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| 1 | Lower Bifidobacteria counts in both duodenal mucosa-associated and fecal microbiota in irritable bowel syndrome patients显示文摘AIM: To determine the composition of both fecal and duodenal mucosa-associated microbiota in irritable bowel syndrome (IBS) patients and healthy subjects using molecular-based techniques. METHODS: Fecal and duodenal mucosa brush samples were obtained from 41 IBS patients and 26 healthy subjects. Fecal samples were analyzed for the composition of the total microbiota using fluorescent in situ hybridization (FISH) and both fecal and duodenal brush samples were analyzed for the composition of bif idobacteria using real-time polymerase chain reaction. RESULTS: The FISH analysis of fecal samples revealed a 2-fold decrease in the level of bifidobacteria (4.2 ± 1.3 vs 8.3 ± 1.9, P < 0.01) in IBS patients compared to healthy subjects, whereas no major differences in other bacterial groups were observed. At the species level, Bifidobacterium catenulatum levels were significantly lower (6 ± 0.6 vs 19 ± 2.5, P < 0.001) in the IBS patients in both fecal and duodenal brush samples than in healthy subjects.CONCLUSION: Decreased bifidobacteria levels in both fecal and duodenal brush samples of IBS patients compared to healthy subjects indicate a role for microbiotic composition in IBS pathophysiology. | Angèle PM Kerckhoffs Melvin Samsom Michel E van der Rest Joris de Vogel Jan Knol Kaouther Ben-Amor Louis MA Akkermans | 2009 | World Journal of Gastroenterology2009，15，23： | 33 |
| 2 | Cerebral ischemia and neuroregeneration显示文摘Cerebral ischemia is one of the leading causes of morbidity and mortality worldwide. Although stroke(a form of cerebral ischemia)-related costs are expected to reach 240.67 billion dollars by 2030, options for treatment against cerebral ischemia/stroke are limited. All therapies except anti-thrombolytics(i.e., tissue plasminogen activator) and hypothermia have failed to reduce neuronal injury, neurological deficits, and mortality rates following cerebral ischemia, which suggests that development of novel therapies again st stroke/cerebral ischemia are urgently needed. Here, we discuss the possible mechanism(s) underlying cerebral ischemia-induced brain injury, as well as current and future novel therapies(i.e., growth factors, nicotinamide adenine dinucleotide, melatonin, resveratrol, protein kinase C isozymes, pifithrin, hypothermia, fatty acids, sympathoplegic drugs, and stem cells) as it relates to cerebral ischemia. | Reggie H.C.Lee Michelle H.H.Lee Celeste Y.C.Wu Alexandre Couto e Silva Harlee E.Possoit Tsung-Han Hsieh Alireza Minagar Hung Wen Lin | 2018 | Neural Regeneration Research2018，13，3： | 30 |
| 3 | Acute appendicitis: Epidemiology, treatment and outcomesanalysis of 16544 consecutive cases显示文摘AIM To investigate the epidemiology,treatment and outcomes of acute appendicitis(AA) in a large population study.METHODS This is a retrospective cohort study derived from the administrative dataset of the Bergamo district healthcare system(more than 1 million inhabitants) from 1997 to 2013.Data about treatment,surgery,length of stay were collected.Moreover for each patients were registered data about relapse of appendicitis and hospital admission due to intestinal obstruction.RESULTS From 1997 to 2013 in the Bergamo district we collected 16544 cases of AA,with a crude incidence rate of 89/100000 inhabitants per year; mean age was 24.51 ± 16.17,54.7% were male and the mean Charlson's comorbidity index was 0.32 ± 0.92.Mortality was < 0.0001%.Appendectomy was performed in 94.7% of the patients and the mean length of stay was 5.08 ± 2.88 d; the cumulative hospital stay was 5.19 ± 3.36 d and 1.2% of patients had at least one further hospitalization due intestinal occlusion.Laparoscopic appendectomy was performed in 48% of cases.Percent of 5.34 the patients were treated conservatively with a mean length of stay of 3.98 ± 3.96 d; the relapse rate was 23.1% and the cumulative hospital stay during the study period was 5.46 ± 6.05 d.CONCLUSION The treatment of acute appendicitis in Northern Italy is slowly changing,with the large diffusion of laparoscopic approach; conservative treatment of non-complicated appendicitis is still a neglected option,but rich of promising results. | Marco Ceresoli Alberto Zucchi Niccolò Allievi Asaf Harbi Michele Pisano Giulia Montori Arianna Heyer Gabriela E Nita Luca Ansaloni Federico Coccolini | 2016 | World Journal of Gastrointestinal Surgery2016，8，10： | 14 |
