Safety and efficacy of laparoscopy-assisted gastrectomy for advanced gastric cancer in the elderly.

To evaluate safety and efficacy of laparoscopy-assisted radical gastrectomy (LARG) for advanced gastric cancer patients aged 70 years or older. Clinical data were retrospectively collected from patients with IIA-IIIC gastric cancer who underwent LARG (n = 30) and open radical gastrectomy (ORG, n = 34) in Department of Gastrointestinal Surgery in the Ningbo First Hospital from January 2012 to December 2013. The mean operative time was longer in the LARG group than in the ORG group but there was no statistical difference between the two groups. The intraoperative blood loss (120 ± 52.7 ml vs 227.3 ± 146.9 ml), incidence of postoperative complication (23.0% vs 47%) were lower in the LARG group than those in the ORG group. In addition, the time to first flatus (2.9 ± 0.8 d vs 4.6 ± 1.2 d), time to first ambulation (1.2 ± 0.4 vs 4.1 ± 1.0 d), time of nasogastric intubation (2.5 ± 1.0 d vs 3.5 ± 1.4 d), and postoperative hospital stay (13.0 ± 4.2 d vs 16.9 ± 4.1 d) were significantly shorter in the LARG group than in the ORG group, respectively. No statistical difference in the number of harvested lymph nodes was noted between the two groups (30.2 ± 12.0 vs 28.1 ± 11.8, P > 0.05). LARG is safer, more effective and less invasive for the elderly patients with advanced gastric cancer.

High fever as an initial symptom of primary gastric inflammatory myofibroblastic tumor in an adult woman.

Inflammatory myofibroblastic tumor, also known as inflammatory pseudotumor, plasma cell granuloma or inflammatory myofibroblastoma, is characterized histopathologically by myofibroblastic spindle cells with inflammatory cell infiltrates composed of plasma cells, lymphocytes and eosinophils. Inflammatory myofibroblastic tumor is typically seen in children or young adults and is most commonly localized to the lungs, but it can occur anywhere in the body. To date, however, only a few cases involving the stomach have been reported. Herein, we present a case of gastric inflammatory myofibroblastic tumor in an adult woman with an initial symptom of high fever.

Adult Hirschsprung's disease: report of four cases.

Adult Hirschsprung's disease (HD) is a rare motor disorder of the gut that is frequently misdiagnosed as refractory constipation. The primary pathogenic defect in adult HD is identical to that seen in infancy or childhood, and is characterized by the total absence of intramural ganglion cells of the submucosal (Meissner) and myenteric (Auerbach) neural plexuses in the affected segment of the bowel. Ninety-four percent of HD cases are diagnosed before the patient reaches 5 years of age, however, on rare occasion, mild cases of HD may go undiagnosed until he or she reaches adulthood. In this study, we describe four cases of adult HD with a history of longstanding recurrent constipation, relieved by laxatives, and presenting to the Department of Gastrointestinal Surgery with progressive abdominal distention, colicky pain or acute intestinal obstruction. Barium enema or computed tomography revealed a grossly distended proximal large colon with fecal retention. Intraoperative frozen section biopsy was performed in all cases and showed aganglionosis of the stenotic segment and a normal distal rectum. In all cases, patient symptoms were completely resolved and there were no complications arising immediately post-surgery or at one-year follow-up. Adult HD should be considered in the differential diagnosis of cases where adult patients present with chronic constipation or even acute intestinal obstruction. The modified one-stage Martin-Duhamel or Rehbein's procedure is a feasible surgical option for treating cases of adult HD involving a segment or the entire bowel.

Lentivirus-mediated RNAi knockdown of VEGFA in RKO colorectal cancer cells decreases tumor formation and growth in vitro and in vivo.

