Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is both clinical and experimental evidence for the antigastric effect of calcitonin. A study was therefore made of gastric secretion after maximum insulin stimulation, and during its inhibition by calcitonin. Evaluation of basal acid flow and the maximum acidity peak in these two tests showed that the difference between the two peaks was related to the increase in gastrin. This was not the case during inhibition. The results show that selective evaluation of gastric secretion enables selective surgical techniques to be employed in the treatment of duodenal ulcer.
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PMID:[Calcitonin inhibition of insulin-stimulated gastric secretion. A possibility of selective evaluation of gastric secretory function]. 39 72

Gastric acidity is influenced by systemic and local peptide effects. Previous work by others has shown that intraluminally secreted peptides may have a role in local control of gastric acidity; however, the response of these peptides to acute changes in gastric pH is unknown. To determine the effects of acute changes in pH on systemic and intraluminal peptide levels, 14 normal volunteers underwent placement of a nasogastric tube after an overnight fast. Blood and gastric fluid were analyzed on a control day, 2 hours after completion of 24 hours of aluminum-magnesium antacid therapy and after 24 hours of H2 blockade. Plasma and acid-alcohol-extracted gastric peptide levels were measured with specific radioimmunoassays. Specimens were subdivided into two groups: 28 gastric fluid specimens with a pH less than 4 and 10 specimens with a pH greater than 4. In the patients with a pH greater than 4, the luminal peptides, motilin, neurotensin, pancreatic polypeptide, somatostatin, substance P, and gastrin, were decreased by 50% to 90% and gastrin-releasing peptide was decreased by 36% compared with specimens with a pH less than 4. Conversely, intraluminal vasoactive intestinal polypeptide and calcitonin levels were elevated by 60% and 27%, respectively, in the samples with a pH greater than 4. Intraluminal peptide concentrations are responsive to changes in intragastric pH; however, this response was not seen in plasma peptide levels.
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PMID:Acute gastric pH changes alter intraluminal but not plasma peptide levels. 172 Sep 3

Regulation of the acidity of osteoclasts was determined in situ on the endocranial surfaces of mouse calvaria using acridine orange, a fluorescent weak base. Osteoclasts could be identified by large size, multiple nuclei, relatively small numbers of cells, and the way and the extent to which they took up the dye. Nonosteoclastic cells were stained mainly in their nuclei and occasionally in a few lysosomes surrounding their nuclei, which were uniformly single in nonosteoclasts. Nuclei in osteoclasts were also stained, but the staining of the nuclei was partially masked by the intensity and completeness of the staining of the cytoplasm. In some cells the cytoplasmic staining appeared to be in discrete granules, giving the cytoplasm a bright, frothy appearance. This fluorescence was present in both treated and untreated cells and aided in identifying the osteoclasts. Acridine orange fluorescence at 624 nm intensity, and hence, osteoclast acidity, was increased by parathyroid hormone and prostaglandin E2. Parathyroid hormone-induced increases in acidity were inhibited by calcitonin, cortisol, sodium fluoride, and prostaglandin E2. Furthermore, osteoclast acidity was dependent largely or partially on maintenance of K+ and Na+ gradients, patent Na+ channels, chloride-bicarbonate exchange, and H+, K+-ATPase. These findings demonstrate that osteoclasts become acidified by mechanisms similar to those occurring in gastric parietal cells.
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PMID:Humoral and ionic regulation of osteoclast acidity. 243 48

We investigated the effects of calcitonin (CT) and parathyroid hormone (PTH) on the distribution of actin, tubulin, vimentin, and on cell size in cultured chick osteoclasts. In addition, we studied the effects of colchicine on intracellular acidity. Osteoclasts were isolated from the endosteum of 2-3-week chick tibias and were maintained under culture conditions for 5 days. The cells were treated with CT for 30 min or PTH for 60 min and were observed after immunocytochemical staining of cytoskeletal proteins. In untreated cells, actin was found in both a filamentous and a punctate staining pattern, with indented or invaginated regions free of punctate spots. The tubulin distribution in untreated cells was characterized by a pattern of microtubules radiating from the cell center and running parallel to the cell edge. Vimentin staining was usually localized to the perinuclear area. There were no changes in cytoskeletal element distribution or morphology attributable to PTH treatment. Osteoclasts treated with CT were more irregularly shaped, contained more retraction fibers, and were more rounded, with a denser array of cytoskeletal elements in the cell center. In addition, the mean area of the CT-treated cells was significantly less than that of the untreated cells. The actin distribution after CT treatment was still characterized by both a filamentous and a punctate pattern. After CT treatment, vimentin staining appeared more centrally localized than in untreated cells and tubulin staining revealed microtubules which now extended to the retracted cell margin. These results indicate that isolated osteoclasts respond to CT by significant morphological changes which are reflected in the distribution of the major cytoskeletal elements. Disruption of the microtubular system by colchicine treatment also resulted in an initial increase in intracellular acidity, suggesting the involvement of microtubules in the movement of acid-laden vesicles to the exterior.
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PMID:Characterization of the cytoskeleton of isolated chick osteoclasts: effect of calcitonin. 277 8

