Objective: To investigate the effect of microcatheter in chemoembolization of HCC. Methods Using 4 - F - 5 - F Yashiro/Kouno and 5 - F Hook catheters as guiding catheter,3 - F microcatheter was put into segmental hepatic artery or tumor feeding artery and chemoembolization was carried out. Results All 35 cases had 50 times chemoembolizations totally, of them, 16 cases with small HCC had segmental TAE and 19 cases with large but localized HCC had right/left hepatic artery or anterio/posterio brtanch of right hepatic artery embolization, 1-2 year survial rates were 100%, 87. 5% and 52. 6%,42. l% respectively after TAE. Liver function damage after TAE was slight and no complications occurred. Conclusion Improving embolization precision by using microcatheter is valuable in the cases with small HCC or large but localized HCC with tortuous hepatic artery,hepatic artery stenosis after injury and variations.

Objective To investigate the effect of microcatheter in chemoembolization of HCC. Methods Using 4-F ～ 5-F Yashiro/Kouno and 5-F Hook catheters as guiding catheter,3-F microcatheter was put into segmental hepatic artery or tumor feeding artery and chemoembolization was carried out. Results All 35 cases had 50 times chemoembolizations totally, of them, 16 cases with small HCC had segmental TAE and 19 cases with large but localized HCC had right/left hepatic artery or anterio/posterio brtaneh of right hepatic artery embolization,1 ～2 year survial rates were 100% ,87.5% and 52.6% ,42. 1% respectively after TAE. Liver function damage after TAE was slight and no complications occurred. Conclusion Improving embolization precision by using microcatheter is valuable in the cases with small HCC or large but localized HCC with tortuous hepatic artery,hepatic artery stenosis after injury and variations.

Objective To detect the synergetic effect and mechanism of arsenic trioxide(As2O3)and Trichostatin A(TSA)during inducing apoptosis of HL-60 cells.Methods MTT method was used to test the proliferation of HL-60 cells.Cell cycle and apoptosis were detected by FCM.Semi-quantitative RT-PCR was used to detect the mRNA expression of Bax and Bcl-2 in the cells treated by As2O3 and(or)TSA.Results As2O3 combined with TSA could inhibit proliferation and induce cell cycle arrest at G0 and G1.The percent of apoptosis induced by combination of As2O3 and TSA was obviously higher than that of either As2O3 or TSA.Bax gene expression was increased,while Bcl-2 gene expression was decreased,Bax/Bel-2 ratio was up-regulated.Conclusion Synergetic effect by As2O3 and TSA is remarkable in inducing apoptosis of HL-60 cells.Cell cycte arrest and Bax/Bcl-2 ratio play an important role in apoptosis of HL-60 cells induced by As2O3,TSA or their combination.

Objective To investigate the effect of euphorbiasteroid on inducing the apoptosis of HL-60 cells and demonstrate whether the Fas/FasL signaling pathway is involved in the induction of apoptosis. Methods HL-60 cells were treated with dose of 2.5,10,40 μg/ml of euphorbiasteroid in vitro for 24 h respectively.After that,cell counting Kit-8 was used to detect cell proliferation.The morphology of HL-60 cells were observed under light and fluorescent microscopy.The early cell apoptosis was detected by using flow cytometry with Annexin Ⅴ-FITC /PI double staining.The expressions of Fas,FasL,caspase-8 and caspase-3 mRNA were analyzed by the method of RT-PCR.The activities of caspase-8 and caspase-3 were examined by chromatometry.Results Compared with 1640 control group,HL-60 cell proliferation was inhibited significant-ly by euphorbiasteroid.The inhibition rates were (34.9 ±3.7)%,(54.6 ±5.2)% and (61.3 ±4.3)%respectively.Moreover,HL-60 cells exhibited typical morphological features.Early cell apoptosis rates of HL-60 cells were (23.4 ±3.1)%,(35.7 ±4.3)% and (53.2 ±3.9)% respectively.Furthermore,the expressions of Fas,FasL,caspase-3 and caspase-8 mRNA were up-regulated significantly after euphorbiasteroid administration in a dose-dependent manner (P<0.01 ).After treated with euphorbiasteroid,the activities of caspase-8 and caspase-3 were significantly enhanced (P<0.01 ).Conclusion The up-regulation effect of euphorbiasteroid on Fas/FasL signaling pathway might contribute to the apoptosis of HL-60 cells.

