bluuebunny/crossref_metadata_2025_split huggingface dataset:
Endoscopic ultrasound guided fine needle aspiration biopsy: a large single centre experience
Authors: Williams D B , Sahai A V , Aabakken L , Penman I D , van Velse A , Webb J , Wilson M , Hoffman B J , Hawes R H 
Published: June 2010

BACKGROUNDEndoscopic ultrasound guided fine needle aspiration biopsy (EUS-FNA) is a recent innovation in the evaluation of gastrointestinal and pulmonary malignancies.AIMSTo review the experience with EUS-FNA of a large single centre.METHODS333 consecutive patients underwent EUS-FNA. Follow up data were available on 327 lesions in 317 patients, including 160 lymph nodes, 144 pancreatic lesions, 15 extraintestinal masses, and eight intramural tumours.RESULTSA primary diagnosis of malignancy was obtained by EUS-FNA in 62% of patients with clinically suspicious lesions. The overall accuracy of EUS-FNA for the diagnosis of malignancy was 86%, with sensitivity of 84% and specificity of 96%. With respect to lesion types, the sensitivity, specificity, and accuracy were 85%, 100%, and 89% for lymph nodes; 82%, 100%, and 85% for pancreatic lesions; 88%, 100%, and 90% for perirectal masses; and 50%, 25%, and 38% for intramural lesions, respectively. Compared with size and sonographic criteria, EUS-FNA in the evaluation of lymph nodes provided superior accuracy and specificity, without compromising sensitivity. Inadequate specimens were obtained from only six patients, including 3/5 with stromal tumors. Only one complication occurred.CONCLUSIONSEUS-FNA is safe and can readily obtain tissue specimens adequate for cytopathological diagnoses. Compared with size and sonographic criteria, it is a superior modality for the detection of nodal metastases. While providing accurate diagnosis of pancreatic and perirectal malignancies, results suggest the technique is less useful for intramural lesions.
Gastric antral vascular ectasia in cirrhotic patients: absence of relation with portal hypertension
Authors: Spahr L , Villeneuve J-P , Dufresne M-P , Tassé D , Bui B , Willems B , Fenyves D , Pomier-Layrargues G 
Published: June 2010

BACKGROUNDPortal hypertensive gastropathy and gastric antral vascular ectasia (GAVE) are increasingly recognised as separate entities. The pathogenic role of portal hypertension for the development of GAVE is still controversial.AIMSTo evaluate the effects of portal decompression on chronic bleeding related to GAVE in cirrhotic patients.METHODSEight patients with cirrhosis and chronic blood loss related to GAVE were included. GAVE was defined endoscopically and histologically.RESULTSAll patients had severe portal hypertension (mean portocaval gradient (PCG) 26 mm Hg) and chronic low grade bleeding. Seven patients underwent transjugular intrahepatic portosystemic shunt (TIPS) and one had an end to side portacaval shunt. Rebleeding occurred in seven patients. In these, TIPS was found to be occluded after 15 days in one patient; in the other six, the shunt was patent and the PCG was below 12 mm Hg in five. In the responder, PCG was 16 mm Hg. Antrectomy was performed in four non-responders; surgery was uneventful, and they did not rebleed after surgery, but two died 11 and 30 days postoperatively from multiorgan failure. In one patient, TIPS did not control GAVE related bleeding despite a notable decrease in PCG. This patient underwent liver transplantation 14 months after TIPS; two months after transplantation, bleeding had stopped and the endoscopic appearance of the antrum had normalised.CONCLUSIONSResults suggest that GAVE is not directly related to portal hypertension, but is influenced by the presence of liver dysfunction. Antrectomy is a therapeutic option when chronic bleeding becomes a significant problem but carries a risk of postoperative mortality.
Effect of Helicobacter pyloriinfection and its eradication on cell proliferation, DNA status, and oncogene expression in patients with chronic gastritis
Authors: Nardone G , Staibano S , Rocco A , Mezza E , D’Armiento F P , Insabato L , Coppola A , Salvatore G , Lucariello A , Figura N , De Rosa G , Budillon G 
Published: June 2010

