Background and purpose:Cervix cancer is the second most common cancer in gynecologic malignant tumors. Chemotherapy has been used more and more lately, and concurrent chemo-radiotherapy are receiving increasing attention. In this study, we investigated the clinical effect of concurrent PCF chemotherapy plus radiotherapy for moderate and advanced cervical cancer. Methods:One hundred and ninty-six patients with moderate and advanced cervical cancer were randomly divided into two groups: only radiotherapy group and chemo-radiotherapy group (98 cases for each group). Two groups underwent the same fractionation irradiation, the chemo-radiotherapy group was given PCF regimen that consisted of (DDP) at the dose of 20 mg daily intravenously for 1-5 days, (5-FU) at the dose of 500 mg daily for 1,3,5 days and (CTX) at the dose of 400 mg daily for 2,4 day for 2-4 cycles. Both groups received radiotherapy with 30 Gy first and were irradiated by the combination of external radiotherapy plus intracavitary irradiation.Results:The immediate response rates of the two groups were 100 %, there was no statistical difference. The 5 year survival rate was 76.5 % in chemo-radiotherapy group and 50 % in only radiotherapy group (P

Objective To study the changes of lactic dehydrogenase (LDH) and ? hydroxybutyric acid (HBD) in atrophic gastritis type A(AAG) patients. Methods Auto biochemistry instrument was used to detect serum LDH and HBD. Hemoglobin, vitamin B 12 and gastrin were also examined routinely. Results All AAG patients had elevated levels of LDH and HBD in serum and 60 percent of patients had a rise of indirect bilirubin. In the first day after supplement with folic acid and vitamin B 12 , LDH and HBD decreased simultaneously by 30% along with a decrease of indirect bilirubin. The changes of LDH and HBD were earlier than changes of reticulocytes. Conclusions Serum LDH and HBD rise significantly in AAG patients. This might be associated with in situ hemolysis of bone marrow. And it may be a good index for differential diagnosis between AAG and atrophic gastritis type B.

Objective To explore the relationship between parental marital quality and depressive behavior in children.Methods Using the method of stratified cluster random sampling,1 311 mothers whose children were 4 to 7 from Shenzhen' s kindergartens were randomnly selected and filled out Achenbach Child Behavior Checklist(CBCL 4/16) and Chinese Marital Quality Questionnaire.The survey results were analyzed using SPSS statistical package.Results ①In 1 311 children,the detection rate of depressive behavior was 3.28％ (43/1 311).Based on the detection rate,the difference of children depressive behavior was not statistically significant between the gender(x2=2.860,P＞0.05),but was statistically significant among different ages(x2 =17.146,P＜0.01).Increasing depressive behavior was observed with age.②The normal group of behavioral and emotional development was better than the group which had depressive behavior in marital quality(63.65±14.86) and 10 indicators of marital quality including personality magnanimous(6.03± 1.49),communication of couple(6.04± 1.48) and family roles (6.03± 1.48).There were statistical significances in marital quality(t=4.415,P＜0.05) and its 10 indicators,which was communication of couple(t=4.891,P＜ 0.05),conflict resolution (t=4.229,P＜0.05) and leisure activities(t=4.084,P＜0.05),were showed significant differences between the two groups.③The relationship between parental marital quality and depressive behavior in children were negatively correlated(r=-0.070--0.352).The better marital quality,the lower incidence of children depressive behavior,and the impact of marital quality for younger children was more significant.④In the indicators of the marital quality,communication of couples(B=-0.318,P＜0.01),and attitude towards offspring and marriage(B=-0.275,P＜0.01) could predict children depressive behavior.Conclusion It is important to improve marital quality and creat harmonious family spiritual enviromnent for reducing the incidence of children's depressive behavior.

