Objective To discuss the clinical value of f iberoptic ductoscopy in the diagnosis and treatment of breast diseases. Methods A total of 3 000 patients with mastalgia, breast mass or ni pple discharge received examinations by fiberoptic ductoscopy. Cytological exami nations were carried out in part of the patients after ductoscopy. Resu lts Of the 3 000 cases, there were 608 cases of intraductal space-occup ying lesions, 1 709 cases of obstructive galactophoritis, 350 cases of galactost asia, 24 cases of acute galactophoritis, 282 cases of simple mammarv duct ectasi a, and 27 cases of normal mammary ducts. Of 1 167 patients with nipple discharge , intraductal space-occupying lesions were clarified by ductoscopy in 585 cases (50%). Surgery was performed in 643 cases while intraductal interventional thera py was adopted in 2 365 cases. Conclusions Fiberoptic ductosco py may be used for the diagnosis and treatment of various breast diseases, not c onfined to nipple discharge.

AIM:to investigate the effects of extract of ginkgo biloba (EGB) on human tubular epithelial-mesenchymal transition induced by transforming growth factor-?1.METHODS: HK2 cells were induced to epithelial-mesenchymal transition by transforming growth factor-?1 (TGF-?1, 10 ?g/L). EGB was added into the medium of HK2 cells 2 h before TGF-?1 was added. The expressions of E-cadherin, ?-smooth muscle actin (?-SMA), NADPH oxidase p67phox and superoxide dismutase (SOD) were determined by Western blotting. Malondialdehyde (MDA) in the mediums of HK2 cells was detected. RESULTS: EGB significantly attenuated the downregulation of E-cadherin, the upregulation of ?-SMA and p67phox, the downregulation of SOD and the upregulation of MDA in HK2 cells induced by TGF-?1.CONCLUSION: EGB significantly attenuates human tubular epithelial-mesenchymal transition induced by TGF-?1, and its underlying mechanism is that EGB attenuates the upregulation of p67phox and the downregulation of SOD induced by TGF-?1.

Objective To compare the effect and toxicity of domestic idarubicin (IDA) and imported daunorubicin (DNR) in the treatment of acute leukemia (AL).Methods According to the random number table method,68 patients were randomly divided in IDA group with 35 patients and DNR group with 33 patients.In IDA group,the patients with acute myelocytic leukemia were treated following IA scheme (domestic idataubicin plus cytosine arabinoside) and the patients with acute lymphoblastic leukemia were treated following VICLP scheme (vincristine,domestic idataubicin,cyclophosphamide,lasparaginase and prednisone).In DNR group,the patients with acute myelocytic leukemia were treated following DA scheme (imported daunorubicin plus cytosine arabinoside) and the patients with acute lymphoblastic leukemia were treated following VDCLP scheme (vincristine,imported daunorubicin,cyclophosphamide,lasparaginase and prednisone).Results In IDA group,21 patients achieved a complete remission(CR),5 patients achieved a partial remission(PR),with a 74.2 ％ (26/35) remission rate (RR).In DNR group,the remission rate was 62.3 ％ (20/33).No differences of the remission rate was found between the two groups (t =0.89,P =0.50).17 patients were found remission over one year in IDA group,and 6 patients were in DNR group.The difference was statistically significant between the two groups (x2 =5.56,P =0.02).Conclusion IDA is more effective than DNR in AL treatment.The higher RR and longer remission time are found in IDA group than DNR group.IDA is effective and safe in the treatment of AL.

Objective To explore the association between genetic polymorphisms and haplotypes of tumor necrosis factor-related apoptosis inducing ligand (Trail) and ulcerative colitis (UC).Methods A total of 331 patients with UC and 832 age and sex-matched healthy controls were collected.After Trail gene was amplified by PCR,the genetic polymorphisms of three single nucleotides (G1525A/G1588A/C1595T) in 3' non coding regions of Trail gene were examined by direct sequencing.The relation between Trail haplotype and UC was analyzed.Results Compared with control group,the frequencies of variant allele A and genotype GA+ AA in Trail G1525A were significantly lower in UC group (both P＜0.01).The frequencies of variant allele A and T in Trail G1588A and C1595T were also significantly lower in UC group than that of control group,and the difference was statistically significant (both P ＜ 0.01 ).In mild and moderate UC patients,the frequencies of variant allele T and CT+TT in Trail C1595T were 49.15％ and 64.51％,in severe UC patients were 72.37％ and 84.21％,and the differences were significant between the two groups (OR=2.710 and 2.935,95％CI:1.598～4.596 and 1.188～7.249,all P ＜0.05).In severe UC patients,the frequency of variant allele A in Trail G1525A was 48.69％,which was higher than that of mild and moderate patients (35.16％,OR=1.750,95％CI:1.082～2.830,P=0.021).In UC group,the frequency of AAT haplotype was significantly lower than that of controls (43.09％ vs 58.41％,P＜0.01).The frequency of GAT haplotype was significantly higher in UC group (10.15％vs 0.18％,95％ CI:0.005 ～ 0.051,P＜ 0.01).Conclusion The genetic polymorphisms and haplotypes of Trail (G1525A/G1588A/C1595T) gene may be closely correlated with the susceptibility to UC.