BACKGROUNDHelicobacter pylori, the main cause of chronic gastritis, is a class I gastric carcinogen. Chronic gastritis progresses to cancer through atrophy, metaplasia, and dysplasia. Precancerous phenotypic expression is generally associated with acquired genomic instability.AIMTo evaluate the effect of H pylori infection and its eradication on gastric histology, cell proliferation, DNA status, and oncogene expression.METHODS/SUBJECTSMorphometric and immunohistochemical techniques were used to examine gastric mucosal biopsy specimens from eight controls, 10 patients withH pylori negative chronic gastritis, 53 withH pylori positive chronic gastritis, and 11 with gastric cancer.RESULTSAll patients with chronic gastritis were in a hyperproliferative state related to mucosal inflammation, regardless of H pyloriinfection. Atrophy was present in three of 10 patients withH pylori negative chronic gastritis and in 26 of 53 with H pylori positive chronic gastritis, associated in 18 with intestinal metaplasia. DNA content was abnormal in only 11 patients with atrophy and H pylori infection; eight of these also had c-Myc expression, associated in six cases with p53 expression. Fifty three patients withH pylori positive chronic gastritis were monitored for 12 months after antibiotic treatment: three dropped out; infection was eradicated in 45, in whom cell proliferation decreased in parallel with the reduction in gastritis activity; atrophy previously detected in 21/45 disappeared in five, regressed from moderate to mild in nine, and remained unchanged in seven; complete metaplasia disappeared in 4/14, and markers of genomic instability disappeared where previously present. In the five patients in whomH pylori persisted, atrophy, metaplasia, dysplasia, and markers of genomic instability remained unchanged.CONCLUSIONSChronicH pylori infection seems to be responsible for genomic instability in a subset of cases of H pylori positive chronic atrophic gastritis; eradication ofH pylori infection can reverse inflammation and the related atrophy, metaplasia, and genomic instability.
T cell specificity and cross reactivity towards enterobacteria,Bacteroides,Bifidobacterium, and antigens from resident intestinal flora in humans
Authors: Duchmann R , May E , Heike M , Knolle P , Neurath M , zum Büschenfelde K-H Meyer 
Published: June 2010

BACKGROUNDT cell responses to normal intestinal bacteria or their products may be important in the immunopathogenesis of chronic enterocolitis.AIMSTo investigate the T cell specificity and cross reactivity towards intestinal bacteria.PATIENTS/METHODST cell clones were isolated with phytohaemagglutinin from peripheral blood and biopsy specimens of inflamed and non-inflamed colon from five patients with inflammatory bowel disease (IBD) and two controls. T cell clones were restimulated with anaerobicBacteroides andBifidobacteria species, enterobacteria, and direct isolates of aerobic intestinal flora. T cell phenotype was analysed by single-cell immunocyte assay.RESULTSAnalysis of 96 T cell clones isolated from peripheral blood and biopsy specimens from two patients with IBD showed that bothBifidobacterium andBacteroides species specifically stimulate proliferation of CD4+TCRαβ+ T cell clones from both sites and that cross reactivity exists between these anaerobic bacteria and different enterobacteria. Analysis of 210 T cell clones isolated from three patients with IBD and two controls showed that indigenous aerobic flora specifically stimulate T cell clones from peripheral blood and biopsy specimens from a foreign subject. Some of these flora specific T cell clones were cross reactive with defined enterobacteria. In addition, T cell clones stimulated by their own indigenous aerobic flora were identified in patients with IBD.CONCLUSIONImmune responses to antigens from the intestinal microflora involve a complex network of T cell specificities.
No association between colon cancer and adenocarcinoma of the oesophagus in a population based cohort study in Sweden
Authors: Lagergren J , Nyren O 
Published: June 2010

BACKGROUNDPrevious reports have indicated an association between Barrett’s metaplasia or adenocarcinoma of the oesophagus and colonic neoplasia, but the findings have been inconsistent. If true, such an association suggests common causal mechanisms.AIMSTo test the hypothesis of an association between Barrett’s metaplasia or adenocarcinoma of the oesophagus and colonic neoplasia.METHODSA population based, retrospective cohort study was performed on all Swedish patients with colon cancer diagnosed between 1958 and 1992. 538 500 person years at risk were reviewed among the 118 030 patients in the cohort (average follow up 4.6 years, median 2.1 years). The standardised incidence ratio (SIR), the ratio of the observed to the expected number of incident oesophageal adenocarcinomas, was used as a measure of relative risk. The expected number was derived from the entire Swedish population.RESULTSEleven oesophageal adenocarcinomas were found during follow up in the cohort, as against 9.5 expected (SIR=1.2; 95% confidence interval 0.6–2.1). Analysis by latency intervals after diagnosis of colon cancer showed no trend towards increasing or decreasing risk over time. There were no important sex differences in relative risk.CONCLUSIONSResults provide no support for a common link between colon cancer and oesophageal adenocarcinoma. Although the direct relation between colon cancer and Barrett’s oesophagus was not looked at, a search for common aetiological factors or genetic defects may not be fruitful. Screening for colonic neoplasia among patients with malignant or premalignant oesophageal mucosa, or vice versa, may not be warranted.
Serum hepatocyte growth factor as an index of extensive catabolism of patients awaiting liver transplantation
Authors: Miki C , Mayer A D , Buckels J A C , Iriyama K , Suzuki H , McMaster P 
Published: June 2010