Aim To investigate the cardiotoxicity of propofol and thiopental. Methods 4day-old contracting neonatal primary myocardial cells obtained from 2-to 3-day-oldWistar rats were divided into 5 groups, with normal contrast group, and the cellcultures in groups PL, PH, TL and TH, were treated with propofol(3 ? 10-5 and3 ? 10-4 mol? L) and thiopental (1 ? 10-5 and 1 ? 10-4 mol?L) for 8 h.The con-tractility and morphology of the cells were observed and the cytoplasmic enzyme(LDH, AST, CK and ALP) release content of myocardial cell and the concentrationof electrolytes (K +, Na +, Cl - and Ca2+ ) in the medium were measured 8 h afterintravenous anesthetics administration. Results In groupPH and TL decreasedsignificantly (P

Dalbergiae Odoriferae Lignum as a traditional Chinese medicine (TCM) has been widely used for promoting blood circulation and removing blood stasis. Flavonoid compounds are main chemical constituents of Dalbergiae Odoriferae Lignum, which exert anti-inflammatory property. However, the underlying anti-inflammatory mechanisms of flavonoid compounds are incompletely understood. It has been reported that isoliquiritigenin, liquiritigenin, naringenin and butein possess anti-inflammatory property. The purpose of this study is to illuminate the anti-inflammatory mechanism of flavonoid compounds based on the protein interaction network (PIN) analysis on molecular network level. 130 targets of the main medicinal ingredients of flavonoid compounds were gained though database retrieval. A protein interaction network of flavonoid compounds was constructed with 589 nodes and 216 interactions. By a graph theoretic clustering algorithm Molecular Complex Detection (MCODE), 26 modules were identified and analyzed by Gene ontology (GO) enrichment. Two modules were associated with anti-inflammatory actions. The most interesting finding of this study was that the anti-inflammatory effect of flavonoid compounds may be partly attributable to inhibite FOS, PTGS2 expression, inhibite of IL-1beta release, and block the MAPK pathway and toll-like receptor pathway.
Anti-Inflammatory Agents ; pharmacology ; Dalbergia ; chemistry ; Drugs, Chinese Herbal ; pharmacology ; Flavonoids ; pharmacology ; Humans ; Protein Binding ; drug effects ; Protein Interaction Maps ; drug effects ; Proteins ; metabolism

Objective: To investigate the epidemiological characteristics of foodborne disease outbreaks in Shaoxing City, Zhejiang Province, from 2012 to 2022, so as to provide the evidence for improving the foodborne disease control strategy. Methods: Foodborne disease outbreaks in Shaoxing City from 2012 to 2022 were collected from National Foodborne Disease Outbreak Monitoring System in China, including populations, places of outbreak, pathogenic factors and suspected foods. The temporal distribution, regional distribution, distribution of outbreak places and pathogenic factors of foodborne disease outbreaks were descriptively analyzed. Results: A total of 89 foodborne disease outbreaks were reported in Shaoxing City from 2012 to 2022, covering totally 699 patients, with an average annual attack rate of 6.35%. The outbreak peaked during the period between June and October (73 outbreaks, 82.02%), and family was the predominant place of outbreak (41 outbreaks, 46.07%). There were 83 outbreaks with known pathogenic factors, including 51 outbreaks caused by microbial factors, with Vibrio parahaemolyticus, Salmonella and norovirus as predominant pathogens, and 29 outbreaks caused by fungi and their toxins, which were all poisonous mushrooms poisoning, resulting in 2 deaths. In addition, there were 3 outbreaks caused by chemical factors. Conclusions The outbreak of foodborne diseases predominantly occurred in summer and autumn in Shaoxing City from 2012 to 2022. Family was the predominant place of outbreak, and toxic mushroom poisoning was the most lethal pathogenic factor.

