Purpose:To study the synergistic inhibitory effects of huachansu plus vinorelbine on cell growth in mice bearing Lewis lung cancer. Methods:Fifty mice bearing Lewis lung cancer were randomly divided into control group,cyclophosphamide group (CTX),huachansu group (HCS), vinorelbine group (VNB) and huachansu plus vinorelbine group (HV). Each group included ten mice. Normal saline (0.2 ml),cyclophosphamide (30 mg/kg),huachansu (5 ml/kg),vinorelbine (6.7 mg/kg),huachansu (5 ml/kg) plus vinorelbine group (6.7mg/kg) were injected intraperitoneally,respectively in the five groups. After the drugs were administered for seven days,all mice were sacrificed and the tumors were weighed. The tumor inhibitory rates were calculated and compared among the five groups of mice. The growth cycles of Lewis lung cancer were analyzed with flow cytometry. Results:The tumor inhibitory rates of HCS,VNB and HV group were 42.86% ,45.68%,53.44%,respectively. The percentage of S phase of cell cycle was increased in HCS and the percentage of G 2 /M phase increased in VNB,and both increased in HV group. Conclusions:There exists synergistic inhibitory effect on Lewis lung cancer between huachansu and vinorelbine and the mechanisms could correlate with their synergistic effect on cell growth cycles.

Objective To observe the renal expression of cyclooxygenase-2(COX-2) in diabetic nephropathy rats and the effects of Losartan as angiotensin II type 1(AT1) receptor antagonist.Methods Twenty-eight diabetic Sprague-Dawley(SD) rats induced with intraperitoneal injection of streptozotocin were randomly divided into two groups: diabetic rats without therapy(group D,n=14) and diabetic rats treated with Losartan(group L,n=14).Twenty SD rats were used as the control(group N).The urine and blood samples in 24h were collected after the treatment with Losartan for 10 weeks.The rats were killed and the renal expression of COX-2 was determined with immunohistochemistry.Results Expression of COX-2 in the nephridial tissue and the concentration of urinary thromboxane B_2(TXB_2) in group D were significantly higher than those in group N(P

Objective To improve the effect of reoperation for postoperative upper gastrointestinal rebleeding due to portal hypertension.[WT5”HZ] Method [WT5”BZ] The operative procedure and effect of reoperation in 29 patients in our hospital within the last 7 years were evaluated and reviewed. [WT5”HZ] Results [WT5”BZ] There was no mortality and short term rebleeding; 8 patients had postoperative complications(8/29) including postoperative gastric bleeding in 4. 23 patients received barium meal examination and gastroscopy on follow up of an average of 35 months. 5 of 23 patients were found to have newly developed esophageal varices. Among them, 3 patients with moderate severe varices had had simple pericardial devascularization; 1 patient with slight varices had before had pericardial devascularization plus esophagus transection and reanastomosis. Only one out of 4 receiving mesocaval shunt developed moderate varices. None of the 7 patients receiving lower part esophagus resection plus proximal gastrectomy developed recurrent esophageal varices.[WT5”HZ] Conclusion [WT5”BZ] The result of simple pericardial devascularization was unsatisfactory. Lower part esophagus resection plus proximal gastrectomy had good short and long term result for the treatment of upper gastrointestinal rebleeding due to portal hypertension.

Drug addiction is a chronic relapsing brain disease that is characterized by compulsive drug use and persistence of drug craving. Drug abuse can lead to changes in the neuron structure and function of plasticity,alterations in molecules and cells,and ultimately to individual abnormal behavior. Current studies have found that epigenetic changes leading to the sustainability of gene expression is an important mechanism of drug addiction. In this review,we will systematically summarize the latest advances in epigenetic mechanisms of drug addiction. This review is expected to provide robust evidence that repeated exposure to drugs of abuse induces changes within the brain′s reward regions in three major modes of epigenetic regulation-histone modifications such as acetylation and methylation , DNA methylation,and non-coding RNAs. It promises a new perspective from which to gain insights into the genetic and epigenetic mechanisms of drug addiction and a new area for epigenetic research on clinical drug addiction treatment.

Objective To clarify if estrogen increases gastric mucosal injury in portal hypertensive rats and its role in the pathogenesis of portal hypertensive gastropathy. Methods Forty SD rats were divided into 4 groups:P + E, P, S + E and S groups. P + E and P groups received portal vein ligation and the S + E and S groups underwent sham operation. P + E and S + E groups were given estrogen intramascularly. All rats were maintained on their indiuidual treatment for 14 days. One hour before the sacrifice rats were orally lavaged with 2 ml 99% ethanol. Gastric mucosal blood flow, degree of gastric mucosal injury and mucosal NO production were determined. Results The P + E group had the highest gastric blood flow of (103?14) U compared with the other 3 groups (P

Objective To evaluate MRI characteristics of solid papillary carcinomas (SPCs) in situ of the breast.Methods A retrospective study included 5 patients with pathologically confirmed SPC in situ was performed.MRI data before operation including conventional MRI,dynamic contrast enhanced MRI (DCE-MRI) and DWI were analyzed.Results All the lesions showed iso/hypointensity on T1 FSPGR sequence,iso/hyperintensity on FSE T2WI sequence and STIR sequence.Mass enhancements were observed for all lesions with oval or irregular shapes on DCE-MRI.The margin of lesions were circumscribed,and internal enhancements were homogeneous or heterogeneous.Time intensity curve appeared a rapid increase in initial contrast phases and platform or outflow types in delayed phases.All the lesions on DWI showed slightly hyperintensity with the ADC value range from 1.34 × 10-3 mm2/s to 1.96)× 10-3 mm2/s.Conclusion MRI manifestations of SPC are characteristics,which may provide valuable information to distinguish SPC in situ from other invasive breast carcinomas.

