Microbiome characteristics and Bifidobacterium longum in colorectal cancer patients pre- and post-chemotherapy.

BACKGROUND: With the development of next generation sequencing technology, a lot of research has focused on the role of human microbiome in regulating immunity. The present study evaluated microbiome changes of colorectal cancer patients who received XELOX regimen (capecitabine plus oxaliplatin) without requiring antimicrobials. METHODS: Stool samples from 7 patients (3 females/4 males) after screening of 11 patients before and after XELOX chemotherapy were subjected to 16S ribosomal RNA (rRNA) sequencing and flora dynamics compared at baseline and after 8 weeks of chemotherapy. Enrolled patients were newly diagnosed with stage IV colorectal cancer and had not received antimicrobial therapy or surgery. XELOX was administered for 2 cycles or 2-weekly treatments for 3 cycles. RESULTS: The patterns of relative abundance of all bacteria isolated from stool samples before or after chemotherapy treatment appeared to be different, but there were no significant differences in the Kyoto Encyclopedia of Genes and Genomes (KEGG) metabolism pathway between the two groups. The top five pathways in patients were the two-component system, phenylalanine metabolism, degradation of aromatic compounds, beta-lactam resistance and folate biosynthesis. More than 99.6% intestinal flora isolates were bacteria, <0.4% were viruses and Archaea. The relative abundances of the 5 most common bacterial phyla in fecal samples before chemotherapy were Bacteroides, Firmicutes, Proteobacteria, Actinobacteria and Verrucomicrobia. The abundance of Actinomycetes in stools after chemotherapy was increased to 2.5 fold higher than before chemotherapy. Bifidobacterium longum species were significantly elevated in stools after chemotherapy (P<0.05), and changes of relative abundance of Bifidobacterium longum species after chemotherapy from baseline in favorable outcome population (stable disease) was significant higher than them in unfavorable outcome population (progressive disease, PD) (P=0.023). CONCLUSIONS: The results indicated that Actinomyces in the gut might have a positive clinical outcome for colorectal cancer patients. This idea needs further studies to examine the actions of Actinomyces on inhibition of tumor growth.

Expression of GCRG213p, LINE-1 endonuclease variant, significantly different in gastric complete and incomplete intestinal metaplasia.

BACKGROUND: Intestinal metaplasia (IM) of the gastric mucosa is classified as complete (Type I) and incomplete IM (Type II and III) subtypes, which showed significantly different risk for developing to gastric adenocarcinoma (GAC). GCRG213, a variant of L1-endonuclease (L1-EN), first identified in our lab, was upregulated in GAC tissue. However, the relationship between GCRG213 and IM subtypes is not clear. Our study explored the association of GCRG213 protein (GCRG213p) with IM subtypes. METHODS: Gastric cancer and/or para-tumor tissue samples were collected from 123 patients who underwent gastrectomy for intestinal type gastric adenocarcinoma. The subtypes of IM were characterized with Alcian blue-periodic acid-Schiff and High Iron Diamine-Alcian blue staining methods. Immunohistochemistry of GCRG213p was performed, and its expression in gastric adenocarcinoma and para-tumor tissue including dysplasia, IM, and normal mucosa were analyzed. RESULTS: GCRG213p was expressed in 48.94% IM, 57.14% dysplasia and 55.32% GAC, respectively. GCRG213p expression was higher in well and moderately differentiated adenocarcinoma (P = 0.037). In IM glands, GCRG213p expressed mainly in the cytoplasm of absorptive enterocytes with defined brush borders, but not in goblet cells. The expression of GCRG213p in type I IM (90.00%) was significantly higher than that in type II (36.36%) and type III (25.00%) (P < 0.001). In normal gastric mucosa, GCRG213p was exclusively positive in the cytoplasm of gastric chief cells. CONCLUSIONS: The expression of GCRG213p in complete IM was significantly higher than in incomplete IM, which implies that GCRG213p may play a role on the developing of IM to adenocarcinoma. GCRG213p was exclusively expressed in chief cells, suggesting that it might be involved in cell differentiation from the chief cells to IM.

