Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori (HP) causes dense gastritis that can be difficult to distinguish morphologically from MALT-type lymphoma (ML). Immunoglobulin heavy chain (IgH) gene analysis by polymerase chain reaction (PCR) is often used to resolve diagnosis. However, monoclonal bands have been reported in nonmalignant cases of gastritis. Retrospectively, 16 gastric ML with both formalin-fixed, paraffin-embedded (FF-PE) and ethanol-fixed samples (EF), and 9 cases of FF-PE HP-gastritis were analyzed by IgH PCR to document the presence of non-reproducible bands in HP-gastritis, but not ML samples. In duplicate analyses, 12 of 16 ML yielded identical monoclonal bands in FF-PE and EF samples whereas 3 of 9 FF-PE gastritis cases yielded different-sized (ie, non-reproducible) "clonal" bands. Sequencing of two PCR products from a gastritis case confirmed IgH gene sequences. To investigate whether FF-PE had a direct effect on producing these non-reproducible bands, 7 gastrectomy samples were prospectively divided into EF and FF-PE halves for IgH PCR. All 7 samples demonstrated polyclonal smears in EF portions while 4 of 7 FF-PE portions yielded either multiple distinct bands or non-reproducible bands. In conclusion, IgH PCR of FF-PE tissue can create artifactual "clonal" bands, which are the appropriate product size, contain IgH sequences, and, if not performed in duplicate, may confuse interpretation of B-cell clonality.
J Mol Diagn 2002 Aug
PMID:IgH PCR of zinc formalin-fixed, paraffin-embedded non-lymphomatous gastric samples produces artifactual "clonal" bands not observed in paired tissues unexposed to zinc formalin. 1216 77

The clinical presentation of patients with vitamin B(12) deficiency varies in a spectrum ranging from haematological disorders to neuropsychiatric diseases. In rare cases, orthostatic hypotension, impotence, constipation and urinary retention have been attributed to autonomic nervous system dysfunction due to vitamin B(12) deficiency. The aim of this study was to evaluate the effect of vitamin B(12) deficiency on autonomic nervous system function by studying gastric emptying times ( T(1/2)). Twenty patients with newly diagnosed vitamin B(12) deficiency and 12 control patients with gastritis and normal vitamin B(12) levels were enrolled in this study. Gastroduodenoscopy, endoscopic biopsy, histopathological evaluation of the biopsy specimens and radionuclide gastric emptying studies were performed. After vitamin B(12) replacement therapy for 3 months, radionuclide gastric emptying studies were repeated. Mean gastric emptying T(1/2) in patients before and after treatment and in controls were 103.83+/-48.80 min, 90.00+/-17.29 min and 74.55+/-8.52 min, respectively. The difference in mean gastric emptying T(1/2) between patients before treatment and controls was statistically significant ( P<0.01). The statistically significant difference persisted after vitamin B(12) treatment ( P<0.05), though mean gastric emptying T(1/2) was somewhat shorter. There were no positive or negative correlations between gastric emptying T(1/2) and the following parameters: haemoglobin, vitamin B(12) level and Helicobacter pylori positivity. In conclusion, gastric emptying T(1/2) was prolonged in patients with vitamin B(12) deficiency and this prolongation was not corrected after vitamin B(12) replacement therapy. Although autonomic nervous system dysfunction due to vitamin B(12) deficiency rarely gives rise to clinical manifestations, latent dysfunction demonstrated by laboratory tests seems to be a frequent phenomenon. The level of vitamin B(12) does not correlate with the degree of autonomic nervous system dysfunction measured by radionuclide gastric emptying studies.
Eur J Nucl Med Mol Imaging 2002 Sep
PMID:Gastric emptying in patients with vitamin B(12) deficiency. 1219 55

