bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diversity of the killer cell immunoglobulin‐like receptor gene KIR2DS4 in the Chinese population
Authors: Yan L.‐X. , Zhu F.‐M. , Jiang K. , He J. 
Published: January 2007

AbstractHuman killer cell immunoglobulin‐like receptors are a subfamily of the immunoglobulin superfamily, which map to the leukocyte receptor complex on chromosome 19. Here, we established polymerase chain reaction–sequence‐based typing (PCR‐SBT) procedures to identify alleles of the KIR2DS4 gene. The method was designed around the specific amplification of exons 4–5 of the KIR2DS4 gene. Genomic DNA from 105 healthy unrelated Chinese Han individuals were typed for the KIR2DS4 alleles. Each sample was assigned the KIR2DS4 alleles combination, consistent with the pairwise combinations of sequences of all the known KIR2DS4 alleles. We observed eleven different genotypes and four KIR2DS4 alleles in the population, with the KIR2DS4*00101 having the highest frequency, 0.576, and also confirmed the new KIR2DS4*007 allele. Our data demonstrated that the established PCR‐SBT method for the KIR2DS4 allele typing was reliable.
Establishment of a sequence‐based typing system for BoLA‐DQA1 exon 2
Authors: Takeshima S. , Miki A. , Kado M. , Aida Y. 
Published: January 2007

AbstractIn cattle, bovine leukocyte antigens (BoLAs) have been extensively used as markers for bovine diseases and immunological traits. Here, we developed a rapid, high‐resolution sequence‐based typing (SBT) system for BoLA‐DQA1. We amplified 355 bp of BoLA‐DQA1 by fully nested polymerase chain reaction (PCR) using the newly constructed primers and then performed direct sequencing of each product. Using this method, we investigated the locus in 51 animals whose BoLA haplotypes had been characterized at the Fifth International BoLA Workshop. We identified 15 distinct DQA1 alleles, and there is no conflict between the typing result of PCR‐SBT and restriction fragment length polymorphism analysis. Together with the previously developed method for typing BoLA‐DRB3, the PCR‐SBT for BoLA‐DQA1 clearly provides a useful tool for detailed class IIa haplotype analysis.
Cavernous hemangioma in the ascending colon treated by endoscopic mucosal resection
Authors: Kimura Shigeru , Tanaka Shinji , Kusunoki Hiroaki , Kitadai Yasuhiko , Sumii Masaharu , Tazuma Susumu , Yoshihara Masaharu , Haruma Ken , Chayama Kazuaki 
Published: January 2007

AbstractHemangioma of the large intestine is rare, but it is a clinically important entity because of the possibility of massive hemorrhage. The case is reported of a patient with a formed, sessile, polypoid‐type cavernous hemangioma in the ascending colon that was removed successfully by endoscopic mucosal resection.
Mechanism of impaired regeneration of fatty liver in mouse partial hepatectomy model
Authors: Murata Hiroshi , Yagi Takahito , Iwagaki Hiromi , Ogino Tetsuya , Sadamori Hiroshi , Matsukawa Hiroyoshi , Umeda Yuzoh , Haga Sanae , Takaka Noriaki , Ozaki Michitaka 
Published: January 2007

AbstractBackground and Aim:  The mechanism of injury in steatotic liver under pathological conditions been extensively examined. However, the mechanism of an impaired regeneration is still not well understood. The aim of this study was to analyze the mechanism of impaired regeneration of steatotic liver after partial hepatectomy (PH).Methods:  db/db fatty mice and lean littermates were used for the experiments. Following 70% PH, the survival rate and recovery of liver mass were examined. Liver tissue was histologically examined and analyzed by western blotting and RT‐PCR.Results:  Of 35 db/db mice, 25 died within 48 h of PH, while all of the control mice survived. Liver regeneration of surviving db/db mice was largely impaired. In db/db mice, mitosis of hepatocytes after PH was disturbed, even though proliferating cell nuclear antigen (PCNA) expression (G1 to S phase marker) in hepatocytes was equally observed in both mice groups. Interestingly, phosphorylation of Cdc2 in db/db mice was suppressed by reduced expression of Wee1 and Myt1, which phosphorylate Cdc2 in S to G2 phase.Conclusions:  In steatotic liver, cell‐cycle‐related proliferative disorders occurred at mid‐S phase after PCNA expression. Reduced expression of Wee1 and Myt1 kinases may therefore maintain Cdc2 in an unphosphorylated state and block cell cycle progression in mid‐S phase. These kinases may be critical factors involved in the impaired liver regeneration in fatty liver.
Experimental investigation of the role of endothelin‐1 in idiopathic portal hypertension
Authors: Yamaguchi Emi , Yamanoi Akira , Ono Takashi , Nagasue Naofumi 
Published: January 2007