Actinomyces and Alimentary Tract Diseases: A Review of Its Biological Functions and Pathology.

Actinomyces are nonmotile, filamentous, Gram-positive bacteria that cause actinomycosis in immunodeficiency patients. Although the prognosis of actinomycosis is good, the diagnosis of actinomycosis is quite difficult. Recent studies on actinomycosis have shown that Actinomyces play an important role in various biological and clinical processes, such as the formation of dental plaque and the degradation of organics in the gastrointestinal tract. Here, the distribution of Actinomyces in the digestive tract, and different biological effects of actinomycosis, and its clinical association with inflammatory diseases are discussed. Furthermore, an overview of the most commonly used treatment methods and drugs used to treat Actinomyces infected alimentary canal diseases is presented.

Management and survival analysis of elderly patients with a cancer in the digestive system who refused to receive anticancer treatments.

Treatment and management of cancers in elderly patients require some special considerations. A better understanding of how cancers progress in those elderly patients who have not received any anticancer treatments could better help us in treating these patients and in making end-of-life decisions. Over the past years, we had encountered 57 elderly patients, aged 75 to 94 years (87.6 on average), with a cancer in the digestive system, who refused to accept anticancer treatment but who did receive the best available supportive and palliative care. Clinicopathological data of these patients were analyzed. Of these 57 cases, 49 were at an advanced or late stage, while the remaining eight were at an early stage at the time of diagnosis. The median overall survival time of all the patients was 11 months, and almost the entire cohort manifested multiple-organ impairments. The average number of malfunctioning organs per patient was 3.68. After carefully predicting, and then preventing or managing complications, only 54.4% of the patients eventually died of multiple-organ functional failure. Nearly 18% of the single organ dysfunctions were finally well-controlled. Our data provide the first statistical information on the survival time and the direct cause of death of the elderly patients with a cancer in the digestive system not treated with chemotherapy or other direct anticancer interventions, but who did receive the best available supportive and palliative cares. During their struggle with cancer, elderly patients clearly could benefit from prophylactic interventions on organ dysfunction.

Gene expression profiling of the mouse gut: Effect of intestinal flora on intestinal health.

The present study aimed to investigate the molecular mechanisms, including potential genes, pathways and interactions, underlying the effect of intestinal flora on intestinal health. The gene expression profiles of GSE22648 were downloaded from the Gene Expression Omnibus database to screen differentially expressed genes (DEGs). The Database for Annotation, Visualization and Integrated Discovery was used for Gene Ontology (GO) functional and pathway enrichment analysis of the DEGs. DEG­associated literature was mined using the GenCLip 2.0 online tool. Finally, GO and pathway enrichment analyses of the DEGs in the literature were processed. By comparing microbiota­depleted mouse samples and control mouse samples, a total of 115 DEGs, including 58 upregulated genes and 57 downregulated genes, were screened. The upregulated genes were enriched into various GO terms, including microsome, oxidation reduction and heme binding, whereas the 57 downregulated DEGs were enriched in different functions, including DNA packaging and linoleic acid metabolism. A total of 19 genes, including baculoviral IAP repeat containing 5, aurora kinase A, angiotensin I converting enzyme 2 and free fatty acid receptor 2 were identified and enriched in four modules, including cell division, chromosome segregation, inflammatory bowel disease and inflammatory response. AURKA, inner centromere protein antigens 135/155 kDa, baculoviral IAP repeat containing 5, aurora kinase B and solute carrier family 22 (organic cation/zwitterion transporter) member 4 were identified as potential important genes for intestinal flora and intestinal disease treatment through their involvement in various functions, including cell division, chromosome segregation, inflammatory bowel disease and inflammatory response.

Transcatheter hepatic arterial chemoembolization and sorafenib for hepatocellular carcinoma: a meta-analysis of randomized, double-blind controlled trials.

