Mycosis fungoides (MF) is the most common subtype of primary cutaneous T-cell lymphoma, and its pathogenesis remains unclear. Recent studies have uncovered high-frequency chromosomal copy number variations in MF, such as gain of chromosomes7q,1q,17q and loss of 9p21,10q,17p, which lead to the gain of proto-oncogenes and loss of tumor suppressor genes, and finally result in tumor development and progression. Moreover, low-frequency single-nucleotide variants have been found in MF, and these mutated genes are mostly enriched in the pathways associated with cell cycle regulation, cell apoptosis, chromatin remodeling as well as T cell activation. Gene-fusion variation is rarely reported in MF. In addition, large cell transformation may occur in some MF cases, and often indicates poor prognoses such as disease progression and drug resistance. In conclusion, MF is a complex disease with highly molecular genetic heterogeneity, and more extensive and intensive researches on its pathogenesis are needed in the future.

Objective To investigate the relationship between anti-trophoblast membrane antigens(TA) antibodies and hypertensive disorders complicating pregnancy(HDCP).Methods Enzyme linked immunosorbent assay(ELISA) was used to detect anti-TA IgG and IgM in both maternal and umbilical serum samples of 40 normal pregnant women and 92 HDCP women(23 gestational hypertension or mild preeclampsia,41 severe preeclampsia and 28 eclampsia).Results The positive rates of anti-TA IgG and IgM in maternal serum samples with HDCP,eclampsia or severe preeclampsia were significantly higher than that in normal pregnant women,the positive rate of anti-TA IgM increased significantly with the aggravation of HDCP(P

County -level public hospitals reform is an important measure of deepening reform of the medical and health system.Medicare payments system reform is therefore an important part of public hospitals reform.By abolishing drugs addition,registration fee,treating fee and setting up medical service fee instead,our hospital carried on a diversified management style in the aspect of medical insurance total prepaid system.The implementation of the reform measures turns out a good result:reasonably keeping a control on the medicare spending and really embodying the transformed of interests patterns.On the premise of ensuring patients interests,medical personnel′s interests are improved to a new level and medical insurance fund are also brought under a reasonable control.The medicare payments system reform puts equity in access and people benefit as the starting point and footing of county -level public hospitals reform,thus lays a foundation of further development of public hospitals reform.

Objective:To study the relationship between alpha seine/threonine-protein kinase (p-Akt)-serine/ threonine-protein kinase (mTOR)-ribosomal protein S6 kinase (p70S6K) signaling pathway and clinicopathological features or chemoresistance of ovarian cancer.Methods:We checked the p-Akt,mTOR and p70S6K protein levels in 18 tissues with chemoresistance or 25 with chemosensitivity of ovarian cancer by immunohistochemistry technique,and analyzed the relationship between those proteins and clinicopathological features or chemoresistance of ovarian cancer.Results:The levels of p-Akt protein in ovarian serous carcinoma,mucinous carcinoma and endometrioid carcinoma were 77.14%,50.00% and 66.67%,respectively,with no significant difference (P>0.05).The levels of these proteins in well-middle differentiated carcinoma and low differentiated carcinoma were 73.33% and 75.00%,respectively,with no significant difference (P>0.05).The levels of these proteins in Ⅰ-Ⅱ stage carcinoma,and Ⅲ-Ⅳ stage carcinoma were 18.18% and 93.75%,respectively,with significant difference (P<0.05).The levels ofmTOR protein in ovarian serous carcinoma,mucinous carcinoma and endometrioid carcinoma were 77.14%,100.00% and 83.33%,respectively,with no significant difference (P>0.05).The levels of this protein in well-middle differentiated carcinoma and low differentiated carcinoma were 80.00% and 78.57%,respectively,with no significant difference (P>0.05).The levels of this protein in Ⅰ-Ⅱ stage carcinoma,and Ⅲ-Ⅳ stage carcinoma were 27.27% and 96.88%,respectively,with significant difference (P<0.05).The levels of p70S6K protein in ovarian serous carcinoma,mucinous carcinoma and endometrioid carcinoma were 80.00%,100.00% and 100.00%,respectively,with no significant difference (P>0.05).The levels of this protein in well-middle differentiated carcinoma and low differentiated carcinoma were 93.33% and 78.57%,respectively,with no significant difference (P>0.05).The levels of this protein in Ⅰ-Ⅱ stage carcinoma,and Ⅲ-Ⅳ stage carcinoma were 45.45% and 96.88%,respectively,with significant difference (P<0.05).The levels of p-Akt protein in tissue of chemoresistance and chemosensitivity of ovarian cancer were 88.89% and 64.00%,respectively,with significant difference (P<0.05).The levels of mTOR protein in tissue of chemoresistance and chemosensitivity of ovarian cancer were 94.44% and 68.00%,respectively,with significant difference (P<0.05).The levels of p70S6K protein in tissue of chemoresistance and chemosensitivity of ovarian cancer were 100.00% and 72.00%,respectively,with significant difference (P<0.05).Conclusion:The p-Akt-mTOR-p70S6K signaling pathway may take part in invasion and metastasis of ovarian cancer.The up-regulation of these proteins may be associated with the chemoresistance of ovarian cancer,and these proteins may have potential to be the prognostic markers for the chemoresistance of ovarian cancer.

