Objective To observe the influence of rational emotional therapy on breast cancer patients preoperation. Methods 50 cases of breast cancer patients were randomly divided into the experimental group and the control group with 25 cases in each group. The control group was provided routine therapy and nursing, health education and general psychological nursing, based upon these routine measures, the experimental group adopted systematic and standardized rational emotional therapy. Zung self rating depression scale(SDS), Zung self rating anxiety scale(SAS), Pittsburgh Sleep Quality Index scale(PSQI)were used to evaluate the effect between two groups. Results No significant differ-ence existed in anxiety, depression and sleep quality between the two groups at admission, but significant difference was seen one day preoperation, also there was statistical significance between at admission and one day preoperation in the experimental group. Conclusions Rational emotional therapy of breast can-cer patients who underwent surgical operation played a significant role on their preoperative short-term e-motions(including anxiety,depression, sleep quality), and worthy of clinical application.

Objective To understand the effect of environmental risk factors exposed in the first trimester of pregnancy on congenital heart disease, then provide scientific evidence for congenital heart disease prevention. Methods A hospital-based 1:1 matched case-control study was conducted. The risk factors were obtained by field investigation with standardized questionnaires. The data was dealt with single factor analysis and conditional Logistic regression using SPSS version 11.5. Results Folic acid(OR=0.340, 95%CI: 0.178-0.649), milk(OR=0.660, 95%CI: 0.460-0.947), meat(OR=0.771, 95%CI: 0.583-0.867) and nausea and vomiting of pregnancy(OR=0.457, 95%CI: 0.271-0.770)were significantly associated with congenital heart disease. Maternal infection(OR=2.736, 95%CI: 1.462-5.121), taking medicine(OR=2.735, 95%CI: 1.483-5.044), poisonous chemicals(OR=2.764, 95%CI: 1.065-7.177) and mental stress(OR=2.211, 95%CI: 1.022-4.782) were risk factors of congenital heart disease. Conclusion To prevent congenital heart diseases, pregnant women should take more nutriment, keep healthy state and avoid infecting, taking medicine and exposing chemical toxicants in the first trimester of pregnancy.

Survivin-D53A (SVV-D53A) is a dominant-negative mutant survivin, which represents a potential promising target for cancer gene therapy. The present study was designed to determine whether SVV-D53A plasmid encapsuled by DOTAP: Chol liposome would have the anti-tumor activity against SPC-A1 lung adenocarcinoma, and to detect the possible mechanisms. In our experiment, SPC-A1 cells were transfected in vitro with SVV-D53A plasmid and examined for protein expression by Western blot, then flow cytometric analysis was used to detect apoptosis. SPC-A1 lung adenocarcinoma xenografts were established in vivo in the nude mice, which received the i. v. administrations of SVV-D53A plasmid/liposome complexes. After mice were sacrificed, the paraffin-embedded tumor tissue sections were used for proliferating cell nuclear antigen (PCNA) expression and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Compared with the control group, the mice treated with SVV-D53A plasmid had an obviously reduced tumor volume, with high level of apoptosis and decreased cell proliferation in tumor tissue. The research results proved that the administration of SVV-D53A plasmid resulted in significant inhibition of SPC-A1 cells both in vitro and in vivo. The functional mechanism is that the anti-tumor response causes and induces tumor cell apoptosis.
Adenocarcinoma ; pathology ; Animals ; Apoptosis ; Apoptosis Regulatory Proteins ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; Heterografts ; Humans ; Inhibitor of Apoptosis Proteins ; metabolism ; Liposomes ; Lung Neoplasms ; pathology ; Mice ; Mice, Nude ; Neoplasm Proteins ; metabolism ; Neoplasm Transplantation ; Plasmids ; Transfection ; Tumor Burden