We performed a meta-analysis of transcatheter hepatic arterial chemoembolization (TACE) combined with sorafenib for hepatocellular carcinoma (HCC), which included 4 double-blind, randomized controlled trials (RCTs) that investigated the effects of TACE combined with sorafenib (experimental groups) on time to disease progression (TTP), overall survival (OS), and various sorafenib-related adverse events, compared to those in the placebo (control) groups. A total of 877 HCC cases from 14 countries, including China and the USA, were included in our meta-analysis. The TTP increased significantly in the experimental groups (hazard ration [HR]: 0.82; 95% CI: 0.69-0.97; p = 0.02), but OS did not improve significantly (HR: 0.97; 95% CI: 0.72-1.29; p = 0.82), compared with the control groups. The risks of hand and foot skin reactions (HFSR), rash, fatigue, and diarrhea were significantly greater in the experimental groups (p < 0.05 for all), compared to those in the control groups, whereas the risk of nausea was statistically similar (p > 0.05). Among these, the risk of HFSR was highest (risk ratio [RR]: 5.93; 95% CI: 2.00-17.53; p = 0.001), and a subgroup analysis of studies that lacked significant heterogeneity in the HFSR data showed a higher risk of HFSR (RR: 10.96; 95% CI: 5.54-21.69; p < 0.05). In conclusion, although TACE plus sorafenib increases TTP, it does not improve OS. Therefore, the risk of the adverse events of TACE plus sorafenib should be considered as a potential therapeutic limitation.

Taurine and tea polyphenols combination ameliorate nonalcoholic steatohepatitis in rats.

BACKGROUND: Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease, for which there is currently no safe and effective drug for therapy. In this study, we explored the effects of taurine, tea polyphenols (TPs), or a combination thereof, on NASH rats. METHODS: Rats were divided into a normal group, a high-fat diet induced model group and a treatment group (including taurine, TPs, or taurine + TPs treatment for 8 weeks). Twelve weeks later, all rats were sacrificed, and serum transaminase, lipid and lipopolysaccharide levels and hepatic oxidative stress levels were determined. Histological changes were evaluated. RESULTS: In NASH rats, hepatocyte damage, lipid disturbance, oxidative stress and elevated lipopolysaccharide levels were confirmed. Taurine treatment alleviated hepatocyte damage and oxidative stress. TPs treatment improved lipid metabolism and increased hepatic antioxidant activity. The therapeutic effects of taurine + TPs treatment on hepatocyte damage, lipid disturbance, and oxidative stress were superior to those of taurine and TPs treatment, respectively. Taurine, TPs and their combination all decreased serum lipopolysaccharide levels in NASH rats, but the combination of the compounds caused these levels to decrease more significantly than taurine or TPs treatment alone. CONCLUSION: Taurine combined with TPs treatment could relieve NASH by alleviating hepatocyte damage, decreasing oxidative stress and improving lipid metabolism and gut flora disturbance partly. Taurine and TPs combination may act as a new effective medicine for treating NASH patients.

MicroRNA-31 inhibits tumor invasion and metastasis by targeting RhoA in human gastric cancer.

Previous studies have shown that microRNA-31 (miR-31) functions as a tumor-suppressor in various types of cancer. In the present study we found that miR-31 was significantly downregulated in gastric cancer (GC) as determined by microRNA (miRNA) array screening analysis. Although aberrant expression of miR-31 has been found in different types of cancer, its pathophysiological effect and role in tumorigenesis still remain to be elucidated. In the present study, we detected miR-31 expression in both metastatic GC cell lines and tissues that are potentially highly metastatic by real-time polymerase chain reaction (PCR). Transwell and scratch healing assays were conducted to examine whether the ectopic expression of miR-31 could modify the invasion and migration abilities of GC cells in vitro. We found that miR-31 inhibited GC metastasis in a nude mouse xenograft model of GC. Luciferase reporter assays demonstrated that miR-31 could directly bind to the 3' untranslated region of RhoA and downregulate the expression of RhoA. Significant downregulation of miR-31 in 78 GC tissues and four GC cell lines was examined by real-time reverse transcription-PCR. Moreover, the decreased expression of miR-31 was demonstrated to be associated with lymph node metastasis, poor pT and pN stage, and invasion ability into lymphatic vessels as determined by the Mann-Whitney U test. We also found that miR-31 could inhibit cell invasion and migration abilities in vitro using the Transwell and scratch healing assays in BGC-823, SGC-7901, MGC-803 as well as AGS cells. Experiments in a nude mouse model revealed that miR-31 suppressed tumorigenicity in vivo. The luciferase activity assay and western blotting indicated that RhoA was the potential target of miR-31 in GC cells. Collectively, our results provide important evidence that the downregulation of miR-31 inhibited the invasion and migration abilities of GC cells through direct targeting of the tumor metastasis­associated gene, RhoA. These findings suggest that miR-31 may be a promising therapeutic candidate in the treatment of GC metastasis.