| 4 | Anti-inflammatory pathways and alcoholic liver disease: Role of an adiponectin/interleukin-10/heme oxygenase-1 pathway显示文摘The development of alcoholic liver disease (ALD) is a complex process involving both the parenchymal and non-parenchymal cells in the liver. Enhanced inflammation in the liver during ethanol exposure is an important contributor to injury. Kupffer cells, the resident macrophages in liver, are particularly critical to the onset of ethanol-induced liver injury. Chronic ethanol exposure sensitizes Kupffer cells to activation by lipopolysaccharide via Toll-like receptor 4. This sensitization enhances production of inflammatory mediators, such as tumor necrosis factor-α and reactive oxygen species, that contribute to hepatocyte dysfunction, necrosis, apoptosis, and fibrosis. Impaired resolution of the inflammatory process probably also contributes to ALD. The resolution of inflammation is an active, highly coordinated response that can potentially be manipulated via therapeutic interventions to treat chronic inflammatory diseases. Recent studies have identif ied an adiponectin/interleukin-10/heme oxygenase-1 (HO-1) pathway that is profoundly effective in dampening the enhanced activation of innate immune responses in primary cultures of Kupffer cells, as well as in an in vivo mouse model of chronic ethanol feeding. Importantly, induction of HO-1 also reduces ethanol-induced hepatocellular apoptosis in this in vivo model. Based on these data, we hypothesize that the development of therapeutic agents to regulate HO-1 and its downstream targets could be useful in enhancing the resolution of inflammation during ALD and preventing progression of early stages of liver injury. | Palash Mandal Michele T Pritchard Laura E Nagy | 2010 | World Journal of Gastroenterology2010，16，11： | 11 |
| 5 | Association between calcium sensing receptor gene polymorphisms and chronic pancreatitis in a US population:Role of serine protease inhibitor Kazal 1type and alcohol显示文摘AIM: To test the hypothesis that calcium sensing receptor (CASR) polymorphisms are associated with chronic pancreatitis (CP), and to determine whether serine protease inhibitor Kazal 1type (SPINK1) N34S oralcohol are necessary co-factors in its etiology. METHODS: Initially, 115 subjects with pancreatitis and 66 controls were evaluated, of whom 57 patients and 21 controls were predetermined to carry the high-risk SPINK1 N34S polymorphism. We sequenced CASR gene exons 2, 3, 4, 5 and 7, areas containing the majority of reported polymorphisms and novel mutations. Based on the initial results, we added 223 patients and 239 controls to analyze three common nonsynonymous single nucleotide polymorphisms (SNPs) in exon 7 (A986S, R990G, and Q1011E). RESULTS: The CASR exon 7 R990G polymorphism was signifi cantly associated with CP (OR, 2.01; 95% CI, 1.12-3.59; P = 0.015). The association between CASR R990G and CP was stronger in subjects who reported moderate or heavy alcohol consumption (OR, 3.12; 95% CI, 1.14-9.13; P = 0.018). There was no association between the various CASR genotypes and SPINK1 N34S in pancreatitis. None of the novel CASR polymorphisms reported from Germany and India was detected. CONCLUSION: Our United States-based study confirmed an association of CASR and CP and for the first time demonstrated that CASR R990G is a signifi cant risk factor for CP. We also conclude that the risk of CP with CASR R990G is increased in subjects with moderate to heavy alcohol consumption. | Venkata Muddana Janette Lamb Julia B Greer Beth Elinoff Robert H Hawes Peter B Cotton Michelle A Anderson Randall E Brand Adam Slivka David C Whitcomb | 2008 | World Journal of Gastroenterology2008，14，28： | 7 |
