Background Paired box gene 6 (Pax6) is a master regulator for eye and brain development.Pax6 mutations or changes in its expression cause a series of ocular diseases including absence of iris,corneal opacity,cataract,glaucoma,abnormal fovea,retinoblastoma,and Wilm's tumor-aniridia-qenital ahormalies-retardation (WAGR).As a transcription factor,it is expressed in the region of anterior surface ectoderm corresponding to the future adenohypophyseal,olfactory and lens placodes,optic vesicle and other parts of the future brain and thus control the development of eye,brain,pituitary grand,nose and pancreas.Pax6 exists in 4 different isoforms,whose functions are subjected to regulation by different post-translation modifications.A complete understanding of the structure and functions of Pax6 and its associations with relevant diseases is helpful for ophthalmologists to investigate the pathogenesis and treatment of implicated ocular diseases caused by Pax6 gene mutation or changing in its expression.

80 NSTE-ACS patients were randomly divided into 2 groups: the control group and the therapy group (40 cases in each group). The therapy group was treated with Tirofiban besides the conventional treatment which received by the control group. The level of HIF-1α and hs-CRP was detected immediately, 12, 24, 48 h,and 7 d after hospitalization. The HIF-1αlevel of both group increased in the first 12 hours and then decreased gradually to the baseline in 7 days. The hs-CRP level of both group increased gradually and reached its peak after 24 h after hospitalization, then decreased. Compared with the control group, the level of HIF-1α and hs-CRP decreased sig-nificantly at 12, 24, 48 h and 7 d after hospitalization in the therapy group.

Objective: To observe the effect of bevacizumab on the proliferation of human heptoma cell line HepG2. Methods: The expression of vascular endothelial growth factor(VEGF) and its receptors (VEGFRs) in HepG2 cells were examined by immunocytochemical staining and RT-PCR; ELISA was used to determine the level of VEGF in culture supernatants of HepG2 cells. The proliferation of HepG2 cells was analyzed by MTT assay after treatment with rh VEGF and bevacizumab separately; the expression of VEGF was examined by RT-PCR and Western blotting. Results: VEGF and VEGFRs (Flt-1 and KDR) were expressed in human HepG2 cells. rhVEGF increased the proliferation of HepG2 cells in a dose-dependent manner within a concentration range of 0-100 ng/ml; bevacizumab inhibited the proliferation of HepG2 cells; the inhibition rates were (8.76% ± 1.15)%, (26.83 ± 1.20)%, (31.87 ± 1.30)% and (28.20 ± 1.28)%, when the concentrations of bevacizumab were 0. 1, 1, 10,and 20 μg/ml,respectively. Expression of VEGF in the HepG2 cells was increased by rhVEGF and inhibited by bevacizumab. Conclusion: Bevacizumab might inhibit the proliferation of HepG2 cells through blocking the effect of VEGF.

Facial Neoplasms ; drug therapy ; Head and Neck Neoplasms ; drug therapy ; Humans ; Mouth Neoplasms ; drug therapy

Objective To investigate the effects of miR-135a on HOXA10 expression,proliferation and apoptosis of SKOV3 cells.Methods (1) Through computer-aided algorithms,the predicted target gene of miR-135a (HOXA10)were determined.(2) miR-135a mimics,miR-135a inhibitor and negative control were transfected into SKOV3 cells,respectively.Reverse transcription (RT)-PCR,western blot analysis were used to examine the expression levels of HOXA10 at different times (24,48 and 72 hours).(3) A luciferase reporter assay was used to confirm the direct regulation between miR-135a and HOXA10.(4) SKOV3 cells proliferation at different times (24,48 and 72 hours) was detected by methyl thiazolyl tetrazolium(MTT) assay [quantified by absorbance(A)].Western blot was used to examine the expression of apoptosis-associated protein bcl-2,bax and caspase-3 in SKOV3 cells after 48 hours transfection.Results (1) HOXA10 was predicted to be the target gene of miR-135a by computer-aided algorithms.(2) RT-PCR shown that HOXA10 mRNA levels were decreased over time (24,48 and 72 hours) after miR-135a mimics transfectionin SKOV3 cells (0.94 ±0.04 vs 0.78 ±0.03 vs 0.70 ±0.03,P ＜0.05).While,the expression of HOXA10 mRNA was increased over time after miR-135a inhibitor transfection (1.14 ± 0.05 vs 1.16 ±0.03 vs 2.60 ±0.08,P ＜0.05).After transfected with miR-135a mimics or miR-135a inhibitor over 48 and 72 hours,the HOXA10 expression levels in SKOV3 cells were significantly lower or higher than each control group,respectively (all P ＜ 0.01).Western blot analysis of HOXA10 expression in SKOV3 cells confirmed the results of RT-PCR detected.(3) After cotransfection of miR-135a plasmid and pMIR-REPORT luciferase plasmid containing HOXA10,luciferase reporter assays showed that the luciferase activity reduced by 67.8％ (P ＜0.01).(4) MTT showed that SKOV3 cells growth after miR-135a mimics transfection for 48 and 72 hours were significantly lower than those in control group (0.38 ± 0.03 vs 0.52 ± 0.05,0.67 ±0.05 vs 0.75 ± 0.06 ; respectively,all P ＜ 0.05).While,SKOV3 cells transfected with miR-135a inhibitor for 72 hours grew significantly faster than that in control group (0.95 ± 0.05 vs 0.75 ± 0.06,P ＜ 0.01).After miR-135a mimics transfection,the level of bcl-2 protein was significantly lower than that in control group (0.28 ±0.06 vs 0.76 ±0.09,P ＜0.01).The activity of caspase-3 was significantly higher than that in control group (115.0 ± 2.4 vs 95.4 ± 2.1,P ＜ 0.01).While,there was no statistical difference of bax expression (P =0.142).However,after miR-135a inhibitor transfection,the expression level of bcl-2 protein was significantly higher than that in control group (0.92 ± 0.03 vs 0.76 ± 0.09,P =0.037) and the activity of caspase-3 was significantly lower than that in control group (59.5 ± 4.1 vs 95.4 ± 2.1,P ＜ 0.01).There was also no statistical difference of bax expression (P =0.066).Conclusion miR-135a may play an important role in cell proliferation and apoptosis of ovarian cancer cells by regulating HOXA10 and its downstream pathways.