Objective To investigate the effects of sevoflurane on inhibition of growth of human lung adenocarcinoma A549 cells by cisplatin and γ ray.Methods The human lung adenocarcinoma cell line A549 was seeded in culture plate.After being cultured for 24 h,the cells were randomly divided into 6 groups (n =6each):control group (group C),sevoflurane group (group S),cisplatin group (group D),cisplatin + sevoflurane group (group DS),γ ray group (group R) and γ ray + sevoflurane group (group RS).A549 cells were exposed to 2.5% sevoflurane for 4 h in group S.Cisplatin with the final concentration of 3 mg/L was added to the culture medium and the cells were then incubated for 4 h in group D.Cisplatin with the final concentration of 3 mg/L was added to the culture medium and the cells were then exposed to 2.5 % sevoflurane for 4 h in group DS.A549 cells were exposed to γ irradiation (2 Gy) for 4 h in group R.A549 cells were exposed to γ irradiation (2Gy) and to 2.5% sevoflurane for 4 h in group RS.The cells were cultured for another 24 h after the end of treatment,the colony formation was detected and the rate of colony formation was calculated by colony formation assay.Proliferation of A549 cells was measured by plate colony formation and MTF assay and the rate of proliferation inhibition was calculated.Cell apoptosis was detected with flow cytometer.The expression of X-linked inhibitor of apoptosis protein (XIAP) and caspase-3 was detected by Western blot.Results Compared with group C,the rate of colony formation was significantly decreased,the rate of proliferation inhibition and percentage of apoptotic cells were increased,XIAP expression was down-regulated and caspase-3 expression was up-regulated in groups S,D,DS,R and RS (P ＜ 0.05).The rate of colony formation was significantly lower,the rate of proliferation inhibition and percentage of apoptotic cells were higher,XIAP expression was lower and caspase-3 expression was higher in group DS than in groups S and D,and in group RS than in groups S and R (P ＜ 0.05).Conclusion Sevoflurane can enhance cisplatin and γ ray-induced inhibition of growth of human lung adenocarcinoma A549 cells,and downregulation of XIAP expression and up-regulation of caspase-3 expression may be involved in the mechanism.

Objective To investigate the correlation between vitamin D receptor gene and bone mass and obesity phenotypes in patients with type 2 diabetes mellitus.Methods 318 patients with type 2 diabetes were chosen as diabetes group,and 50 healthy people were selected as healthy control group.Vitamin D receptor gene Apa Ⅰ type was detected in the two groups.Height,weight and body mass index(BMI)biochemical index,fat content(FM),lean tissue content(LM)and bone mineral density were detected in patients with type 2 diabetes mellitus.The relationship between vitamin D receptor gene(Apa Ⅰ)polymorphism and BMD and obesity phenotypes in type 2 diabetes was analyzed.Results The VDR gene distribution between the diabetes group and healthy control group showed no signif-icant difference(Z =0.561,P >0.05).The vitamin D receptor genotype in the diabetes group included AA 31 cases (9.7%),Aa type 108 cases(34.0%),aa type 179 cases(56.3%),while the vitamin D receptor genotype in the healthy control group comprised AA 7 cases(9.3%),Aa type 29 cases(38.7%),aa type 39 cases(52.0%).The percentage of AA in both groups was significantly less than that of Aa and aa(χ2 diabetic group =4.127,3.976,all P <0.05;χ2 healthy control group =5.129,4.213,all P <0.05).Proportion of normal bone mass and average bone density in AA,Aa,aa type decreased(χ2 =15.552,P <0.05;F =5.127,P <0.05),the genotype AA was not detec-ted in osteoporosis group.BMI and FM were the highest in AA,which were significantly higher than those of Aa,aa (F =4.319,4.263,all P <0.05).Conclusion Vitamin D receptor gene Apa Ⅰ type polymorphism is related with BMD and obesity in type 2 diabetes mellitus,and it has predictive value on bone mass changes.The increase of BMI and FMmay be beneficial to bone mineral density.