| 6 | The hypoxia-inducible factor-1α activates ectopic production of fibroblast growth factor 23 in tumor-induced osteomalacia显示文摘Tumor-induced osteomalacia(TIO) is a rare paraneoplastic syndrome in which ectopic production of fibroblast growth factor 23(FGF23) by non-malignant mesenchymal tumors causes phosphate wasting and bone fractures. Recent studies have implicated the hypoxia-inducible factor-1α(HIF-1α) in other phosphate wasting disorders caused by elevated FGF23, including X-linked hypophosphatemic rickets and autosomal dominant hypophosphatemia. Here we provide evidence that HIF-1α mediates aberrant FGF23 in TIO by transcriptionally activating its promoter. Immunohistochemical studies in phosphaturic mesenchymal tumors resected from patients with documented TIO showed that HIF-1α and FGF23 were co-localized in spindleshaped cells adjacent to blood vessels. Cultured tumor tissue produced high levels of intact FGF23 and demonstrated increased expression of HIF-1α protein. Transfection of MC3T3-E1 and Saos-2 cells with a HIF-1α expression construct induced the activity of a FGF23 reporter construct. Prior treatment of tumor organ cultures with HIF-1α inhibitors decreased HIF-1α and FGF23 protein accumulation and inhibited HIF-1α-induced luciferase reporter activity in transfected cells. Chromatin immunoprecipitation assays confirmed binding to a HIF-1α consensus sequence within the proximal FGF23 promoter, which was eliminated by treatment with a HIF-1α inhibitor. These results show for the first time that HIF-1α is a direct transcriptional activator of FGF23 and suggest that upregulation of HIF-1α activity in TIO contributes to the aberrant FGF23 production in these patients. | Qian Zhang Michele Doucet Ryan E Tomlinson Xiaobin Han L Darryl Quarles Michael T Collins Thomas L Clemens | 2016 | Bone Research2016，4，2： | 6 |
| 7 | Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: the PCI-CURE study显示文摘 | Shamir R Mehta Salim Yusuf Ron JG Peters Michel E Bertrand Basil S Lewis Madhu K Natarajan Klas Malmberg Hans-Jürgen Rupprecht Feng Zhao Susan Chrolavicius Ingrid Copland Keith AA Fox | 2001 | The Lancet . 2001 (9281)2001，，9281： | 4 |
| 8 | Control of stem cell fate by engineering their micro and nanoenvironment显示文摘Stem cells are capable of long-term self-renewal and differentiation into specialised cell types, making them an ideal candidate for a cell source for regenerative medicine. The control of stem cell fate has become a major area of interest in the field of regenerative medicine and therapeutic intervention. Conventional methods of chemically inducing stem cells into specific lineages is being challenged by the advances in biomaterial technology, with evidence highlighting that material properties are capable of driving stem cell fate. Materials are being designed to mimic the clues stem cells receive in their in vivo stem cell niche including topographical and chemical instructions. Nanotopographical clues that mimic the extracellular matrix(ECM) in vivo have shown to regulate stem cell differentiation. The delivery of ECM components on biomaterials in the form of short peptides sequences has also proved successful in directing stem cell lineage. Growth factors responsible for controlling stem cell fate in vivo have also been delivered via biomaterials to provide clues to determine stem cell differentiation. An alternative approach to guide stem cells fate is to provide genetic clues including delivering DNA plasmids and small interfering RNAs via scaffolds. This review, aims to provide an overview of the topographical, chemical and molecular clues that biomaterials can provide to guide stem cell fate. The promising features and challenges of such approaches will be highlighted, to provide directions for future advancements in this exciting area of stem cell translation for regenerative medicine. | Michelle F Griffin Peter E Butler Alexander M Seifalian Deepak M Kalaskar | 2015 | World Journal of Stem Cells2015，7，1： | 3 |
| 9 | Reproducibility of thrombus volume quantification in multicenter computed tomography pulmonary angiography studies显示文摘AIM To evaluate reproducibility of pulmonary embolism(PE) clot volume quantification using computed tomography pulmonary angiogram(CTPA) in a multicenter setting.METHODS This study was performed using anonymized data in conformance with HIPAA and IRB Regulations(March 2015-November 2016). Anonymized CTPA data was acquired from 23 scanners from 18 imaging centers using each site's standard PE protocol. Two independent analysts measured PE volumes using a semi-automated region-growing algorithm on an FDA-approved image analysis platform. Total thrombus volume(TTV) was calculated per patient