bluuebunny/crossref_metadata_2025_split huggingface dataset:
Controlled Trial of the Effect of Cinnamon Extract on Helicobacter pylori
Authors: Nir Yael , Potasman Israel , Stermer Eddi , Tabak Mina , Neeman Isaac 
Published: March 2003

Background. Helicobacter pylori has been associated with the pathogenesis of antral gastritis, duodenal ulcer, and gastric lymphoma. Eradication of H. pylori has been shown to reverse or prevent relapse of these diseases. Antimicrobials employed in the eradication of H. pylori are not without adverse effects. Newer treatment modalities, therefore, are required. In vitro studies have shown the effectiveness of cinnamon extract against H. pylori and its urease. In this pilot study, we tested the activity of an alcoholic extract of cinnamon in a group of patients infected with H. pylori.Materials and Methods. Fifteen patients (11 women, 4 men) aged 16 to 79 years were given 40 mg of an alcoholic cinnamon extract twice daily for 4 weeks; eight patients aged 35 to 79 (7 women, 1 man) received placebo. The amount of H. pylori colonization was measured by the 13C urea breath test before and after therapy.Results. The mean urea breath test counts in the study and control groups before and after therapy were 22.1 and 23.9 versus 24.4 and 25.9, respectively. The cinnamon extract was well tolerated, and side effects were minimal.Conclusions. We concluded that cinnamon extract, at a concentration of 80 mg /day as a single agent, is ineffective in eradicating H. pylori. Combination of cinnamon with other antimicrobials, or cinnamon extract at a higher concentration, however, may prove useful.
Factors That Affect Results of the 13C Urea Breath Test in Japanese Patients
Authors: Chen Xing , Haruma Ken , Kamada Tomoari , Mihara Mitsuhiro , Komoto Kunihiko , Yoshihara Masaharu , Sumii Koji , Kajiyama Goro 
Published: March 2003

Background. The 13C urea breath test (UBT) is considered to be the most accurate way of diagnosing Helicobacter pylori infection. Our objective was to investigate the accuracy of the UBT in Japanese patients and the association of UBT values with histological findings.Materials and Methods. A total of 169 consecutive patients were studied by endoscopy with histology, by serology with IgG antibody and test serum pepsinogen (PG), and by UBT. The association between UBT values and histological findings and the PG I / II ratio were analyzed in H. pylori–positive patients.Results. Of 169 Japanese patients, 135 were H. pylori–positive on both histology and serology analysis, 27 were H. pylori–negative on both histology and serology analysis, and 7 patients showed differing results. Using a cutoff value of 2.5‰, test sensitivity was 100%, while specificity was 96%. Among the 135 H. pylori–positive patients, a significant relation was observed between UBT value and H. pylori colonization density of the corpus and antrum, neutrophil activity of the antrum, atrophy, and intestinal metaplasia of the corpus in the H. pylori–positive patients. Also, UBT values correlated with the PG I /II ratio. In multivariate analysis, the PG I /II ratio was the most important factor related to UBT values (odds ration [OR], 4.99; 95% confidence interval, 1.60–15.55).Conclusions. The UBT is an accurate method for detecting H. pylori infection in the Japanese population, which shows a high prevalence of atrophic gastritis. Values are affected by H. pylori infection and by the severity of atrophic gastritis.
Differentiation of Clinical Helicobacter pullorum Isolates from Related Helicobacter and Campylobacter Species
Authors: Melito Pasquale L. , Woodward David L. , Bernard Kathryn A. , Price Lawrence , Khakhria Rasik , Johnson Wendy M. , Rodgers Frank G. 
Published: March 2003

