Objective To explore the efficiency of arterial perfusion chemotherapy combined with embolization for the treatment of giant carcinoma of the kidney. Methods Arterial perfusion chemotherapy combined with embolization was performed through the renal artery in 21 cases of giant carcinoma of the kidney from April 1992 to April 2006. The chemotherapeutic agents contained carboplatin(300 mg), mitomycin(20 mg) and cyclophosphamide(800 mg). The embolization was conducted with anhydrous alcohol, sodium morrhuate, and lipiodol plus gelatin sponge. Results The arterial perfusion with embolization was successfully obtained in all 21 cases. Surgical resection was accomplished in 15 cases, 1 - 8 weeks after the embolization; revealing severely less or no blood supply to the tumor. Pathological findings showed marked necrosis of tumor cells with peripheral inflammatory infiltration, fibrous proliferation as well as capillary embolization. The survival rates at 1-, 2-, and 3-, year were 80%(12/15), 53.33%(8/15) and 40%(6/15) respectively. Conclusions Combination of perfusion chemotherapy and embolization through the renal artery for the treatment of giant carcinoma of the kidney offers promising clinical effects.

Adult ; Facial Neoplasms ; Facial Nerve ; Humans ; Male ; Neurilemmoma

Aim To study the anti-inflammatory activity of the Channa argus bile.Methods The bile was isolated and purified by extraction and silica gel column chromatography.Then the compounds were identified by hydrogen and carbon spectra.The spleen lymphocytes proliferation assay and Lipopolysaccharide(LPS) induced mouse macrophage RAW264.7 releasing Nitrogen Monoxide(NO) experiment were used to evaluate the anti-inflammatory activity.Results Compound(C1) of sodium taurocholate and compound(C2) of sodium taurochenodeoxycholate were isolated by activity tracing.The cell relative viabilities of the two compounds on Concanavalin A(Con A) induced spleen lymphocytes proliferation assay were 65.9%±11.7% and 60.5%±9.4%, which were significantly different from the result of model group (P<0.01), respectively.The NO production of LPS-induced RAW264.7 release of NO was (16.4±1.9) μmol·L-1 and (15.5±1.7) μmol·L-1, which were significantly different from the result of model group(P<0.01).Conclusion Sodium taurocholate and sodium taurochenodeoxycholate from Channa argus perform the anti-inflammatory activities but have no cytotoxic effect on spleen lymphocytes and macrophage.

Tunnel endoscopy is a new therapeutic technique developed from natural orifice endoscopic transluminal surgery and endoscopic submucosal dissection. With the quick development in the passing 5 years, tunnel endoscopy has been applied in the treatment of clinical diseases. In this article, our aim was to clarify the indication and method, evaluate the efficacy and safety of tunnel endoscopy for the treatment of esophagogastric diseases, including esophageal achalasia and submucosal tumors originating from the muscularis propria layer.
Endoscopy, Digestive System ; adverse effects ; methods ; Esophageal Diseases ; surgery ; Humans ; Stomach Diseases ; surgery

Aged ; Aged, 80 and over ; Endoscopy ; Epistaxis ; diagnosis ; surgery ; therapy ; Female ; Humans ; Male

Purpose:To determine the efficacy of paclitaxel in human bladder cancer lines and to investigate the mechanism by which paclita xel induce apoptosis in human bladder cancer cells. Methods:BIU-87, 5637, T24 and EJ bladder cancer cell lines wer e cultured by techniques of cell culture in vitro. The cytotoxic activity an d apoptosis induction abilities of paclitaxel were analyzed by MTT and Annexin- V assay as well as DNA cytometry , respectively. The effects on the cell cycle w ere assessed by flow cytometry of propidium iodide. The expressions of Bcl-2, B ax, p53 and Caspase3 proteins were determined by flow cytometry immunofluorescen ce. Results:Paclitaxel dose-dependent inhibition of cell prolifera tion was seen.Paclitaxel induced G_2/M arrest (71.29% and 64.57%) which was maximal in 5637 and EJ cell lines. While paclitaxel at 1?g/ml concentration ex posure to 5637 12h, 14h and 48h respectively, the apoptosis rates of the respect ive times were 5.0%, 12.9%, 27.6%. The expression of genes p53 and Bcl-2 was no t influenced, whereas the expression of Bax and Caspase3 had increases time-dep endently after exposure to paclitaxel. The analysis of Annexin-V showed a drama tic dose-dependent increase of apoptosis. Conclusions:Paclitaxel inhibited bladder cancer cells prolifera tion and had more effect on those cells whose grade was lower and doubling time was longer. Paclitaxel could block G_2/M arrest, and induce apoptosis by th e path of Bcl-2/Bax in bladder cancer cell lines.

