Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We compared the cutaneous reaction to intradermal injection of substance P, gastrin and histamine in asymptomatic atopic subjects with a history of hay fever and/or asthma versus non-atopic healthy volunteers. We also studied in these two groups the basophilic histamine release induced by substance P and gastrin with that obtained with anti-human IgE and Con A. Intradermal injection of substance P (3-300 pM) and gastrin (3-30 pM) caused a wheal and flare reaction which was comparable in both groups of subjects. Substance P 10(-4)M caused a mean basophilic histamine release of about 15% in atopic and non-atopic subjects. Gastrin was not effective in this model. Anti-IgE and Con A-induced histamine release was significantly higher in atopic than in non-atopic volunteers.
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PMID:Cutaneous and basophilic sensitivity to substance P and gastrin in non-atopic versus atopic subjects. 170 11

Serum IgE level and blood levels of gastrin, insulin, C peptide and glucagon have been studied in 34 patients with chronic opisthorchiasis (18 females and 16 males aged 36.5 +/- 2.6 years) prior to treatment and 10 days, 6 months and 12 months after recovery from the invasion. Blood levels of gastrin, insulin and C peptide remained unchanged. A trend towards normalization of glucagon levels about a year after recovery from opisthorchiasis has been observed. Serum IgE level a year after recovery was normal.
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PMID:[The serum immunoglobulin E level and the endocrine activity of the stomach, duodenum and pancreas after recovery from opisthorchiasis]. 223 34

Serum IgE, gastrin, and insulin levels were measured by radioimmunoassay and gastric secretion was studied by the method of submaximal histamine stimulation in 59 inhabitants of Sverdlovsk and 51 former inhabitants of Tyumen Province, who had chronic opisthorchiasis. In the hypoendemic focus, increased IgE content was observed mostly in young people, and in the hyperendemic focus it was in middle-aged and old people, this parameter correlating with decreased levels of gastrin and insulin in the serum. Gastric basal acid secretion was decreased in more than 70% patients from the both groups. However, hyperimmunoglobulinemia tends to show elevated hydrochloric acid debit.
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PMID:[The secretory activity of the stomach, duodenum and pancreas in patients with chronic opisthorchiasis]. 261 1

A radioimmunoassay of the carcinoembryonic antigen, gastrin and immunoglobulin E was performed in the blood serum of more than 300 esophageal and gastric cancer patients. It has been noted that the CEA study makes it possible to determine the severity of disease and may serve as a yard-stick of radical therapy. Hypogastrinemia develops in 82-84% of patients with tumors of these sites. The gastrin level after therapy depends on the nature and type of antitumor therapy. An increase in the IgE level is a risk factor which makes it possible to identify patients with an "unfavorable" or complicated course of disease and to determine, to some extent, prognosis, to control therapeutic measures in combined treatment. The use of the radioimmunoassay for CEA, gastrin and IgE in the combined study of esophageal and gastric cancer patients allows one to evaluate the patients's status before treatment and to determine their response to tumor therapy.
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PMID:[Radioimmunoassay of carcinoembryonic antigen, gastrin and immunoglobulin E in evaluating different methods of treatment of patients with esophageal and stomach cancer]. 650 53