Objective To explore the role of 14-3-3σ in cell cycle arrest,proliferation inhibition of HaCaT cells after UVB exposure.Methods Crystal violet assay was used to determine the viable density of HaCaT,HaCaTKD cells after being irradiated with UVB of different doses (10,20,30,40,50,60 and 80 mJ/cm2) for 48 h.After HaCaT and HaCaTKD being treated with 30 mJ/cm2irradiation,cell growth and cell cycle distribution were detected by CCK-8 assay and PI staining combined with flow cytometry,respectively.Western blot was used to evaluate the protein expression of 14-3-3σ,Cdc2,Cdc25c and Cyclin B1.Results After 48 h,the survival rate of both HaCaT and HaCaTKD decreased in a dosedependent manner.Especially,HaCaTKD cells had drastically low proliferation rate compared with normal HaCaT at 10 mJ/cm2 (t =8.83-49.63,P ＜ 0.05).The proliferation rate of HaCaTKD cells was significantly lower than that of HaCaT cells (F =32.89,P ＜ 0.05).After treatment with 30 mJ/cm2 UV irradiation,the ability of proliferation in normal HaCaT cells was recovered after 24 h while there was no proliferation in HaCaTKD cells within 72 h after the same treatment.The distribution of cell cycle has little change in HaCaTKD (P ＞ 0.05).UVB treatment led to cell cycle arrest from 6 to 18 h in HaCaT cells(t =7.41,9.22,9.16,P ＜0.05)while no cell cycle arrest could be observed in the HaCaTKID cell.Western blot detection indicated that the expression of 14-3-3σ in HaCaT cells was upregulated(t =5.42-9.57,P ＜0.05)while the Cdc25c and Cyclin B1 proteins were downregulated in both HaCaT and HaCaTKD cells (t =3.95-11.21,P ＜0.05).Specifically,Cdc2 protein decreased in HaCaT cells(t =4.93-5.37,P ＜ 0.05)but there was no change in HaCaT~ cells.Conclusions 14-3-3σ protein affects the proliferation and cell cycle of HaCaT cells after UVB irradiation.14-3-3oσ co-activates the expression of Cdc2,Cdc25cand Cyclin B1 to mediate UVB-induced G2/M arrest in HaCaT cells.

Objective To investigate the carcinogeic role of miR-365 in cuntanerous squamous cell carcinoma (cSCC).Methods Normal HaCaT cells were divided into control and irradiation groups,the later was exposed by UVB irradiation (50 J/m2).MicroRNA expression profiles of the two groups were analyzed by microRNA array.The expression variations of miR-365 in HaCaT,A431,Tca8113 and HSC-1 cells were validated by qRT-PCR analysis.The colony-forming and invasion capacities were dectected by colony forming assay and Transwell migration assay in vitro,respectively.HaCaTpre-miR365-2 highly expressing miR-365 was constructed by retroviral vector infection.Tumorigenicity evaluation was carried out by subcutaneously inject of the cells at the right back flank of nude mice.Results There were 30 microRNAs differentially expressed in HaCaT cells after UVB irradiation and miR-365 was one of the most sensitive miRNAs(as high 6.7 times as control).Expression of miR-365 in all the cSCC cell lines A431,Tca8113 and HSC-1 were significantly higher than that in HaCaT cell,in which the maximum was A431 (15.67 ±1.12 times,P ＜ 0.01),and the minimum was TcaS113 (4.72 ± 0.85 times,P ＜ 0.05).Knockdown of miR-365 in cSCC cell lines significantly inhibited the colony forming ability (t =13.68,P ＜ 0.05) and cell migration (t =19.98,P ＜ 0.05) in vitro.HaCaT cells overexpressing miR-365 by transient transfection significantly increased the ability of colony formation (t =7.11,P ＜ 0.05) and cell migration (t =22.03,P ＜0.05) in vitro.In addition,HaCaTpre-miR-365-2 cell line stably expressing miR-365 could successfully establish tumors in nude mice.Conclusions MiR-365 is an oncogene for cutaneous squamous cell carcinoma.

