Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Solid and papillary epithelial neoplasms of the pancreas from six female patients were studied using immunohistochemistry and electron microscopy to define better their histogenesis. The tumors ranged in diameter from 5 to 15 cm (average: 9 cm), and, on cross section, most had areas of hemorrhage and necrosis, sometimes extensive. Microscopically, there was a solid and pseudopapillary pattern, with tumor cells typically having ovoid nuclei with delicate folding and indistinct nucleoli. Of note were the following: a relatively low mitotic rate (range: 0-6/20 hpf), the presence of hyaline globules (four of six cases), and collections of foam cells (three of six cases). Staining for cytoplasmic argyrophil granules was negative in each case. Ultrastructurally, the solid and papillary epithelial neoplasms of the pancreas showed evidence of acinar or ductular differentiation. Two contained zymogen granules, one had intermediate filaments (probably keratin), and three had abundant rough endoplasmic reticulum and mitochondria. Immunostaining was positive for chymotrypsin (six of six cases), trypsin (four of six), and amylase (three of six). None was positive for alpha-1-antitrypsin, neuron-specific enolase, pancreatic polypeptide, gastrin, glucagon, somatostatin, or insulin. The findings support an origin from exocrine pancreas, and follow-up indicates a low rate of malignancy, with local recurrence in two of the six patients.
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PMID:Solid and papillary epithelial neoplasm of the pancreas. An ultrastructural and immunocytochemical study of six cases. 381 76

1. Analytical subcellular fractionation techniques have been applied to endoscopic human rectal biopsies to study the localization of enteroglucagon, somatostatin, vasoactive intestinal peptide and the properties of the principal subcellular organelles. 2. The peptide hormones, detected by radioimmunoassay, showed particulate localizations with single peaks in the density gradients for enteroglucagon (modal density 1.25) and somatostatin (modal density 1.23). Vasoactive intestinal peptide showed a less discrete localization but demonstrated a major peak (modal density, 1.17) with a small subsidiary peak (modal density 1.24). 3. The following organelles, characterized by their marker enzymes, were located in the density gradients; plasma membrane (5'-nucleotidase), mitochondria (malate dehydrogenase), peroxisomes (catalase), lysosomes (beta-N-acetyl-D-glucosaminidase), endoplasmic reticulum (neutral alpha-D-glucosidase) and cytosol (lactate dehydrogenase). 4. This technique can be used to investigate disease of the human rectum at a subcellular level.
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PMID:Subcellular fractionation studies of human rectal mucosa: localization of the mucosal peptide hormones. 610 76

1. Analytical subcellular fractionation techniques have been applied to endoscopic human gastric antral biopsies to study the localization of gastrin, somatostatin, vasoactive intestinal peptide and the properties of the principal subcellular organelles. 2. The peptide hormones, detected by radioimmunoassay, showed particulate localizations with single peaks in the density gradients for somatostatin (modal density 1.23) and vasoactive intestinal peptide (modal density 1.17). Gastrin showed a more complex distribution with a distinct peak (modal density 1.18) and a substantial shoulder extending into the denser regions of the gradient. 3. The following organelles, characterized by their marker enzymes, were located in the density gradients: plasma membrane (5'-nucleotidase), mitochondria (malate dehydrogenase), peroxisomes (catalase), lysosomes (beta-N-acetyl-D-glucosaminidase), endoplasmic reticulum (neutral alpha-aminidase), cytosol (lactate dehydrogenase). 4. This technique can be applied to investigate disease of the gastric antrum at a subcellular level.
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PMID:Subcellular fractionation studies of human gastric antrum: localization of the mucosal peptide hormones. 611 May 6

Optical diffraction analysis was carried out on crystalline inclusions in the rough endoplasmic reticulum of the insulin and somatostatin cells in the islet organ of the hagfish. A striking difference in crystalline arrangement was observed between the inclusions of the insulin and somatostatin cells. The crystallographic arrangement of the inclusions observed in situ in the insulin cells differed from that previously found by means of X-ray diffraction analyses of hagfish insulin crystals formed in vitro.
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PMID:Optical diffraction analysis of crystalline inclusions in the rough endoplasmic reticulum of islet parenchymal cells of the hagfish, Myxine glutinosa. 612 67

