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)

Novel islet cell, duct cell, and acinar cell markers have been identified by monoclonal autoantibodies (Maab) derived from prediabetic BB rats. Spleen cells from two rats that both developed diabetes after splenectomy were fused with mouse myeloma cells. A cellular immunoradiometric assay for differential reactivity toward the surface of two closely related, insulin- and non-insulin-producing rat islet tumor cell lines was used to select and clone several IgM-producing hybridomas. The supernatants were finally characterized by two-color immunofluorescence with islet hormone antisera on frozen sections of human, monkey, and rat pancreas. Maab EB52 stained PP cells, but also few A cells on rat pancreas. Maab CA812 identified a subpopulation of islet D cells on rat, human and monkey pancreas. Although the CA812-reactive antigen and somatostatin were coexpressed in most D cells in adult rat pancreas, only a few islet D cells were stained in the newborn pancreas. The CA812-reactive antigen was not detected in somatostatin-producing cells in the duct epithelium. Maab H37 and IF5 selectively stained acinar cells in rat, human, and monkey pancreas, whereas Maab DA39 identified the rat ductal epithelium including the scattered endocrine cells of the ducts. In summary, B lymphocytes producing autoantibodies to pancreatic endocrine, exocrine, and ductal markers are present in prediabetic BB rats and can be detected by use of transformed pluripotent islet cells as target. Such B lymphocytes can be immortalized to produce monoclonal antibodies to study their role in insulin-dependent diabetes mellitus pathogenesis and to clarify the development of the pancreas.
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PMID:Novel islet, duct, and acinar cell markers defined by monoclonal autoantibodies from prediabetic BB rats. 212 46

Spleen cells from acutely diabetic (AD) and non-diabetic but diabetes prone (DP) BB/Wor rats lysed insulinoma target cells to a significantly greater degree than did diabetes resistant (DR) cells as determined using a 51Cr release cytotoxicity assay. There were no differences between the AD and DP groups. Lysis was not target cell specific, since somatostatin secreting RIN 14B cells, Wistar Furth leukemia cells designated LW12, PC12 cells and NK sensitive YAC-1 cells were also lysed. Lysis of all target cells was significantly reduced by pretreatment of the effector lymphocytes with antiserum to NK cells (anti-asialo GM1) and complement suggesting that NK cells mediated destruction of these cells. These data demonstrate a generalized increase in non-specific NK cell activity in BB/Wor rats. Since NK cells have been shown to mediate antibody dependent cell mediated cytotoxicity (ADCC), splenic lymphoid cells from AD rats were tested for their ability to lyse insulinoma target cells in the presence of diabetic rat sera which were demonstrated to contain islet cell surface antibodies. Three different ADCC protocols were tested but in each case the addition of serum dilutions from AD rats reduced the lysis of insulinoma cells by AD spleen cells in a dose dependent manner. This inhibition was also demonstrated when sera and effector cells from control rats were used. As a positive control, DR spleen cells were incubated with 51Cr labelled target cells that were untreated or pre-treated with anti-rat class 1 antibody (OX18). Pre-treatment of the target cells resulted in a marked increase in their subsequent lysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vitro natural killer cell activity in the spontaneously diabetic BB/Wor rat: effects of serum on lysis of insulinoma cells. 285 69

