115 were down-regulated; 119 differential metabolites were screened out in the 500 mg·L⁻¹ PbAc group, of which 42 were up-regulated and 77 were down-regulated. The results of the KEGG enrichment analysis on the differential metabolites revealed alterations in metabolic pathways mainly involving primary bile acid biosynthesis, bile secretion, and cholesterol metabolism. Among the differential metabolites, norethisterone was positively correlated with the number of central region crossings (r=0.406, P<0.05); dihydrothymine was negatively correlated with the number of central region crossings (r=−0.346, P<0.05); lysophosphatidylcholine 22∶1 and lysophospholipid 14∶0 were negatively correlated with time spent in central region (r=−0.429, P<0.05; r=−0.374, P<0.05). Conclusion Chronic lead exposure induces anxiety-like behavior in mice, and this altered behavior is associated with altered metabolites in serum, with differential metabolites enriched primarily in the metabolic pathways of primary bile acid biosynthesis, bile acid secretion, and cholesterol metabolism.

Objective:To explore the learning guidance model and its influencing factors of undergraduates in medical schools.Methods:Based on the developmental learning guidance theory, 1 117 undergraduates from two undergraduate medical universities were selected as the research objects, through questionnaire surveys to collect their knowledge learning, curriculum learning and other core variables, and balanced guidance, compound guidance and other outcome variables, using Smart PLS 3.0 to test the validity of the samples.Results:There were statistical significance in the path relationship affecting the core variables and the outcome variables of the learning guidance model, P<0.05, indicating that the influencing factors of the learning guidance model had a significantly positive effect on the learning guidance model construction. Conclusion:Constructing a "balanced-compound-special" learning guidance model suitable for undergraduates' learning activities in medical universities provides a reference for the application and promotion of learning guidance model in medical undergraduate stage.

Objective To promote the research innovative capacity for the academic medical graduate student to adapt to the development of modern medicine,life science,as well as the trend of interdisciplinary integration.Methods The curriculum reform of the medical graduate student was carried out by taking into account of the knowledge context and systematic implementation,which covered the latest development of global life science and scientific research methodologies from the context perspective,also the interdisciplinary integration and the consistency and extension of knowledge from the structure perspective.Results A totally new core curriculum system for medical graduated students,which including four modules:public courses,core courses,professional courses and elective courses,was set up.Furthermore,related administrative mechanism reform was also carried out.Conclusions The new curriculum constructed is based on the integration of research and teaching,highlighted the needs for research innovation which is well adapted with the development trend of life science,break down the traditional barriers of different disciplines,contributes to the integration of interdisciplinary,as well as the promotion of research innovative capacities of graduate students.

Objective:To investigate the effect of epigallocatechin gallate (EGCG) on the activation of human Tenon fibroblasts (HTFs) and its mechanism.Methods:Tenon capsule tissues from nine eyes of nine advanced primary open angle glaucoma patients during trabeculectomy were obtained for primary cell culture.HTFs harvested were identified by immunofluorescence staining for vimentin and keratin.Cells at passage 4-6 were used for experiment.Viability of HTFs treated with EGCG at 0, 10, 20, 30, 40, 50, 60, 70 and 80 μmol/L was detected by cell counting kit-8 (CCK-8) assay.The cells were divided into blank control group, transforming growth factor (TGF)-β1-induced group, and EGCG-treated group, which were cultured in normal medium, medium containing 10 ng/ml TGF-β, medium containing 10 ng/ml TGF-β+ 50 μmol/L EGCG, respectively.The proliferation rate of HTFs was detected by BrdU labeling assay.Cell migration was observed by scratch wound healing assay.The expression of α-smooth muscle actin (α-SMA) was measured by immunofluorescence staining.The protein relative expression levels of Smad2/3, phosphoinositide-3-kinase (PI3K), protein kinase B (Akt) as well as the phosphorylated Smad2/3 (p-Smad2/3) and phosphorylated Akt (p-Akt) were measured by western blot.This study was approved by the Ethics Committee of Guangdong Provincial People's Hospital (NO.GDREC2019331H[R1]).Results:The HTFs harvested had spindle shape, grew regularly and were vimentin-positive.CCK-8 assay showed that there was no significant difference in the variability of HTFs treated with EGCG at 10, 20, 30, 40 and 50 μmol/L in comparison with 0 μmol/L EGCG treatment (all at P<0.05). BrdU labeling assay showed that cell proliferation in the TGF-β1-induced group was (66.37±12.65)%, which was significantly higher than (14.75±12.33)% in EGCG-treated group ( P<0.05). Three days after scratch, the relative scratch area in the TGF-β1-induced group was (47.33±12.22)%, which was significantly lower than (92.67±4.04)% in the EGCG-treated group ( P<0.05). Immunofluorescence assay showed that α-SMA fluorescence was significantly enhanced in the TGF-β1-induced group in comparison with the blank control group, which was reduced to blank control group level in EGCG-treated group.Western blot analysis showed that there were significant differences in the relative expression levels of p-Smad2/3, PI3K and p-Akt protein among the various groups ( F=58.820, 121.153, 69.289; all at P<0.001). The relative expressions of p-Smad2/3, PI3K and p-Akt in the TGF-β1-induced group were significantly higher than those in the blank control group, 10 μmol/L and 50 μmol/L EGCG-treated groups (all at P<0.05). Conclusions:EGCG can suppress TGF-β1-induced HTFs activation through Smad and PI3K/Akt signaling pathways.

Objective:To explore the mechanism of Huangqi Jiedu Decoction (HQJD) in the treatment of breast cancer with the syndrome of Zheng deficiency and toxic incandescence by network pharmacology and molecular docking technology.Methods:The main active ingredients and targets of HQJD were screened through the traditional Chinese medicine (TCM) systematic pharmacology database and analysis platform. The relevant targets of breast cancer with the syndrome of Zheng-deficiency, toxic-incandescence were obtained using OMIM, GeneGards and Drugbank databases, and the relevant targets of HQJD for the treatment of breast cancer with the syndrome of Zheng-deficiency and toxic incandescence were obtained by intersection; The Cytoscape 3.9.1 software was used to build the protein protein interaction (PPI) network and the " drug active component target disease" network on the basis of String 11.0 database, and the core active components and core targets of HQJD in treating breast cancer with the syndrome of Zheng-deficiency and toxic-incandescence were inferred according to the topological parameters. gene ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed on core targets using R language; and molecular docking verification on the main active ingredients and core targets were conducted.Results:230 effective targets of active ingredients of HQJD were screened, and 15 467 active ingredients of breast cancer with syndrome of Zheng-deficiency/toxic-incandescence were obtained; 217 intersection targets; GO function enrichment analysis showed that the treatment of HQJD for breast cancer with the syndrome of Zheng-deficiency and toxic-incandescence mainly involved oxidative stress and cytochemical stress; The enrichment analysis of KEGG pathway showed that HQJD treatment of breast cancer with the syndrome of Zheng-deficiency and toxic-incandescence was mainly related to phosphatidylinositol 3-protein kinase B (PI3K-Akt), interleukin-17 (IL-17) and other signal pathways. The molecular docking results showed that the main active ingredients such as β-sitosterol, stigmasterol, luteolin had good binding ability with core targets.Conclusions:HQJD has the characteristics of multi-component, multi target and multi pathway in the treatment of breast cancer with syndrome of Zheng-deficiency and toxic-incandescence, and its main mechanism may be related to PI3K-Akt, IL-17, P53 and other signal pathways.