Tubulointerstitial fibrosis (TIF) is a common pathological feature of end-stage kidney disease. Previous studies showed that upregulation of TGFbeta1 notably contributed to the chronic renal injury and irbesartan halted the development of TIF in rats with 5/6 renal mass reduction. This study was to investigate the effects of irbesartan on chronic TIF and the mechanism involved TGFbeta1 in the rodent model of chronic renal failure involving 5/6 nephrectomy. The results showed that irbesartan significantly attenuated the rise in blood pressure and tubulointerstitial injury observed in this model. Masson staining of the renal tissue revealed that there appeared severe renal tubule atrophy and fibrosis in operation group, but the lesion was attenuated mostly in irbesartan-treated group. Immunohistochemistry showed that irbesartan treatment apparently decreased the protein expression of TGFbeta1 which was up-regulated in operation groups. Western blot showed that irbesartan treatment down-regulated the expression of TGFbeta1, phosphorylated smad2 (p-smad2), AT1R and phosphorylated p38 (p-p38) MAPK, but significantly up-regulated the protein expression of smad6 as compared with operation group. These findings suggest that irbesartan attenuates hypertension and reduces the development of TIF in rats with 5/6 renal mass reduction via changes in the expression of these proteins at least including smad6, TGF-beta1, p-smad2, AT1 and p-p38 MAPK.

Objective To investigate the application value of Photoshop in grading invasive risk of gastric stromal tumors (GSTs). Methods EUS image of 97 cases of GSTs confirmed by pathological and immunohistochemical examination were collected. GSTs were divided into four groups (very low risk, low risk, intermediate risk, high risk) by tumor size, mitotic count and rupture of tumor. Mean gray value (intensity of echo) and gray value standard deviation (uniformity of echo) of EUS images of the lesions were determined by Photoshop and then the differences of each group were found by statistical analysis. Results It is difficult to differentiate EUS images of GSTs from each group by visual observation. The mean gray value of EUS image of very low risk group,low risk group, intermediate risk group and high risk group of GSTs respectively were (56.54 ± 6.10), (59.20 ± 7.51), (77.77 ± 10.90) and (83.43 ± 12.47). There was no significant difference between very low risk group and low risk group (P > 0.05). There was no significant difference between intermediate risk group and high risk group (P > 0.05). In addition, the others all had significantly different from that of each group (P < 0.05). The mean gray value standard deviation of EUS image of very low risk group, low risk group, intermediate risk group and high risk group of GSTs respectively were (8.46 ± 2.59), (12.57 ± 5.89), (12.84 ± 4.15) and (16.69 ± 4.69). There was no significant difference between low risk group and intermediate risk group (P > 0.05). In addition, the others all had significantly different from that of each group (P < 0.05). Conclusions The higher risk of GSTs, the higher of echo intensity and the worse of echo uniformity under EUS. Photoshop combined with EUS is helpful for differentiating different risk of GSTs by analyzing mean gray value and gray value standard deviation of the lesions.

AIM: To observe the effects of cimetidine(Cim) on platelet function and thrombosis. METHODS: After incubated with Cim in vitro , rat platelets were activated with ADP or thrombin. The platelet aggregation, platelet malondialdehyde(MDA) formation, platelet intracellular free calcium([Ca 2+ ] i), and thromboxane B 2 (TXB 2) were measured. The effects of Cim on electric-induced thrombosis in rat carotid artery were examined. RESULTS: Cim potentiated ADP induced platelet aggregation , increased the thrombin induced [Ca 2+ ] i and MDA formation, decreased TXB 2. Also, Cim shortened the duration of electric-stimulated occlution time in rat carotid artery. CONCLUSION: Cim increased platelet function and accelerated thrombosis.

