bluuebunny/crossref_metadata_2025_split huggingface dataset:
“Cag PAI HAVE A FUNCTION RELATED WITH ADHESION TO GASTRIC EPITHELIAL CELLS”
Authors: Mizushima Takuji , Sugiyama Toshiro , Komatsu Yoshito , Ishizuka Jun , Kumagai Ayae , Oda Hirasashi , Kagaya Hidetoshi , Hokari Kaku , Sukegawa Makoto , Saito Nagahito , Takeda Hiroshi , Asaka M. 
Published: March 2003

ObjectiveThe cag pathogenecity island (PAI) is a major virulence factor of Helicobacter pylori (H.p). Andherent ability of H. pylori to the gastric epithelial cells is an important initial step for bacterial virulance. The hpaA and bab A2 genes are thought to be major adherent‐associated genes. Some of cag genes have partial homology to the flagellar aparatus or other adhesion related gene. It is not fully investigated whether cag PAI is related with the adherent ability to the gastric epithelial cells. To evaluate the interaction between the structure of Cag PAI and adherent ability to the gastric epithelial cells.MethodsThe polymerase chain reaction (PCR) and Southern blot analysis were used to determine the structure of cag PAI in Japanese 236 clinical isolates. The PCR and Southern blot analysis were used to verity the presence or absence of hpaA and bab A2. Adherent ability H. pylori to the gastric epithelial cells (KATO cells) was examined in the tested strains by flow‐cytometric analysis (FACS) using anti‐H. pylori antibody.ResultsSeven cag PAI partial deleted strains of tested 236 strains (3.0%) were found by PCR and southern blot analysis, and which showed 3 pattern in deleted region within cag PAI. All cagG‐deleted strains showed less ability of adhesion than CagG positive strains. The peak counts of the cells adhered with cagG deleted strains ( n = 4 ) were significantly lower than that of cagG positive strains ( n = 8 ) ( mean peak count ± SE ; 27.3 ± 2.9 vs 54.8 ± 4.9 ) by FACS analysis. All of cagG‐deleted strains posessed hpaA gene. Six of them possesed babA2 gene.ConclusionsOur results demonstrated that cagG‐deleted clinical isolates had less ability of adhesion to the gastric epithelial cells, even if hpaA and babA2 gene are present.
EVALUATION OF DYSPEPTIC SYMPTOMS AND ACID SUPPRESSIVE DRUG (ASD) CONSUMPTION IN SUCCESFULLY ERADI CATED AND HEALED DUODENAL ULCER (DU) PATIENTS; RESULTS OF A ONE YEAR PROSPECTIVE STUDY
Authors: Gy Pecsi , Szabo  , Csondes A. , P M. Abraham , I. Racz 
Published: March 2003

Aim:To determine the upper abdominal symptoms, the use of ASD and the recurrence‐rate of Helicobacter pylori in DU (Hp) patients one year after ulcer healing and successful HP eradication.Patient and methods:37 endoscopically proven healed and successfully eradicated DU patients were successfully recruited in the study. All patients had active ulcer and showed HP positivity both by rapid urease test and histology 5 weeks before the enrollement endoscopy. The severity and character of dyspeptic symptoms and the use of ASD‐s were checked by questionnaires at the start and one year after successful eradication therapy. NSAID users and reflux oesophagitis patients were excluded at inclusion. Eradication was performed by a one week LAC combination followed by 4 week ranitidine therapy. HP reinfection was controlled by C13 urea breath test at the 12 month visit.Results:7 patients were lost for follow up by the end of the one year program. A together the data of 30 eligible patients (17 females, 13 males, mean age 49 years) were analyzed. The questionnaires represent the symptoms and ASD use of the whole year program. Only 12 out of 30 patients (40%) were permanently and completely symptoms free after the cessation of the short‐term therapy. 16 patients (53.3%) had temporary and 2 patients (6.7%) had persistant symptom. About half of the patients (n=17) were taking absolutely no ASD during the follow up. The number of occasional and continuous ASD users were 7 (23.4%) and 6 (20%) respectively. HP reinfections occurred in one patient and no ulcer relaps was proven.Conclusions:1. More than half of the patients had clinically relevant dyspeptic symptoms during the year after successful HP eradication and ulcer healing. 2. The majority of them required occasional or long term ASD therapy in this period. 3. Recurrences rate of HP was low.
EXPRESSION OF CYCLOOXYGENASE‐2 (COX‐2) IN PRE‐MALIGNANT GASTRIC LESIONS BEFORE AND AFTER H. PYLORI ERADICATION
Authors: Leung W.k , To K.F. , Chan Francis K.L. , Go Minnie Y.Y. , Cheng Alfred S.L. , Ng Enders K.W. , Sung. Joseph J.y 
Published: March 2003