Sialyl-Tn antigen (STn) is a mucin-type carbohydrate normally present in goblet cells of small and large bowel. STn expression has been demonstrated to occur in complete and incomplete intestinal metaplasia as well as in many carcinomas but in no normal gastric cell. The aim of our present study was to evaluate the distribution of STn in Helicobacter pylori chronic gastritis (HpCG) of pediatric patients. Eighteen gastric biopsies from 15 children (mean age: 11.5 years) with HpCG, 9 gastric biopsies from 9 children without H. pylori infection, and 1 heterotopic gastric mucosa in Meckel's diverticulum were immunostained using the anti-STn antibody STn1 (18/18), NCL-MUC-1 (7/18), and NCL-MUC-2 (18/18) antibodies. Also, sulfated mucosubstances were investigated with the Alcian Blue-Periodic Acid Schiff (AB-PAS), pH 1.0 stain. Although with different intensity (weak in 5/18, moderate 9/18, and intense 4/18) all cases with HpCG exhibited STn immunoreactivity. The expression of STn was found to be located mainly to the supranuclear region of the epithelial cells at the foveolae and glandular necks, with occasional cells showing diffuse cytoplasmic staining. When reactivity was intense, it was for the most part found in the cells at the neck of the glands. The mucus out of the luminal border above the positive cells was usually also stained. MUC-1 was negative (2/7) or weakly positive (5/7) in a few surface mucous cells. MUC-2 was negative (16/18) or occasionally detected in some foveolar and surface cells (2/18). AB-PAS pH 1.0 revealed the presence of sulfomucins in the cytoplasm of isolated cells of gastric pits and glands of most cases (11/15). None of these findings was observed in the control group. We conclude that STn can be identified in gastric cells of pediatric patients with HpCG and that this does not correlate with other mucosubtances markers. The findings could indicate that minimal intestinal metaplasia takes place in children with HpCG.
Pediatr Pathol Mol Med
PMID:SIALYL-Tn antigen distribution in Helicobacter pylori chronic gastritis in children: an immunohistochemical study. 1255 92

Somatic mutations of the mitochondrial DNA (mtDNA) are associated with development of various types of human cancer. To elucidate the significance of somatic mutations of the mtDNA in gastric carcinogenesis, we examined mtDNA mutations in gastric cancers and in Helicobacter pylori-associated chronic gastritis (H. pylori-CG), which is associated with an increased risk for gastric cancer development. Specimens of gastric cancer and gastric mucosa were obtained from 73 gastric cancer patients with H. pylori-CG, 75 cancer-free H. pylori-CG patients and 30 H. pylori-negative healthy subjects. Mutations of a specific mononucleotide repeat (D310) of the mtDNA were examined by microsatellite assay. mtDNA mutations were detected in 9 of 56 (16%) gastric cancers, in 10 of 148 (7%) H. pylori-CG and none of the 30 H. pylori-negative healthy subjects. mtDNA mutations in H. pylori-CG were significantly more frequent in gastric cancer patients than in cancer-free patients (12% vs. 1%, p=0.008). In addition, mtDNA mutations in H. pylori-CG were significantly more frequent in patients with mtDNA mutated gastric cancer than in patients with mtDNA unmutated gastric cancer (66% vs. 4%, p<0.001). These data suggest that somatic mutations of the mtDNA may be involved in the early stages of gastric carcinogenesis.
Int J Mol Med 2003 Aug
PMID:Somatic mutation of mitochondrial DNA in Helicobacter pylori-associated chronic gastritis in patients with and without gastric cancer. 1285 12

Helicobacter pylori is a causative agent of severe diseases of the gastric tract ranging from chronic gastritis to gastric cancer. Cellular proteins of H. pylori were separated by high resolution two-dimensional gel electrophoresis. A dataset of 384 spots was automatically picked, digested, spotted, and analyzed by matrix-assisted laser desorption ionization mass spectrometry peptide mass fingerprint in triple replicates. This procedure resulted in 960 evaluable mass spectra. Using a new version of our data analysis software MS-Screener we improved identification and tested reliability of automatically generated data by comparing with manually produced data. Antigenic proteins from H. pylori are candidates for vaccines and diagnostic tests. Previous immunoproteomics studies of our group revealed antigen candidates, and 24 of them were now closely analyzed using the MS-Screener software. Only in three spots minor components were found that may have influenced their antigenicities. These findings affirm the value of immunoproteomics as a hypothesis-free approach. Additionally, the protein species distribution of the known antigen GroEL was investigated, dimers of the protein alkyl hydroperoxide reductase were found, and the fragmentation of gamma-glutamyltranspeptidase was demonstrated.
Mol Cell Proteomics 2003 Dec
PMID:Analysis of automatically generated peptide mass fingerprints of cellular proteins and antigens from Helicobacter pylori 26695 separated by two-dimensional electrophoresis. 1451 19