Background. Helicobacter pullorum, first detected in the liver and intestinal contents of poultry, was defined as a new species in 1994. This organism has since been isolated from humans with gastroenteritis. Phenotypic as well as genotypic methods have been used to identify H. pullorum associated with cases of human disease.Materials and Methods. Clinical isolates were submitted for identification to the National Laboratory for Enteric Pathogens by Provincial Public Health Laboratories within Canada. Phenotypic characterization was conducted using a variety of growth and biochemical tests including oxidase, catalase, indoxyl acetate, H2S production in triple sugar iron (TSI) agar, antimicrobial susceptibility testing, and fatty acid analysis. Genotypic identification was performed using a polymerase chain reaction–restriction fragment–length polymorphism (PCR‐RFLP) analysis of a 1‐kb fragment of the Helicobacter 16S rRNA gene.Results. During the last 7 years (1993–1999) a total of 11 isolates of H. pullorum were detected from patients with gastroenteritis for inclusion in this study. Typically, these isolates were oxidase and catalase positive, produced optimal growth at 42°C, and produced H2S in TSI. Of these 11 isolates, 1 showed DNase activity, while another did not produce H2S in TSI, and only 2 showed tolerance to 1% bile. Antimicrobial susceptibility assays indicated that 6 of the 11 strains were resistant to nalidixic acid. The fatty acid profiles of the isolates were similar to each other and provided a distinguishing profile from the other related species. Genetically identical and distinct species‐specific restriction fragment–length polymorphism (RFLP) patterns were produced using the restriction enzymes Bsr I and Dde I.Conclusion. Phenotypic and genotypic procedures were used to identify H. pullorum. Interspecies phenotypic variability was apparent and supported the use of a polyphasic approach for identification. Similarities to the more prominent human pathogens Campylobacter coli and C. lari were also noted. The use of a combination of phenotypic and, in particular, genotypic markers for H. pullorum should prove valuable both for epidemiological investigations and for the diagnosis of disease related to this emerging human pathogen.
Helicobacter pylori Entry into Human Gastric Epithelial Cells: A Potential Determinant of Virulence, Persistence, and Treatment Failures	1
Authors: Björkholm Britta , Zhukhovitsky Vladimir , Löfman Carl , Hultén Kristina , Enroth Helena , Block Mats , Rigo Robert , Falk Per , Engstrand Lars 
Published: March 2003

Background and Objectives. Intracellular location of Helicobacter pylori in human gastric epithelial cells has been observed in biopsies. Whether this reflects an ability to invade host cells and establish an intracellular niche remains to be determined.Methods. The interactions between a clinical isolate of H. pylori and primary cell cultures from human gastric epithelium or the human epithelial cell line HEp‐2 were monitored using time‐lapse photography. This technique allows studies of the dynamics of host‐microbial interactions.Results. H. pylori cells readily approached and established close contacts with epithelial cells followed by uptake of the bacteria into the cellular cytoplasm. Entry into epithelial cells was achieved through an active process of bacterial motility and penetration of the cell membranes. In conventional invasion assays using HEp‐2 cells, an increased internalization in a strain producing the vacuolating cytotoxin was observed, compared to the isogenic VacA knockout mutant.Conclusion. Invasion of gastric epithelium represents a hitherto unappreciated trait of H. pylori that could contribute to the bacterium's ability to establish persistent infection that evades the mucosal immune defense and sometimes also antimicrobial therapy. A small number of bacterial cells with a transient intracellular habitat could serve as a seeder population, providing a backup for a constantly challenged and fluctuating luminal population.
Distinction of GastricHelicobacterspp. in Humans and Domestic Pets by Scanning Electron Microscopy
Authors: Stoffel Michael H. , Friess Armin E. , Burnens André , Schmassmann Adrian , Neiger Reto 
Published: March 2003

Background.A number of differentHelicobacterspp. can colonize the stomach of humans and domestic pets. Difficulties encountered with primary isolation of these spiral microorganisms and their unusual inertia with respect to biochemical reactions still represent considerable obstacles to their characterization with classic tools. In addition, the high degree of similarity in the 16S rRNA sequence hampers differentiation ofHelicobacterspp. using routine molecular biological assays.Materials and Methods.Samples from experimentally monoinfected mice, of naturally infected hosts, and of cultured strains were examined by scanning electron microscopy (SEM). In parallel, all samples were analyzed by molecular techniques to ascertain theHelicobacterspp. involved.Results.Using the mouse samples as a reference, microorganisms found in naturally infected hosts were identified by SEM as belonging toH. pylori,H. felis, or a group consisting ofH. bizzozeroniiandH. heilmannii.A further spiral microorganism with unique morphology was found in a dog that was positive forH. salomonis, but the organism could not be recovered from experimentally infected mice. In culture, mostHelicobacterstrains lost their ultrastructural characteristics.Conclusions.When gastricHelicobacterspp. were collected from their natural habitat and examined by SEM, relevant differences could be detected betweenH. felis,H. bizzozeroniiandH. heilmannii, andH. salomonis, respectively. SEM, therefore, seems to be a useful auxillary tool for the distinction of various gastricHelicobacterspp. as based on their ultrastructure.
Helicobacter pylori Infection in the Cat: Evaluation of Gastric Colonization, Inflammation and Function
Authors: Simpson Kenneth W. , Strauss‐Ayali Dalit , Straubinger Reinhard K. , Scanziani Eugenio , McDonough Patrick L. , Straubinger Alix F. , Chang Yung‐Fu , Esteves Maria I. , Fox James G. , Domeneghini Cynzia , Arebi Naila , Calam John 
Published: March 2003

