AlM: To find out the weaknesses of the cultivation of the Chinese ophthalmology physicians and the gap between Chinese and the international ophthalmology physicians, so that provide the advice on the future cultivation of the Chinese ophthalmology physicians.
METHODS: The passrate of the 2013 lCO examinations taken by worldwide examiners by common statistical methods was analyzed.
RESULTS:The results indicated that the test scores of Chinese candidates' were lower than that of the international average level, there was a obvious gap existed between Chinese and other countries' ophthalmology physicians. lt showed that Chinese candidates were not quite adaptable to this examination, basic science and clinical level needed to be improved.
CONCLUSlON:lt may shows that the effects on the mid-anaphase of our country's ophthalmology residency training are not so good, which area we should pay more attentions.

Objective To investigate the signaling pathway and the key signal molecules of protein kinase (RIPK)3 in SH-SY5Y cells. Methods SH-SY5Y cells were transfected with RIPK3 expression plasmid vector to upregulate intracellular RIPK3, while the SH-SY5Y cells were transfected with empty vector plasmid, which was considered as control group. Western blot assay was used to check the expression of exogenous RIPK3 in cells. The proliferation rate of SH-SY5Y cells was determined by MTT assay at designated time to detect exogenous RIPK3 activity. Whole transcriptome sequencing (RNAseq) was used to detect the transcription of genes. Whole-transcriptomic gene transcription was measured by following Ingenuity Pathway Analysis (IPA) to obtain downstream signaling pathways and the key molecule, which were partly confirmed by following droplet digital PCR (ddPCR). Results Exogenous RIPK3 showed biological activity in SH-SY5Y, which inhibited the proliferation of cells. IPA showed that znic finger protein 36 (ZFP36) was significantly up-regulated as compared with that of the control group. The tran?scription levels of ZFP36 downstream genes such as tumor necrosis factor (TNF), brain derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF) and mRNA-decapping enzyme 2 (DCP2) were affected at the same time. Conclusion Within the limitations of this study, it seems that RIPK3 is notable for the development, inflammation and tumorigenesis of the nervous system as an independent regulator of ZFP36 gene and downstream effectors.

control group from the high to the low. When the typeⅢand type Ⅳglomerular function was changed (BUN and BCr in high value),the drainage quantity of the enzymes evidently increased.Conclusions Urine enzyme series can sensitively reflect the damage of renal tubules in early stage, even if BUN and BCr value is on the normal level , and the drainage quantity of these enzymes are changed more or less, which show that renal tubule damage exists. The value of BUN and BCr is positively correlated with the drainage quantity of these enzymes.the more urine enzymes are drained out, the more renal tubule function is involved, therefore, the more renal globe function is damaged.

Brain Neoplasms ; metabolism ; Cell Line, Tumor ; Glioma ; metabolism ; Humans ; Neoplastic Stem Cells ; drug effects ; metabolism ; Reactive Oxygen Species ; metabolism ; Sodium Selenite ; pharmacology

Objective To investigate the effects of synuclein-γ (SNCG) gene silencing on the proliferation and apoptosis of glioma U87-MG cells.Methods Five small hairpin RNA templates targeting SNCG and a negative control were synthesized and cloned into the lentiviral vector system and all the constructs were sequenced.Then the recombinant lentiviral vectors were used to infect U87-MG cells.The lentiviruses which can effectively inhibit protein expression levels of SNCG were selected by RT-PCR for further study.Colony formation and flow cytometry assay were used to investigate the effects of SNCG downregulation by RNA interference on the clony formation,proliferation,and apoptosis of U87-MG cells,respectively.Results The lentiviral vectors carrying 5 shRNAs targeting the SNCG gene were successfully constructed,and SNCG siRNA3 and siRNA5 showed higher interfering efficiency than other vectors.In comparison with the group of negative control,SNCG siRNA3 and siRNA5 were observed to significantly inhibit SNCG expression at the mRNA levels (the relative mRNA levels:siRNA3 (0.17± 0.01)％,siRNA5 (0.13±0.01)％ vs (1.00±0.10)％,P＜0.05).Also,SNCG suppression mediated by RNAi significantly inhibited the clone formation (colony number:siRNA3 (66± 12),siRNA5 (1 ± 1) vs (80± 5),P＜0.05),and the proliferation (ratio of cells in S phase:siRNA3 (41.2±0.7) ％,siRNA5 (39.9±0.5) ％ vs (47.6±2.2) ％,P ＜0.05),but promoted the apoptosis (cell apoptosis:siRNA3 (22.9± 0.4) ％,siRNA5 (28.6± 0.9) ％ vs (1.1 ± 0.1) ％,P＜0.01) of transfected U87-MG cells.Conclusion SNCG suppression at the mRNA level mediated by RNAi can inhibit the proliferation and the clony formation,but induce the apoptosis of glioma U87-MG cells in vitro,suggesting that SNCG suppression mediated by an RNAi strategy may become a novel approach for treating human gliomas.