BACKGROUND:Glucocorticoids may induce local bone trabecular and bone marrow necrosis, femoral head col apse and deformation, thus resulting in hip dysfunction. However the pathological mechanisms and treatment of glucocorticoids-induced osteonecrosis of the femoral head remain unclear, and the pathogenesis mechanisms are controversial. The current studies focus on the understanding of the pathological mechanisms.
OBJECTIVE:To summary the research progress of adipogenic differentiation theory of glucocorticoids-induced osteonecrosis of the femoral head and the treatment.
METHODS:The first author searched literature from CNKI and PubMed database from 1988 to 2010, by using the key words is“Glucocorticoids, osteonecrosis of femoral head, bone marrow stromal stem cells, adipogenic differentiation, differentiation factors, treatment, choices”in English, and“glucocorticoids induced osteonecrosis of femoral head, adipogenic differentiation, treatment, research progress”in Chinese. Articles regarding the adipogenic differentiation theory of glucocorticoids-induced osteonecrosis of the femoral head and the treatment were included.
RESULTS AND CONCLUSION:A total of 112 literatures were screened out, according to inclusion and exclusion criteria for literature screening, 54 articles were included. Modern researches emphasize the celland molecular biology level, and show that the biological base of glucocorticoids-induced osteonecrosis of the femoral head is abnormal adipogenic differentiation of bone cells, glucocorticoids cause the variations of adipogenic differentiation factors, leading to adipogenic differentiation of bone marrow stromal cells. But glucocorticoids affects multiple differentiation factors, it may cause great error in the evaluation of the pathogenesis of glucocorticoids-induced osteonecrosis of the femoral head purely from one factor. The abuse of glucocorticoids is the leading cause for the osteonecrosis of femoral head. Further studies are needed to investigate the pathogenesis of osteonecrosis of the femoral head and treatment programs.

Objective To evaluate the role of protein kinase Cα( PKCα)?nuclear factor E2?related factor 2 ( Nrf2)?heme oxygenase?1 ( HO?1) signaling pathway on endotoxic shock?induced acute lung injury ( ALI) in rabbits. Methods Thirty healthy male New Zealand white rabbits, aged 2 months, weighing 2?0-2?5 kg, were randomly divided into 3 groups ( n=10 each) using a random number table: normal control group ( group C);ALI group ( group ALI);PKCα inhibitor chelerythrine group ( group CHE) . In group CHE, chelerythrine 8 mg∕kg ( in 0?5 ml of DMSO) was injected intraperitoneally, and 30 min later, LPS 5 mg∕kg ( in 2 ml of normal saline) was injected via the auricular vein to induce ALI in ALI and CHE groups. The rabbits were then sacrificed at 6 h after injection of LPS or normal saline, and the lungs were removed for examination of the pathological changes which were scored and for determination of wet∕dry lung weight ratio ( W∕D ratio) , and the expression of Nrf2 and HO?1 protein and mRNA. Results Compared with group C, the pathological score and W∕D ratio were significantly increased, and the expression of Nrf2 and HO?1 protein and mRNA was up?regulated in ALI and CHE groups. The pathological score and W∕D ratio were significantly higher, and the expression of Nrf2 and HO?1 protein and mRNA was lower in group CHE than in group ALI. Conclusion The PKCα?Nrf2?HO?1 signaling pathway is one of the endogenous protective mechanisms underlying endotoxic shock?induced ALI in rabbits.

Objective To study the changes of DNA repair genes and enhanced anti-tumor effect of cisplatin induced by mifepristone in human ovarian cancer drug resistance cells.Methods The alterations of cisplatin concentration producing 50％inhibition(IC50)in the COC1/DDP cell lines were examined by methyl thiazolyl tetrazolium(MTT)assay.RT-PCR and flow cytometry were used to analyze the changes of the mRNA of ERCC1,BRCA1,hMLH1 genes and cell cycle and apoptosis.Subcutaneous implantation of COC1/DDP was established in nude mice and the enhanced anti-tumor effect of cisplatin by mifepristone was observed in vivo.ResultsCisplatin IC50 values of COC1/DDP cell were decreased from(3.71±0.38)μg/ml to(3.18±0.46),(1.95±0.14),(0.64±0,18)μg/ml respectively when treated with 2.5,5.0,10.0 μmol/L mifepristone.Mifepristone could down-regulate the mRNA levels of ERCC1,BRCA1,hMLH1 genes and enhance G0/G1 phase block effect pf cisplatin,and 2.5,5.0,10.0 μmol/L mifepristone combined with cisplatin increased rate of cell apoptosis from 0.08％to 5.11％,9.13％and 12.24％ respectively.The percentage of inhibition of xenograft tumor volume in combined treatment group was 70.1％,which was significantly different(P＜0.05).Conclusion By down-regulating ERCC1,BRCA1,hMLH1 genes,blocking G0/G1 phase,and increasing apoptosis rate,mifepristone could enhance anti-tumor effect of cisplatin.