AbstractBackground and Aim:  The authors' previous report revealed that endothelin‐1 might be released from B lymphocytes in cirrhotic patients with hypersplenism. Other investigators have shown that persistent exposure to environmental contaminants including arsenic might induce idiopathic portal hypertension. The aim of this study was to experimentally identify how endothelin‐1 is involved in the development of idiopathic portal hypertension and which cells produce endothelin‐1 in the spleen.Methods:  Portal pressure and venous endothelin‐1 concentrations were measured in rats that were given sodium arsenate orally for long periods, and endothelin‐1 expression levels in the spleen were assessed by staining. In a second experiment, B and T lymphocytes and monocyte‐derived macrophages cultured from healthy human peripheral blood were stimulated with sodium arsenite, sodium arsenate, lipopolysaccharide and interferon‐γ. Endothelin‐1 concentrations in the supernatants were measured by ELISA.Results:  Arsenic exposure gradually increased portal pressure and venous endothelin‐1 levels in rats. Endothelin‐1 concentration in the supernatant did not change in every cell type stimulated with arsenic, but it increased in B lymphocytes and monocyte‐derived macrophages treated with lipopolysaccharide and interferon‐γ.Conclusions:  The in vivo study indicated that arsenic might elevate portal pressure through mechanisms involving endothelin‐1. In the in vitro study, lipopolysaccharide and interferon‐γ clearly induced endothelin‐1 synthesis not only in monocyte‐derived macrophages but also in B lymphocytes, although arsenic treatment did not affect those cells. This study partially supports the hypothesis that idiopathic portal hypertension might be promoted by endothelin‐1 overproduction from splenic B lymphocytes in response to certain substances. © 2007 The Authors; Journal compilation © 2007 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd
Prospective evaluation of indeterminate ERCP findings by intraductal ultrasound
Authors: Varadarajulu Shyam , Eloubeidi Mohamad A , Wilcox C Mel 
Published: January 2007

AbstractBackground and Aim:  Although the role of intraductal ultrasound (IDUS) in the evaluation of specific disease entities is well known, its utility in evaluating indeterminate findings in a heterogeneous group of patients undergoing endoscopic retrograde cholangiopancreatography (ERCP) is unknown. This study evaluates the diagnostic accuracy of IDUS in patients with indeterminate findings at ERCP.Methods:  This was a prospective study of all patients who underwent IDUS for evaluation of an indeterminate biliary stricture or main pancreatic duct (MPD) dilation noted at ERCP over an 8‐month period. The accuracy of IDUS was established based on long‐term follow‐up, surgery, or further investigations.Results:  Twenty‐nine (5%) of 600 patients who underwent ERCP had an indeterminate finding that warranted further evaluation by IDUS: this was biliary stricture in 19 patients and MPD dilation in 10. Technical success was 100%. Mean duration of follow‐up was 435 days (range 192–614 days). In patients with biliary stricture, IDUS diagnosed 11 as benign and eight as malignant. In patients with MPD dilation, IDUS diagnosed intraductal papillary mucinous tumor in six patients and chronic pancreatitis in four. Findings on IDUS supported the correct diagnosis in 27 of 29 patients (93%). In two patients with dominant hilar stricture in the setting of primary sclerosing cholangitis, IDUS was false positive in one and false negative in the other. One patient died of multiorgan failure due to post‐ERCP pancreatitis.Conclusions:  A technically easy procedure, IDUS offers unique advantages in the evaluation of patients with indeterminate findings at ERCP.
Clinical relevance of Helicobacter pylori sabA genotype in Japanese clinical isolates
Authors: Yanai Ayako , Maeda Shin , Hikiba Yoko , Shibata Wataru , Ohmae Tomoya , Hirata Yoshihiro , Ogura Keiji , Yoshida Haruhiko , Omata Masao 
Published: January 2007