ObjectiveCOX‐2 is frequently expressed in gastric cancer, which may play a active role in carcinogenesis, tumor invasion and metastatis. To evaluate the distribution and expression of COX‐2 in various stages of gastric carcinogenesis and monitor the changes of COX‐2 in intestinal metaplasia (IM) after H. pylori eradication.MethodsGastric biopsies were selected from a group of H. pylori infected patients with various histological diagnosis of chronic active gastritis (CAG, n=40), gastric atrophy (GA, n=20), IM (n=51) and adenocarcinoma (CA, n=25). Non‐infected (n=40) were included as control. Expression of COX‐2 was examined by immunohistochemistry and scored in a semiquantitative manner: 0 = negative , 1 = <5% cells with positive staining, 2 = 5‐30%, 3 = 30‐60% and 4 = >60%. Cellular localization of COX‐2 was further confirmed by in‐situ hybridization of COX‐2 mRNA using an anti‐sense RNA probe. In subgroup of patients with IM, the experissions of COX‐2 one‐year after successful H. Pylori eradication was compared with pre‐treatment level.ResultsCOX‐2 expressions were detected in all H.Pylori‐infected patients irrespective of histological diagnosis. In Contrast, only 14 (35%) H. Pylori‐negative control expressed weak COX‐2 expression (median score 0 vs 2; P<0.0001). However, there was no difference in the intensity of COX‐2 expression between CAG, GA, IM and CA patients. Among the 17 IM patients who had received successful H. Pylori eradication therapy, there was a modest reduction of COX‐2 expressions in both epithelial (P=0.049) and stromal cells (P=0.001) at one‐year. However, there was no significant change in the severity of IM, not any correlation between changes in IM and COX‐2 expression, at one‐year follow‐up.ConclusionBoth premalignant and malignant gastric lesions show strong COX‐2 expression. Although successful eradication of H. pylori reduces the level of COX‐2 expression, there is no association with regression of IM at one year.
MANAGEMENT OF HELICOBACTER PYLORI INFECTION
Authors: Manan Chudahman 
Published: March 2003

Background:Some diseases of UGI, like chronic active gastritis, peptic ulcer, cancer, strongly related to H. pylori infection. Before H. pylori was found, the problem of management PU, recurrent rate was very high. This condition come from healing of PU only clinical and endoscopic findings, but the criteria of healing must be confirm by eradicate of H. pylori infection.Aim:To prove efficacy of some regimens to eradicate H. pylori infection.Method:Some samples included this study with diagnosis Chronic active gastritis, duodenal ulcer, gastric ulcer, and on laboratory findings H. pylori positive. Each group of cases got some regimens of therapy, like triple, dual quadruple therapy. The duration of treatment 2 weeks, and after that to perform the endoscopic and laboratory examination to find H. pylori infection. The data presented with descriptive analysis.Result:Eradication rate triple therapy (omeprazole, clarithromycin & amoxycilin), for chronic active gastritis 90‐100%, gastric ulcer and for dual therapy (omeprazole, amoxycillin, omeprazole, ceftibuten) 83.3%. Micro organism sensitivity test in vitro found that resistency for clarithromycin 18.2%, Metronidazole 90.9% and amoxycilin 31.2%.Conclusion:Omeprazole, Amoxycilin and Clarithromycin (triple therapy) were the drug of choice to eradicate H. pylori infection.
MULTIPLE STRAIN HELICOBACTER PYLORI INFECTION IN PATIENTS WITH DYSPEPSIA
Authors: Achwan Wenny Astuti , Muttaqin Zainul , Isnaningsih Sri , Sumoharjo Suwignyo 
Published: March 2003

ObjectiveSome author reported that infection by more than one strain of Helicobacter pylori in the same patient is not rare. The objective of this study is to explore the possibility of multiplicity of Helicobacter pylori strain in patients with dyspepsia using Random Amplified Polymorphic DNA (RAPD) technique.Material and MethodUpper GI Endoscopy and gastric mucosal biopsy were done on 81 patiens with dyspepsia in Endoscopy Unit Department of Internal Medicine Mataram General Hospital. Gastric Mucosal biopsy was done on three different sites of antrum. Primary culture of Helicobacter pylori was done from each biopsy specimen separately. RAPD was done by Polymerase Chain Reaction using single primer (5’AACGCGCAAC3’) on the colonies grown from secondary culture of each biopsy specimen.ResultsHelicobacter pylori can be grown in 23 patients (28.3%). Helicobacter pylori was grown from single biopsy specimen in 17 patients, while in 6 patients from 2 or 3 biopsy specimens. Heterogenity of RAPD pattern was found in 3 cases, while in the other 3 cases RAPD patterns were identical. Pattern of antibiotic sensitivity of strains found in the same patients was identical.Conclusion:Infection with more than one strain with different genetic pattern can be found in patients with dyspepsia caused by Helicobacter pylori infection.
PRE CANCER LESION H. pylori CHRONIC INFECTION
Authors: Yoewono Vera D. , Krinuhoni E. , Marwoto W , Widodo S.O. Sri 
Published: March 2003