Objective To investigate changes in high mobility group box-1 protein ( HMGB1 ) level in brain tissues with severe sepsis, and the relationship between HMGB1 and septic brain injury.Methods Forty wild C57BL/6 mice were randomly ( random number) divided into 4 groups: sham group, sepsis group, cerebroventricular injection control group, and sepsis with BoxA ( HMGB1 inhibitor) cerebroventricular injection group.Septic model was reproduced by cecal ligation and puncture, and the cerebroventricular catheterization model was established by motorized mice brain stereotaxic instruments.After septic challenge, 1 μg BoxA was injected into the ventricle of brain via cerebroventricular catheter immediately.Mice were sacrificed and brains were harvested at 24 h after sepsis, and hippocampus tissue was separated immediately.Expressions of brain HMGB1 and caspase-3 changed in apoptotic neurons and brain injury were determined by brain tissue immunofluorescence, Western blotting, TUNEL and HE staining respectively.One-way analysis of variance ( ANOVA) for analyzing inter-group differences, student t test for comparing difference between two groups . Results (1) HMGB1 expression in hippocampus was significantly enhanced in the septic group compared to the sham group [ (22.74 ±9.29) vs.4.57 ±2.18, P<0.01].(2) Compared to the sham group, neuronal apoptosis [ (35 ±9.17) vs.(1.67 ±1.53) , P<0.01) and caspase-3 expressions [ (16.79 ±8.17) vs.( 3.39 ±2.09), P<0.05] were significantly increased in hippocampus with aggravated brain injury in the septic group.(3) Cerebroventricular injection of BoxA significantly inhibited HMGB1 in hippocampus [ (2.66 ± 2.06) vs.( 22.74 ±9.29), P<0.01];(4) Cerebroventricular injection of BoxA obviously alleviated acute brain injury, and decreased neuronal apoptosis [ ( 12 ±4.36 ) vs.( 35 ±9.17 ) , P <0.01 ] as well as caspase-3 activity [ (4.10 ±2.11) vs.(16.80 ±8.17), P<0.05].Conclusions The elevated expression of brain HMGB1 is closely related to pathogenesis and development of septic brain injury, and treatment with antagonist towards brain HMGB1 can markedly attenuate acute brain injury following severe sepsis.

Objective To investigate the effect of high mobility group box-1 protein (HMGB1) on cytokine expression in splenic dendritic cell (DCs). Method DCs isolated from the spleens of male Wistar rats were seed-ed on 96-well (1×10s cells/well) cell culture plates, and the cells were stimulated with HMGB1 for various length of time or in different concentrations. (1) The time-dependent response between HMGB1 and tumor necrosis factor-α(TNF-α) as well as interleukin-12 (IL-12) gene/protein expressions: 24 wells of DCs were dividedly into six groups including 24 h-normal controls (n=4), 48 h-normal controls (n=4), 72 h-normal controls (n=4), and 24 h-HMGB1 treated group (n=4), 48 h-HMGB1 treated group (n=4) as well as 72 h-HMGB1 treated group (n=4), respectively. Among three HMGB1-treated groups, DCs were stiraulated by 1 μg/mL HMGB1. DCs were denatured in cell culture plates to determine gene expression of IL-12 as well as TNF-α, and supernatants were harvested to determine Il-12 as well as TNF-α protein levels. (2) The dose-dependent response between HMGB1 and TNF-α as well as IL-12 gene/protein expressions: 16 wells of DCs were dividedly into four groups in-cludingnormal controls (n=4), 0.1 μg/mL HMGB1 treated group (n=4), 1 μg/mL HMGB1 treated group (n =4), and 10 μg/mL HMGB1 treated group (n=4), respectively. After stimulated for 48 h, DCs were dena-tured in cell culture plates to determine gene expression of IL-12 as well as TNF-α, and supernatants were harvest-ed to determine IL-12 as well as TNF-α protein levels. Total RNA was extracted from cells using the single-step technique of acid guanidinium thiocyanate-chloroform extraction according to the manufacturer' s instruction (Promega, Madison, WI). mRNA for TNF-α and IL-12 were quantified by SYBR Green two-step, real-time re-verse transeription-polymerase chain reaction taking glyceraldehyde-3-phesphate dehydrogenase (GAPDH) as an internal standard. Levels of IL-12 and TNF-α in cell culture supernatants were determined with ELISA, strictly fol-lowing the protocols provided by the manufacturer. Data were analyzed with a one-way ANOVA. A P-values <0.05 were considered statistically significant. Results After stimulation with 1 μg/mL HMGB1, IL-12 and TNF-α protein and gene expressions in rat splenic DCs were markedly up-regulated at 24 h to 72 h (P<0.05 or P<0.01), and the expression levels of IL-12 and TNF-α peaked at 48 h (P<0.01). When DCs were cultured in the presence of 0.1 μg/mL, 1 μg/mL, and 10 μg/ml HMGBI for 48 h, expressions of IL-12 and TNF-α were also significantly up-regulated (P<0.01), and values of these cytokines were highest in 1 μg/mL HMGB1-treated group (P<0.01). Conclusions These data suggest that HMGB1 appears to be a potential immunostimulatory signal that induced DC maturation, and HMGB1 stimulation can result in marked up-regulation of IL-12 as well as TNF-α synthesis and release in splenic DCs.