as the primary endpoint. Secondary endpoints were individual thrombus volume(ITV), Qanadli score and modified Qanadli score per patient. Inter-and intra-observer reproducibility were assessed using intra-class correlation coefficient(ICC) and BlandAltman analysis. RESULTS Analyst 1 found 72 emboli in the 23 patients with a mean number of emboli of 3.13 per patient with a range of 0-11 emboli per patient. The clot volumes ranged from 0.0041-47.34 cm3(mean +/-SD, 5.93 +/-10.15 cm3). On the second read, analyst 1 found the same number and distribution of emboli with a range of volumes for read 2 from 0.0041 – 45.52 cm3(mean +/-SD, 5.42 +/-9.53 cm3). Analyst 2 found 73 emboli in the 23 patients with a mean number of emboli of 3.17 per patient with a range of 0-11 emboli per patient. The clot volumes ranged from 0.00459-46.29 cm3(mean +/-SD, 5.91 +/-10.06 cm3). Inter-and intraobserver variability measurements indicated excellent reproducibility of the semi-automated method for quantifying PE volume burden. ICC for all endpoints was greater than 0.95 for inter-and intra-observer analysis. Bland-Altman analysis indicated no significant biases.CONCLUSION Semi-automated region growing algorithm for quantifying PE is reproducible using data from multiple scanners and is a suitable method for image analysis in multicenter clinical trials. | Audrey E Kaufman Alison N Pruzan Ching Hsu Sarayu Ramachandran Adam Jacobi Indravadan Patel Lee Schwocho Michele F Mercuri Zahi A Fayad Venkatesh Mani | 2018 | World Journal of Radiology2018，10，10： | 3 |
| 10 | Changes in the colon microbiota and intestinal cytokine gene expression following minimal intestinal surgery显示文摘AIM: To investigate the impact of minor abdominal surgery on the caecal microbial population and on markers of gut inflammation.METHODS: Four week old piglets were randomly allocated to a no-surgery 'control' group(n = 6) or a 'transection surgery' group(n = 5).During the transection surgery procedure, a conventional midline incision of the lower abdominal wall was made and the small intestine was transected at a site 225 cm proximal to the ileocaecal valve, a 2 cm segment was removed and the intestine was re-anastomosed.Piglets received a polymeric infant formula diet throughout the study period and were sacrificed at two weeks post-surgery.Clinical outcomes including weight, stool consistency and presence of stool fat globules were monitored.High throughput DNA sequencing of colonic content was used to detect surgery-relateddisturbances in microbial composition at phylum, family and genus level.Diversity and richness estimates were calculated for the control and minor surgery groups.As disturbances in the gut microbial community are linked to inflammation we compared the gene expression of key inflammatory cytokines(TNF, IL1 B, IL18, IL12, IL8, IL6 and IL10) in ileum, terminal ileum and colon mucosal extracts obtained from control and abdominal surgery groups at two weeks post-surgery.RESULTS: Changes in the relative abundance of bacterial species at family and genus level were confined to bacterial members of the Proteobacteria and Bacteroidetes phyla.Family level compositional shifts included a reduction in the relative abundance of Enterobacteriaceae(22.95 ± 5.27 vs 2.07 ± 0.72, P < 0.01), Bacteroidaceae(2.54 ± 0.56 vs 0.86 ± 0.43, P < 0.05) and Rhodospirillaceae(0.40 ± 0.14 vs 0.00 ± 0.00, P < 0.05) following transection surgery.Similarly, at the genus level, changes associated with transection surgery were restricted to members of the Proteobacteria and Bacteroidetes phyla and included decreased relative abundance of Enterobacteriaceae(29.20 ± 6.74 vs 2.88 ± 1.08, P < 0.01), Alistipes(4.82 ± 1.73 vs 0.18 ± 0.13, P < 0.05) and Thalassospira(0.53 ± 0.19 vs 0.00 ± 0.00, P < 0.05).Surgeryassociated microbial dysbiosis was accompanied by increased gene expression of markers of inflammation.Within the ileum IL6 expression was decreased(4.46 ± 1.60 vs 0.24 ± 0.06, P < 0.05) following transection surgery.In the terminal ileum, gene expression of TNF was decreased(1.51 ± 0.13 vs 0.80 ± 0.16, P < 0.01) and IL18(1.21 ± 0.18 vs 2.13 ± 0.24, P < 0.01), IL12(1.04 ± 0.16 vs 1.82 ± 0.32, P < 0.05) and IL10(1.04 ± 0.06 vs 1.43 ± 0.09, P < 0.01) gene expression increased following transection surgery.Within the colon, IL12(0.72 ± 0.13 vs 1.78 ± 0.28, P < 0.01) and IL10(0.98 ± 0.02 vs 1.95 ± 0.14, P < 0.01) gene expression were increased following transection surgery.CONCLUSION: This study suggests that minor abdominal surgery in infants, results in long-term alteration of the colonic microbial composition and persistent gastrointestinal inflammation. | Susan Lapthorne Julie E Bines Fiona Fouhy Nicole L Dellios Guineva Wilson Sarah L Thomas Michelle Scurr Catherine Stanton Paul D Cotter Prue M Pereira-Fantini | 2015 | World Journal of Gastroenterology2015，21，14： | 3 |