AbstractBackground.Further elucidation of the consequences of Helicobacter pylori infection on gastric mucosal inflammation and gastric secretory function would be facilitated by an animal model that is susceptible to infection with H. pylori, is broadly similar in gastric physiology and pathology to people, and is amenable to repeated non‐invasive evaluation. The goal of this study was to examine the interrelationship of bacterial colonization, mucosal inflammation and gastric secretory function in cats with naturally acquired H. pylori infection.Materials and Methods.Twenty clinically healthy cats with naturally acquired H. pylori infection (cagA−, picB) and 19 Helicobacter‐free cats were evaluated. Gastric colonization was determined by tissue urease activity, light microscopy, culture and PCR. The mucosal inflammatory response was evaluated by light microscopy, and by RT‐PCR of the pro‐inflammatory cytokines IL‐1α, IL‐1β, IL‐8 and TNF‐α in gastric mucosa. Gastric secretory function was assessed by measuring pentagastrin‐stimulated acid secretion, fasting plasma gastrin, and antral mucosal gastrin and somatostatin immunoreactivity.Results. H. pylori colonized the pylorus, fundus and cardia in similar density. Bacteria were observed free in the lumen of gastric glands and were also tightly adherent to epithelial cells where they were associated with microvillus effacement. Mononuclear inflammation, lymphoid follicle hyperplasia, atrophy and fibrosis were observed primarily in H. pylori‐infected cats, with the pylorus most severely affected. Neutrophilic and eosinophilic infiltrates, epithelial dysplasia, and up‐regulation of mucosal IL‐1β and IL‐8 were observed solely in infected cats. Fasting plasma gastrin concentrations and pentagastrin‐stimulated acid output were similar in both infected and uninfected cats. There was no relationship of bacterial colonization density or gastric inflammation to plasma gastrin concentrations or gastric acid output.Conclusions.The pattern of colonization and the mucosal inflammatory response in cats with naturally acquired H. pylori are broadly similar to those in infected people, particularly children, and non‐human primates. The upregulation of IL‐8 in infected cats was independent of cagA and picB. Our findings argue against a direct acid‐suppressing effect of H. pylori on the gastric secretory‐axis in chronically infected cats.Abbreviations:RT‐PCR, reverse transcriptase polymerase chain reaction, HLO; Helicobacter‐like organisms.
Helicobacter pylori CagA: Analysis of Sequence Diversity in Relation to Phosphorylation Motifs and Implications for the Role of CagA as a Virulence Factor
Authors: Evans Doyle J. , Evans Dolores G. 
Published: March 2003

AbstractCagA is transported into host target cells and subsequently phosphorylated. Clearly this is a mechanism by which Helicobacter pylori could take control of one or more host cell signal transduction pathways. Presumably the end result of this interaction favors survival of H. pylori, irrespective of eventual damage to the host cell. CagA is noted for its amino acid (AA) sequence diversity, both within and outside the variable region of the molecule. The primary purpose of this review is to examine how variation in the type and number of CagA phosphorylation sites might determine the outcome of infection by different strains of H. pylori. The answer to this question could help to explain the widely disparate results obtained when H. pylori CagA status has been compared to type and severity of disease outcome in different populations, that is in different countries. Analysis of all available CagA sequences revealed that CagA contains both tyrosine phosphorylation motifs (TPMs) and cyclic‐AMP‐dependent phosphorylation motifs (CPMs). There are two potential CPMs near the N‐terminus of CagA and at least two in the repeat region; these are not all equally well conserved. We also defined a 48‐residue AA sequence, which includes the N‐terminal TPM at tyrosine (Y)‐122, which distinguishes between Eastern (Hong Kong‐Taiwan‐Japan‐Thailand) H. pylori isolates and those from the West (Europe‐Africa‐the Americas‐Australia). All 28 of the Eastern type CagA proteins have a functional N‐terminal TPM whereas 11 of 47 (23.4%) of the Western type contain an inactive motif, with threonine (T) replacing the critical aspartic acid (D) residue. Only 13 of 24 (54%) known CagA sequences have an active TPM in the repeat region and only one has two TPMs in this region. The potential TPM near the C‐terminus of CagA is not likely to be important since only 3 of 24 (12.5%) sequences were found to be intact. Protein database searches revealed that the AA sequence immediately following the TPM at Y‐122 in CagA is homologous with a pair of PDZ domains which are common in signal transducing proteins, particularly tyrosine phosphatases. This provides a theoretical link between CagA and many of the observed responses of host cells to H. pylori. In summary, not all CagA proteins are equal in their potential for initiating host cell responses via signal transduction pathways. The degree of functional diversity of this protein depends upon which phosphorylation motifs are critical to the biological activity of CagA.
Atrophic Gastritis and Intestinal Metaplasia in Japan: Results of a Large Multicenter Study
Authors: Asaka Masahiro , Sugiyama Toshiro , Nobuta Aichiro , Kato Mototsugu , Takeda Hiroshi , Graham David Y. 
Published: March 2003