Previous studies in our laboratory have shown that substance P (SP), injected into benzylpenicilloyl-keyhole limpet hemocyanin (BPO-KLH) sensitized mice at the peak of the benzylpenicilloyl (BPO)-specific IgE response, suppressed these responses in isotype-specific fashion within 48 h. These studies also showed that SP, but not neurotensin (NT), serotonin (5-HT), somatostatin (SOM) or gastrin, suppressed BPO-specific memory IgE antibody-forming cell (AFC) responses induced in vitro, also in isotype-specific fashion. To investigate the mechanisms by which SP suppressed BPO-specific IgE AFC responses were induced in vitro, these responses were induced by culturing spleen cells from BPO-KLH sensitized mice for 5 days with BPO-KLH with or without whole SP, amino terminal SP (SP 1-4: Arg-Lys-Pro-Lys), or carboxy terminal SP (SP 8-11: Phe-Gly-Leu-Met). In some experiments, the SP receptor antagonist (D-Pro2, D-Phe7, D-Trp9)-SP (D-SP) was included in culture. In other experiments anti-interferon monoclonal antibody (anti-IFN gamma mAb) was in culture. Whole SP and SP 8-11, but not SP 1-4, suppressed BPO-specific IgE AFC responses induced in vitro. The suppression obtained was IgE isotype-specific and dose-dependent. Inclusion of SP receptor antagonist (D-Pro2, D-Phe7, D-Trp9)-SP inhibited suppression of BPO-specific memory IgE AFC responses by SP or SP 8-11. The SP-mediated suppression of BPO-specific memory IgE responses appeared to involve interferon gamma (IFN gamma).
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PMID:Neuropeptide-mediated regulation of hapten-specific IgE responses in mice. II. Mechanisms of substance P-mediated isotype-specific suppression of BPO-specific IgE antibody-forming cell responses induced in vitro. 750 99

The ability of substance P (SP) to regulate peak benzyl-penicilloyl (BPO)-specific IgE antibody-forming cell (AFC) responses in vivo and the ability of SP and other neuropeptides to regulate BPO-specific memory IgE AFC responses induced in vitro was determined. SP injected subcutaneously into BPO-keyhole limpet hemocyanin (BPO-KLH)-sensitized mice at the time of peak IgE responses suppressed these responses within 48 h (> 90%). The suppression obtained was IgE isotype-specific, dose-dependent, and transient. When spleen cells from immunized mice were cultured for 5 days with BPO-KLH, peak memory IgE AFC responses were induced in vitro. Inclusion of either SP or vasoactive intestinal peptide (VIP), but not neurotensin, serotonin, somatostatin, or gastrin, in cultures suppressed these responses in isotype-specific, dose-dependent fashion (approximately 70%). SP-, but not VIP-mediated suppression of IgE responses was abrogated by inclusion of anti-IFN gamma culture.
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PMID:Neuropeptide-mediated regulation of hapten-specific IgE responses in mice. I. Substance P-mediated isotype-specific suppression of BPO-specific IgE antibody-forming cell responses induced in vivo and in vitro. 753 Feb 76

The prevalence of high total IgE serum levels was evaluated in 232 consecutive patients suffering from peptic ulcer. Twenty-one percent of the patients presented total IgE serum levels above 200 KU/L compared with the 5% found in a healthy control population (p < 0.004). Similar prevalence was found in gastric and/or duodenal ulcers. No significant differences in the duration of the disease, smoking habits, familiarity for peptic ulcer, symptomatology and frequency of complications were observed between patients with high and with normal total IgE serum levels. Gastric function studies (gastric acid secretion, serum pepsinogen and gastrin levels) did not show any significant differences between the two groups. The incidence of Helicobacter pylori infection was 65% in patients with normal IgE levels and 75% in those with high IgE levels (p: n.s.). The response to treatment with full dose of H2-receptor antagonists was comparable in both groups (91.25% and 90.7% of ulcer healing after 6-8 weeks of treatment). A relapse of the ulcer after 6 months of maintenance therapy (half dose of H2-receptor antagonists) was observed in 39.5% of the patients with ulcer and high total IgE serum as against the 11.9% observed in patients with normal IgE (p < 0.001). These data lend further support to the hypothesis of an underlying immuno-allergic reaction in some forms of gastric or duodenal ulcer.
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PMID:High IgE serum levels and "peptic" ulcers: clinical and functional approach. 791 69