| 11 | Liver angiogenesis as a risk factor for hepatocellularcarcinoma development in hepatitis C virus cirrhotic patients显示文摘AIM: To evaluate the predictive value of hepatocyte proliferation and hepatic angiogenesis for the occurrence of Hepatocellular carcinoma (HCC) in hepatitis C virus (HCV) cirrhotic patients. METHODS: One hundred-five patients (69 males, 36 females; age range, 51-90 year; median 66 year) with biopsy proven HCV cirrhosis were prospectively monitored for HCC occurrence for a median time of 64 mo. Angiogenesis was assessed by using microvessel density (MVD), hepatocyte turnover by MIB1 and PCNA indexes at inclusion in liver biopsies. RESULTS: Forty six patients (43.8%) developed HCC after a median time of 55 (6-120) mo while 59 (56.2%) did not. Patients were divided into two groups according to the median value of each index. The difference between patients with low (median MVD = 3; range 0-20) and high (median MVD = 7; range 1-24) MVD was statistically significant (χ2 = 22.06; P < 0.0001) which was not the case for MIB1 or PCNA (MIB-1: χ2 = 1.41; P = 0.2351; PCNA: χ2 = 1.27; P = 0.2589). The median MVD was higher in patients who developed HCC than in those who did not. HCC-free interval was significantly longer in patients with the MVD ≤ 4 (P = 0.0006). No relationship was found between MIB1 or PCNA and MVD (MIB-1 r2 = 0.00007116, P = 0.9281; PCNA: r2 =0.001950; P = 0.6692). MVD only was able to predict the occurrence of HCC in these patients. Among other known risk factors for HCC, only male sex was statistically associated with an increased risk. CONCLUSION: Liver angiogenesis has a role for in HCV- related liver carcinogenesis and for defining patients at higher risk. | Roberto Mazzanti Luca Messerini Camilla E Comin Lorenzo Fedeli Nathalie Gannè-Carrie Michel Beaugrand | 2007 | World Journal of Gastroenterology2007，13，37： | 3 |
| 12 | Macrophage secretory products induce an inflammatory phenotype in hepatocytes显示文摘AIM:To investigate the influence of macrophages on hepatocyte phenotype and function.METHODS:Macrophages were differentiated from THP-1 monocytes via phorbol myristate acetate stimulation and the effects of monocyte or macrophageconditioned medium on HepG2 mRNA and protein expression determined.The in vivo relevance of these findings was confirmed using liver biopsies from 147 patients with hepatitis C virus(HCV)infection.RESULTS:Conditioned media from macrophages,but not monocytes,induced a transient morphological change in hepatocytes associated with upregulation of vimentin(7.8±2.5-fold,P=0.045)and transforming growth factor(TGF)-β1(2.6±0.2-fold,P<0.001)and downregulation of epithelial cadherin(1.7±0.02-fold,P=0.017)mRNA expression.Microarray analysis revealed significant upregulation of lipocalin-2(17-fold,P <0.001)and pathways associated with inflammation,and substantial downregulation of pathways related to hepatocyte function.In patients with chronic HCV,realtime polymerase chain reaction and immunohistochemistry confirmed an increase in lipocalin-2 mRNA(F0 1.0 ±0.3,F1 2.2±0.2,F2 3.0±9.3,F3/4 4.0±0.8,P= 0.003)and protein expression(F1 1.0±0.5,F2 1.3± 0.4,F3/4 3.6±0.4,P=0.014)with increasing liver injury.High performance liquid chromatography-tandem mass spectrometry analysis identified elevated levels of matrix metalloproteinase(MMP)-9 in macrophageconditioned medium,and a chemical inhibitor of MMP-9 attenuated the change in morphology and mRNA expression of TGF-β1(2.9±0.2 vs 1.04±0.1,P<0.001) in macrophage-conditioned media treated HepG2 cells.In patients with chronic HCV infection,hepatic mRNA expression of CD163(F0 1.0±0.2,F1/2 2.8±0.3,F3/4 5.3±1.0,P=0.001)and MMP-9(F0 1.0±0.4,F1/2 2.8±0.3,F3/4 4.1±0.8,P=0.011)was significantly associated with increasing stage of fibrosis.CONCLUSION:Secreted macrophage products alter the phenotype and function of hepatocytes,with increased expression of inflammatory mediators,suggesting that hepatocytes actively participate in liver injury. | Michelle Melino Victoria L Gadd Gene V Walker Richard Skoien Helen D Barrie Dinesh Jothimani Leigh Horsfall Alun Jones Matthew J Sweet Gethin P Thomas Andrew D Clouston Julie R Jonsson Elizabeth E Powell | 2012 | World Journal of Gastroenterology2012，18，15： | 3 |
