A new method skim milk proteolysis ager diffusion test (SMPAD) was established. Extracelluar proteases in supernatants produced by Aeromonas hydrophila J-l in different mediums were detected by SMPAD and the Azocasein substrat method. It was demonstrated that the two methods agreed with each other and the SMPAD test was charactered by more easily operated, more sensitive and better repeated.

A new method agar diffsive hemolysis test (ADHT)was esteblished to measure thd hemlytic titer of HEC toxin produced by Aeromonas hydrophila.The ADHT had also been compared with the spectrophotometry and the microhemolyses test The results shows that the hemlytic titer detected by ADHTwas hither than the former methods and the ADHT was charactered by better and more easily determined.

A new method agar diffsive hemolysis test (ADHT)was esteblished to measure thd hemlytic titer of HEC toxin produced by Aeromonas hydrophila. The ADHT had also been compared with the spectrophotometry and the microhemolyses test The results shows that the hemlytic titer detected by ADHTwas hither than the former methods and the ADHT was cha ractered by better and more easily determined.

Objective To evaluate the clinical value of 3.0T magnetic resonance imaging (MRI) diffusion weighted imaging (DWI) on evaluation effect of neoadjuvant chemotherapy in advanced gastric cancer. Methods 3.0 T MRI DWI examination was performed in 42 cases of advanced gastric cancer diagnosed by gastroscopy and pathology, including 32 patients were examined with DWI both before and after chemotherapy. Lymph nodes of gastric cancer lesions and display ability of stomach were measured, and the area of the apparent diffusion coefficient (ADC) values in normal stomach and tumors were compared. ADC values were compared in the same patients before and after neoadjuvant chemotherapy and analyzed along with postoperative pathological examinations. Results In a total of 40 patients who received 74 DWI examinations, ADC values in tumor and lymph nodes were significantly higher than those in normal tissue. The ADC value in tumors was (1.348 ±0.278) ×10-3 mm2/s, and in 12 cases of stomach lymph node enlargement was (1.329±0.188) ×10-3 mm2/s. However, the average ADC value of normal stomach was (2.081± 0.189) ×10-3 mm2/s with significantly lower DWI than that of the former (P< 0.001). After chemotherapy, the ADC value in tumors was increased, which was (1.572 ±0.261) ×10-3 mm2/s (P< 0.001). After neoadjuvant chemotherapy, 16 patients received gastric cancer radical prostatectomy, and postoperative pathological TRG ratings of tumor were decreased with different extent. Tumor cell density (TCD) before treatment with an average of 4.45 ×10-5 / px2, which was downgraduated to 2.48 ×10-5 / px2 after chemotherapy and surgery. Negatively correlation between TCD values and ADC values were observed. Conclusion MRI DWI examination can effectively detect advanced stomach cancer and the associated lymph node enlargement. Comparison of tumor morphology and ADC values in advanced gastric cancer before and after neoadjuvant chemotherapy has clinical value in prognosis.

Background and purpose:It has be reported that the activation of EGFR-STAT3 signal transduction pathway is involved in oncogenesis of many cancers.This study was to investigate whether EGFR-STAT3 pathway plays a role in the carcinogenesis of hepatoma in rats.Methods:Hepatoma induced by 3'Me-DAB was used as a model.EGFR,TGF?,STAT3,p-STAT3 in different stages of carcinogenesis were detected by immunohistochemistry and Western blot.In situ hybridization was applied to investigate the expression of STAT3 mRNA.The slides were assessed by Carl Zeiss Image Analysis system.The data were statistically evaluated.Results:EGFR,TGF?,STAT3 were highly expressed at the stages of liver necrosis and repair.the expression of EGFR,TGFa,STAT3 and p-STAT3 has been found in all hepatomas and the levels of EGFR and TGFa were statistically higher than that in normal tissue,similarlly the STAT3 mRNA and protein level in hepatoma was much higher than in normal tissue(P

Objective To evaluate the efficacy and toxicity of the protocol of FOLFOX4 for advanced colorectal cancer. Methods 27 patients received FOLFOX4oxaliplatin 85 mg/m2 as a 2-hour infusion on day 1 and a 2-hour infusion of LV (200 mg?m-2?d-1) followed by a 5-Fu bolus (400 mg?m-2?d-1) and 22-hour infusion (600 mg?m-2?d-1) for 2 consecutive days every 2 weeks. Four courses were carried out with an interval of one month. Results The total effective rate was 44.44 %, CR(3.70 %), PR(40.74 %). Median survival of all patients was 10.0 months. Mean Survival was 11.5 months. One year survival rate was 30.02 %. Median duration of 12 effective patients were 5.3 months. Median survival of effective patients and non-effective was 11.8 and 8.5 months respectively(P