The effects of acetazolamide, calcitonin (CT), and parathyroid hormone (PTH) on acid production in isolated osteoclasts has been investigated. Osteoclasts were isolated from the endosteum of 3-week chick tibias and were maintained under culture conditions for 5 days. The cells were treated with acetazolamide (10 x 4 M and 10(-7) M), CT (1 mU/ml and 0.31 mU/ml) and PTH (6.5 U/ml and 0.40 U/ml) for 1, 3, 6, and 18 hr. The cells were stained with acridine orange and the intensity of fluorescence measured by a light microscope photometer. Acetazolamide treatment resulted in a steady decline in intracellular acidity, suggesting that carbonic anhydrase plays a major role in acid production in isolated osteoclasts. Treatment with PTH produced a decline in acidity at 1 hr, followed by a peak at 3 hr and then a decline at 6 and 18 hr. The transient increase in acidity may be due to activation of carbonic anhydrase by PTH. Calcitonin treatment also resulted in a decline in cell acidity which was similar, but less pronounced than that resulting from acetazolamide treatment. These results indicate that calcitonin may mediate osteoclast activity by alterations in intracellular acid production.
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PMID:Characterization of isolated and cultured chick osteoclasts: the effects of acetazolamide, calcitonin, and parathyroid hormone on acid production. 314 73

The effect of intracerebroventricular injection of rat calcitonin gene-related peptide (CGRP), human calcitonin (CT) and [Asu1,7]-eel CT on the volume and acidity of gastric juice was examined in the pylorus-ligated male rats. These 3 peptides were effective in suppressing both the volume and acidity of secreted gastric juice. Their potency on a molar basis, however, was markedly different; [Asu1,7]-eel CT was most potent, followed by human CT and finally by rat CGRP. These finding suggest that CGRP could not substitute for [Asu1,7]-eel or human CT in exerting the suppressive effect of gastric acid secretion.
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PMID:Effect of intracerebroventricular administration of rat calcitonin gene-related peptide (CGRP), human calcitonin and [Asu1,7]-eel calcitonin on gastric acid secretion in rats. 348 10

After vagotomy (truncal, highly selective, superselective) in rats, basal gastric secretion, gastric mucosal blood flow, associated fasting blood glucose and a variety of hormones were measured. All forms of vagotomy reduce acid (volume, acidity, output), but highly selective and superselective--though not truncal--procedures stimulate basal pepsin secretion, whereas mucosal blood flow roughly parallels acid production. Spontaneous gastric mucosal lesions increase after highly selective vagotomy. Both highly selective and superselective--but not truncal--vagotomy tend to increase plasma glucose and somatostatin, while only the former reduces insulin and glucagon. Common to all vagotomies is the development of virtually undetectable calcitonin (less than 25 pg/ml) and of hypergastrinemia. It is concluded that in the rat with draining gastric fistula in response to vagotomy there are moderate differences in regard to gastric mucosal ulcer index, gastric secretion, glucose, glucose-regulating hormones, while lowered calcitonin may be a general feature of low vagal tone.
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PMID:Basal gastric secretion, mucosal blood flow and associated fasting blood hormones in the rat. Effects of various forms of vagotomy. 612 15

We evaluated protocols for the extraction of calcitonin gene-related peptide, neuropeptide Y, substance P, peptide YY and beta-endorphin from rat lung tissue for subsequent radioimmunoassay. The effects of varying acidity of the extraction solution and repeating extraction on the recovery of peptide immunoreactivity and non-specific tracer-binding were compared by analysis of variance. Moreover, variability of immunoreactivity was quantified for comparison. Considering all three criteria, the optimal acidity for extraction was: 0.1 M or 1 M acetic acid for CGRP and beta-endorphin, 0.1 M acetic acid for NPY, 1 M acetic acid for substance P and phosphate buffer for peptide YY. Double or combined extraction unambiguously improved assay results only for substance P. Reversed-phase high-performance liquid chromatography of CGRP-, NPY- and SP-immunoreactivity obtained from selected extracts suggested that differences in recovery of these peptides are not explainable by differential peptide fragmentation during extraction.
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PMID:Analytical extraction of regulatory peptides from rat lung tissue. 943 21