Manganese Superoxide Dismutase Gene-Modified Mesenchymal Stem Cells Attenuate Acute Radiation-Induced Lung Injury.

Radiation-induced lung injury (RILI) is a major clinical complication for radiotherapy in thoracic tumors. An immediate effect of lung irradiation is the generation of reactive oxygen that can produce oxidative damage to DNA, lipids, and proteins resulting in lung cell injury or death. Currently, the medical management of RILI remains supportive. Therefore, there is an urgent need for the development of countermeasures. The present study aimed to evaluate the protective effect of manganese superoxide dismutase (MnSOD) gene-modified mesenchymal stem cells (MSCs) to facilitate the improved recovery of RILI. Here, nonobese diabetic/severe combined immunodeficiency mice received a 13 Gy dose of whole-thorax irradiation, and were then transfused intravenously with MnSOD-MSCs and monitored for 30 days. Lung histopathologic analysis, plasma levels of inflammatory cytokines (interleukin [IL]-1, IL-6, IL-10, and tumor necrosis factor-α), profibrotic factor transforming growth factor-ß1, and the oxidative stress factor (hydroxyproline) were evaluated after MnSOD-MSC transplant. Apoptotic rates were evaluated by terminal deoxynucleotidyl transferase-mediated nick-end labeling immunohistochemical method. Colonization and differentiation of MnSOD-MSCs in the irradiated lung were analyzed by immunofluorescence staining. Consequently, systemic administration of MnSOD-MSCs significantly attenuated lung inflammation, ameliorated lung damage, and protected the lung cells from apoptosis. MnSOD-MSCs could differentiate into epithelial-like cells in vivo. MnSOD-MSCs were effective in modulating RILI in mice and had great potential for accelerating from bench to bedside.

MicroRNA-137 represses FBI-1 to inhibit proliferation and in vitro invasion and migration of hepatocellular carcinoma cells.

The pro-oncogene factor that binds to inducer of short transcripts-1 (FBI-1), which is encoded by ZBTB7A gene and belongs to POK (POZ/BTB and KrÜppel) protein family, has been shown to enhance hepatocellular carcinoma (HCC) cells proliferation and multi-drug resistance (MDR) process. However, the possibility that FBI-1 is a therapeutic target for further HCC treatment remains poorly determined. In the current study, two microRNA (miRNA) target prediction programs (TargetScan and MiRanda) were used to identify miR-137 as a potential regulator of FBI-1. Our results showed that expression of miR-137 was downregulated, while FBI-1 was upregulated in clinical HCC specimens, compared with paired non-tumor specimens. Overexpression of miR-137 via adenoviral vector inhibited the proliferation and anchorage-independent growth of HCC cells, HepG2 and MHCC-97H. Our data also showed that miR-137 repressed endogenous expression level of FBI-1, as well as Notch-1 and Survivin. MiR-137 also inhibited in vitro invasion and migration of HCC cells and attenuated their epithelial-mesenchymal transition (EMT) process. Moreover, miR-137 suppressed the growth rate of HepG2 cells in nude mice model. Overexpression of miR-137 via its adenoviral vector enhanced the sensitivity of HepG2 cells to anti-tumor drugs and attenuated the MDR process of a resistance cell line HepG2/adriamycin (ADR). Thus, FBI-1 downregulation mediated by miR-137 overexpression may be a potential strategy for HCC treatment.

Rifaximin for Irritable Bowel Syndrome: A Meta-Analysis of Randomized Placebo-Controlled Trials.