Recently, some studies revealed that gastric cancer and precancer, were more frequent in individuals with H. pylori antibodies.Histological studies, found that the relationship between H. pylori infection and gastric cancer were in wide range (19% ‐ 80%).In our department, from 1999 Jan 1st to 1999 Dec 31thNo biopsy, showed severe atrophic/dysplasia, or lymphoid follicle.Age, ethnic and location were also studied, correlated to malignant and premalignant lesions.
Helicobacter pylori induces apoptosis in gastric epithelial cells through inducible nitric oxide
Authors: Watanabe Sumio , Takagi Atsushi , Koga Yasuhiro , Kamiya Shigeru 
Published: March 2003

Abstract
Background
: Gastric mucosal injury by Helicobacter pylori has been suggested to be mediated by various cytokines induced by this organism. Nitric oxide (NO) is an important effector molecule involved in immune regulation and defence. To clarify the mechanisms by which H. pylori induces gastric mucosal cell injury, we examined whether H. pylori induces gastric epithelial death via NO production.
Methods
: Cytotoxic and non‐cytotoxic strains of H. pylori were used. The death of MKN45 cells caused by H. pylori was examined by the 3‐(4,5‐dimethyl‐thiazole‐2yl)‐2,5‐diphenyl tetrazolium bromide (MTT) assays. Aminoguanidine was used to inhibit inducible nitric oxide synthase (iNOS) activity. Expression of iNOS mRNA was determined by the reverse transcriptase–polymerase chain reaction and the DNA fragmentation analysis was performed by using agarose gel electrophoresis.
Results
: The MTT assay revealed that neither viable H. pylori nor other components of the microorganism induced cell death. Both preincubation of MKN45 cells with interferon‐γ for 6 h and coculture with TNF‐α significantly increased the cytotoxicity of H. pylori. Both cytotoxic and non‐cytotoxic strains of H. pylori induced cell death. Expression of iNOS mRNA was observed in MKN45 cells at 6, 8 and 12 h after H. pylori inoculation. The cytotoxicity of H. pylori was inhibited by aminoguanidine and DNA fragmentation analysis showed that H. pylori induced apoptosis.
Conclusions
: These findings suggested that viable H. pylori induces apoptosis of gastric epithelial cells via nitric oxide. Our study indicated that iNOS expression plays an important role in gastric cell injury.
Endoscopic [13C]‐urea breath test for quantification of Helicobacter pylori infection
Authors: Suto Hiroyuki , Azuma Takeshi , Ito Shigeji , Ito Yoshiyuki , Miyaji Hideki , Yamazaki Yukinao , Kohli Yoshihiro , Kuriyama Masaru 
Published: March 2003

Abstract
Background
: We previously developed a new diagnostic method for Helicobacter pylori infection and called it the endoscopic [13C]‐urea breath test (EUBT). Here we evaluate the relationship between the EUBT results and the histological findings.
Methods
: The EUBT was performed on 137 patients with gastroduodenal diseases. After the collection of a baseline breath sample, gastroduodenal endoscopy was performed. Twenty milliliters of 0.05% phenol red solution containing 100 mg of [13C]‐urea was sprayed over the entire gastric mucosa under endoscopic observation. A breath sample was collected 15 min after spraying. The content of 13CO2 in the breath samples was measured by ratio mass spectrometry. Two biopsy specimens each from the antrum and the middle corpus were obtained for culture and histology. Helicobacter pylori colonization, activity, inflammation, atrophy and intestinal metaplasia were classified on a four‐point scale according to the Updated Sydney System.
Results
: We found positive correlations between the EUBT values and the H. pylori colonization and activity score in the antrum and corpus, and negative correlations between the EUBT values and the atrophy and intestinal metaplasia scores in the corpus.
Conclusions
: The EUBT can be an indicator of the intragastric bacterial load and the histological findings for H. pylori.
Role of steroid priming in the treatment of chronic hepatitis B
Authors: Yokosuka Osamu 
Published: March 2003