AbstractBackground and Aim:  The clinical outcome of Helicobacter pylori infection is strongly affected by the bacterial genotype. The aim of this study was to assess the relationship between the status of H. pylori sialic acid‐binding adhesin (sabA) and the severity of gastric inflammation and diseases.Methods:  Clinical isolates from 108 patients with duodenal ulcer, gastric ulcer, gastric cancer, or chronic gastritis were analyzed by sequencing and PCR assay. The degree of neutrophil infiltration in the antral region was evaluated by histopathological examination. The extent of atrophic change was evaluated using serum pepsinogen levels and the pepsinogen I/II ratio.Results:  Functional sabA was present in 88 (81%) of the 108 patients. Although there was no correlation between the sabA status and gastric diseases, severe neutrophil infiltration and atrophy were associated with functional sabA.Conclusions:  The results show a high prevalence of functional sabA in Japanese clinical isolates. The status of sabA may be an important virulence factor in inducing chronic gastric inflammation.
REG Iα protein expression in Barrett's esophagus
Authors: Chinuki Daisuke , Amano Yuji , Ishihara Shunji , Moriyama Nobuyuki , Ishimura Norihisa , Kazumori Hideaki , Kadowaki Yasunori , Takasawa Shin , Okamoto Hiroshi , Kinoshita Yoshikazu 
Published: January 2007

AbstractBackground and Aim:  Accelerated cellular proliferation in Barrett's esophagus has been implicated in Barrett's elongation and malignant transformation. Therefore, growth factors may play important roles in the pathophysiology of Barrett's esophagus. Regenerating gene (REG), an epithelial growth factor, has been reported to link mucosal inflammation and subsequent carcinogenesis in the gastrointestinal tract. The aim of this study was to investigate whether REG is expressed in Barrett's esophagus and to elucidate the relationship between REG protein expression and clinicopathological factors of Barrett's esophagus.Methods:  Between July 2003 and June 2004, 266 patients with endoscopically and histologically proven Barrett's esophagus were enrolled in this study. Before endoscopic examination, all participants were requested to answer structured questionnaires on gastroesophageal reflux symptoms and drugs usage. Mucin phenotype, cyclooxygenase‐2 expression, cellular proliferation, apoptosis and REG Iα protein expression were investigated in the biopsy samples taken from Barrett's esophagus. Clinicopathological factors that correlated with REG Iα protein expression in patients with Barrett's esophagus were evaluated using multivariate logistic regression analysis.Results:  REG Iα protein expression was observed in 48 (18.0%) of 266 patients with Barrett's esophagus by immunohistochemistry. Newly developed squamous re‐epithelialization of Barrett's esophagus at biopsy sites, presence of hiatal hernia and aging were shown to correlate with REG Iα protein expression.Conclusions:  The present study is the first to show REG expression in Barrett's esophagus. Expression of REG Iα was more frequently observed in patients who showed squamous re‐epithelialization of Barrett's esophagus at biopsy sites.
Effects of bariatric surgery on nonalcoholic fatty liver disease: Preliminary findings after 2 years
Authors: Furuya Carlos K , De Oliveira Claudia P M S , De Mello Evandro S , Faintuch Joel , Raskovski Alessandra , Matsuda Mitsunori , Vezozzo Denise C P , Halpern Alfredo , Garrido Arthur B , Alves Venâncio A F , Carrilho Flair J 
Published: January 2007

AbstractBackground and Aim:  Although nonalcoholic fatty liver disease (NAFLD) is very common among morbidly obese patients, the effect of weight loss after bariatric surgery on inflammation and fibrosis related to NAFLD is still a matter of debate. The aim of this study was to evaluate the impact of Roux‐en‐Y gastric bypass (RYGB) surgery on NAFLD with a follow up of 2 years.Methods:  Eighteen consecutive NAFLD patients with body mass index >40 kg/m2 undergoing gastroplasty with RYGB were enrolled, and wedge liver biopsy was obtained at the operation. After 2 years, these patients underwent percutaneous liver biopsy.Results:  At baseline, 67% of patients had nonalcoholic steatohepatitis (NASH) and 33% had steatosis, according to the NASH Clinical Research Network Scoring System (NAS) for biopsy. Cirrhosis was present in 5.5% of the patients with NASH. After a mean excess weight loss of 60%, steatosis disappeared in 84% and fibrosis disappeared in 75% of the patients. Hepatocellular ballooning disappeared in 50%. A slight lobular inflammatory infiltrate remained in 81%, apparently unrelated to fatty degeneration. As liver biochemical variables had been found within normal limits in 92.3% of patients at initial biopsy, no difference was found 2 years later. Lipid profile and blood sugar plasma concentration were closer to normal in all patients after 2 years (P < 0.05).Conclusions:  Aspects of NAFLD including steatohepatitis improved significantly with massive weight loss at 2 years after RYGB surgery. No patient in this series had progression of hepatic fibrosis.
Insulin resistance and lichen planus in patients with HCV‐infectious liver diseases
Authors: Nagao Yumiko , Kawasaki Katsuya , Sata Michio 
Published: January 2007