Vascular endothelial growth factors (VEGF) play important roles in angiogenesis, vasculogenesis and endothelial cell growth. In endothelial cancers, secreted VEGF proteins induce endothelial cell proliferation, promote cell migration, inhibit apoptosis and induce blood vessel permeabilization. VEGFA is frequently overexpressed in human colorectal cancers (CRC) and its expression correlates with tumor progression and invasiveness. In this study we examine the effect of knocking down VEGFA expression by infecting RKO colorectal cancer cells with lentiviral particles containing VEGFA-targeting RNAi constructs. We found that suppressing VEGFA dramatically decreased RKO cell proliferation, colony formation, invasion, migration and tumor growth. Furthermore, VEGFA knock-down reduced MAPK pathway signaling and Smac/DIABLO expression. These results suggest that lentivirus-mediated RNAi knock-down of VEGFA could be an effective therapy for the treatment of CRC.

[Diagnosis, treatment, and prognosis of primary appendiceal tumors: analysis of 37 cases].

OBJECTIVE: To investigate the pathology, diagnosis,treatment, and prognosis of primary appendiceal tumors. METHODS: The clinical data of 37 patients with primary tumors of the appendix, 16 males and 21 females, aged 56 +/- 13 (35-87) hospitalized Jan. 1977 to Feb. 2007 were analyzed retrospectively. RESULTS: Appendicitis and abdominal mass were the major clinical manifestations. All 37 cases received surgical operation with the diagnosis confirmed by pathology. The pathological types included carcinoid tumor (n=12), mucinous tumor (n=17), and adenocarcinoma (n=8). Only 4 cases were diagnosed pathologically by biopsy before operation, 28 cases were diagnosed by intra-operative frozen section, and 5 cases were diagnosed after operation. Single appendectomy were performed in 17 cases, ileocecalectomy in 9 cases, right hemicolectomy in 8 cases, and other operation patterns in 3 cases. The 1, 3, and 5-year survival rates of the primary appendix carcinoid tumor, mucinous tumor, and adenocarcinoma were 100.0%, 100.0%, and 91.7%, 100.0%, 86.7%, and 71.5%, and 75.0%, 50.0%, and 50.0% respectively. CONCLUSION: A rare disease, appendiceal tumors lack specific clinical features. Intra-operative exploration and frozen section are very important for diagnosis and operation choice. The prognosis of primary appendix carcinoid tumors is better.

Cystamine ameliorates liver fibrosis induced by carbon tetrachloride via inhibition of tissue transglutaminase.

AIM: To investigate the anti-fibrosis effect of the tissue transglutaminase (tTG) specific inhibitor cystamine on liver fibrosis. METHODS: Sixty-eight male Sprague Dawley rats were divided into three groups: normal control, liver fibrosis control and cystamine-treated group. Liver fibrosis was induced by intraperitoneal injection of carbon tetrachloride (CCl(4)), and Cystamine was administrated by intraperitoneal injection starting 2 d before the first administration of CCl(4). Animals in each group were further divided into 2 subgroups according to two time points of 4 wk and 8 wk after treatment. Hepatic function, pathological evaluation (semi-quantitative scoring system, SSS) and liver hydroxyproline (Hyp) content were examined. Real-time PCR was used to detect the expression of tTG, smooth muscle alpha actin (alpha-SMA), tissue inhibitor of metalloproteinase 1 (TIMP-1) and collagen-1 mRNA. The expressions of tTG and alpha-SMA protein were detected by Western Blotting. RESULTS: Eight weeks after treatment, the SSS score of liver was significantly less in the cystamine group than that in the fibrosis control group (P < 0.01). The levels of alanine aminotransferase (ALT) and total bile acid (TBA) at the 4 wk and 8 wk time points were decreased in the cystamine group compared with those in fibrosis controls (P < 0.01). Liver hydroxyproline content at the 4 wk and 8 wk time points showed a substantial reduction in the cystamine group compared to fibrosis controls (P < 0.01). The expression of tTG, alpha-SMA, collagen-1, TIMP-1 mRNA and tTG, as well as alpha-SMA protein was downregulated in the cystamine group compared to fibrosis controls. CONCLUSION: Cystamine can ameliorate CCl(4) induced liver fibrosis and protect hepatic function. The possible mechanism is related to the reduced synthesis of the extracellular matrix (ECM) caused by the inhibition of hepatic stellate cell activation and decreased expression of TIMP-1.