ABSTRACTBackground.This study evaluated the relationship between Helicobacter pylori infection, atrophic gastritis and intestinal metaplasia in Japan.Materials and Methods.This was a multicenter study performed in 21 centers in Japan. A total of 2455 individuals were enrolled. H. pylori status was determined by validated ELISAs. Atrophic gastritis was diagnosed by histology, endoscopy with Congo Red dye scattering or the Kimura‐Takemoto endoscopic classification.Results.Atrophic gastritis increased from 9.4% in those less than 20 years of age to > 70% in those aged 60 or older and was strongly associated with H. pylori infection. The overall prevalence of atrophic gastritis in H. pylori infection was 82.9% (1272/1534) compared with 9.8% (90/921) among uninfected (OR = 44.8; 95% CI = 34.7–57.8). Intestinal metaplasia was present in 43.1% (542/1258) of H. pylori positive persons compared with 6.2% (51/823) among the uninfected (OR = 11.5; 95% CI = 8.5–15.5). Atrophic gastritis in H. pylori positive Japanese was very high in the younger generation (38.5% in those aged 20 or less and 58.5% in those 21–30).Conclusions.Atrophic gastritis and intestinal metaplasia were strongly associated with H. pylori and not with aging. The fall in prevalence of H. pylori in Japan has not been associated with a corresponding fall in the prevalence of atrophic gastritis among those with H. pylori infection. The high prevalence of the precursor lesion, atrophic gastritis with intestinal metaplasia, among those with H. pylori infection suggests that the risk of development of early gastric cancer will continue to remain high in Japan.
Significance of the Caspase Family in Helicobacter pylori Induced Gastric Epithelial Apoptosis
Authors: Potthoff A. , Ledig S. , Martin J. , Jandl O. , Cornberg M. , Obst B. , Beil W. , Manns M. P. , Wagner S. 
Published: March 2003

AbstractBackground and Aims.  H. pylori infection results in an increased epithelial apoptosis in gastritis and duodenal ulcer patients. We investigated the role and type of activation of caspases in H. pylori‐induced apoptosis in gastric epithelial cells.Methods.  Differentiated human gastric cancer cells (AGS) and human gastric mucous cell primary cultures were incubated with H. pylori for 0.5–24 hours in RPMI 1640 medium, and the effects on cell viability, epithelial apoptosis, and activity of caspases were monitored. Apoptosis was analyzed by detection of DNA‐fragments by Hoechst stain®, DNA‐laddering, and Histone‐ELISA. Activities of caspases were determined in fluorogenic assays and by Western blotting. Cleavage of BID and release of cytochrome c were analyzed by Western blot. Significance of caspase activation was investigated by preincubation of gastric epithelial cells with cell permeable specific caspase inhibitors.Results.  Incubation of gastric epithelial cells with H. pylori caused a time and concentration dependent induction of DNA fragmentation (3‐fold increase), cleavage of BID, release of cytochrome c and a concomittant sequential activation of caspase‐9 (4‐fold), caspase‐8 (2‐fold), caspase‐6 (2‐fold), and caspase‐3 (6‐fold). No effects on caspase‐1 and ‐7 were observed. Activation of caspases preceded the induction of DNA fragmentation. Apoptosis could be inhibited by prior incubation with the inhibitors of caspase‐3, ‐8, and ‐9, but not with that of caspase‐1.Conclusions.  Activation of certain caspases and activation of the mitochondrial apoptotic pathway are essential for H. pylori induced apoptosis in gastric epithelial cells.
Helicobacter pylori CagA Containing ITAM‐Like Sequences Localized to Lipid Rafts Negatively Regulates VacA‐Induced Signaling In Vivo
Authors: Asahi Momoyo , Tanaka Yukie , Izumi Toshimasa , Ito Yoshiyuki , Naiki Hironobu , Kersulyte Dangeruta , Tsujikawa Kazutake , Saito Masakazu , Sada Kiyonao , Yanagi Shigeru , Fujikawa Akihiro , Noda Masaharu , Itokawa Yoshinori 
Published: March 2003

