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.

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 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 changes of cisplatin sensitivity by RNA interfering the excision repair cross-complementing (ERCC) 1 gene in ovarian cancer cell lines. Methods The small interference RNA (siRNA) targeting ERCC1 gene was designed and synthesized by transcription in vitro, and transfected to ovarian cancer cell line ES-2. The mRNA and protein of ERCC1 were evaluated by means of RT-PCR, western blot and immunocytochemistry. The changes of cisplatin sensitivity after interference were examined by methyl thiazolyl tetrazolium (MTT) assay. Results In ES-2 cell, the mRNA and protein levels of ERCC1 were dramatically decreased 24, 48 and 72 hours after transfection. The sensitivity to cisplatin of ES-2 cell line was increased by 53.88 times after disturbing the ERCC1 gene. Conclusion The sensitivity to cisplatin of ovarian cancer cell lines ES-2 could be enhanced by RNA interfering ERCC1 gene.

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

Objective Based on real-time PCR technique and ring primers,to establish a simple,accurate,cost-effective and easily standardized quantitative assay for quantification of HER2 mRNA,and apply to provide medication guidance for clinical tumor personalized molecular targeted therapy.Methods Screening reference gene which was stable expression in breast cancer,and optimizing the PCR reaction system.Then a real-time PCR with Eva Green for quantification of the mRNA expression levels of HER2 gene was developed.The specificity,sensitivity and reproducibility of the method were evaluated 87 specimens including 55 liquid nitrogen-frozen breast cancer tissues and 32 normal tissues were detected by the real-time quantitative reverse transcription (FQ RT)-PCR and immunohistochemistry(IHC).Results The standard curve of the method indicated a good linear relationship between the Ct value and the template concentration with the correlation coefficient being 0.997.The linear range of the system was from 101 to 106 copies/μl and the lower detection limit was 101 copies/μl.It had a high sensitivity and good specificity.The inter-assay coefficients of variation of HER and RPL37A genes were (5.93 ± 0.57)％ and (5.11 ± 0.59)％,(2.49 ±0.81)％ and (2.98 ±0.97)％ respectively.The intra-assay coefficients of variation were (5.76 ±0.58)％and (7.71 ±0.61)％,(3.75 ±0.76)％ and (4.40 ±0.96)％ respectively.Using the optimized FQ RTPCR system,HER2 gene of 87 specimens was quantificated.The sensitivity of the assay was 96.36％ (53/55),the specificity was 78.13％ (25/32),the positive predictive value was 88.33％ (53/60),the negative predictive value was 92.59％ (25/27),and the total coincidence rate between FQ RT-PCR and IHC was 89.66％ (78/87).The correlation of the results between the FQ RT-PCR and IHC was good (Kappa =0.770,P ＞ 0.05).Conclusions The method can quantify the mRNA expression levels of HER2 gene rapidly and cost-effictively with high sensitivity and specificity.It can be applied to clinical molecular diagnosis with attractive prospect.

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.

Objective To determine the possible differences in DNA methylation of benign and malignant thyroid tumors and its role in tumorgenesis and tumor progression. Methods Infinium human methylation 450 bead chip platform was utilized to screen the whole-genome of benign and malignant thyroid tumor tissues surgically removed from a patient for the determination of their DNA methylation levels. The genes with significant differences in methylation were analyzed for their functional pathways with bioinformatics. Results There were significant differences in DNA methylation between benign and malignant thyroid tumor. The inflammation-related pathways, such as T cell, Jak-STAT and cytokine-cytokine receptor signaling pathways involved in the biological process of tumorgenesis and tumor progression. Conclusions The differences in DNA methylation between benign and malignant reveal a close relationship between inflammation and tumorgenesis and tumor progression and provide a novel method for investigation of thyroid cancer development and target drug discovery.