Paeonol has inhibitory effect on a variety of tumor cells, whereas cadherin is a kind of glycoprotein that is associated with the occurrence and development of different tumor.In this study, the interactions of paeonol and E-cadherin have been investigated by fluorescence spectrometry and atomic force microscopy (AFM).Fluorescence spectrometry results revealed that the addition of paeonol significantly quenched the fluorescence of E-cadherin.Based on the results of the quenching constant, it was inferred that the interaction of paeonol and E-cadherin was a static quenching process.The thermodynamic parameters ΔH and ΔS were calculated to be -4.3×10.5 J/mol and -1.3×10.3 J/(mol·K), respectively, which proved the involvement of weak interactive forces such as hydrogen bond van der Waals force.AFM results revealed that cadherin molecules were assembled into the long-chain structure.The addition of paeonol could significantly disrupt these assembling structures into short chains, which could be ascribed to the damage of the interdigitation model from the adjacent cadherin molecules.All these results reveal that cadherin is an important target of paeonol to modulate its activity.

Objective To investigate the correlation between methylation status of UNC 5C gene promoter with colorectal cancer UNC5C .Methods 54 cases of sporadic colorectal cancer and related normal mucosal tissue ,as well as 6 colon cancer cell lines and fiber cell lines(FCL) in the oncology department of the Kailuan General Hospital from February 2010 to March 2013 were selected as the research objects and performed the mRNA and methylation analysis for exploring the correlation between the netrin‐1 receptor UNC5C defects with colorectal cancer disease .Results mRNA of UNC5A and UNC5B was expressed in the detected colorectal cancer cell lines .Except FCL for UNC5C ,all of the cancer cell lines had no mRNA expression .In colorectal cancer tissue , UNC5C methylation was significantly higher than that in the normal mucosa ,the difference was statistically significant (P<0 .05) . The methylation levels of UNC5C gene in the stage Ⅰ to Ⅱ ,and the stage Ⅲ to Ⅳwere significantly higher than non‐methylation levels ,the differences were statistically significant (P<0 .05) .The correlation analysis by the Spearman method showed that the UNC5C defects was positively correlated with colorectal cancer disease (r= 0 .856 ,P< 0 .05) .Conclusion Netrin‐1 receptor UNC5C defect has certain correlation with colorectal cancer disease .

Objective To study the protective effect of Xingnaojing combined with alprostadil on brain after acute ischemic stroke in rats.MethodsSixty patients with acute ischemic stroke were enrolled in zhejiang xin'an international hospital from March 2014 to March 2016.They were randomly divided into control group and treatment group, 30 cases in each group.The control group received conventional treatment plus alprostadil, the treatment group in the control group based on the combination of Xingnaojing treatment.Two groups of patients after treatment, are given nursing intervention, such as routine diet guidance, nutritional support, health education.The levels of serum oxidative stress (MDA), vascular endothelial growth factor (VEGF) and vascular endothelial growth factor (VEGF) were compared between the two groups before and after treatment.The levels of cerebral blood flow (CBFV) were recorded before and after treatment Observe the adverse reactions during treatment.ResultsAfter 14 days of treatment, the NIHSS score of the treatment group was lower than that of the control group and the ADL score was higher than that of the control group.The difference between the two groups was statistically significant (P<0.05).Before treatment, the oxidative stress indexes MDA and Hcy were no significant difference between the two groups.After treatment, the oxidative stress indexes MDA and Hcy were lower than the control group(P<0.05).Before treatment, the levels of VEGF and CBFV in the two groups were no significant difference between the two groups.After treatment, the levels of VEGF and CBFV in the two groups were significantly higher than those in the control group (P<0.05).The adverse reaction rate between the 2 groups was similar, and there was no significant adverse reaction, there was no significant difference between the two groups.ConclusionXingnaojing combined with alprostadil has a certain clinical effect on acute ischemic stroke, and has a good protective effect on brain tissue after reperfusion.