Objective To investigate the effect of high glucose and losartan on cell proliferation and cyelooxygenase-2 (COX2) expression in normal human mesangial cells (NHMCs), and to examine the effect of losartan on COX2 and transforming growth factor-betal (TGF-β1) expression in a model of diabetic nephropathy (DN). Methods NHMCs were cultured in vitro in high glucose media with or without losartan. NHMCs proliferation and COX2 expression were determined by WST-1, Western blot,and RT-PCR. The rat model of DN was produced by injections of streptozocin (STZ). After the treatment with losartan for 4 weeks, glomerular hypertrophy, urinary thromboxane B2(TXB2) and 24 h urinary pro-tein counts were measured,and COX2 and TGF-β1 expressions were investigated using immunohistochem-ical techniques and RT-PCR. Results Losartan dose-dependently inhibited the proliferation of NHMCs in response to high glucose. Losartan also decreased COX2 expression in NHMCs at high or low glucose concentrations. In vivo experiments found kidney weight/body weight (KW/BW), urinary TXB2 and 24 hurinary protein counts increased significantly in the DN group. Losartan reduced KW/BW, urinary TXB2,and 24 h urinary protein counts and significantly suppressed the over-expression of COX2 and TGF-β1.Conclusion Losartan reduces COX2 expression in NHMCs, especially at high glucose concentrations.Losartan could suppress the expression of COX2 and TGF-β1 in the kidney of DN rats and attenuate the renal lesions caused by DN.

Aim To explore the apoptotic effect of mimics of manganese superoxide dismutase(MnSODm)on human leukemia cell line K562 in vitro and the possible molecular mechanisms.Methods Human leukemia K562 cells were used as the target cells.The cell proliferating activity was examined by a MTT colorimetric assay,and the apoptosis of K562 cells was assessed with FITC-Annexin V and propidium iodide(PI)double staining and morphological changes.The expressions of bcl-2 and bax mRNA were detected by reverse transcription polymerase chain reaction(RT-PCR),and flow cytometry(FCM)was employed to measure the expressions of Bcl-2 and Bax protein,mitochondrial inner membrane potential(??m),Cytochrome C(Cyt C)release and Caspase-3 activity.Results The proliferation of K562 cells was obviously inhibited by 0.5~10 mg?L-1 MnSODm(P

Objective To investigate effects of total flavonoids of litchi (TFL) on the proliferation of rat hepatic stellate cells (HSC-T6) in comparison with western medicine rosiglitazone, and to explore the mechanism of anti hepatic fibrosis of TFL. Methods Effect of TFL on proliferation of HSC-T6 was examined by MTT. The expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) mRNA, connective tissue growth factor (CTGF) mRNA in HSC-T6 cells exposured were examined by real-time quantitative PCR. Effects on HSC-T6 CTGF protein from TFL and rosiglitazone were detected by Western bloting. Results The expression of PPAR-γ mRNA was upregulated and the expression of CTGF mRNA and protein was downregulated after exposure to TFL and rosiglitazone for 72 hours. And the effect of TFL increased with the increase of concentration. Conclusion TFL can inhibit the proliferation of HSC-T6 and antagonizing liver fibrosis. This mechanism may be associated with the upregulation of PPAR-γ expression and the downregulation of CTGF expression.

Objective To explore the impact of hyperglycemia on Hypersensitive C-reaction protein (hsCRP),B-type natriuretic peptide(BNP) and ventricular remodeling in elder patients with acute myocardial infarction(AMI).Methods One hundred and twenty elder patients with AMI are divided into hyperglycemia group(blood sugar in admission ＞ 7.8 mmol/L) and non-glycemia group(blood sugar in admission ≤7.8 mmol/L).The levels of blood sugar in admission,hsCRP,BNP were detected.LVEF,LVEDD,LVESD,WMS were observed by cardiac echo in admission and two weeks after therapy.Results The blood sugar in admission,hsCRP and BNP of the patients in hyperglycemia group were (9.6 ± 0.6) mmol/L,(1 750.6 ±677.1) ng/L,(56.1 ±38.6) ng/L,higher than those in non-glycemia group (t =38.679 and P =0.000; t =11.941 and P =0.000; t =3.288 and P ＜0.01,respectively).LVEF,LVEDD,LVESD and WMS of patients in hyperglycemia group didn't show statistical significance before and after therapy.However,there were significant in hyperglycemia group (t =2.049 and P =0.043,t =2.836 and P =0.005,t =3.814 and P =0.000,t =2.086 and P =0.039,respectively).Conclusion Hyperglycemia can reduce the increase of hsCRP and BNP,which has an impact on hsCRP,BNP and ventricular remodeling in elder patients with acute myocardial infarction,but the mechanism need to further research.