Objective To screen altered proteins of hippocampus in the stress-induced depression (STRID) rat model, and explore the potential molecular mechanism. Methods Twenty Sprague-Dawley rats were randomly divided into the control group and STRID group, 10 rats in each group. Chronic unpredictable mild stress (CUMS) methods including fasting for solids and liquids, electric foot-shock, reversing day and night, cold water swimming, cage tilt, scare stimulation and tail pinch were conducted on STRID rats with no repeats for 28 days to make up the depression animal model. The control group was normally fed during this period. After the stress stimulation, the hippocampus protein samples were used for two dimensional electrophoresis to screen the differentially expressed protein, and then mass spectrum identification and function analyze were conducted. Results Compared with the control group, 34 proteins were altered in STRID group. Among which, 18 were up-regulated, and 16 were down-regulated. The differentially expressed proteins mainly located in cytoplasm, mitochondrion, extracellular exosome and myelin sheath. The involved signaling pathways included metabolic pathway, oxidative phosphorylation pathway, and Alzheimer's disease, Parkinson's disease and Huntington's disease pathways. Conclusion The altered proteins and dysfunction of nerve signaling, and the excess of oxidative phosphorylation in hippocampus of STRID rats may be one of the pathogenesises.

Objective To observe the change of stanniocalcin 1 (STC1) and calcium content in brain of coal-burning-borne fluorosis rats,and to explore the role of STC1 in brain injury of coal-burning-borne fluorosis.Methods Twenty four male SD rats were randomly divided into control,low,medium,and high fluoride groups according to body mass.Control group was fed conventional rat chow(fluorinated 1.3 mg/kg),and low,medium and high fluoride groups fed with fluorinated feed(20.0,40.0,60.0 mg/kg).All rats were given distilled water and feed ad libitum.One hundred and eighty days after modeling,STC1 protein and gene expression in the brain tissue of rats were detected using immunohistochemistry and RT-PCR and calcium content of brain tissue was detected.Results The cell positive rates of STC1 in low,medium,high fluoride groups [(48.10 + 2.11)％,(54.90 ± 1.73)％,(79.30 ± 3.71)％] were significantly higher than that of the control group[(24.70 + 3.53)％,all P ＜ 0.05],the cell positive rate of high fluoride group was significantly higher than that of the low and medium fluoride groups (all P ＜ 0.05).The STC1 mRNA expression of low,medium and high fluoride groups (0.58 ± 0.09,0.85 ± 0.17,1.75 ± 0.04) were significantly higher than that in the control group(0.37 ± 0.12,all P＜ 0.05),the STC1 mRNA expressions of high fluoride group was significantly higher than that of the low and medium fluoride groups (all P ＜ 0.05).The brain cortex calcium ion concentrations of low,medium and high fluoride groups[(138.62 + 4.19),(167.43 + 6.57),(189.45 + 3.72)nmol/L] were significantly higher than that in the control group [(101.47 + 9.46)nmol/L,all P ＜ 0.05],the brain cortex calcium ion concentrations of high fluoride group was significantly higher than that of the low and medium fluoride groups(all P ＜ 0.05),and the medium fluoride groups was higher than the low groups (P ＜ 0.05).Conclusion STC 1 may be involved in brain damage of coal-burning-borne fluorosis rats through regulating calcium balance.

E2A is involved in promoting forkhead box P3 (FOXP3) and retinoid-related orphan receptor gamma t (RORγt) gene transcription,which are pivotal transcription factors of T regulatory cells and Thl7 cells,respectively.Little is known about the involvement of E2A in pregnancy process.This study aimed to investigate the expression of E2A,cytotoxic T-lymphocyte-associated protein 4 (CTLA-4),and Foxp3 in luteal phase endometrium of women suffering recurrent miscarriage (RM) (n=21) and control group (n=11) by immunohistochemistry,with the Vectra(R) automated quantitative pathology imaging system for analysis.The percentage of E2A+ cells and CTLA-4+ cells was significantly higher in the endometrium of women with RM than in the controls.There was positive correlation between E2A and CTLA-4 (r=0.523,P=0.002),E2A and FOXP3 (r=0.380,P=0.032),and FOXP3 and CTLA-4 (r=0.625,P=0.000) in the mid-secretory phase of endometrium for all subjects.It was concluded that the abnormal expression of endometrial E2A existed in mid-secretory endometrium of women with RM,and there was a positive correlation between E2A and FOXP3,and E2A and CTLA-4,suggesting the possible regulation role of E2A involved in regulating endometrium receptivity.