Although dermatology now has the most extensive group of systemic medications available for the treatment of skin diseases at any time, GCSs remain the most important agents for managing inflammatory disorders. It is important that the dermatologist have a broad knowledge of guidelines for clinical use, pharmacology, and adverse effects of these drugs. Acute and chronic side reactions should be well recognized. An understanding of the HPA axis and reasons for administering GCSs in different ways is of great value. A good medical history should be taken on any patient treated with GCSs, including knowledge of conditions that would make GCSs inadvisable and other concomitant systemic medications that might produce drug interactions. During the course of therapy, physical examination should include all systems pertinent to side effects caused by these agents, including frequent evaluations of weight and blood pressure. Blood chemistries should be performed on a regular basis, including glucose, electrolytes, and serum lipids. Osteoporosis is one of the most significant adverse affects to be evaluated, with bone mineral density studies recommended on an annual basis for persons continuing on GCS therapy. If hip or other joint pain develops, MR imaging is the most specific and sensitive radiologic examination for evaluating the possibility of osteonecrosis. An ophthalmology examination should be performed every 6 to 12 months to detect early cataract or glaucoma development. Any early signs of infection should be evaluated by appropriate smears, wet preparations, and cultures. Many other studies, including gastrointestinal and pulmonary examinations, may be dictated by specific acute situations. It is important to begin early prevention of the bone loss that occurs with GCS-induced osteoporosis. The 1996 guidelines of the American College of Rheumatology, including adequate calcium and vitamin D intake, should be followed. Hormonal replacement, a bisphosphonate, calcitonin, or a thiazide diuretic may be indicated. Restriction of sodium in the diet is important, as well as adequate potassium intake. The diet should be low in saturated fat and calories and should be high in vegetable protein. Because osteoporosis is so prevalent with GCSs, keeping the patient as active as possible with mild-to-moderate exercise is important. Whenever possible, exposure to persons with infectious processes should be avoided, and proper treatment should be instituted at the initial signs of systemic or cutaneous infection. Oral doses of GCSs are best taken with food to prevent gastrointestinal irritation, and agents for gastric acidity occasionally may be indicated. Significant trauma should be prevented, as should severe exposure to the sun. Many situations may call for consultation with other medical or surgical subspecialists. The patient must be aware of the importance of regular physician evaluations and reporting of any adverse effects while on long-term GCSs. A good relationship and understanding between the patient and physician are vital in minimizing potential problems from these agents. If the dermatologist maintains the proper guidelines of care, patients on GCSs have the highest benefits and lowest risks possible.
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PMID:Update on systemic glucocorticosteroids in dermatology. 1115 87

The gastrointestinal mucosa serves as the interface between the luminal contents, including nutrients and injurious substances, and submucosal structures. Secreted gastric acid is one of the principal injurious components of the luminal contents. To be protected against harm from this acid, the epithelium has an "early warning" system that can activate potent defense mechanisms. We studied the mechanisms that defend the epithelium against luminal acid-induced injury, including the regulation of epithelial intracellular pH (pHi), blood flow, and mucus gel secretion in the perfused rat duodenum, and the pathways involved in the activation and regulation of these mechanisms. Physiological concentrations of luminal acid acidified the epithelial cells and increased blood flow (hyperemic response) and mucus gel thickness. The hyperemic response to acid was abolished by inhibitors of the Na+/H+ exchange, vanilloid receptors (VR), calcitonin gene-related peptide (CGRP) receptors, and nitric oxide (NO) synthase, and also by sensory afferent denervation, but not by pretreatment with a nonselective cyclooxygenase (COX) inhibitor. Mucus secretion in response to luminal acid was delayed by an interruption to the capsaicin pathway, which includes VR, capsaicin-sensitive afferent nerves, CGRP, and NO, and was abolished by COX inhibition. These observations support the hypothesis that the capsaicin pathway is an acid-sensing pathway that promotes hyperemia and mucus secretion in response to luminal acid. The COX pathway is a secondary regulatory system for mucus secretion. A similar acid-sensing capsaicin pathway is also present in the colon, suggesting that the gastrointestinal mucosa "tastes" luminal acidity through epithelial-VR communication.
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PMID:Acid-sensing pathways in rat gastrointestinal mucosa. 1257 81


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