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)

Somatostatin was compared with intensive antacid and thrombin in a randomised controlled study on 15 patients with severe haemorrhages of the upper digestive tract deriving from peptic ulcers and identified endoscopically in order to assess the efficacy of the two drugs. The results in both groups were similar but somatostatin appeared more effective than antacids and thrombin in terms of blood transfusions required and the average time it took to stop the bleeding. The insignificance of these results is in contrast with the data from similar studies using other drugs (anti-H2) and reported by others. This shows the need for controlled polycentric studies conducted on large groups of homogeneous patients.
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PMID:[Somatostatin in severe peptic ulcer hemorrhage]. 286 63

The effect of somatostatin on haemostasis in the dogs was tested. The following data could be found: marked shortening of clotting time, decrease of platelet count, decrease of fibrinogen, level, an increase of plasma euglobulin fibrinolytic activity, prolongation of thrombin time and consumption of plasminogen. The obtained results indicate a biphasic haemostatic reaction, first hypercoagulability and then hypocoagulability. The presented results are briefly discussed with some remarks to clinical practice.
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PMID:The effect of somatostatin on haemostasis in dogs. 616 6

The heterodimer Ku, first described as a nuclear autoantigen, is a regulatory factor of DNA replication and transcription. We have expressed the p86 subunit of Ku in Escherichia coli as a fusion protein with glutathione-S-transferase, using the vector pGEX-2T. After splitting up by thrombin, p86 was isolated by Sephacryl S200 gel filtration. The recombinant protein was found to have the same electrophoretic migration and to react with the same monoclonal antibody as the somatostatin-binding protein we recently isolated from the human gastric tumor cell HGT1 [7]. Furthermore, using the analog [125I]Tyr-11 somatostatin-14 as a tracer, we found that, like the HGT1 cell-purified protein, recombinant p86 specifically bound somatostatin with high affinity (KD = 2.3 +/- 0.3 nM) and large capacity (10,300 +/- 1,700 pmol/mg protein). These findings suggest that p86 subunit of Ku stands for the protein we previously isolated from the HGT1 cell. It could represent a new somatostatin receptor subtype perhaps involved in the antimitogenic effect of this peptide.
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PMID:Somatostatin specifically binds p86 subunit of the autoantigen Ku. 752 16

Fig 2 gives an algorithm for the treatment of bleeding oesophageal varices. Initial resuscitation of the patient is of paramount importance, ideally followed by early interventional endoscopy. Recent advances in available endoscopic techniques enable the endoscopist to suit the therapeutic approach to the clinical situation. Injection sclerotherapy remains the initial treatment of choice in bleeding patients. Endoscopic banding ligation is an alternative, best used in patients who have spontaneously stopped bleeding or as a complementary treatment a few days after the initial session of injection sclerotherapy. The tissue adhesives and thrombin can be used to treat bleeding gastric varices. [table: see text] Should the endoscopic expertise not be available, drug treatment (with somatostatin or octreotide) or balloon tamponade are the treatments of choice. Transjugular intrahepatic portal-systemic stent shunt is a new effective technique, not yet widely available, which has a documented complication rate that has yet to be fully defined. It is a good alternative to surgery as a "rescue" procedure for patients who continue to bleed despite two sessions of endoscopic intervention.
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PMID:Management of variceal haemorrhage. 818 May 41

Fastidious resuscitation is essential in the initial management of acute variceal bleeding and requires adequate monitoring. Where endoscopic services are available diagnostic endoscopy should be performed ideally within 4-6 hours of admission and endoscopic therapy with injection sclerotherapy or binding ligation performed. Treatment to prevent early rebleeding will require further endoscopic treatment and possibly adjuvant vasoconstrictor therapy (somatostatin/octreotide or glypressin). Where endoscopy is unavailable vasoconstrictor therapy and/or balloon tamponade should be started prior to transfer to a centre with endoscopic facilities. Treatment failures should be considered for TIPSS or surgery. Gastric varices are better treated endoscopically with bovine or human thrombin than sclerotherapy. For prevention of rebleeding, variceal obliteration with endoscopic band ligation or prophylactic beta blockade are the two optimal treatments, although candidates may be identified for TIPPS if rebleeding recurs. Only beta blockers have so far been shown to be of value as primary prophylaxis.
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PMID:The management of variceal bleeding. 880