| 13 | Pulse pressure and aortic pulse wave are markers of cardiovascular risk in hypertensive populations显示文摘 | Roland Asmar Annie Rudnichi Jacques Blacher Gérard M London Michel E Safar | 2001 | American Journal of Hypertension2001，，2： | 3 |
| 14 | Towards a standard diet-induced and biopsy-confirmed mouse model of non-alcoholic steatohepatitis: Impact of dietary fat source显示文摘BACKGROUND The trans-fat containing AMLN(amylin liver non-alcoholic steatohepatitis,NASH)diet has been extensively validated in C57BL/6J mice with or without the Lep^ob/Lep^ob(ob/ob)mutation in the leptin gene for reliably inducing metabolic and liver histopathological changes recapitulating hallmarks of NASH.Due to a recent ban on trans-fats as food additive,there is a marked need for developing a new diet capable of promoting a compatible level of disease in ob/ob and C57BL/6J mice.AIM To develop a biopsy-confirmed mouse model of NASH based on an obesogenic diet with trans-fat substituted by saturated fat.METHODS Male ob/ob mice were fed AMLN diet or a modified AMLN diet with trans-fat(Primex shortening)substituted by equivalent amounts of palm oil[Gubra amylin NASH,(GAN)diet]for 8,12 and 16 wk.C57BL/6J mice were fed the same diets for 28 wk.AMLN and GAN diets had similar caloric content(40%fat kcal),fructose(22%)and cholesterol(2%)level.RESULTS The GAN diet was more obesogenic compared to the AMLN diet and impaired glucose tolerance.Biopsy-confirmed steatosis,lobular inflammation,hepatocyte ballooning,fibrotic liver lesions and hepatic transcriptome changes were similar in ob/ob mice fed the GAN or AMLN diet.C57BL/6J mice developed a mild to moderate fibrotic NASH phenotype when fed the same diets.CONCLUSION Substitution of Primex with palm oil promotes a similar phenotype of biopsyconfirmed NASH in ob/ob and C57BL/6J mice,making GAN diet-induced obese mouse models suitable for characterizing novel NASH treatments. | Michelle L Boland Denise Oro Kirstine S T■lb■l Sebastian T Thrane Jens Christian Nielsen Taylor S Cohen David E Tabor Fiona Fernandes Andrey Tovchigrechko Sanne S Veidal Paul Warrener Bret R Sellman Jacob Jelsing Michael Feigh Niels Vrang James L Trevaskis Henrik H Hansen | 2019 | World Journal of Gastroenterology2019，25，33： | 3 |
| 15 | Stratification of outcomes for mucinous appendiceal adenocarcinoma with peritoneal metastasis by histological grade显示文摘AIM To investigate the importance of a three-tiered histologic grade on outcomes for patients with mucinous appendiceal adenocarcinoma(MAA).METHODS Two hundred and sixty-five patients with MAA undergoing cytoreductive surgery and hyperthermic intraperitoneal chemotherapy were identified from a prospective database from 2004 through 2014. All pathology was reviewed by our gastrointestinal subspecialty pathologists and histological grade was classified as well-differentiated, moderately differentiated, and poorly differentiated. Survival analysis was performed using Cox proportional hazards regression.RESULTS There were 201(75.8%) well-, 45(16.9%) moderatelyand 19(7.2%) poorly-differentiated tumors. Histological grade significantly stratified the 5-year overall survival(OS), 94%, 71% and 30% respectively(P < 0.001) as well as the 5-year disease-free survival(DFS) 66%, 21% and 0%, respectively(P < 0.001). Independent predictors of DFS included tumor grade(HR = 1.78, 95%CI: 1.21-2.63, P = 0.008), lymph node involvement(HR = 0.33, 95%CI: 0.11-0.98, P < 0.02), previous surgical score(HR = 1.31, 95%CI: 1.1-1.65, P = 0.03) and peritoneal carcinomatosis index(PCI)(HR = 1.05, 95%CI: 1.02-1.08, P = 0.002). Independent predictors of OS include tumor grade(HR = 2.79, 95%CI: 1.26-6.21, P = 0.01), PCI(HR = 1.10, 95%CI: 1.03-1.16, P = 0.002), and complete cytoreduction(HR = 0.32, 95%CI: 0.11-0.92, P = 0.03). Tumor grade and PCI were the only independent predictors of both