Objective To investigate the expression of gastric and intestinal phenotypic markers in Siewert typeⅡand Ⅲ early gastroesophageal junction(GEJ) cancer, and to explore its correlation with clinic-pathological features.Methods From April 2010 to July 2015, 53 cases diagnosed as early GEJ cancer were enrolled.The gastric and intestinal phenotypic markers such as mucin5AC(MUC5AC),mucin6(MUC6),mucin2(MUC2),caudal related homeodomain transcription 2(CDX2) and cluster of differentiation 10(CD10) were detected, and then the patients were divided into gastric type, gastrointestinal type, intestinal type and non-classified type according to the results of immunohistochemical staining.Combined with Siewert classification the clinicopathological features were analyzed.Chi square test or Fisher′s exact test was performed for statistical analysis.Results In the cancer tissues of 47 patients with Siewert type Ⅱand Ⅲ early GEJ cancer, the case numbers of positive expression of MUC5AC,MUC6,MUC2, CDX2 and CD10 were 21(44.7%),19(40.4%),31(66.0%),27(57.4%) and 17(36.2%),respectively;the case numbers of gastric type, gastrointestinal type, intestinal type and non-classified type were 11(23.4%),14(29.8%),21(44.7%) and one(2.1%), respectively.The positive expression rates of MUC5AC and MUC6 in Siewert typeⅡwere 55.9%(19/34) and 50.0%(17/34),which were higher than those of Siewert typeⅢ(2/13), and the positive expression rate of MUC2 was 55.9%(19/34), which was lower than that of Siewert typeⅢ(12/13), and the differences were statistically significant (x2=6.240,4.679 and 4.053;all P<0.05).In Siewert typeⅡ, the proportion of intestinal type was 32.4%(11/34), which was lower than that of Siewert typeⅢ(10/13), and the differences were statistically significant (x2=7.142,P=0.010).In patients with Siewert typeⅡand Ⅲ early cancer, males predominated in intestinal type which were mostly well differentiated type with less submucosal carcinoma.The maximum diameter of tumor was less than those of gastric type and gastrointestinal type.In paracancerous mucosal tissues, the incidences of intestinal metaplasia in gastrointestinal type and intestinal type were 11/14 and 81.0%(17/21), which were higher than that of gastric type (3/11);the incidences of atrophy in gastrointestinal type and intestinal type were 12/14 and 85.7%(18/21),which were higher than that of gastric type (4/11),and the differences were statistically significant (Fisher′s exact test,all P<0.05).Conclusions Siewert typeⅡand Ⅲ early GEJ cancer can directly originated not only from gastric mucosa, but also from gastrointestinal and intestinal mucosa.Atrophy and intestinal metaplasia could exist before cancer genesis.

OBJECTIVETo explore the apoptosis resistance induced by Leptin and its mechanism in breast cancer cells in vitro.

METHODSThe leptin-mediated reduction of docetaxel-induced apoptosis in human breast cancer T47D cells was evaluated by TransAM ELISA, MTT and caspase-9 assay. The leptin-promoted survivin expression was analyzed by Western-blot and RT-PCR. The reversing effect of STAT3 knockdown on leptin-induced survivin upregulation was measured by Western-blot and RT-PCR.

RESULTSLeptin promoted T47D cells proliferation and the inhibitory rate was -63.6%. It reduced docetaxel-induced apoptosis in T47D cells by 31.9%. Leptin at different concentrations promoted survivin protein and mRNA expression in T47D cells. The expression of survivin mRNA was 4.6 fold compared with the T47D cells not treated with leptin(10 nmol/L). The expression of survivin mRNA in T47D cells was 0.55 +/- 0.15 fold after transfected with small interfering RNA (siRNA) of STAT3. The expression of survivin mRNA in STAT3 siRNA group and mock transfected group were 0.56 +/- 0.18 fold and 1.61 +/- 0.22 fold after treated by leptin, respectively. The survivin protein level of T47D mock transfected cells was increased after treated by leptin, but the protein level of T47D transfected with STAT3 siRNA cells were not changed significantly.

CONCLUSIONLeptin/STAT3 signaling is a novel pathway for up-regulation of survivin expression in breast cancer cells.

Apoptosis ; drug effects ; Breast Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Female ; Humans ; Inhibitor of Apoptosis Proteins ; Leptin ; pharmacology ; Microtubule-Associated Proteins ; genetics ; metabolism ; RNA, Messenger ; metabolism ; RNA, Small Interfering ; STAT3 Transcription Factor ; genetics ; metabolism ; Signal Transduction ; Transfection ; Up-Regulation