ABSTRACTBackground. Helicobacter pylori CagA is injected into the host cell and tyrosine‐phosphorylated. We examined tyrosine‐phosphorylation sites of CagA, as well as the function of CagA proteins in vivo and in vitro.Methods. After proteolytic digestion of CagA with lysyl endopeptidase, CagA tyrosine‐phosphorylation sites were determined using quadropolar time‐of‐flight (Q‐TOF) mass spectrometry analysis. Specific anti‐pY CagA polyclonal and anti‐CagA monoclonal antibodies were used to examine gastric mucosal biopsy specimens from H. pylori infected patients.Results. Mass spectrometry identified five crucial tyrosine‐phosphorylation sites of CagA at Tyr893, Tyr912, Tyr965, Tyr999, and Tyr1033 within the five repeated EPIYA sequences of H. pylori (NCTC11637)‐infected AGS cells. CagA protein also had an immuno‐receptor tyrosine‐based activation motif (ITAM)‐like amino acid sequences in the 3′ region of the cagA, EPIYATIx27EIYATI, which closely resembled the ITAM. CagA proteins: (i) were localized to the 1% TritonX‐100 resistant membrane fraction (lipid rafts); (ii) formed a cluster of phosphorylated CagA protein complexes; (iii) associated with tyrosine‐phosphorylated GIT1/Cat1 (G protein‐coupled receptor kinase‐interactor 1/Cool‐associated tyrosine‐phosphorylated 1), substrate molecules of receptor type protein‐tyrosine phosphatase (RPTPζ/β), which is the receptor of VacA; and (iv) were involved in a delay and negative regulation of VacA‐induced signal. Furthermore, immunohistochemical staining of gastric mucosal biopsy specimens provided strong evidence that tyrosine‐phosphorylated CagA is found together with CagA at the luminal surface of gastric foveola in vivo.Conclusion. These findings suggest an important role for CagA containing ITAM‐like sequences in the pathogenesis of H. pylori‐related disease.
Pathogenesis of Helicobacter pylori infection
Authors: Gerhard Markus , Rad Roland , Prinz Christian , Naumann Michael 
Published: March 2003

AbstractFive years after publication of the complete genome sequence of Helicobacter pylori, research interest is shifting from the descriptive association of virulence factors with clinical outcome in infected patients to the molecular mechanisms of virulence factor action. This is particularly noticeable for VacA and CagA, for both of which detailed understanding of the interaction with host signalling pathways has accumulated over the last year. The role of H. pylori Lewis antigens for clinical outcome was further substantiated. Various strategies of H. pylori to fool or evade the human immune system are described, which all lead to the dysfunction of specific compartments of the host cellular immune system. Finally, a number of animal models indicate that inflammation is a key factor for gastric carcinogenesis, which is finally supported by a large prospective study identifying corpus atrophy and intestinal metaplasia as precancerous conditions.
Perceptions of Quality of Life in Hispanic Patients with Cancer
Authors: Juarez Gloria , Ferrell Betty , Borneman Tami 
Published: March 2003

PURPOSE
: The purpose of this study was to describe perceptions of quality of life (QOL) of Hispanic patients with cancer pain.
DESCRIPTION OF STUDY
: This qualitative pilot study is guided by the conceptual framework of pain and QOL. From interviews with 17 Hispanic patients with cancer pain, data on perceptions of QOL were analyzed and are reported here.
RESULTS
: The study demonstrated the influence of culture on perceptions of QOL and the impact of pain on QOL. Several themes were identified for each domain of QOL, including physical, psychological, social, and spiritual well‐being. The role of the family and faith in God were important components of QOL for all patients.
CLINICAL IMPLICATIONS
: It is important for clinicians to devote greater attention to cultural assessment and to include cultural beliefs in cancer care to improve QOL for Hispanic patients. The role of the family and religious beliefs should be included in the planning and evaluation of each patient's care.