AbstractChronic hepatitis B is the result of the immunological response of the host to persistently replicating hepatitis B virus. Steroids can modulate this response; after steroid administration, viral replication increases and after drug withdrawal, it decreases in conjunction with a temporal increase in the transaminase level. Long‐term decrease of the viral level is observed in some patients, but the beneficial effect of steroid withdrawal alone has not been confirmed. Interferon and other anti‐viral agents can suppress virus replication, but the effect of these agents is still unsatisfactory. The combination of steroid priming and anti‐viral treatment may be beneficial. Recent large‐scale controlled trials indicate the utility of the combination therapy, but other randomized trials show no significant difference between therapy with or without steroid priming. Although steroid priming in combination with antiviral agents may be useful in some patients, it should be carefully performed due to the potential risk of liver failure.
Serum total bile acid level as a sensitive indicator of hepatic histological improvement in chronic hepatitis C patients responding to interferon treatment
Authors: Shima Toshihide , Tada Hisashi , Morimoto Michio , Nakagawa Yoshihiro , Obata Hirozumi , Sasaki Toshiyuki , Park Hyohun , Nakajo Shinobu , Nakashima Toshiaki , Okanoue Takeshi , Kashima Kei 
Published: March 2003

Abstract
Background and Methods
: Serum total bile acid (TBA) levels are used clinically as a sensitive and reliable index of hepatobiliary diseases. In the present study, to assess the clinical usefulness of determining TBA in interferon (IFN)‐treated patients, changes in liver function test values, including TBA and liver histology, were examined in 36 chronic hepatitis C patients for 3 years after a sustained response to IFN treatment.
Results
: Alanine aminotransferase and gamma‐glutamyl transpeptidase values significantly decreased during the period of IFN treatment compared to the same measures before IFN treatment. Albumin, cholinesterase, total cholesterol and platelet count values temporarily decreased during IFN treatment, then increased significantly and reached a plateau 6–12 months after the end of IFN treatment. The zinc sulphate turbidity test and TBA values began to decrease during IFN treatment and continued to decrease during the 3‐year follow‐up period. The histological activity index of the liver (Knodell’s score) significantly decreased, whereas the staging score was unchanged 1 year after the end of IFN treatment. In patients who had a TBA value > 10 μmol/L before IFN treatment, a significant correlation was observed between the decrease of TBA and liver histology grading score.
Conclusions
: A decrease in serum TBA level reflected histological improvement in the liver more precisely than did changes in the other liver function test values following IFN therapy.© 2000 Blackwell Science Asia Pty Ltd
Metronidazole‐resistant Helicobacter pylori in an urban Asian population
Authors: Teo Eng‐Kiong , Fock Kwong‐Ming , Ng Tay Meng , Khor Christopher Jen Lock , Tan Ai Ling 
Published: March 2003

Abstract
Background
: Helicobacter pylori eradication is the mainstay in the treatment of H. pylori‐associated peptic ulcer disease. Metronidazole is an important component in most eradication regimens. However, the presence of metronidazole‐resistant H. pylori adversely affects the efficacy of such regimens. We aimed to study the prevalence of metronidazole resistance in our population, and the factors associated with its presence.
Methods and Results
: From September 1993 to September 1996, 459 H. pylori isolates were collected and analysed. The overall resistance rate was 62.7%. The rate was significantly higher among women compared with men (P < 0.05). When the results were analysed according to each year, there was a significant increase in the resistance rate from 50.5% in the first year to 72.7% in the third year (P = 0.0039).
Conclusions
: There was a significant rise in the prevalence of metronidazole resistance over a 3‐year period. The presence of metronidazole resistance adversely affects the eradication rates of nitroimidazole‐based regimens. Hence, in a population with a high prevalence of metronidazole resistance, the use of non‐nitroimidazole‐based therapy may be more efficacious. This information on resistance rates is important for the empirical choice of antibiotic against H. pylori in a population.
Identification of a pre‐S2 mutant in hepatocytes expressing a novel marginal pattern of surface antigen in advanced diseases of chronic hepatitis B virus infection
Authors: Fan Yu‐Fen , Lu Chen‐Chan , Chang Yu‐Chuang , Chang Ting‐Tsung , Lin Pin‐Wen , Lei Huan‐Yao , Su Ih‐Jen 
Published: March 2003