The current treatments for irritable bowel syndrome (IBS) are suboptimal. The findings of previous studies of rifaximin treatment for IBS may have differed due to variations in study design. Our study aimed to determine the therapeutic and adverse effects of rifaximin treatment for IBS based on a meta-analysis of published randomized controlled trials (RCTs). We searched the MEDLINE, EMBASE, EBSCO, Springer, Ovid, and Cochrane Library databases for RCTs investigating the effects of rifaximin on IBS. Data from each selected RCT was evaluated individually based on an intention-to-treat analysis, and a meta-analysis was performed in which the odds ratios (ORs) and 95% confidence intervals (CIs) of clinical outcomes and adverse events were calculated using fixed-effects models. Four eligible studies were identified. Overall relief of IBS symptoms in the rifaximin groups was greater than that in the placebo groups at the ends of both the treatment and follow-up periods (OR = 1.19; 95% CI: 1.08-1.32 and OR = 1.36; 95% CI: 1.18-1.58, respectively, P < 0.05 for both). Significant relief of abdominal distention was observed at the follow-up endpoint (OR = 1.69; 95% Cl: 1.27-2.23; P < 0.05), but not at the treatment endpoint (OR = 1.19; 95% CI: 0.96-1.49; P > 0.05). Abdominal pain (OR = 1.01; 95% CI: 0.98-1.03; P > 0.05), nausea (OR = 1.00; 95% CI: 0.98-1.02; P > 0.05), vomiting (OR: 0.99; 95% CI: 0.98-1.01; P > 0.05), and headache (OR = 1.01; 95% CI: 0.98-1.03; P > 0.05) did not differ significantly between the rifaximin and placebo groups. In the RCTs selected, our meta-analysis showed that the efficacy of rifaximin for the resolution of overall IBS symptoms was greater than that of the placebos, and that rifaximin was well-tolerated. The course of relief from abdominal distention in IBS patients treated with rifaximin may be delayed in some patients, compared with that of overall IBS symptom relief.

The role of serum intestinal fatty acid binding protein levels and D-lactate levels in the diagnosis of acute intestinal ischemia.

BACKGROUND AND OBJECTIVE: To evaluate the clinical usefulness of serum intestinal fatty acid binding protein (I-FABP) and D-lactate measurements in the early diagnosis of acute intestinal ischemia. METHODS: A total of 272 patients with a clinical diagnosis of acute abdomen were recruited for this trial over a 24-month period, and 37 healthy people were included in the study as controls. Serum I-FABP and D-lactate levels were measured by an enzyme-linked immunosorbent assay and compared in patients with intestinal ischemia vs. non-intestinal ischemia. RESULTS: Of the 272 patients, 39 were diagnosed with intestinal ischemia and 233 were diagnosed with other cause of acute abdomen. The mean serum I-FABP and D-lactate levels in the patients with intestinal ischemia were 149.74±57.81ng/mL and 52.73±26.46 ug/mL, respectively, and were significantly higher compared with patients with non-intestinal ischemia (36.78±11.25ng/mL and 15.58±5.17 ug/mL, respectively) and with levels in the healthy control group (8.33±6.25 ng/mL and 5.47±1.64 ug/mL, respectively). Area under the curve for I-FABP and D-lactate were 0.85 and 0.69, and cut-off values of 93.07 ng/mL and 34.28 ug/mL, respectively. CONCLUSION: Serum I-FABP and D-lactate can improve the diagnosis of intestinal ischemia in patients with acute abdomen who are at risk.

[Effect of miR-92b on migration, adhesion and invasion of human gastric cancer cell line SGC7901].

OBJECTIVE: To investigate the effect of miR-92b on the migration, adhesion and invasion of gastric cancer cell line SGC7901. METHODS: The miR-92b inhibitor and mimics were transiently transfected in SGC7901 cells. The changes in the migration, adhesion and invasion of the transfected cells were tested with wound healing assay, Transwell migration assay, matrigel adhesion and Transwell invasion assay. The cellular expression of E-cadherin, vimentin, Akt and p-Akt were analyzed by Western blotting. RESULTS: The migration, adhesion and invasion assays showed that transfection with the inhibitor of miR-92b obviously decreased the numbers of gastric cancer cells. The expression of E-cadherin, AKT, and pAKT increased and vimentin decreased significantly in the cells transfected with the inhibitor of miR-92b. Transfection with the mimics of miR-92b produced opposite effects in SGC7901 cells. CONCLUSION: miR-92b promotes the migration, adhesion and invasion of human gastric cancer cell line SGC7901 by mediating epithelial-mesenchymal transition, and may accelerate tumor cell metastasis via signaling pathways other than PI3K/Akt pathway.