BACKGROUNDWhole body catabolism as the result of intrahepatic metabolic derangement is common in liver transplant candidates. However, individual nutritional assessment parameters lack sensitivity and specificity in determining energy status of these patients. Recently, serum hepatocyte growth factor (HGF) has been shown to reflect the recovery of hepatic energy metabolism after liver transplantation.AIMSThe relation between preoperative levels of serum HGF and metabolic variables was investigated to clarify the clinical value of measuring HGF in evaluations of the catabolism.PATIENTS/METHODSBlood samples were obtained from 30 liver transplant recipients, and biopsy specimens were taken from each recipient’s rectus muscle and the explanted liver. Preoperative serum concentration of HGF was determined. Whole body energy metabolism was assessed by measuring glycogen contents of biopsy specimens and plasma or serum levels of glucose, insulin, total ketone bodies, total carnitine, and amino acids.RESULTSSerum HGF concentration was elevated in 22 of 30 patients and correlated with the Child-Pugh score. It showed a negative association with muscle glycogen content, and a positive correlation with serum levels of glucose, total carnitine, and total ketone bodies. Patients with elevated serum HGF concentrations had higher preoperative plasma levels of aromatic amino acids and branched chain amino acids, associated with lower branched chain to aromatic amino acid ratios.CONCLUSIONSThe elevated serum concentration of HGF in liver transplant candidates reflected inhibition of peripheral glucose storage, enhanced lipid oxidation, and increased peripheral release of branched chain amino acids, and thus extensive energy catabolism.
Cholinergic effects on human gastric motility
Authors: Parkman H P , Trate D M , Knight L C , Brown K L , Maurer A H , Fisher R S 
Published: June 2010

BACKGROUNDCholinergic regulation of chronotropic (frequency) and inotropic (force) aspects of antral contractility and how these impact on gastric emptying are not well delineated.AIMSTo determine the effects of cholinergic stimulation and inhibition on myoelectric, contractile, and emptying parameters of gastric motility.METHODSTen normal subjects underwent three studies each, using simultaneous electrogastrography (EGG), antroduodenal manometry, and gastric emptying with dynamic antral scintigraphy (DAS). After 30 minutes of baseline fasting manometry and EGG, subjects received saline intravenously, atropine (0.6 mg then 0.25 mg/hour intravenously), or bethanechol (5 mg subcutaneously). This was followed by another 30 minutes’ recording and by three hours of postprandial recording after ingestion of a technetium-99m labelled solid meal.RESULTSDuring fasting, atropine decreased, whereas bethanechol increased, the antral manometric motility index and EGG power. Postprandially, atropine decreased the amplitude of antral contractions by DAS, decreased the postprandial antral manometric motility index, and slowed gastric emptying. Atropine caused a slight increase in postprandial frequency of antral contractions by DAS and gastric myoelectrical activity by EGG. Bethanechol slightly increased the amplitude, but slightly decreased the frequency of antral contractions by DAS and decreased the frequency of gastric myoelectrical activity by EGG, with no significant increase in the motility index or gastric emptying.CONCLUSIONSCholinergic antagonism with atropine reduces antral contractility and slows gastric emptying. Cholinergic stimulation with bethanechol increases antral contractility, but decreases the frequency of antral contractions, without altering the antral motility index or gastric emptying.
Serum concentrations and peripheral secretion of the beta chemokines monocyte chemoattractant protein 1 and macrophage inflammatory protein 1α in alcoholic liver disease
Authors: Fisher N C , Neil D A H , Williams A , Adams D H 
Published: June 2010