Background and purpose: Aurora kinases, frequently detected to be over-expressed in some human tumors, regulate many essential events during tumor cell mitosis progression and have been regarded as potentially important targets for cancer therapy. This study was designed to detect Aurora-B expression in cervical carcinoma, explore the relation Aurora-B expression and clinicopathologic feature. So, Aurora-B kinase inhibition ZM447439 was used to investigate the effect of ZM447439 on SiHa cell line and the synergy effect with paclitaxel. Methods:Detected Aurora-B protein in cervical carcinoma(70 patients), CINⅡ(46 patients) and normal cervix(21patients) by immunohistochemistry. The inhibitory effects of ZM447439 and paclitaxel in SiHa cell line were investigated by MTT based assay, The expression of apoptosis associated protein was measured by Western blot. Results:The rate of Aurora-B expression is 71.43%in cervical cancer, with no signiifcant correlation to clinical stage, age, lymph node metastasis, vascular invasion (P>0.05). Aurora-A protein expression has significant correlation to pathological type and grade(P<0.05). Enhanced antiproliferative effects were found when SiHa cells were cultured with ZM447439. Synergic effect of ZM447439 combined with paclitaxel was found in SiHa cell line(Q>1.15). The level of P53 was increased significantly through ZM447439 treatments with Western blot. Conclusion: Our data provides strong evidence that high expression of Aurora-B in cervical cancer. The targeted Aurora-B inhibitors, ZM447439, can enhance paclitaxel anti-tumor activity in cervical cancer.

ibits tyrosinase activity and melanogenesis in murine B16 melanoma cells. Hence, N-acetylglucosamine may serve as a skin lightening agent in the future.

Due to the particularity of marine ecological environment, many marine lives have developed and accumulated a large amount of biological molecules with special chemical structures and physiological activities, representing an important resource for the development of marine drugs. Generally, the marine antibacterial proteins are mainly identified from the marine microorganisms, invertebrates and fish.In this review, the progresses on marine antibacterial peptides and antimicrobial activity proteins are briefly summarized.

Objective To investigate the expression of Jagged1 in human epithelial ovarian carcinoma tissues and the effect of Jagged1 on growth of xenograft in nude mice. Methods (1) Forty-eight cases of ovarian cancer and 30 cases of patients with benign epithelial ovarian tumor in the Henan Province Xinxiang Central Hospital during Feb. 2011 to Mar. 2014 were enrolled in this study. The mRNA expression of Jagged1, Notch1 and the downstream target genes Hes1, Hey1 were analyzed by using realtime PCR method. (2) The ovarian cancer xenograft models in nude mice were constructed by injecting SKOV3 cells in axillary subcutaneouswere. The nude mice were randomly divided into Jagged1 interference group, blank plasmid group and control group. Each group had 10 mice. They were transfected with pcDNA3.1(+)-siRNA-Jagged1, blank plasmid pDC3.1 and phosphate buffer, respectively. The tumor volumes and tumor masses were measured 14 days after transfection and the inhibition rate was calculated. The relative mRNA expression of Jagged1, Notch1, Hes1 and Hey1 in xenograft tissues after transfection in each group was detected by using realtime PCR technique and the relative protein expression of Jagged1, Notch1, Hes1 and Hey1 in xenograft tissues was detected by utilizing western blot method. Results (1) The relative mRNA expression of Jagged1, Notch1, Hes1 and Hey1 in ovarian cancer tissues were higher than benign ovarian tumor tissues, the differences were statistically significant (P<0.01). (2) The tumor volume was (491 ± 68) mm3 and tumor mass was (2.6±0.4) g in Jagged1 interference group, which were significantly lower than that in the blank plasmid group [(842 ± 88) mm3 and (4.4 ± 0.8) g, respectively] and that in the control group [(851 ± 90) mm3 and (4.5 ± 0.9) g, respectively;P<0.05], the tumor inhibition rate was 42.2% in Jagged1 interference group, which was significantly higher than that in the blank plasmid group and that in the control group (2.2%and 0, respectively), the differences were statistically significant (P<0.05). The relative mRNA and protein expression of Jagged1, Hes1 and Hey1 in xenograft tissues of nude micein Jagged1 interference group were lower than that in the other two groups, the differences were statistically significant (P<0.05). There were no differences of relative mRNA and protein expression of Notch1 in xenograft tissues of nude mice among the three groups (P>0.05). Conclusions Jagged1 is highly expressed in epithelial ovarian carcinoma. Jagged1 gene interference in xenograft tumor can inhibit ovarian cancer cell growth and improve tumor suppressor rate, which probably play roles by inhibiting Notch1 signaling pathway.