[An analysis of clinical characteristics and risk factors for ulceration in ischemic colitis].

OBJECTIVE: To investigate the clinical manifestations and risk factors related to ulcer in patients with ischemic colitis (IC). METHODS: Clinical data of sixty-three IC patients with definite diagnosis from June 2002 to June 2012 in the PLA General Hospital were retrospectively analyzed. All patients were classified into ulcer group (23 cases) and non-ulcer group (40 cases) according to the presence of ulcer or not. Clinical manifestations and risk factors related to ulcer lesions were compared in the two groups. Logistic regression model was used for statistical analysis. RESULTS: There were 50 men and 13 women enrolled, with an average age of 70 years old. The main clinical manifestations included abdominal pain [85.7% (54/63) ], diarrhea [54.0% (34/63)], hematochezia [41.3% (26/63)]. In comparison with non-ulcer group, the ulcer group showed higher incidences of chronic constipation [34.8% (8/23) vs 12.5% (5/40) , P = 0.03], enteric-coated aspirin intake [52.2% (12/23) vs 25.0% (10/40), P = 0.03] and abdomen tenderness [82.6% (19/23) vs 52.5% (21/40), P = 0.02]. Chronic constipation and enteric-coated aspirin intake were independent risk factors related to ulcer lesions (OR = 3.38, P = 0.04; OR = 5.91, P = 0.03). Patients with abdomen tenderness had higher incidence of ulcer lesion (OR = 3.12, P = 0.04). The most common location of IC was left colon [69.8% (44/63)]. No difference of site distribution was found in ulcer and non-ulcer group (P = 0.066). Splanchnic atherosclerosis in the ulcer group was more common than in non-ulcer group [88.2% (15/17) vs 58.3% (14/24), P = 0.038]. The duration of hospitalization was significantly longer in ulcer group [ (14.3 ± 7.1) d vs (6.2 ± 4.1) d, P < 0.01]. Higher white blood cell (WBC) count and lower hemoglobin (Hb) were seen in ulcer group than those in non-ulcer group [(10.17 ± 3.32) ×10(9)/L vs (7.25 ± 3.15)×10(9)/L, P = 0.018; (98 ± 27) g/L vs (126 ± 35) g/L, P = 0.041]. CONCLUSIONS: Chronic constipation, enteric-coated aspirin intake and splanchnic atherosclerosis are risk factors related to ulcer in IC patients. Abdomen tenderness, high WBC and low Hb strongly indicate possible IC with ulcer.

Application of human bone marrow-derived mesenchymal stem cells in the treatment of radiation-induced Gastrointestinal syndrome.

Nuclear accidents and terrorism present a serious threat for mass casualty. Accidental or intended radiation exposure leads to radiation-induced gastrointestinal (GI) syndrome. However, currently there are no approved medical countermeasures for GI syndrome. Thus, developing novel treatments for GI syndrome is urgent. Mesenchymal stem cells (MSCs) derived from bone marrow are a subset of multipotent adult somatic stem cells that have the ability to undergo self-renewal, proliferation and pluripotent differentiation. MSCs have advantages over other stem cells; they can be easily isolated from patients or donors, readily expanded ex vivo, and they possess reparative and immunomodulatory properties. Moreover, MSCs have been shown to be powerful tools in gene therapy and can be effectively transduced with vectors containing therapeutic genes. Therefore, the therapeutic potential of MSCs has been brought into the spotlight for the clinical treatment of GI syndrome. In this review, we discuss the possible role of MSCs in radiation-induced GI syndrome.

[The clinical analysis for 43 cases of acute superior mesenteric artery thrombosis confirmed by angiography and surgery].