BACKGROUNDAlcoholic liver disease is associated with increased hepatic expression of monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein 1α (MIP-1α).AIMSTo determine whether concentrations of chemokines in the peripheral circulation reflect disease activity, and whether chemokine secretion is restricted to the liver or is part of a systemic inflammatory response in alcoholic liver disease.PATIENTSFifty one patients with alcoholic liver disease and 12 healthy controls.METHODSPeripheral vein (and hepatic vein in patients undergoing transjugular liver biopsy) chemokine concentrations were measured by ELISA. Chemokine secretion and transcription in isolated peripheral mononuclear cells were assessed using ELISA and in situ hybridisation in patients with severe alcoholic hepatitis.RESULTSSerum MCP-1 concentrations were higher in alcoholic hepatitis compared with cirrhosis or healthy controls. MIP-1α concentrations were below the assay sensitivity in most patients. Serum MCP-1 concentrations correlated significantly with serum aspartate aminotransferase and creatinine. In severe alcoholic hepatitis, MCP-1 concentrations were higher in hepatic compared with peripheral veins; in mild alcoholic hepatitis there was no difference. Mononuclear cell secretion of both MCP-1 and MIP-1α was higher in severe alcoholic hepatitis compared with healthy controls, and chemokine mRNA was identified in monocytes.CONCLUSIONSSerum MCP-1 concentrations are raised in alcoholic liver disease and reflect severity of hepatic inflammation. Monocyte secretion of both MCP-1 and MIP-1α is increased in severe alcoholic hepatitis. Both intrahepatic sources and peripheral mononuclear cells contribute to the raised serum MCP-1 concentrations.
The effect of business improvement districts on the incidence of violent crimes
Authors: MacDonald John , Golinelli Daniela , Stokes Robert J , Bluthenthal Ricky 
Published: June 2010

ObjectiveTo examine whether business improvement districts (BID) contributed to greater than expected declines in the incidence of violent crimes in affected neighbourhoods.MethodA Bayesian hierarchical model was used to assess the changes in the incidence of violent crimes between 1994 and 2005 and the implementation of 30 BID in Los Angeles neighbourhoods.ResultsThe implementation of BID was associated with a 12% reduction in the incidence of robbery (95% posterior probability interval −2 to 24) and an 8% reduction in the total incidence of violent crimes (95% posterior probability interval −5 to 21). The strength of the effect of BID on robbery crimes varied by location.ConclusionThese findings indicate that the implementation of BID can reduce the incidence of violent crimes likely to result in injury to individuals. The findings also indicate that the establishment of a BID by itself is not a panacea, and highlight the importance of targeting BID efforts to crime prevention interventions that reduce violence exposure associated with criminal behaviours.
Translocation of Helicobacter pylori CagA into Human B Lymphocytes, the Origin of Mucosa-Associated Lymphoid Tissue Lymphoma
Authors: Lin Wei-Cheng , Tsai Hwei-Fang , Kuo Sung-Hsin , Wu Ming-Shiang , Lin Chung-Wu , Hsu Ping-I , Cheng Ann-Lii , Hsu Ping-Ning 
Published: June 2010

Abstract
Infection by cagA-positive Helicobacter pylori (H. pylori) is strongly associated with gastric carcinomas and gastric mucosa–associated lymphoid tissue (MALT) lymphomas. H. pylori translocates the bacterial protein CagA into gastric epithelial cells, and the translocated CagA deregulates intracellular signaling pathways and thereby initiates pathogenesis. This in turn raised the possibility that H. pylori is associated with the development of MALT lymphomas during persistent infection by direct interaction with B lymphocytes. In this work, we showed that CagA can be directly translocated into human B lymphoid cells by H. pylori, and the translocated CagA undergoes tyrosine phosphorylation and binds to intracellular SH-2. Meanwhile, the translocated CagA induces activation of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase in human B lymphoid cells, and upregulates the expressions of Bcl-2 and Bcl-XL, which prevents apoptosis. These results provide the first direct evidence for the role of CagA as a bacterium-derived oncoprotein that acts in human B cells, and further implies that CagA is directly delivered into B cells by H. pylori and is associated with the development of MALT lymphomas. Cancer Res; 70(14); 5740–8. ©2010 AACR.
Integrated Profiling Reveals a Global Correlation between Epigenetic and Genetic Alterations in Mesothelioma
Authors: Christensen Brock C. , Houseman E. Andres , Poage Graham M. , Godleski John J. , Bueno Raphael , Sugarbaker David J. , Wiencke John K. , Nelson Heather H. , Marsit Carmen J. , Kelsey Karl T. 
Published: June 2010