The biosynthesis of somatostatin has been studied at the ultrastructural level in pancreatic islets by using rabbit antiserum against synthetic somatostatin. To document that the antiserum specifically bound preprosomatostatin, we have tested the ability of the antiserum to precipitate the product synthesized in vitro. Poly(A) enriched RNA isolated from catfish islets was translated in both the wheat germ extract and nuclease-treated reticulocyte lysate systems. It was found that the in vitro translation product, preprosomatostatin, could be recognized by the antibody against synthetic somatostatin. The morphological study was then performed by immunoelectron microscopy by using the Fab-peroxidase conjugate technique. In dog pancreatic islets, somatostatin immunoreactive reaction product was seen only in the delta cells. In these cells, they were detected on bound ribosomes, in the cisternae of the rough endoplasmic reticulum (ER) and Golgi apparatus, in the Golgi associated vesicles, and in secretory vesicles. These findings suggest that somatostatin precursor molecules are synthesized on bound ribosomes and discharged into the cisternae of the rough ER. They are then transported to the Golgi apparatus and transferred to the secretory vesicles for secretion. The different staining intensities in the secretory vesicles would suggest that the processing of the precursor molecules of somatostatin probably takes place in the secretory vesicles.
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PMID:Immunoelectron microscopic study of somatostatin biosynthesis in dog pancreas. 613 5

An unusual thyroid carcinoma is described, showing structural, histochemical and radioimmunologic features of both a follicular and a parafollicular cell carcinoma. Radioimmunoassay revealed high levels of thyroglobulin in the patient's serum and in extracts from metastatic tumor tissue. Immunoreactive thyroglobulin was demonstrated histochemically in tumor cells. On scanning, pulmonary metastases showed uptake of 131I. Somatostatin and neurotensin immunoreactivity was also revealed histochemically in the tumor and a large proportion of the neoplastic cells were argyrophil. Serum calcitonin level was normal and no immunoreactive calcitonin was found in tumor tissue by radioimmunoassay or histochemically. Light microscopy showed cribriform patterns suggestive of follicular carcinoma as well as solid areas reminiscent of medullary carcinoma. Electron microscopy revealed two types of tumor cells. One type had electron dense granules resembling secretory granules characteristic of polypeptide hormone and/or monoamine producing endocrine cells. The other type had no such granules but showed a prominent vesicular rough endoplasmic reticulum similar to that seen in neoplastic follicular cells. The results suggest two alternative possibilities regarding the histogenesis of the tumor. One would be a mixed neoplasm, resulting from a coincidental malignant change in both follicular and parafollicular thyroid cells. The other, more likely alternative would be that the tumor cells are derived from a common stem cell with the potentiality of differentiating into both follicular and parafollicular adult cells. The finding that both thyroglobulin and somatostatin or neurotensin immunoreactivity occurred together in some tumor cells supports the latter possibility and suggests that at least some follicular and parafollicular cells may have a common precursor origin.
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PMID:A compound follicular-parafollicular cell carcinoma of the thyroid: a new tumor entity? 613 20

Apart from the known hypothalamic controls, which have been well documented, a myriad of compounds both endogenous and exogenous have proved effective in influencing secretion of prolactin (PRL). Recent studies have shown that somatostatin (SRIF), when injected intra-atrially as a bolus, is able to inhibit PRL secretion in vivo. However, the inhibitory effect of SRIF occurs only in adenohypophyses previously primed with estradiol. This research was undertaken to examine the ultrastructural effects of that inhibition using male Sprague-Dawley rats primed for three weeks with subcutaneous implants of estradiol. Within 2 min of injection of SRIF (1 mg/kg), the adenohypophyses were removed and processed for electron microscopy. We found dramatic changes in the estradiol-primed mammotrophs, including 1) an apparent rearrangement of rough endoplasmic reticulum (RER) into concentric cisternae, and 2) the appearance of intracellular bodies closely associated with granules. These changes were not observed in non-estradiol-primed male rats injected with SRIF which is consistent with the fact that in the normal male rats, SRIF failed to inhibit PRL secretion. These findings suggest that SRIF causes reorganization of cellular organelles so that PRL granules are sequestered thereby inhibiting secretion of PRL.
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PMID:Ultrastructural changes rapidly induced by somatostatin may inhibit prolactin release in estrogen-primed rat adenohypophysis. 613 30