Objective To explore the effects of mitogen-activated protein kinase (MAPK) pathway by estradiol induced vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in endometrial cancer Ishikawa cells.Methods The experiments were divided into 4 groups:E2 group (Ishikawa cells treated with 1 p mol/L estradiol for 30 minutes); inhibitor group:including Ishikawa cells treated with 10 μmol/L Bibf1 120 (Bibf1 120 group),or treated with 2.5 μmol/L Ponatinib (Ponatinib group),or treated with 10 p mol/L U0126 (U0126 group) for 60 minutes; inhibitor + E2 group:including Ishikawa cells treated with 10 μmol/L Bibf1120 (Bibf1120 + E2 group),or treated with 2.5 μmol/L Ponatinib (Ponatinib + E2 group),or treated with 10 μmol/L U0126 (U0126+ E2 group) for 60 minutes following incubation with 1 μmol/L estradiol for 30 minutes; control group:only adding the culture medium without serum DMEM.(1) Western blot analysis was used to detect phosphorylation extracellular signal-regulated kinase 1/2(p-ERK 1/2) protein expression with stimulation in different concentrations of estradiol (0.01,0.1,1,10,100 μmol/L).(2) Quantitative fluorescent reverse transcription (qRT)-PCR and western blot analysis was used to test the level of mRNA and protein of VEGF,bFGF,MAPK kinase 1/2 (MEK1/2),extracellular signal-regulated kinase 1/2 (ERK1/2),p-ERK1/2 and phosphorylation MEK1/2 (p-MEK1/2).Flow cytometry were used to examine the cell cycle,and transwell chamber assay were used to detect the cell migration in different groups.Results The expression of the p-ERK1/2 protein at 0.01,0.1,1,10,100 μ mol/L were 0.16±0.03,0.10±0.03,0.41 ±0.04,0.19±0.03,0.19±0.03,there were significantly higher than that in control group(0.05±0.00,P＜0.05),and which was more obvious at the concentration of 1 μmol/L estradiol.The expression level of VEGF,bFGF mRNA and protein in E2 group were higher than those in the control group (P＜O.05).VEGF mRNA and protein in Bibf1120+E2 group were higher than those in E2 group.The expression of MEK1/2,ERK1/2 mRNA protein in E2 group were higher than those in control group (P＜0.05).The expression of MEK1/2,ERK1/2 mRNA or p-MEK1/2,p-ERK1/2 protein in Bibf1120 + E2 group,Ponatinib+E2 group or U0126+E2 group were lower than those in E2 group(all P＜0.05).Percentage of G1 phase [(53.6±3.2)％] and S phase[(29.2±4.2)％] in E2 group was significantly different with those in control group respectively(P＜0.05).Percentage of G1 phase[(66.8±2.6)％,(63.1±2.6)％ and (63.3±0.4)％] and S phase [(25.4±1.9)％,(25.0±3.8)％ and(23.8±0.5)％] in U0126+E2 group,Bibf1120+E2 group or Ponatinib +E2 group was also significantly different with those in control group (all P＜0.05); percentage of G1 phase and S phase in U0126+E2 group was significant difference with those in Bibf1120+E2 group or ponatinib+E2 group (P＜0.05).The number of cell colony in E2 group (110± 17) was more than those in control group (65±8) ;the number of cell colony in U0126+E2 group(28±4),Bibf1120+E2 group(38±5) or Ponatinib+E2group(42±6) were significant different with those in E2 group (P＜0.05),the number of cell colony in U0126+E2 group was significant difference with those in Bibf1 120+E2 group or Ponatinib+E2 group (all P＜0.05).The results shown that the abilities of proliferation and cell migration were significantly increased in cells after estradiol stimulation.Conclusion Estradiol inducing the production of VEGF and bFGF could activate MAPK pathway through ER-independent manner,further promote development.