OBJECTIVE: To investigate the clinical manifestations and mortality related risk factors in patients with acute superior mesenteric artery embolism (ASMAE). METHODS: Clinical data of forty-three confirmed ASMAE patients in the PLA General Hospital from June 2002 to June 2012 were retrospectively analyzed. All patients were classified into the survival group (28 cases) and the death group (15 cases) according to the prognosis. The prognosis associated factors were further analyzed. RESULTS: The study group consisted of 31 men (72.1%) and 12 women (27.9%), with average age of (63 ± 11) years. The majority patients with ASMAE in our study had history of atherosclerotic diseases. The main clinical manifestations included abdominal pain [100% (43/43)], nausea and vomitting [55.8% (24/43)], hematochezia [32.6% (14/43)]. Abdominal CT scan was performed in 74.4% (32/43) patients with a high positive result of 96.9% (31/32).Weight loss occurred more frequently in survival group than in death group [32.1% (9/28) vs 6.7% (1/15) , P = 0.001]. Moreover, weight loss has been shown as a protective factor for ASMAE survival (OR = 0.75, P = 0.038) by logistic analysis. Compared with the death group, the incidence of either peritoneal irritation sign or ascites was significantly lower in survival group [respectively 7.1% (2/28) vs 66.7% (10/15), 14.3% (4/28) vs 73.3% (11/15), P < 0.05], which were two independent risk factors of mortality (OR = 8.51, P = 0.014; OR = 3.07, P = 0.028) . The incidence of main artery embolism of superior mesentery artery (SMA) in death group was higher than that in survival group [93.3% (14/15) vs 60.7% (17/28), P = 0.023]. Main artery embolism of SMA was also an independent mortality risk factor of ASMAE patients (OR = 5.05, P = 0.039) . A total of 18 patients were treated with enterectomy.Intestine excision length was shorter in survival group than in death group [(82.8 ± 25.2)cm vs (141.0 ± 18.1) cm, P = 0.017]. The time from onset to operation in survival group was shorter than that in death group [(44.8 ± 29.7) h vs (69.1 ± 28.0) h, P = 0.013]. CONCLUSIONS: Patients with ASMAE based on chronic ischemia have a relative good prognosis for survival. Peritoneal irritation sign, ascites and main artery embolism of SMA were independent risk factors for death in ASMAE.Intestine excision length and the interval from onset to operation may affect the mortality of ASMAE patients.

Classification, clinicopathologic features and treatment of gastric neuroendocrine tumors.

Gastric neuroendocrine tumors (GNETs) are rare lesions characterized by hypergastrinemia that arise from enterochromaffin-like cells of the stomach. GNETs consist of a heterogeneous group of neoplasms comprising tumor types of varying pathogenesis, histomorphologic characteristics, and biological behavior. A classification system has been proposed that distinguishes four types of GNETs; the clinicopathological features of the tumor, its prognosis, and the patient's survival strictly depend on this classification. Thus, correct management of patients with GNETs can only be proposed when the tumor has been classified by an accurate pathological and clinical evaluation of the patient. Recently developed cancer therapies such as inhibition of angiogenesis or molecular targeting of growth factor receptors have been used to treat GNETs, but the only definitive therapy is the complete resection of the tumor. Here we review the literature on GNETs, and summarize the classification, clinicopathological features (especially prognosis), clinical presentations and current practice of management of GNETs. We also present the latest findings on new gene markers for GNETs, and discuss the effective drugs developed for the diagnosis, prognosis and treatment of GNETs.

[Expression of Foxa2 and its early alarm value of cancerous in gastric polyps].

