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 made a mutated progastrin cDNA construct that contains a cleavage site (-Arg(-4)-Arg(-3)-Lys(-2)-Arg-1) specific for the Kex2-like endoprotease furin, located ahead of the bioactive gastrin. For expressing the mutated progastrin cDNA, we used two non-endocrine cell lines, CHO and COS-7. CHO cells exhibit amidating enzyme activity and levels of amidation enzyme mRNA as high as those in the pituitary-derived endocrine cell line GH3, whereas COS-7 cells have far less amidating activity and lower amounts of mRNA. Mutant progastrin-expressing CHO cells produced mostly amidated gastrin. Gel filtration showed the size of this gastrin corresponded to that of the synthetic human gastrin-17. In contrast, COS-7 cells produced glycine-extended gastrin and only a small amount of amidated gastrin. The difference in the amount of amidated gastrin products produced by the two non-endocrine cell lines is due to differing amounts of the amidation enzyme contained in each cell line.
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PMID:Production of bioactive gastrin from the non-endocrine cell lines CHO and COS-7. 827 7

A 4-yr-old cheetah (Acinonyx jubatus) with a 2-yr history of chronic intermittent vomiting and spiral bacteria-associated gastritis presented with dramatically increased vomiting frequency and marked intermittent abdominal distention. Physical examination revealed loss of muscle mass and poor fur coat quality. Contrast radiography was consistent with delayed gastric emptying due to presumed gastric outlet obstruction. Both Y-U pyloroplasty and incisional gastropexy were performed, and no subsequent vomiting has been observed for 3 yr with the exception of three episodes during the immediate postoperative period. The cause of delayed gastric emptying was not determined, although a gastric motility disorder associated with gastric bacterial infection and elevated gastrin levels was suspected.
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PMID:Use of pyloroplasty (Y-U) to treat presumed delayed gastric emptying in a cheetah (Acinonyx jubatus). 1142 4

Neuroendocrine tumors (NETs) represent a large group of neoplasms deriving from pluripotent stem cells or from differentiated neuroendocrine cells that are characterized by the expression of different peptides and biogenic amines. These rare tumors tend to grow slowly and are notoriously difficult to localize, at least in the early stages. Diagnostics involve blood, urine and biochemical examination as well as imaging modalities. Imaging is achieved by a variety of techniques such as radiological morphological imaging methods, for example, sonography, computerized tomography (CT)/magnetic resonance imaging (MRI), angiography and finally, nuclear functional imaging methods such as metaiodobenzylguanidine (MIBG), somatostatin receptor scintigraphy (SRS), vasoactive intestinal peptide receptor scintigraphy (VIPRS) and positron emission tomography (PET) using (18)F labeled deoxyglucose (FDG) and fluorinated dihydroxyphenylalanine ((18)F-DOPA) as a radioisotopic marker. (131)I-labeled MIBG is a well-established radiopharmaceutical for localization and therapy of phechromocytoma and paraganglioma. The majority of neuroendocrine tumors possess a high density of somatostatin receptors. This observation provided the basis for the development of various radiolabeled somatostatin peptide analogs as imaging agents and therapeutics in nuclear medicine. FDG-PET is now performed in a wide variety of tumors and indications, including diagnosis, staging, re-staging and evaluation of the response to treatment. (18)F-DOPA-PET may be useful if (18)F-FDG-PET scan result is negative. (99m)Tc-pentavalent dimercaptosuccinic acid ((99m)Tc-DMSA-V) or (99m)Tc sestamibi ((99m)Tc-MIBI) or (99m)Tc-tetrofosmin is used only for diagnosis of certain NETs such as medullary thyroid cancer. The expiences with other nuclear medicinie imaging and therapy modalities such as cholecystokinin (CCK)-B/gastrin-receptors, bombesin/gastrin-releasing peptide receptor scintigraphy are still limited, and further clinical studies are needed. The studies using vascular endothelial growth factor (VEGF) for tumor angiogenesis imaging, annexin-V for imaging apoptosis and agents for hypoxia imaging are still in an early stage and the clinical role for these agents needs to be defined. In conclusion, no single imaging technique identifies all the metastatic sites of NETs. The best results may be obtained with a combination of functional imaging such as PET or/and SRS and morphologic imaging with CT and/or MR imaging. Many molecular imaging and therapy modalities fur NETs are recently under investigation or being developed, the usefulness of these modalities, however, has to be evaluated by well-designed and multicentre studies.
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PMID:The radionuclide molecular imaging and therapy of neuroendocrine tumors. 1581 Aug 78