AIM: To study the effect of TGF-? 1 and TN F-? antisense PS-ODNS on ex vivo expansion of hematopoietic stem/progenitor cell s (HSPC). METHODS: CD 34 + cells were purified from fres h umbilical cord blood by immunomagnetic beads, and mononuclear cells were purifi ed from bone marrow by Ficoll-hypaque . The effects of TGF-? 1 and /or TNF-? an tisense PS-ODNS on ex vivo expansion of CD 34 + cells、CFU-GEMM、CFU-G M、CFU-E and BFU-E were detected by using liquid and semi-solid culture systems . RESULTS: TGF-? 1 antisense PS-ODNS cooperated with cytokines increased the number of CD 34 + cells,CFU-GEMM,CFU-GM,CFU-E and BFU-E , which was as 4,2.6,2.7,1.8,2.1 times as that of the control (the cytokine s combination), respectively. TNF-? antisense PS-ODNS cooperated with cytokines respectively increased the number of CD 34 + cells, CFU-GEMM, CFU-GM, CF U-E and BFU-E by 4, 2 9, 2 6, 1 7, 1 8 times as that of the control. The ab ove two antisense PS-ODNS cooperated with cytokines could respectively increased the number of CD 34 + cells, CFU-GEMM, CFU-GM, CFU-E and BFU-E by 5 3,2 1, 2 7, 1 9, 1 8 times as that of the control. CONCLUSION: I nhibition of endogenous TGF-? 1 and TNF-? by antisense PS-ODNS will be one of the effective methods to expand HSPC ex vivo.

Objective To study the localizations and the quantity of GnRH receptor in stomach of Sprague-Dawley (SD) rats under stress.Methods The model of stress SD rats was established by fear. Then, stomachs were taken from the rats in acute stress group (2h-12h), chronic stress group (1d-4w) and the control group respectively.The localizations and the quantity of GnRH receptor in stomachs were detected using immunohistochemistry and Western blotting.Results The results of immunohistochemistry showed that immunoreactivity of GnRH receptor was displayed in the gastric parietal cells and the epithelial cells of the gastric pits in stomachs of rats in all groups. The immunoreactive materials were distributed in membrane and cytoplasm of all positive cells, but not in nuclei. Meanwhile, the results of Western blotting showed that the number of GnRH receptor decreased significantly when SD rats were in stress from 2h to 2w (P

Objective To investigate the efficacy and safety of a novel biologies-infliximab in the treatment of patients with Crohn's disease (CD). Methods A prospective study was conducted in 10 patients with CD(8 with active refractory CD and 2 with severe lower gastrointestinal bleeding caused by CD). All patients were intravenously infused with infliximab of 5 mg/kg body weight in an induction regimen of 3 doses at week 0, 2 and 6, followed by maintenance dosing every 8 weeks beginning at week 14. The clinical and endoscopic efficacy of infliximab were evaluated by follow-up of 30 weeks. Results ① Five out of 8 patients with active CD had initial clinical response at week 2. Clinical remission was found in 4 patients at week 30, (3 of them in symptomatic remission without corticosteroids). ② Two patients with severe lower gastrointestinal bleeding caused by CD were in control of bleeding and absence of further recurrence by 30 weeks follow-up. ③ Endoscopy was performed in 6 patients at week 30 to evaluate the healing of mucosal ulceration. Four patients were evaluated for complete or almost mucosal healing. ④ Adverse events were seen in 7 out of 10 patients with infliximab treatment, among whom 2 cases had severe side effect including pneumonia in one and delayed hypersensitirity reaction in the other. Conclusion Infliximab has efficacy for the induction and maintenance of remission in part of patients with active CD. Some patients achieved mucosal healing with infliximab therapy and low incidence of serious adverse events.