Abstract
Background and Aims
: The expression of hepatitis B viral (HBV) antigens in liver tissue reflects the replicative status of chronic HBV infection. We have previously recognized a novel marginal pattern of hepatitis B surface antigen (HBsAg) in hepatocytes, which usually clusters in groups and emerges at the late non‐replicative phase. This study was designed to investigate whether the marginal‐type HBsAg represented the gene product of a specific HBV‐surface mutant.
Methods
: Microdissection of cirrhotic nodules homogeneously expressing marginal HBsAg was performed on two of 12 resected livers from HBsAg‐seropositive patients with hepatocellular carcinoma. The gene presumably encoding marginal HBsAg was polymerase chain reaction (PCR)‐cloned, sequenced and analysed. In vitro transfection and expression of the cloned surface mutant plasmids were performed on the Huh7 cell line to illustrate intrahepatic HBsAg expression.
Results
: Immunohistochemical staining revealed that the marginal HBsAg was positive for pre‐S1 and thus contained large surface proteins. The PCR cloning and sequencing of the genes presumably encoding marginal‐type HBsAg in both cases revealed the same deletion at the 5′ terminus (nt 2–55) of pre‐S2. A point mutation on the small‐surface (S) antigen was also found in one case. The pre‐S2 deletion sequence and the mutation sites of the S gene coincide with human lymphocyte antigen‐restricted T‐ and/or B‐cell epitopes. In vitro transfection of the mutant plasmid revealed a blot‐like retention or accumulation of HBsAg in the cytoplasm or at the periphery of hepatocytes, accompanied by a decreased secretion of HBsAg in the culture supernatant, mimicking intrahepatic expression.
Conclusion
: A natural pre‐S2 deletion mutant was identified in hepatocytes expressing a novel marginal pattern of HBsAg, which probably contains mutant, large, surface proteins. The biological significance of the pre‐S2 deletion mutant should be interesting in view of the clustering proliferation of hepatocytes expressing marginal HBsAg.
School absenteeism after upper gastrointestinal endoscopy in children
Authors: Treepongkaruna S , Lee K , Giltinan D , Catto‐Smith Anthony G 
Published: March 2003

Abstract
Background and Aims
: To examine the functional impact of upper gastrointestinal endoscopy as a day procedure, particularly in relation to subsequent school attendance.
Methods
: Symptoms and morbidities were prospectively recorded from school‐aged children during observation in hospital and for 3 days at home after endoscopy by using a structured questionnaire. Reasons for school absence were identified.
Results
: Sixty children (31 boys, 29 girls) were enrolled in the study (mean age 10.6 ± 2.8 years, range 6.1–16.2 years). Following the procedure, symptoms were reported at home in 68.3% (same day), 56.7% (day 1) and 20% (day 2). The commonest symptoms were sore throat, tiredness and dizziness. Twenty‐nine children (48.3%) did not attend school on the day following the procedure but most (26 of 29) had returned to school by the second day. The main reason for their absence was residual physical discomfort related to the procedure (55.2%).
Conclusions
: Persisting physical discomfort and school absenteeism are common following upper gastrointestinal endoscopy in children.
Bilirubin and bile acids may modulate their own metabolism via regulating uridine diphosphate‐glucuronosyltransferase expression in the rat
Authors: Li Yan Q , Prentice David A , Howard Monique L , Mashford Maurice L , Desmond Paul V 
Published: March 2003

Abstract
Background and Aims
: Uridine diphosphate (UDP)‐glucuronosyltransferase (UGT) is a critical enzyme in the elimination of bilirubin and it also plays a role in the metabolism of bile acids. The aim of this study was to determine whether bilirubin and bile acids could modulate their own metabolism by regulating UGT levels in cultured rat hepatocytes.
Methods and Results
: Incubation of hepatocytes with bilirubin (48 μmol/L) for 24 h significantly increased the mRNA expression of UGT1A1 and UGT1A5, two UGT isoforms responsible for the conjugation of bilirubin. The induction of UGT1A1 and UGT1A5 by bilirubin was concentration and time dependent. Treatment with chenodeoxycholic acid, cholic acid, deoxycholic acid, hyodeoxycholic acid and lithocholic acid at a concentration of 100 μmol/L for 48 h significantly enhanced the mRNA expression of UGT2B1, a UGT isoform responsible for the glucuronidation of bile acids. The UGT2B3 mRNA level was also increased by hyodeoxycholic acid. The regulation of UGT2B1 mRNA by chenodeoxycholic acid and hyodeoxycholic acid was dose and time dependent.
Conclusion
: Our results suggest that bilirubin and bile acids can induce UGT expression and as a result, these compounds may modulate their own metabolism. Such regulation could play a compensatory role in the pathological increased concentrations of these compounds in some hepatobiliary diseases.