OBJECTIVE: To explore the expression of Foxa2 in different pathological types of gastric polyps and examine the correlation with cancerous risk. METHODS: According to computerize random number, a total of 2000 patients were selected to receive endoscopic biopsy during November 2011 to October 2012. Tissues were harvested from 170 with gastric polyps and suspicious cancerous lesions and their histological types detected. There were hyperplastic polyps(n = 35), adenomatous polyps(n = 31), fundic gland polyps(n = 42), advanced gastric cancer tissues (n = 32)and normal gastric mucosa tissues (n = 30). ABC immunohistochemical staining and reverse transcription(RT)-PCR were employed to detect the expression of Foxa2 in these different types of tissues. Imagepro plus was used for quantitative and statistical analyses. RESULTS: A low-level expression of Foxa2 was 3.6% ± 1.3% in normal gastric mucosa group. And its expreesion gradually higher in proliferative inflammatory polyp group(33.1% ± 8.0%), adenomatous polyp group (71.4% ± 1.7%) and gastric cancer group(96.3% ± 0.9%, all P < 0.05). Its expression was 35.6% ± 5.6% in fundic gland polyps, similar to that of proliferative inflammatory polyp group (P > 0.05), it was markedly lower than the gastric cancer group (P < 0.05) and higher than the normal gastric mucosa group (P < 0.05). Correlation analyses of clinicopathological parameters showed that no significant correlation existed between its expression and patient gender, age, predilection, Helicobacter. pylori infection or proton pump inhibitor used (all P > 0.05). However, the size of polyps was correlated with Foxa2 (rs = 0.69, P < 0.05). CONCLUSION: The expression level of Foxa2 in different types of gastric polyps may be used as a clinical predicator of polyps risk.

Manganese superoxide dismutase gene therapy protects against irradiation- induced intestinal injury.

Radiation-induced intestinal injury is a common complication in radiotherapy for solid organ malignancies in abdomen or pelvis. However, currently there are no approved medical countermeasures for radiation-induced intestinal injury. Therefore, it is urgent to develop new treatments for radiation-induced intestinal injury. In the present study, we demonstrated that bone marrow derived mesenchymal stem cells (MSCs) and overexpression of human manganese superoxide dismutase (MnSOD) could ameliorate radiation-induced intestinal syndrome. NOD/SCID mice received abdominal irradiation at a selected dose of 5 Gy, and then infused intravenously with MnSOD-MSCs. Mice body weight, survival and diarrhea were monitored for 30-days. Colonization and differentiation of MnSOD-MSCs in the irradiated intestine were analyzed by histological and immunohistochemical methods. Consequently, our data demonstrated that intravenous administration of MnSOD-MSCs improved survival, decreased diarrhea occurrence and protected the small intestinal structural integrity of irradiated mice. Moreover, intravenously transplanted MnSOD-MSCs could colonize the irradiated intestine and repair injured sites. These findings suggested that MnSOD-MSCs may be an attractive and potential option for radiation-induced intestinal injury.

[Differential proteomic analysis of rat hepatic stellate cells treated by oxymatrine liposomes using two-dimensional electrophoresis].

OBJECTIVE: To analyze differentially expressed proteins of hepatic stellate cells (HSCs) treated with oxymatrine (OMT) liposomes, thus further exploring the molecular mechanism of OMT liposomes for treating liver fibrosis. METHODS: A rat model of CCl4 induced chronic liver fibrosis was established. HSCs were perfusion isolated from modeled SD rats and cultured in vitro . Passage 2 HSCs were divided into the model group (Group A), the OMT-liposome-treated group (Group B), and the liposome-treated control group (Group C). HSCs from normal rats were taken as the normal control group (Group D). The total proteins of HSCs cells were extracted from Group B and D after 7 days of treatment, and separated with isoelectrofocusing two-dimensional electrophoresis (2-DE). A 2-DE system was established to analyze the differences in the protein profile between Group B and Group C. Tow protein dots with most obvious difference were selected to determine the structures and functions of different proteins using peptide mass fingerprinting (PMF). RESULTS: (1) The total number bf proteins decreased after treated with OMT liposomes, with 864 spots before treatment and 756 spots after treatment, and the matching rate was 63%. (2) According to 2-DE results, 10 differential protein spots were found by image analysis of magnifying images in local regions. (3) Two most differently expressed proteins were identified to be ATM (46. 236 kD) and Miz1 (54. 051 kD) by PMF and SWISS-PROT protein database retrieval. CONCLUSION: Action of OMT liposomes on HSCs of rats with chronic liver fibrosis caused different protein expressions, which might be involved in the signaling pathways of inducing the apoptosis of HSCs.