Background and purpose:The occurrence of endometrial cancer may be related to the persistent stimulus of endogenous and exogenous estrogen without progesterone antagonist. But how does estrogen regulate cell proliferation is still unknown. AKT pathway is the most important signal transduction way to mediate proliferation in the cells. The main aim was to study whether estradiol induces the expression of VEGF, bFGF and IL-8 in the endometrial cancer HEC-1A cells by activating AKT, and its effect on proliferation. Methods:Western blot was used to detect the expression of AKT protein in HEC-1A cells after estradiol stimulation, AKT inhibitor or ER inhibitor stimulation followed by estradiol. Real-time PCR and ELISA were used to detect the gene and protein expression of VEGF, bFGF and IL-8 in different inhibitors. Cell colony formation assay, lfow cytometry and CFSE assay were used to examine the proliferation in HEC-1A cells. Results:The expression of p-AKT protein in HEC-1A cells after stimulation with estradiol was markedly higher than that in the control group (P=0.006 2);the expression of p-AKT protein in AKT inhibitor group and ER inhibitor group were signiifcantly decreased than that in estradiol group (P=0.006 0, P=0.006 4). qPCR and ELISA showed the mRNA and protein expression of VEGF, bFGF, IL-8 in estradiol group were signiifcantly increased than that in control group (P<0.05);The expressions of VEGF, bFGF, IL-8 in AKT inhibitor group and ER inhibitor group were signiifcantly decreased than that in estradiol group (P<0.01). The abilities of proliferation and cell cycle were signiifcantly increased in HEC-1A cells after estradiol stimulation. Conclusion:Estrogen induces the production of VEGF, bFGF and IL-8 through activating AKT signal pathway.

objective To study the TCR gene mutation in peripheral blood lymphocytes induced by X-ray exposure using cultured lymphocytes cloning method.Methods Freshly isolated peripheral lymphocytes from healthy aduh donors were irradiated with X-ray in doses ranging from 0 to 8 Gy and cultured with interleukin2 and phytohemagglutinin for 7 days.The mutant frequencies of TCR gene(TCR MF)were detected by flow cytonletry and the dose response curves were fitted.Results TCR MF increased with the dose going up.An aquadratic polynomial dose response model was fitted.Conclusions TCR gene mutation could which serve as a potential biological dosimeter.It might be applied for the estimation of biological dose in emergency exposure.

Objective: To explore effect of AMP-activated protein kinase (AMPK) /mammalian target of rapamycin (mTOR) /ribosomal protein S6 kinase-1 (S6K1) signaling pathways and the insulin-sensitizing effect by adiponectin in endometrial cancer HEC-1B cells. Methods: The experiments were divided into 4 groups, adiponectin (Ad) group (HEC-1B cells treated with 20 μg/ml adiponectin for 30 minutes) , inhibitor group (HEC-1B cells treated with 10 μmol/L compound C for 30 minutes) , inhibitor+ Ad group (HEC-1B cells treated with 10 μmol/L compound C for 30 minutes following incubation with 20 μg/ml adiponectin for 30 minutes) , control group (only added the culture medium without serum DMEM) . (1) Real-time quantitative PCR and western blot analysis were used to detect the level of mRNA and protein of adiponectin receptor (AdipoR) 1 and AdipoR2. (2) Western blot analysis were used to detect phosphorylation of AMPK, mTOR, S6K1 or insulin receptor substrate 1 (IRS1) protein expression with stimulation in different concentrations of adiponectin (2.5, 5, 10, and 20 μg/ml) , or following incubation with insulin 50 nmol/L for 5 minutes; or treated with 20 μg/ml adiponectin for different times (15, 30, 45, and 60 minutes) , or following incubation with insulin 50 nmol/L for 5 minutes. (3) Cell counting kit-8 (CCK-8) assay was performed to investigate the cell proliferation, and transwell chamber assay was used to detect the cell migration in different groups. Results: (1) The relative expression level of AdipoR1 mRNA and protein were higher than AdipoR2 in HEC-1B cell (8.50±0.09 to 1.00±0.00, and 0.91±0.03 to 0.69±0.03; P<0.05) . (2) The phosphorylation level of p-AMPK was significantly induced, and the phosphorylation level of p-mTOR and p-S6K1 proteins, and 20 μg/ml adiponectin at 30 minutes, AMPK protein had the highest level of activation. (3) Adiponectin induces increased tyrosine phosphorylation of IRS1 in a time-and concentration-dependent manner. (4) The proliferation inhibition ratio in Ad group (0.68±0.34) % was much more than that in inhibitor+Ad group (0.24±0.04) % (t=17.88, P<0.05) . The number of cell migration in Ad group (77±8) was much more than that in inhibitor+Ad group (132±13; t=-7.34, P<0.05) . Conclusions Adiponectin maybe inhibit proliferation and migration of endometrial cancer cells through AMPK/mTOR/S6K1 signal pathway. Adiponectin insensitizes insulin signaling may by regulating by the AMPK/S6K1/IRS1 pathway.