Abstract
Development of mesothelioma is linked mainly to asbestos exposure, but the combined contributions of genetic and epigenetic alterations are unclear. We investigated the potential relationships between gene copy number (CN) alterations and DNA methylation profiles in a case series of pleural mesotheliomas (n = 23). There were no instances of significantly correlated CN alteration and methylation at probed loci, whereas averaging loci over their associated genes revealed only two genes with significantly correlated CN and methylation alterations. In contrast to the lack of discrete correlations, the overall extent of tumor CN alteration was significantly associated with DNA methylation profile when comparing CN alteration extent among methylation profile classes. Further, there was evidence that this association was partially attributable to prevalent allele loss at the DNA methyltransferase gene DNMT1. Our findings define a strong association between global genetic and global epigenetic dysregulation in mesothelioma, rather than a discrete, local coordination of gene inactivation. Cancer Res; 70(14); 5686–94. ©2010 AACR.
A C-terminal amino acid substitution in the γ-chain caused by a novel heterozygous frameshift mutation (Fibrinogen Matsumoto VII) results in hypofibrinogenaemia
Authors: Haneishi Ayumi , Yamauchi Kazuyoshi , Terasawa Fumiko , Ito Toshiro , Ishida Fumihiro , Okumura Nobuo , Fujihara Noriko 
Published: June 2010

SummaryWe found a novel hypofibrinogenemia designated as Matsumoto VII (M-VII), which is caused by a heterozygous nucleotide deletion at position g.7651 in FGG and a subsequent frameshift mutation in codon 387 of the γ-chain. This frameshift results in 25 amino acid substitutions, late termination of translation with elongation by 15 amino acids, and the introduction of a canonical glycosylation site. Western blot analysis of the patient’s plasma fibrinogen visualised with anti-γ-chain antibody revealed the presence of two extra bands. To identify the extra bands and determine which of the above-mentioned alterations caused the assembly and/or secretion defects in the patient, 11 variant vectors that introduced mutations into the cDNA of the γ-chain or γ′-chain were transfected into Chinese hamster ovary cells. In vitro expression of transfectants containing γΔ7651A and γΔ7651A/399T (γΔ7651A with an amino acid substitution of 399Asn by Thr and a variant lacking the canonical glycosylation site) demonstrated a reduction in secretion to approximately 20% of the level seen in the transfectants carrying the normal γ-chain. Furthermore, results from other transfectants demonstrated that eight aberrant residues between 391 and 398 of the M-VII variant, rather than the 15 amino acid extension or the additional glycosylation, are responsible for the reduced levels of assembly and secretion of M-VII variant fibrinogen. Finally, the results of this study and our previous reports demonstrate that the fibrinogen γ-chain C-terminal tail (388–411) is not necessary for protein assembly or secretion, but the aberrant amino acid sequence observed in the M-VII variant (especially 391–398) disturbs these functions.
mRNA levels of CD31, CD144, CD146 and von Willebrand factor do not serve as surrogate markers for circulating endothelial cells
Authors: Strijbos Michiel , van Krimpen Brigitte , Debets Reno , Kraan Jaco , Sleijfer Stefan , Gratama Jan Willem , Lamers Cor 
Published: June 2010

SummaryCirculating endothelial cells (CEC) are considered a promising marker to determine the extent of vascular damage. However, currently available and validated CEC enumeration assays are laborious, time consuming and costly, which limits their clinical utility. Here, we evaluated the feasibility of quantifying mRNA levels of the endothelium-associated markers CD31, CD144, CD146 and von Willebrand factor (vWf) in peripheral blood (PB) of healthy donors, patients, and human umbilical veins by real-time reverse transcriptase polymerase chain reaction (RTPCR) and their use as surrogate markers for CEC. Whole blood samples and CD146+ cell-enriched fractions were assessed for mRNA and protein expression of CD31, CD144, CD146 and vWf by RT-PCR and flow cytometry, respectively. We showed the feasibility to detect endothelial mRNA isolated from HUVEC numbers as low as 10. However, no endothelial mRNA could be measure in whole blood samples, and only low levels of CD31 and CD146 mRNA were detected in suspensions of isolated CEC with numbers up to 4,450 CEC per sample. We conclude that mRNA levels of CD31, CD144, CD146 and vWf in whole blood as detected by real time RT-PCR cannot be used as biomarkers for endstage endothelial cells such as CEC.