Objective To determine the expression of cathepsin D (CD), cathepsin H (CH) and cathepsin L (CL) in human primary hepatocellular carcinoma (HCC), and to investigate their mechanisms. Methods The protein expression of CD, CH and CL in hepatic specimens consisted of control (n = 17), HCC (n = 37) and paracancerous (n = 28) tissues were detected by immunohistochemistry. The relative values of CD, CH and CL protein expression were examined with absorbent density analysis. Data were analyzed using SPSS11. 5 software. The univariate analysis was used to compare the difference among groups. Results The mean absorbance of CD, CH and CL proteins in HCC tissues (1.21± 0.33, 0. 89 ± 0.22 and 1.16± 0. 25, respectively) were significantly higher in comparison with those in control tissues (0. 19 ± 0. 07, 0. 24 ± 0. 12 and 0. 28 ± 0. 14,respectively) and in paracancerous tissues (0.27±0.13,0. 31± 0.14 and 0. 36±0.15)(all P values =0.0001). Whereas there was no difference between control and paracancerous tissues with respect to CD, CH and CL proteins (P ＞0. 05). Three proteins immunohistochemically appeared as a lot of diffused spots and stripes staining in cytoplasma of HCC tissues,but only a few scatted spots staining was found in control and paracancerous tissues. Conclusion The high expression of CD, CH and CL protein in primary HCC may be important markers for carcinogenesis and malignant progress.

Objective To investigate the association between the genetic polymorphisms of methylenetetrahydrofolate reductase (MTHFR) and ulcerative colitis (UC) of Han ethnic population in Zhejiang, China. Methods Two hundred and seventy-four consecutive patients with UC and 726 healthy controls (HC) were studied. The genetic polymorphisms of MTHFR (C677T and A1298C) were genotyped using PCR-RELP methods. Results The frequencies of variant allele and genotype in MTHFR A1298Cgene were higher in UC patients than in the HC (35.77% vs 29. 96%, P =0. 013; 52. 19% vs 44. 90%,P=0.039; respectively). However, there were no significant discrepancies of the allele and genotype frequencies in the MTHFR C677T gene between the UC patients and the HC (P ＞ 0. 05 ). In addition, the MTHFR 677Tr homozygote, T allele and 677CT/1298AC compound genotype were more prevalent in patients with extensive colitis than in those with distal colitis (37. 66% vs 14. 72% ,P = 0. 0002; 49. 35% vs 32.99% ,P =0. 0004; 29. 87% vs 15.23% ,P =0. 006; respectively). Furthermore,the variant allele in the MTHFR A1298C gene (C) in severe UC patients was significantly lower than in mild and moderate UC patients (18.97% vs 33. 88% ,P =0. 022). Conclusion The genetic polymorphisms of MTHFR C677T and A1298C are obviously associated with Han ethnic population with UC in Zhejiang province.

BACKGROUND:Previous studies have found that electroacupuncture can delay articular cartilage degeneration mediated by JAK-STAT signaling pathway through upregulating the expression level of transforming growth factor β1 as well as mRNA expression levels of STAT3, Smad3 and LepR. In the meanwhile, electroacupuncture can inhibit the mRNA expression of p38 and Fas mRNA mediated by MAPK signaling pathways, further inhibiting the apoptosis of chondrocytes. OBJECTIVE: To explore the effect of electroacupuncture on the degeneration of articular cartilage in rats with knee osteoarthritis based on Ras-Raf-MEK1/2-ERK1/2 signaling pathway. METHODS:120 male healthy Sprague-Dawley rats aged 2 months olds were selected and randomly divided into normal, model, 15-minite electroacupuncture and 30-minute electroacupuncture groups (n=30 per group). The rats in the latter three groups received the intra-articular injection of 4% papain bilaterally, and the remaining rats received no intervention. At 2 weeks after modeling, the latter two groups were respectively given 15- and 30-minute electroacupuncture, five times weekly for consecutive 12 weeks. The morphology of the cartilage was observed by hematoxylin-eosin staining, the expression level of interleukin-1β in the synovium was detected by ELISA assay, and the protein expression levels of Ras, Raf, MEK1/2, ERK1/2, C-MYC, C-FOS, and C-JUN were detected by western blot analysis. RESULTS AND CONCLUSION: Hematoxylin-eosin staining showed that: in the model group, the cartilage surface was rough, the cartilage layer became thinner, and the cartilage structure was damaged with incomplete tidal line; in the 15- and 30-minute electroacupuncture groups, the cartilage structure was complete with clear layers and complete tidal line. ELISA showed that the expression level of interleukin-1β in the model group was significantly higher than that in the normal group (P< 0.01), and the level in the 15- and 30-minute electroacupuncture groups was significantly lower than that in the model group (P < 0.05). Western blot assay found that compared with the normal group, the protein expression levels of Ras, Raf, MEK1/2, ERK1/2, C-MYC, C-FOS, and C-JUN were increased in the model group. However, all above protein levels except ERK1/2 in the 15- and 30-minute electroacupuncture groups were significantly lower than those in the model group (P < 0.01,P < 0.05). To conclude, electroacupuncture inhibits the degeneration of articular cartilage in osteoarthritisvia Ras-Raf-MEK1/2-ERK1/2 signaling pathway and downregulating the expression level of interleukin-1β.