AbstractBackground and Aim:  Hepatitis C virus (HCV) causes liver diseases and extrahepatic manifestations, and also contributes to insulin resistance and type 2 diabetes mellitus (DM). The aims of the present study were to examine the incidence of extrahepatic manifestations including lichen planus in HCV‐infected patients and to evaluate the relationship between lichen planus and insulin resistance.Methods:  Of 9396 patients with liver diseases presenting to the study hospital, 87 patients (mean age 60.0 ± 11.5 years) with HCV‐related liver diseases were identified and examined for the incidence of extrahepatic manifestations. Insulin resistance and the presence of Helicobacter pylori antibodies were also measured.Results:  The prevalence of DM was 21.8% (19/87), hypertension was 28.7% (25/87), thyroid dysfunction was 20.7% (18/87), and extrahepatic malignant tumor was 9.2% (8/87). The prevalence of lichen planus at oral, cutaneous, pharyngeal, and/or vulval locations was 19.5% (17/87). Characteristics of 17 patients with lichen planus (group A) were compared with 70 patients without lichen planus (group B). Prevalence of smoking history, presence of hypertension, extrahepatic malignant tumor, and insulin resistance (HOMA‐IR) were significantly higher in group A than in group B. Significant differences were not observed for age, sex, body mass index, diagnosis of liver disease, alcohol consumption, presence of DM, thyroid dysfunction, liver function tests, or presence of H. pylori infection between the two groups.Conclusions:  Infection with HCV induces insulin resistance and may cause lichen planus. It is necessary for an HCV‐infected patient to be assayed for insulin resistance, and to be checked for different extrahepatic manifestations of this infection, particularly lichen planus.
Influence of Helicobacter pylori genotype on triple eradication therapy
Authors: Zhao Jian Jun , Wang Jiang Bin , Yang Lei , Li Yan 
Published: January 2007

AbstractBackground:  The efficiency of Helicobacter pylori eradication varies geographically, as do many parameters that might affect therapeutic efficiency. The aims of this study were to investigate the relationship between different genotypes of H. pylori and bacterium‐related histopathological lesions in patients with duodenal ulcer and to determine the effect of genotype on triple eradication therapy.Methods:  Helicobacter pylori infections were analyzed in 78 duodenal ulcer patients. The cytotoxin‐associated gene (cagA) and vacuolating cytotoxin gene (vacA) subtype status of cultured strains were studied by PCR. Histopathological findings were graded using a described grading system. The patients were treated with triple‐therapy regimens consisting of a proton pump inhibitor and two antibiotics twice daily for 7 days. Endoscopy was repeated at 4 weeks post‐therapy to monitor ulcer healing and H. pylori eradication.Results:  The bacteria were genotyped from 66 patients, 57 of whom had H. pylori eradicated. The absence of cagA was associated with unsuccessful treatment. No difference was found with regard to vacA subtype between the successful and unsuccessful eradication groups. On histopathological examination, high H. pylori colonization density and intestinal metaplasia were associated with low eradication rate, while a high grade of neutrophil infiltration was associated with a significantly higher eradication rate.Conclusions:  The data confirm the importance of cagA positivity as a predictor of successful eradication. When high H. pylori colonization density and intestinal metaplasia are present, therapy appears to be less effective. Therefore, these histopathological features may be involved in an unsuccessful therapeutic outcome.
Examination of normal intestine using confocal endomicroscopy
Authors: Odagi Isao , Kato Tomohiro , Imazu Hiroo , Kaise Mitsuru , Omar Salem , Tajiri Hisao 
Published: January 2007