[Protective effects of vasoactive intestinal peptide on septic shock rats].

OBJECTIVE: To investigate the protective effects of vasoactive intestinal peptide (VIP) on septic shock rats and explore its possible mechanism. METHODS: Cecal ligation and puncture (CLP) was performed to produce septic shock rat model. Thirty adult Sprague-dawley rats were randomly divided into 3 groups with 10 animals in each group: sham operation group, CLP group and VIP group. The rats in VIP group were given intravenous injection of VIP (5 nmol per rat) instantly after the CLP operation. Then the mean arterial pressure (MAP) was monitored consistently and survival rate was observed. Blood samples were obtained from femoral artery for measuring the serum concentrations of tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) by using enzyme-linked immunosorbent assays (ELISA). Organs (lung, kidney and intestine) were harvested for pathological examination. RESULTS: At each time point after 8 h, the MAP of VIP rats was significantly higher than that in CLP rats (P<0.05). In VIP group rats, the serum TNF-alpha concentration was decreased meanwhile IL-10 level was increased with markedly alleviated organic pathological injuries and the survival rate was obviously raised. CONCLUSIONS: VIP exerts protective effects on septic shock rats through inhibiting production of proinflammatory factors and stimulating the production of anti-inflammatory cytokines.

Construction and identification of polycistron adenoviral expression vector PCA13/FasL-IRES-iNOS.

OBJECTIVE: To construct the Fas ligand (FasL) and inducible nitric oxide synthase (iNOS) coexpressed PCA13 plasmid used for packing of adenovirus, so as to observe the immunoprotective effect of FasL on the adenovirus vector. METHODS: By way of the internal ribosome entry site (IRES), gene engineering techniques such as preparation and transformation of competent cells, plasmid extraction, agarose gel electrophoresis and restriction enzymolysis were used for the construction of the polycistron adenoviral expression vector PCA13/FasL-IRES-iNOS, which could coexpress FasL and the iNOS gene after multisubcloning steps. RESULTS: FasL and iNOS connected with the IRES were successfully cloned to the PCA13 plasmid and verified by enzymolysis (600 bp FasL, 1000 bp IRES and 4000 bp iNOS) and the gene sequence was concordant with the gene bank. CONCLUSIONS: The polycistron adenoviral expression vector PCA13/FasL-IRES-iNOS was successfully constructed.

[Experimental study on iNOS gene transfer mediated by liposome to treat portal hypertension in cirrhotic rats].

OBJECTIVE: To evaluate the effects of iNOS gene transfer on portal hypertensive rats. METHODS: Eukaryotic expression plasmid pcDNA(3)/iNOS was used to transfect sinusoidal endothelial cells (SEC) mediated by Lipofectamine. Transfection rate and gene exspression were detected. Hepatic cirrhosis was induced in male Sprague-Dawley rats by intraperitoneal injection of carbon tetrachloride, and the cirrhotic rats were divided into three groups:Liposome-pcDNA(3)/iNOS (n = 10), Tris buffer (n = 10) and nude plasmid (n = 10), which were injected into the portal vein of experiment cirrhotic rats respectively. Five days later, animals were killed, immunohistochemistry and spectrophotometry methods were used to measure the expression of iNOS and the amount of NO production. RESULTS: Eukaryotic expression plasmid pcDNA(3)/iNOS could effectively transfect SEC and express corresponding gene products. Following iNOS gene transfer, compared with the two controlled groups, iNOS expression and the NO production were significantly increased meanwhile portal pressure was decreased significantly. CONCLUSIONS: The iNOS gene transfer is a feasible and an effective approach to treat portal hypertension in cirrhotic rats which could increase the expression of intra-hepatic iNOS and the amount of NO production thus leading to a remarkable reduction of portal venous pressure.