Objective To study the effect and toxicity of COX-2 selective inhibitor, celecoxib, plus doxetaxel + epirubicin regimen for LABC as neoadjuvant chemotherapy. Methods 59 women with LABC staged ⅡB～ⅢB were allotted and randomly divided into 2 groups: the control group consisted of 29 patients and with the dosage: doxetaxel (75 mg/m2, d1), epirubicin(75 mg/m2, d1) every 3 weeks; the experiment group consisted of 30 patients and with the dosage: doxetaxel (75 mg/m2, d1), epirubicin(75 mg/m2, d1) and celeeoxib (40Omg, twice daily, d1～21) every 3 weeks. After 2 cycles, the efficacy and toxicity of each group were evaluated. Results The control group achieved an overall response rate (RR) of 72.41%(21/29), and consisted of clinical complete remission (cCR) 2 cases, partial remission (PR) 19 cases, stable disease (SD) 8 cases; the experiment group achieved a RR of 80.00 %(24/30), and consisted of eCR 3 cases, PR 21 cases, SD 6 cases. Both of the group had no pathological complete remission (pCR) and progressive disease (PD) case, and the difference of RR between 2 groups showed no statistical signifieance(χ2=0.469, P=0.493). There was no difference of the diameter of tumor between 2 groups before neoadjuvant ehemotherapy(t=0.569, P= 0.570), but showed statistieal significance after neoadjuvant chemotherapy (t=7.300, P=0.000). Incidence of myalgia and arthralgia of the experiment group was lower than that of control group and had statistical significance (P=0.013). Conclusion Doxetaxel plus epirubiein regimen is effective for LABC with tolerable toxicity. Celeeoxib can enhance the effect and reduce the incidence of myalgia and arthralgia.

AIM:To study the effect of Hand2 (one of basic helix-loop-helix proteins’ transcription factors) expression on the development of the cardiac tissues in the fetal rats from gestational diabetes mellitus ( GDM) parents, and to investigate the potential pathogenesis of GDM-induced congenital cardiac defects in rats.METHODS: The adult Spra-gue-Dawley female rats were randomly divided into blank control group (n=24), GDM group (n=30), negative control group ( n=30) and insulin intervened group ( n=30) .The GDM model was established by intraperitoneal injection of 2%streptozotocin (STZ, 40 mg/kg body weight) to the pregnant rats on the successive day.The rats in insulin intervened group were injected with intermediate-acting insulin in order to keep the fasting blood glucose in the normal range.The rats in negative control group were injected with citric acid-sodium citrate buffer solution in the same position.Blood glucose and body weight were examined every day 72 h after STZ injection.On E12, E15 and E19, the rats were anesthetized and the embryonic cardiac tissues were collected after caesarean section.The histopathological changes of the cardiac tissues were observed under microscope with HE staining.The expression of Hand2 was analyzed by the method of immunohisto-chemistry.The expression of Hand2 in the cardiac tissues at mRNA and protein levels was determined by real-time fluores-cence quantitative PCR and Western blotting.RESULTS:During the development of embryonic heart, the protein expres-sion of Hand2 in the cardiac tissues was showed dynamic changes.Observed on E12, obviously increased on E15, and at the highest level on E19.Compared with the other 3 groups, the protein and mRNA expression of Hand2 in GDM group was decreased at the time points of E12 and E15.CONCLUSION:The morbidity of fetal cardiac malformation is significantly increased in GDM group, suggesting that Hand2 may be involved in the development of cardiac malformation in GDM.

The purpose of the study was to investigate the impact of rat cytomegalovirus(RCMV) infection on the development of the nervous system in rat embryos,and to evaluate the involvement of Wnt signaling pathway key molecules and the downstream gene neurogenin 1(Ngn1) In RCMV infected neural stem cells(NSCs).Infection and control groups were established,each containing 20 pregnant Wistar rats.Rats in the infection group were inoculated with RCMV by intraperitoneal injection on the first day of pregnancy.Rat E20 embryos were taken to evaluate the teratogenic rate.NSCs were isolated from E13 embryos,and maintained in vitro.We found:1) Poor fetal development was found in the infection group with low survival and high malformation rates.2) The proliferation and differentiation of NSCs were affected.In the infection group,NSCs proliferated more slowly and had a lower neurosphere formation rate than the control.The differentiation ratio from NSCs to neurons and glial cells was significantly different from that of the control,showed by immunofluorescence staining.3) Ngn1 mRNA expression and the nuclear β-catenin protein level were significantly lower than the control on day 2 when NSCs differentiated.4) The Morris water maze test was performed on 4-week pups,and the infected rats were found worse in learning and memory ability.In a summary,RCMV infection caused abnormalities in the rat embryonic nervous system,significantly inhibited NSC proliferation and differentiation,and inhibited the expression of key molecules in the Wnt/β-catenin signaling pathway so as to affect NSCs differentiation.This may be an important mechanism by which RCMV causes embryonic nervous system abnormalities.