The human intestinal tract is constantly exposed to an enormous indigenous bacterial flora. It has recently been recognised that antimicrobial peptides of the defensin family likely play a role in protection against microbial invasion at a variety of mucosal epithelial surfaces, including that of the intestinal tract. To date, six alpha-defensins have been identified in humans. Four of these, designated Human Neutrophil Peptides (HNP) 1,2,3 and 4, form part of the armoury of neutrophils, where they participate in systemic innate immunity. The remaining two, Human Defensin (HD) 5 and 6, are expressed in intestinal Paneth cells, and probably contribute to innate defense of the GI mucosal surface. Murine intestinal alpha-defensins (the 'cryptdins') have been extensively studied, but less is known about their human counterparts. The putative mature HD-5 was chemically synthesised and used to raise polyclonal antiserum. Using this anti-HD-5 antiserum, the expression of HD-5 in normal and inflamed intestinal mucosal samples was studied using immunohistochemistry. HD-5 is expressed in Paneth cells and also in some villous epithelial cells in normal duodenum, jejunum and ileum. HD-5 is not expressed in the normal stomach or colon. In cases of gastritis, colonic Crohn's disease and ulcerative colitis, HD-5 is expressed in metaplastic Paneth cells. Utilizing the anti-HD-5 antiserum, native HD-5 was isolated and purified from acid extracts of normal terminal ileal mucosal epithelial cells using cation exchange and reverse phase high pressure liquid chromatography. The purified peptide was characterised using N-terminal amino acid sequence and mass spectral analysis. Antimicrobial activity of the peptide was assessed using a sensitive colony forming unit antimicrobial assay. HD-5 is stored in the predicted precursor form in Paneth cells, and this form does not have antimicrobial activity against a defensin sensitive Salmonella. Potential processing of the precursor form of the HD-5 peptide into a mature active form, was studied by stimulating Paneth cell granule secretion in freshly isolated, cultured ileal crypts. A truncated form of the precursor form of HD-5, but not the predicted mature form, was present in the culture supernatant. Recently published studies suggest that further processing of the molecule occurs in vivo. The expression of HNP 1-3 in the normal intestinal mucosa and in cases of inflammatory bowel disease was studied. In the normal intestinal mucosa, HNP are expressed only in sparse lamina propria neutrophils, and not in Paneth cells. In cases of active ulcerative colitis and Crohn's disease, scattered surface epithelial cells, as well as numerous lamina propria neutrophils, were seen to express HNP. In conclusion, HD-5 is stored only in its precursor form in normal ileal Paneth cells, and partial processing of the peptide to a mature form occurs during and/or after secretion. In inflammatory bowel disease, HD-5 is expressed in metaplastic Paneth cells in the colon, and HNP is expressed by some surface epithelial cells. These studies suggest that antimicrobial defensin peptides may be important in protection of the host against microbial invasion in states of intestinal inflammation.
Mol Immunol 2003 Nov
PMID:Alpha-defensins in the gastrointestinal tract. 1456 93

Gastritis and peptic ulcers result from Helicobacter pylori (H. pylori) infection. To analyze the influence of Helicobacter on inflammatory responses and cell proliferation, we used an animal model of H. pylori-induced gastritis in p53-knockout mice. H. pylori were introduced by gastric intubation into p53-knockout C57BL/6 mice. The animals were then followed-up for 1 year and compared with uninfected controls of the same genotype. Serum levels of anti-H. pylori antibody and histopathological changes were analyzed according to the updated Sydney System. Immunohistochemistry for proliferating cell nuclear antigen (PCNA) and TUNEL staining were also performed. The infected mice showed significantly increased levels of anti-H. pylori antibody in serum. Histologically, p53-knockout mice exhibited increased scores of chronic and active inflammation compared with uninfected controls. The PCNA and TUNEL indices were 25.5% and 10/mm, respectively, in the inflammatory foci of infected mice, and were increased compared with the controls. In the p53-knockout mice, H. pylori infection caused severe inflammatory reactions. The p53 gene may play an important role in inflammatory responses including cell proliferation and apoptosis.
Int J Mol Med 2004 Jun
PMID:Helicobacter pylori induces chronic active gastritis in p53-knockout mice. 1513 11