Animals ; Ear Canal ; surgery ; Female ; Gene Expression ; Hypothalamus ; metabolism ; Nerve Block ; Pregnancy ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate ; genetics ; metabolism

Animals ; Female ; Gene Expression Regulation, Developmental ; Inferior Colliculi ; metabolism ; N-Methylaspartate ; genetics ; metabolism ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate ; genetics ; metabolism

Objective To investigate the expression and clinicopathological features of gene associated with retinoid-interferon mortality-19 (GRIM-19) in epithelial ovarian carcinoma.Methods The expression of GRIM-19 gene in tissues from 138 cases of epithelial ovarian carcinoma,102 cases of benign ovarian epithelial tumor and 46 cases of normal ovarian tissues were detected by Immunohistochemistry and Western blot methods.Assembled clinical survival data were analyzed with Kaplan-Meier and Cox regression models.Results The expression level of GRIM-19 in epithelial ovarian carcinoma (3.4 ± 2.0) was lower than that in benign ovarian tumor tissues (4.7 ± 2.9) and that in normal ovarian tissues (7.5 ± 2.2 ; P ＜0.01).The level of GRIM-19 expression was related to the survival time of epithelial ovarian carcinoma patients by Kaplan-Meier analysis (P =0.002).The shorter survival time of epithelial ovarian carcinoma patients was significantly associated with the level of GRIM-19 expression (P =0.001),clinical stage (P =0.001),volume of ascites (P =0.023) and the largest diameter of the primary tumor lesion (P =0.044) by Cox regression models.Conclusions The low expression of GRIM-19 in the epithelial ovarian carcinoma suggests that GRIM-19 may be a key gene involved in its carcinogenesis.The expression level of GRIM-19 may be also an independent prognostic factor for epithelial ovarian carcinoma patients.

Objective To understand the molecular mechanism by which protein kinase C? mediates multidrug resistance of human glioma cell line SHG-44.Methods SHG-44/ADM was constructed by stepwise concentration increasing method and intermittent administration method.SHG-44/WT and SHG-44/ADM were treated by PKC? reactivator PMA and PKC? inhibitor staurosporine,then the expressions of PKC? and MDR-1 were detected by Western blotting,the PKC? activity was assayed by kinase,and ADM accumulation was determined by fluorescence spectrometry.Results PMA increased PKC? activity and MDR-1 protein expression and activity.Staurosporine was able to block PKC? activity and decrease MDR-1 expression and activity.Conclusion Multidrug resistance in human glioma cells is mediated by PKC? via MDR-1 pathway.

Objective:To investigate the expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor-C (VEGF-C) in papillary thyroid carcinoma and their relationship to cervical lymph metastases.Method:In this study, the expressions of COX-2 and VEGF-C were examined by immunohistochemistry in papillary thyroid carcinoma tissues of 40 patients, and analysis was performed on the correlation of cervical lymph metastases with COX-2 and VEGF-C expression.Result:Positive expressions of COX-2 and VEGF-C were 70.0%(28/40)and 75.0%(30/40)respectively in papillary thyroid carcinoma. The positive rates of COX-2 and VEGF-C expression were 80.8%(21/26)and 84.6%(22/26)respectively in patients with cervical lymph metastases, and 50.0%(7/14)and 57.1%(8/14)respectively in patients without cervical lymph metastases, with a statistically significant difference between two groups(P<0.05, all). COX-2 was positively correlated to VEGF-C expression in papillary thyroid carcinoma(r=0.378, P<0.05).Conclusion:The results suggest that COX-2 and VEGF-C were highly expressed in papillary thyroid carcinoma, with possible interaction of their expressions, and may play a critical role in the cervical lymph metastases of papillary thyroid carcinoma.