The idea presented here is that, in gastric mucosa, two independent regulatory systems use the same transmitter: histamine molecules. The IgE/mast cell system is dispersed throughout the body, while the other regulates the gastric acid secretion. IgE molecules in gastric mucosa are attached to the mast cells. Mast cells release histamine molecules after the antigen has been recognized by IgE. These molecules normally act on vascular H1 receptors to promote extravasation and chemotaxy. Gastrin molecules are released from antral G cells to stimulate gastric acid secretion. Their influence on parietal cells is indirectly augmented by gastrin governed release of histamine molecules from enterochromaffin-like cells. These histamine molecules normally act on H2 receptors of parietal cells to promote gastric acid secretion. Chronic infection of gastric mucosa (i.e. with Helicobacter pylori), autoimmune disorders or repetitive mucosal exposure to the same antigen, can develop chronic inflammation of gastric mucosa. Gastric acid secretion is diminished with secondary hypergastrinemia and increased release of histamine from enterochromaffin-like cells in an attempt to stimulate the few remaining parietal cells. Hypothetically, increased concentrations of released histamine in gastric mucosa might activate the vascular H1 receptors with extravasation and aggravated inflammation. This can further decrease the number of active parietal cells, reduce gastric acid secretion and potentiate hypergastrinemia. In this hypothetical setting, H1 blockers might reduce the damage by abolishing the vascular reactions. The prolonged antigen load on gastric mucosa can promote production of specific IgE antibodies. Further exposures to the same antigen degranulate sensitized mucosal mast cells. Liberated histamine can produce extravasation through the vascular H1 receptor and, hypothetically, local hyperacidity through the parietal cell H2 receptors. The result would be hyperacidity and hypogastrinemia with possible ulcer disease. Some individuals are more predisposed to IgE production or have increased numbers of mast cells that might explain why only some people develop ulcer disease after H. pylori infection.
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PMID:The role of gastric mast cells, enterochromaffin-like cells and parietal cells in the regulation of acid secretion. 877 Oct 47

A relationship between allergic diseases and Helicobacter pylori infection has recently been noted. We report a case of atopic dermatitis and H. pylori infection in a 14-year-old girl. She had had widespread diffuse skin erythema with erosions and pigmentation since the age of 3 years. Endoscopically, there was chronic antral gastritis with H. pylori infection and histological eosinophilic infiltration. A high titer of H. pylori-specific IgG was present in serum. She was treated with a proton pump inhibitor (lansoprazole 60 mg), an antibiotic (clarithromycin 800 mg), and plaunotol (a mucosal protective agent, 480 mg) for 2 weeks to eliminate the infection. After 10 days of treatment, erythema and itching were more widespread and vesicle formation was seen on the foot. Generalized skin lesions abated a few days later. After eradication of the bacterium by the treatment, eosinophils decreased from 38.8% to 19.0%, and the clinical signs of atopic dermatitis almost disappeared. Serum gastrin level and the pepsinogen I/II ratio were normalized and histological findings of gastric mucosa showed improvement. H. pylori-specific IgE antibody, analyzed by the Western blot method, gradually decreased with the eradication treatment.
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PMID:Atopic dermatitis successfully treated by eradication of Helicobacter pylori. 895 27

Expression of 25 mRNAs in a single human lymphocyte was investigated using the reverse transcription nested polymerase chain reaction (RT nested PCR) method. Proteins corresponding to the mRNA investigated were mucin antigen, melanoma antigen, pregnancy-specific beta-1 glycoprotein 4, phenylethanolamine-N-methyl-transferase, beta B3-crystallin, homeobox 4A, interleukin 2, cluster of differentiation 8, progesterone receptor, parathyroid hormone, gastrin, cholecystokinin/pancreozymin, glucagon, insulin, enkephalin, thyroid stimulating hormone, adrenocorticotropic hormone, synapsin I, immunoglobulin (Ig)M, IgD, IgG1, IgG3, IgE, IgA, and T cell receptor alpha. All mRNAs were detected in single lymphocytes of two individuals, without exception. In addition, transcripts of IgM, IgD, IgG1, IgG3, IgE, IgA, and the T cell receptor a gene were detected in single sperms. The results strongly suggest the possibility that all mRNAs may be expressed in a single human cell, of both somatic and germ lineage. Thus, cells can consume energy in vain to produce functionally meaningless gene transcripts. However, this basal or illegitimate transcription may be essential for the birth of living matter: the arrow of time in a cell. Moreover, the phenomenon implies the potential of using lymphocytes in place of inaccessible tissue for the diagnosis of genetic diseases.
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PMID:A single human cell expresses all messenger ribonucleic acids: the arrow of time in a cell. 964 29


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