BACKGROUND: Eosinophilic gastritis is related to eosinophilic gastroenteritis, varying only in regards to the extent of disease and small bowel involvement. Common symptoms reported are similar to our patient's including: abdominal pain, epigastric pain, anorexia, bloating, weight loss, diarrhea, ankle edema, dysphagia, melaena and postprandial nausea and vomiting. Microscopic features of eosinophilic infiltration usually occur in the lamina propria or submucosa with perivascular aggregates. The disease is likely mediated by eosinophils activated by various cytokines and chemokines. Therapy centers around the use of immunosuppressive agents and dietary therapy if food allergy is a factor. CASE PRESENTATION: The patient is a 31 year old Caucasian female with a past medical history significant for ulcerative colitis. She presented with recurrent bouts of vomiting, abdominal pain and chest discomfort of 11 months duration. The bouts of vomiting had been reoccurring every 7-10 days, with each episode lasting for 1-3 days. This was associated with extreme weakness and cachexia. Gastric biopsies revealed intense eosinophilic infiltration. The patient responded to glucocorticoids and azathioprine. The differential diagnosis and molecular pathogenesis of eosinophilic gastritis as well as the molecular effects of glucocorticoids in eosinophilic disorders are discussed. CONCLUSIONS: The patient responded to a combination of glucocorticosteroids and azathioprine with decreased eosinophilia and symptoms. It is likely that eosinophil-active cytokines such as interleukin-3 (IL-3), granulocyte macrophage colony stimulating factor (GM-CSF) and IL-5 play pivotal roles in this disease. Chemokines such as eotaxin may be involved in eosinophil recruitment. These mediators are downregulated or inhibited by the use of immunosuppressive medications.
Clin Mol Allergy 2004 May 14
PMID:Eosinophilia in a patient with cyclical vomiting: a case report. 1514 61

Recent advances in gene-amplification technology and molecular phylogenetics have provided the means of detecting and classifying bacteria directly from their natural habitats without the need for culture. These techniques have revolutionized environmental microbiology, and it is now apparent that the global diversity of microorganisms is much greater than previously thought. In the context of clinical microbiology, this molecular-based approach has facilitated the characterization of culture-resistant bacteria associated with human disease. Examples include Helicobacter heilmannii, a cause of gastritis, Tropheryma whippeli (the agent of Whipple's disease), and the agents of human ehrlichiosis and bacillary angiomatosis. Molecular-based techniques also provide a means of investigating complex bacterial flora within the human ecosystem, such as feces and dental plaque, without the bias of culture-based isolation. This has given a new perspective to the study of polymicrobial infections such as gingivitis, and offers the potential for the detection and identification of novel bacterial pathogens from among complex and numerous endogenous microbial flora.
Methods Mol Biol 2004
PMID:Discovering new pathogens: culture-resistant bacteria. 1514 25

Helicobacter pylori is a major human pathogen causing gastritis and chronic superficial infection (CSG). It colonizes the stomach of more than 50% of humans and causes disease. This microorganism is associated with the gastric antral epithelium in patients with active chronic gastritis, peptic (gastric) or duodenal ulcers, and gastric adenocarcinoma H. pylori is present in feces, sewage, and water but is killed by routine chlorination. Therefore, in developing countries, consumption of sewage-contaminated drinking water and vegetables may pose a risk; properly cooking foods and chlorinating water reduces the risk of transmitting H. pylori to humans. In South America the consumption of raw vegetables fertilized with human feces has been found to be a risk factor for infection, and consumption of water from a municipal supply has been suggested as a risk factor for children. Epidemiological studies have found that H. pylori organisms colonize the stomach and duodenum of humans and many animal species and family clusters; it is believed to be orally transmitted person to person. This transmission is the major, if not exclusive, source of infection.H. pylori has been detected in the mouth from dental plaque. Recent observations in persons infected with H. pylori caused to vomit or have diarrhea showed that an actively unwell person with these symptoms could spread H. pylori in the immediate vicinity by aerosol, splashing of vomitus, infected vomitus, and infected diarrhea. In summary, H. pylori is usually spread by the fecal-oral route but possibly also by the oral-oral route and the spread of contaminated secretions. Thus, in developing countries, individuals catch H. pylori at a very young age from other persons (children) in their environment. In developed countries, H. pylori is more difficult to acquire and is usually transmitted from one family member to another, possibly by the fecal-oral route, or by the oral-oral route, e.g., kissing, vomitus. On occasion, transmission occurs from person to person via contaminated endoscopes. Other gastric Helicobacter-like organisms have now been observed in a variety of animals, including rodents, primates, swine, and ferrets, but, with the exception of primates and possibly cats, these isolates are clearly different from human isolates. Foodborne transmission would not be unusual.
Methods Mol Biol 2004
PMID:Helicobacter pylori and food products: a public health problem. 1515 39


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