AbstractBackground and Aim:  Endoscopy is an important clinical tool for the diagnosis and treatment of gastrointestinal disorders. However, biopsy tissue is still required in many cases to obtain a definitive histopathological diagnosis. The aim of this study was to evaluate confocal endomicroscopy (CEM) as a tool for conducting virtual biopsies of the colon by comparing CEM images with biopsy samples from normal colon.Methods:  The study cohort comprised 45 patients who underwent investigative colonoscopy between April 2004 and January 2006, 25 of whom also had biopsy due to suspected diseases such as inflammation and neoplasm. The small and large intestine were examined with CEM using an intravenous injection of fluorescein, and CEM images were compared with conventional histopathological results from biopsied samples. In addition, the injected fluorescein was localized immunohistochemically to further analyze the CEM images taken in vivo.Results:  A total of 46 biopsies were taken, of which 24 demonstrated no histopathological abnormality and were regarded as normal. All of the CEM images observed from the surface to the deeper layers were concordant histopathologically with the biopsy results. Furthermore, CEM allowed observation of physiological functions such as blood flow in the capillaries of the surrounding crypts and mucus release from crypts. The immunohistochemical localization of fluorescein was consistent with the CEM images.Conclusions:  CEM provides endoscopists with a valuable new diagnostic tool, not only for observing tissue in situ at the histopathological level, but also for the coincident evaluation of physiological function during endoscopic examination.
Effect of heme oxygenase‐1 induction by octreotide on TNBS‐induced colitis
Authors: Erbil Yeşim , Giriş Murat , Abbasoğlu Semra Doğru , Barbaros Umut , Yanık Burcu Tulumoğlu , Necefli Ahmet , Olgaç Vakur , Toker Gülçin Aykaç 
Published: January 2007

AbstractBackground and Aim:  Ulcerative colitis is a chronic inflammatory disease of the colon and rectum. Although the precise etiology of ulcerative colitis remains unknown, it is believed to involve an abnormal host response to endogenous or environmental antigens, genetic factors, and oxidative damage. The aim of the present study was to investigate whether heme oxygenase‐1 (HO‐1) induction by octreotide could protect against oxidative and inflammatory damage from induced colitis.Methods:  Rats received octreotide 50 µg/kg per day intraperitoneally for 5 days before 2,4,6 trinitrobenzene sulfonic acid (TNBS) solution administration and for 15 days following TNBS solution administration. Rats were killed on day 21, and colonic malondialdehyde (MDA) levels, glutathione (GSH) levels and HO‐1 expression were measured. Nuclear factor (NF)‐κB and HO‐1 expression was evaluated by immunohistochemical examination of the colonic tissue.Results:  Rats with TNBS‐induced colitis had significantly increased colonic MDA levels and HO‐1 expression in comparison to the control group. Octreotide treatment was associated with increased HO‐1 expression and GSH levels, but decreased MDA levels. Histopathological examination revealed that the intestinal mucosal structure was preserved in the octreotide‐treated group. In addition, treatment with octreotide significantly increased HO‐1 expression and decreased NF‐κB expression by immunohistochemistry when compared to the TNBS‐induced colitis group.Conclusion:  Octreotide appears to have protective effects against colonic damage in TNBS‐induced colitis. This protective effect is, in part, mediated by modification of the inflammatory response and the induction of HO‐1 expression.
Further studies on the arrest of cell proliferation in tumor cells at the invading front of colonic adenocarcinoma
Authors: Rubio Carlos A 
Published: January 2007

AbstractBackground and Aim:  The author has previously reported that neoplastic glands at the leading invading edge of colorectal carcinomas often display flat tumor cells and cellular gaps called glandular pores. The aim of this study was to audit cell proliferation and p53 mutation in flat tumor cells and in tumor cells at the tip of glandular pores at the leading invading front of colonic carcinomas.Methods:  Sections from 40 colonic adenocarcinomas were immunostained with the proliferation marker Ki67 and with p53 protein. Expression was assessed at the leading invading front in consecutive neoplastic glands having flat tumor cells and epithelial pores and in neoplastic glands showing neither flat tumor cells nor glandular pores.Results:  Flat tumor cells in neoplastic glands usually showed no Ki67 expression but overexpressed p53 mutation. In neoplastic glands with pores 40% of the tumor cells at the tip of the pores showed no Ki67, but they overexpressed p53 mutation.Conclusions:  The results showed, for the first time, that p53‐positive flat neoplastic colonic cells arrest their proliferation at the invading front. It is possible that these p53‐positive/Ki67‐negative neoplastic cells were temporarily removed from the cell cycle (G0). This paradoxical biological behavior of tumor cells might be connected with the formation of glandular pores and appears to indicate that arrest of cell proliferation at the advancing tumor front in colonic carcinomas occurs independently of p53 mutation. The possible existence of two independent molecular systems at the advancing tumor edge of colonic carcinomas, one supervising cell proliferation and the other zealously transferring the p53 mutation to daughter cells, is suggested.