Objective To study the effects of ibuprofen on the growth and development of oligodendrocytes. Methods A total of 6 clean and healthy adult female SD (Sprague Dawley) rats were used for extracting and culturing of oligodendrocytes(OLs).Lysophosphatidic acid(LPA)was then added,and the morphological changes of OLs pre-treatment and post-treatment were observed. Then 6 newborn rats (born 24-48 h) were used for mixed glial cell extraction from the cortex, then the OPCs were inoculated into the culture plates and randomly divided into control group, ibuprofen group, lysophosphatidic acid(LPA)group and LPA+ibuprofen group.After the adhering of the cells in each group for three days, cell morphology was observed,and the drugs were added as interventions.The control group was treated with normal saline, and the other 3 groups were added with saline solution of ibuprofen(100 μmol/L),LPA(1.0 μmol/L)and the mixture of them. The cell morphological changes were observed after 7-day intervention.The morphology of OPCs and OLs were observed by immunofluorescence staining through OPCs'specific immune markers (platelet-derived growth factor receptor alpha, PDGFR-α)and OLs'specific immune markers(myelin basic protein,MBP)along with cell count of mature OLs.Western blot assay was used to detect the relative expression level of MBP in each group. Results After the treatment with LPA to the mature OLs,protrusions were shrinking and became very sparse.The morphology of cells developed well in each group after cell adhering for 3 days. After drug intervention for 7 days, more cell protrusions and branches were observed in ibuprofen group and LPA+ibuprofen group than those of the control group and LPA group.The results of cell count showed that the number of MBP positive cells was significantly higher in the ibuprofen group and LPA+ibuprofen group than that in the control group and LPA group(P<0.01).The results of Western blot assay showed that the MBP protein expression was significantly less in LPA group than the other three groups (P<0.01), and the expression was significantly higher in the ibuprofen group than that of LPA+ibuprofen group (P<0.01). Conclusion LPA has a toxic effect on the growth and development of OPCs, and it has an inhibitory effect on the normal growth of mature OLs. A certain concentration of ibuprofen can significantly inhibit the cytotoxicity of LPA on OPCs and OLs,and promote the formation and maintenance of mature OLs.

In order to clarify the pharmacodynamic substances and mechanism of Xiangju Preparations (Xiangju Tablets, Xiangju Drops) in the treatment of rhinitis and sinusitis, the multi-level network integration analysis of "ingredients-targets-pathways" was conducted. 137 chemical constituents were identified in Xiangju Preparations by high pressure liquid chromatography-quadrupole-time of flight mass spectrometry (HPLC-QTOF/MS) for the first time. Network pharmacology analysis was performed on 59 potential active components. The results of network pharmacology analysis demonstrated that the medicinal ingredients in Xiangju Preparations included caffeic acid, senkyunolide F, rosmarinic acid, ligustilide, prim-O-glucosylcimifugin, linarin, magnolin, luteolin, senkyunolide I and gallic acid. These ingredients act on the crucial targets of tumor necrosis factor (TNF), interleukin 1B (IL1B), protein kinase B (AKT1), vascular endothelial growth factor A (VEGFA), signal transducer and activator of transcription 3 (STAT3) and participate in the regulation of advanced glycosylation end products-receptor of AGEs (AGE-RAGE), TNF, nuclear factor kappa B (NF-κB), and cyclic guanosine monophosphate-protein kinase G (cGMP-PKG) signaling pathways to effectively treat rhinitis and sinusitis. The excellent binding performance between above 10 active components and 5 key target proteins was further confirmed by molecular docking, indicating that these 10 ingredients are pharmacodynamic substances of Xiangju preparations. In conclusion, this study preliminarily clarified the effective components and mechanism of Xiangju preparations in the treatment of rhinitis and sinusitis, and provided a theoretical basis for the clinical application of Xiangju preparations.