DFS and OS. Furthermore, histological grade and lymphovascular invasion stratified the risk of lymph node metastasis into a low(6%) and high(40%) risk groups. CONCLUSION Our data demonstrates that moderately differentiated MAA have a clinical behavior and outcome that is distinct from well-and poorly-differentiated MAA. The threetier grade classification provides improved prognostic stratification and should be incorporated into patient selection and treatment algorithms. | Travis Edward Grotz Richard E Royal Paul F Mansfield Michael James Overman Gary N Mann Kristen Ashlee Robinson Karen A Beaty Safiea Rafeeq Auerlio Matamoros Michelle W Taggart Keith Francis Fournier | 2017 | World Journal of Gastrointestinal Oncology2017，9，9： | 2 |
| 16 | Psychosocial mechanisms for the transmission of somatic symptoms from parents to children显示文摘AIM: To examine familial aggregation of irritable bowel syndrome(IBS) via parental reinforcement/modeling of symptoms, coping, psychological distress, and exposure to stress.METHODS:Mothers of children between the ages of8 and 15 years with and without IBS were identified through the Group Health Cooperative of Puget Sound.Mothers completed questionnaires,including the Child Behavior Checklist(child psychological distress),the Family Inventory of Life Events(family exposure to stress),SCL-90R(mother psychological distress),and the Pain Response Inventory(beliefs about pain).Children were interviewed separately from their parents and completed the Pain Beliefs Questionnaire(beliefs about pain),Pain Response Inventory(coping)and Child Symptom Checklist[gastrointestinal(GI)symptoms].In addition,health care utilization data was obtained from the automated database of Group Health Cooperative.Mothers with IBS(n=207)and their 296 children were compared to 240 control mothers and their 335 children,while controlling for age and education.RESULTS:Hypothesis 1:reinforcement of expression of GI problems is only related to GI symptoms,but not others(cold symptoms)in children.There was no significant correlation between parental reinforcement of symptoms and child expression of GI or other symptoms.Hypothesis 2:modeling of GI symptomsis related to GI but not non-GI symptom reporting in children.Children of parents with IBS reported more non-GI(8.97 vs 6.70,P<0.01)as well as more GI(3.24 vs 2.27,P<0.01)symptoms.Total health care visits made by the mother correlated with visits made by the child(rho=0.35,P<0.001 for cases,rho=0.26,P<0.001 for controls).Hypothesis 3:children learn to share the methods of coping with illness that their mothers exhibit.Methods used by children to cope with stomachaches differed from methods used by their mothers.Only 2/16 scales showed weak but significant correlations(stoicism rho=0.13,P<0.05;acceptance rho=0.13,P<0.05).Hypothesis 4:mothers and children share psychological traits such as anxiety,depression,and somatization.Child psychological distress correlated with mother’s psychological distress(rho=0.41,P<0.001 for cases,rho=0.38,P<0.001 for controls).Hypothesis 5:stress that affects the whole family might explain the similarities between mothers and their children.Family exposure to stress was not a significant predictor of children’s symptom reports.Hypothesis 6:the intergenerational transmission of GI illness behavior may be due to multiple mechanisms.Regression analysis identified multiple independent predictors of the child’s GI complaints,which were similar to the predictors of the child’s non-GI symptoms(mother’s IBS status,child psychological symptoms,child catastrophizing,and child age).CONCLUSION:Multiple factors influence the reporting of children’s gastrointestinal and non-gastrointestinal symptoms.The clustering of illness within families is best understood using a model that incorporates all these factors. | Miranda AL van Tilburg Rona L Levy Lynn S Walker Michael Von Korff Lauren D Feld Michelle Garner Andrew D Feld William E Whitehead | 2015 | World Journal of Gastroenterology2015，21，18： | 2 |