Previous studies showed a rapid decrease of somatostatin concentration in the gut and an increase in serum gastrin levels after a single dose of the duodenal ulcerogen cysteamine. An attempt was made to identify morphologic changes that would correlate with these functional changes. Rats were killed 1, 4, 8, or 24 hr after a single dose of cysteamine and sections of gastric mucosa and pancreas were processed for electron and light microscopy. Subtle ultrastructural alterations were seen in D cells of the stomach (e.g., dilation of mitochondrial cristae and endoplasmic reticulum, and apparent increase in electron density of secretory granules) after cysteamine administration. The number of somatostatin-positive cells visualized by the immunoperoxidase technique using light microscopy was decreased in 1-4 hr but returned to normal by 24 hr. The alterations observed in the G cells after cysteamine administration are consistent with release of gastrin from mature granules and increased synthesis of the hormone. The lack of major morphologic changes in the D cells suggests that cysteamine affects somatostatin without causing cell necrosis or alteration in lysosome formation. The effect of the drug may thus be mediated at the biochemical level without marked morphologic alterations.
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PMID:The effect of the duodenal ulcerogen cysteamine on somatostatin and gastrin cells in the rat. 613 3

Twelve cases of thymic carcinoid were studied by electron microscopy and immunohistochemistry. Clinically, all of them presented either as asymptomatic, radiographically detected mediastinal masses or as neoplasms producing symptoms of thoracic structural displacement or Cushing's syndrome. By light microscopic examination, the carcinoids manifested an organoid growth pattern, being composed of uniform polygonal cells with central, oval nuclei and finely dispersed chromatin. Immunohistochemical analysis disclosed the presence of cytoplasmic adrenocorticotropic hormone in four cases (three associated with Cushing's syndrome), of somatostatin in seven cases, and of serotonin in one case. Ultrastructurally, these tumors generally showed short, blunt, interdigitating cell processes; focal, scanty basement membrane material; infrequent but well-formed junctional complexes; moderate to large numbers of dense-core granules; and lipoautophagosomes. Six tumors contained small numbers of type I microfilaments, and three demonstrated perinuclear whorls of type II microfilaments. Rough and smooth endoplasmic reticulum was well developed in each tumor, the smooth form being prominent in cases with clinical Cushing's syndrome.
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PMID:Thymic carcinoid. A histologic, immunohistochemical, and ultrastructural study of 12 cases. 614 Oct

After finding that ergocristine and somatostatin can cause extensive changes in mammotroph ultrastructure within 2 min of administration, we chose dopamine, the putative physiological prolactin-inhibiting factor, to correlate ultrastructural changes to inhibition of prolactin release. In order to choose a dose of dopamine for this study we tested the effects of 2 doses of dopamine (10 and 1,000 micrograms/kg) on inhibition of prolactin release. The higher dose of dopamine (1,000 micrograms/kg) completely inhibited prolactin release immediately (in less than 2 min) and maintained complete blockage for a period of 14 min. For the ultrastructural study we injected dopamine (1,000 micrograms/kg) in the right atrium of conscious free-moving rats through indwelling cannulae, and killed the rats by decapitation 2 min after dopamine administration. The following changes in mammotrophs were observed after the dopamine treatment: (1) increased numbers of secretory granules, (2) peripheral relocation of rough endoplasmic reticulum, and (3) increased numbers of 'intracellular bodies' (putative prolactin granule disposal system) associated with secretory granules. Because these rapid ultrastructural changes have been observed after treatment with three different compounds (dopamine, somatostatin and ergocristine), we do not believe that they are the unique effect of any one compound but the common denominator of the three compounds, i.e., inhibition of prolactin secretion being closely linked to the ultrastructural changes. We thus propose that the extensive ultrastructural changes that occurred in such a short period of time following dopamine administration are the mechanism of inhibition of prolactin release.
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PMID:Dopamine creates a physical barrier to inhibit prolactin release in mammotrophs of estradiol-primed male rats. 683 77


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