Substance P (SP) and somatostatin 1-14 (SOM) have immunoregulatory properties. Cells within the granulomas of murine schistosomiasis mansoni make both. SP enhances, whereas SOM inhibits soluble egg Ag (SEA)-induced, IFN-gamma production. IFN-gamma is important during IgG2a isotype switching. Thus, we investigated whether SP or SOM could affect IgG2a production in murine schistosomiasis. Our results show that SEA and rIFN-gamma stimulate splenic IgG2a secretion in murine schistosomiasis. Moreover, SP at > or = to 10(-10) M substantially increased both polyclonal as well as SEA-specific, IgG2a secretion from spleen cells challenged with SEA. However, cells exposed to SOM at > or = 10(-10)M showed strong inhibition. Also, both SP and SOM modulated the frequency of IgG2a-producing cells. Splenic IgG2a production in response to SEA, SP, and SOM required the presence of Thy 1.2+ cells, whereas, rIFN-gamma- induced IgG2a synthesis did not. Also, experiments using irradiation lymphocytes showed that SP, SOM, or rIFN-gamma modulation of IgG2a release was not dependent on cell proliferation. The highly specific SP receptor antagonist, CP-96,345, completely inhibited the effect of SP but not SOM on IgG2a release. This suggests that SP acted through an authentic NK-1 receptor and that SOM required a different receptor interaction. Granuloma cells secreted IgG2a constitutively. Yet, neither SEA, SP, SOM, rIFN-gamma, nor blocking anti-IFN-gamma mAb could modulate this constitutive IgG2a release during short term culture conditions. Moreover, the IgG2a secretion also continued in the absence of Thy 1.2+ lymphocytes. However, mice treated with CP-96,345 or octreotide (SOM agonist) in vivo produced granulomas that made little or no IgG2a. Spleen cell experiments showed that SEA, SP, SOM, and rIFN-gamma could only affect SEA-induced, IgG2a production during early stages of Ag stimulation. Thus, unlike the spleen, it is probable that the granulomas contain mostly activated B cells that have completed switch recombination.
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PMID:Substance P and somatostatin can modulate the amount of IgG2a secreted in response to schistosome egg antigens in murine schistosomiasis mansoni. 750 19

Spleen cells from a Robertsonian mouse immunized with rat alpha-CGRP were fused with FOX-NY cells to induce hybridoma cells. Antibody activities were screened by radioimmunoassay, and hybridomas producing high affinity antibodies were cloned by limiting dilutions. Ascites were produced from the highest affinity clone in pristine-primed Balb/c mice. Ascites fluid contained approximately 20 mg/ml IgG which was of subclass IgG2a as determined by immunodiffusion analysis. The titer of this IgG2a antibody titled #4901, was 1:2,000,000 and the ID50 for rat alpha-CGRP, rat beta-CGRP and human alpha-CGRP were 350, 4000, and 4500 pg/ml respectively. Protein A purified CGRP antibody #4901 (5-10 mg/kg) completely abolished the portal release of somatostatin and the inhibition of gastric acid secretion induced by intravenous infusion of rat alpha CGRP (15-20 micrograms/kg/h) in anesthetized rats. The unpurified antibody (25 mg/kg) also prevented the fall in mean arterial blood pressure and the increase in heart rate caused by intravenous injection of rat alpha-CGRP. Immunohistochemistry showed that CGRP monoclonal antibody stains nerve fibers and endocrine-like cells in the pancreas, and neuronal elements in the gastrointestinal tract. These results show that CGRP monoclonal antibody #4901, which is relatively specific for rat alpha-CGRP, is useful for in vivo immunoneutralization of CGRP and is also an excellent reagent for immunohistochemical localization of alpha- and beta-CGRP in mammals.
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PMID:Monoclonal antibody to rat alpha-CGRP: production, characterization, and in vivo immunoneutralization activity. 809 20

Cystic neoplasms of the pancreas are an uncommon entity comprising fewer than 1 per cent of all pancreatic neoplasms. The guidelines for management of these tumors, specifically, the extent of resection, are unclear. Formerly, a distal pancreatectomy including the spleen was performed for tumors in the tail of the pancreas. The importance of preserving the spleen has been well documented; however, there are few reports of spleen-preserving pancreatectomy for cystic neoplasms of the distal pancreas. We report two patients who underwent spleen-preserving pancreatectomy for mucinous cystic neoplasms in the tail of the pancreas. Both patients were female, ages 39 and 65 years. Preoperative preparation included administration of vaccinations and subcutaneous somatostatin. Operative technique emphasized division of the splenic artery and vein beyond the tip of the distal pancreas without mobilization of the spleen. The pancreas was transected with a vascular stapler. Fibrin glue was applied to the margin of the pancreas. The operative blood loss, duration of operation, and postoperative hospital stay were 150 and 250 mL, 150 and 180 minutes, and 7 and 9 days, respectively. The pathology revealed both lesions to be mucinous cystic neoplasms. The patients recovered and at 6-month follow-up were without complaints and in good health. Spleen-preserving pancreatectomy is rapid and associated with minimal morbidity. This procedure should be considered in the surgical management of cystic neoplasms in the tail of the pancreas.
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PMID:Spleen-preserving pancreatectomy for cystic pancreatic neoplasms. 1036 17