| 17 | Senescent human hepatocytes express a unique secretory phenotype and promote macrophage migration显示文摘AIM:To develop a model of stress-induced senescence to study the hepatocyte senescence associated secretory phenotype(SASP).METHODS:Hydrogen peroxide treatment was used to induce senescence in the human Hep G2 hepatocyte cell line.Senescence was confirmed by cytochemical staining for a panel of markers including Ki67,p21,heterochromatin protein 1β,and senescence-associated-β-galactosidase activity.Senescent hepatocytes were characterised by gene expression arrays and quantitative polymerase chain reaction(q PCR),and conditioned media was used in proteomic analyses,a human chemokine protein array,and cell migration assays to characterise the composition and function of the hepatocyte SASP.RESULTS:Senescent hepatocytes induced classical markers of senescence(p21,heterochromatin protein1β,and senescence-associated-β-galactosidase activity);and downregulated the proliferation marker,Ki67.Hepatocyte senescence induced a 4.6-fold increase in total secreted protein(P=0.06)without major alterations in the protein profile.Senescence-induced genes were identified by microarray(Benjamini Hochbergcorrected P<0.05);and,consistent with the increase in secreted protein,gene ontology analysis revealed a significant enrichment of secreted proteins among inducible genes.The hepatocyte SASP included characteristic factors such as interleukin(IL)-8 and IL-6,as well as novel components such as SAA4,IL-32and Fibrinogen,which were validated by q PCR and/or chemokine protein array.Senescent hepatocyteconditioned medium elicited migration of inflammatory(granulocyte-macrophage colony stimulating factor,GM-CSF-derived),but not non-inflammatory(CSF-1-derived)human macrophages(P=0.022),which could contribute to a pro-inflammatory microenvironment in vivo,or facilitate the clearance of senescent cells.CONCLUSION:Our novel model of hepatocyte senescence provides insights into mechanisms by which senescent hepatocytes may promote chronic liver disease pathogenesis. | Katharine M Irvine Richard Skoien Nilesh J Bokil Michelle Melino Gethin P Thomas Dorothy Loo Brian Gabrielli Michelle M Hill Matthew J Sweet Andrew D Clouston Elizabeth E Powell | 2014 | World Journal of Gastroenterology2014，20，47： | 2 |
| 18 | Label-retaining liver cancer cells are relatively resistant to sorafenib显示文摘 | Hong-Wu Xin Chenwi M Ambe Danielle M Hari Gordon W Wiegand Tyler C Miller Jin-Qiu Chen Andrew J Anderson Satyajit Ray John E Mullinax Tomotake Koizumi Russell C Langan Douglas Burka Michelle A Herrmann Paul K Goldsmith Alexander Stojadinovic Udo Rudloff S | 2013 | Gut2013，，12： | 2 |
| 19 | Vulvar granular cell tumor显示文摘Granular cell tumors are rare,usually benign,soft tissue neoplasms of neural origin.They occur more often in females than males,the peak age incidence is in the fourth through fifth decades.They can occur anywhere in the body with up to 15% situated in the vulva.The commonest presentation is as an asymptomatic mass.Microscopic findings are usually sufficient,but immunohistochemistry can also be helpful in confirming the diagnosis.The vulvar tumors are benign in 98% of cases with 2% reported as malignant.In this case report we describe a woman with a granular cell tumor confirmed by biopsy who underwent excision of the mass but with focal extension to the resection margin on microscopy.Our recommendation of re-excision was declined.Since it is not uncommon with these tumors to find groups of tumor cells extending beyond the macroscopic limits of growth,we conclude that it is advisable to have margins assessed intraoperatively by frozen section such that further excision can be performed for positive margins.Our patient has been followed for 18 mo without recurrence,should the tumor recur,re-excision,with frozen section control,is indicated.Recurrence rates are reported as 2%-8% with clear margins and 20% with positive margins. | Michel E Rivlin G Rodney Meeks Mohamed A Ghafar Jack R Lewin | 2013 | World Journal of Clinical Cases2013，1，4： | 2 |
| 20 | Effect of donor–recipient HLA matching at HLA A, B, C, and DRB1 on outcomes after umbilical-cord blood transplantation for leukaemia and myelodysplastic syndrome: a retrospective analysis显示文摘 | Mary Eapen John P Klein Guillermo F Sanz Stephen Spellman Annalisa Ruggeri Claudio Anasetti Maria Brown Richard E Champlin Joan Garcia-Lopez Gareth Hattersely Gesine Koegler Mary J Laughlin Gerard Michel Samir K Nabhan Franklin O Smith Mary M Horowitz Eli | 2011 | Lancet Oncology2011，，13： | 2 |
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