To investigate the RNA interference (RNAi) effect induced by vector-derived small interfering RNA (siRNA) targeting the three gatekeeper genes (Rad52, Ku70, Ku80) and screen the more effective target sites from candidates for further research, by using siRNA design tools online, we selected 2 candidate sequences directed to every gatekeeper gene. According to the sequences, six vector-derived siRNAs (denoted psiRNA1-6) and one mocking psiRNA7 were constructed. Among them, psiRNA1 and psiRNA2 targeted Rad52, psiRNA3 and psiRNA4 to Ku70, psiRNA5 and psiRNA6 to Ku80. The mocking psiRNA7 was used as control. After sequence identification, the seven plasmids were transfected into HepG2 cell line. siRNA-induced silencing of gatekeeper genes was determined by using RT-PCR at RNA level and Western Blot at protein level. The results showed that the six plasmids specifically targeting the coding region of gatekeeper genes were successfully designed and constructed. To some extent, the six plasmids could reduce the expression of target gene. Comparatively, the plasmid-derived siRNA psiRNA1, psiRNA4 and psiRNA5 were more effective than their counterparts. The results suggest that the gene silencing efficiency of siRNA is different, depending on their targeted region, and siRNA may provide us with practical tools for further study on the three gatekeeper genes, i.e. Rad52, Ku70, Ku80.

Objective:To investigate the effect of DKK1 on linearly patterned programmed cell necrosis (LPPCN) and vasculogenic mim-icry (VM) and the related molecular mechanism in non-small cell lung cancer (NSCLC). Methods:A total of 173 human NSCLC speci-mens were collected to detect LPPCN by H&E staining, detect VM with CD31/PAS double staining, and investigate DKK1 and related protein expression by immunohistochemistry. The clinical pathological significance of LPPCN, VM, and DKK1 and the correlation of them were analyzed. Human NSCLC H460-DKK1 cells were engrafed in nude mice to evaluate the influence of DKK1 up-regulation on VM and LPPCN in vivo. Results:Approximately, 14.45%(25/173) of NSCLC had VM and 49.71%(86/173) had LPPCN. 25.6%(22/86) of NSCLC cases in LPPCN-positive group formed VM. Both of VM and LPPCN were all correlated with poor differentiation, late TNM stage, easy recurrence and metastasis and poor prognosis in NSCLC. DKK1 expression in the VM-positive group and the LPPCN-positive group was higher than that in the VM-negative group and the LPPCN-negative group, respectively. DKK1, LPPCN, and VM were positive-ly correlated with VE-cadherin, MMP-2,β-catenin nuclear expression and Twist1. H460-DKK1 transplantation tumor model confirmed that DKK1 promotes the expression of VM and LPPCN and related proteins in NSCLC. Conclusion:The increase of theβ-catenin and Twist1 expression induced by DKK1 may promote the formation of LPPCN and VM in NSCLC.