Endoscopic treatments for bleeding gastroesophageal varices include injection sclerotherapy, variceal obturation with tissue adhesives, and variceal rubber band ligation. Acute injection sclerotherapy remains a quick and simple technique for the control of active bleeding from esophageal varices. Although few trials have been published so far, some evidence suggests that the early administration of vasoactive drugs (somatostatin, octreotide, or terlipressin) is safe and may increase the efficacy of endoscopic treatments. Banding ligation is the optimal endoscopic treatment for the prevention of rebleeding from esophageal varices. The use of tissue adhesives and thrombin as injectates to treat bleeding fundal gastric varices and esophageal varices not responding to vasoactive drugs or sclerotherapy is promising but needs further assessment by means of randomized controlled trials. As of today, endoscopic treatments are not recommended for the primary prophylaxis of variceal bleeding.
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PMID:Endoscopic treatments for portal hypertension. 1064 28

Somatostatin regulates multiple biological functions by acting through a family of five G protein-coupled receptors, somatostatin receptors (SSTRs) 1-5. Although all five receptor subtypes inhibit adenylate cyclase activity and decrease intracellular cAMP levels, specific receptor subtypes also couple to additional signaling pathways. In CCL39 fibroblasts expressing either human SSTR1 or SSTR2, we demonstrate that activation of SSTR1 (but not SSTR2) attenuated both thrombin- and integrin-stimulated Rho-GTP complex formation. The reduction in Rho-GTP formation in the presence of somatostatin was associated with decreased translocation of Rho and LIM kinase to the plasma membrane and fewer focal contacts. Activation of Rho resulted in the formation of intracellular actin stress fibers and cell migration. In CCL39-R1 cells, somatostatin treatment prevented actin stress fiber assembly and attenuated thrombin-stimulated cell migration through Transwell membranes to basal levels. To show that native SSTR1 shares the ability to inhibit Rho activation, we demonstrated that somatostatin treatment of human umbilical vein endothelial cells attenuated thrombin-stimulated Rho-GTP accumulation. These data show for the first time that a G protein-coupled receptor, SSTR1, inhibits the activation of Rho, the assembly of focal adhesions and actin stress fibers, and cell migration.
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PMID:Somatostatin, acting at receptor subtype 1, inhibits Rho activity, the assembly of actin stress fibers, and cell migration. 1204 95

Although the interleukin (IL)-1 receptor is densely distributed in the leptomeninges constituting the blood/cerebrospinal fluid barrier, its physiologic significance has remained unclear. In the present study, we show that in cultured leptomeningeal cells, IL-1beta, tumor necrosis factors, or lipopolysaccharide causes a prominent increase in the synthesis and release of prostaglandin (PG) D synthase, which catalyzes the final step in the biosynthesis of PGD2. Although significant increases in the amount of PGD synthase were also observed with cells exposed to somatostatin, thrombin, or ciliary neurotrophic factor, these were much smaller than were those induced by the proinflammatory cytokines. Other agents tested including IGF-I had no effect upon the enzyme levels in the culture media. Furthermore, we found that the increased secretion of PGD synthase by IL-1beta was completely inhibited by 10(-7) M PGE2. The same dose of PGD2 or 15-deoxy-Delta(12-14)PGJ2 had no effect upon the IL-1beta action. In addition, PGE2 increased the level of fibronectin and eliminated the expression of zonula occludentes-1, a tight junction-associated protein from cultured cells, effects likely reflecting a loss of barrier integrity. These results demonstrate the importance of inflammatory stimuli as a physiologic regulator of the leptomeningeal cell function.
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PMID:Effects of interleukin-1beta and prostaglandin E2 on prostaglandin D synthase production in cultivated rat leptomeningeal cells. 1508 10

The tissue factor (TF) pathway is the primary mechanism for initiation of blood coagulation. Circulating blood contains TF, which originates mainly from monocytes and is thrombogenic. The presence of somatostatin (SMS) receptors on monocytes suggests the possibility that SMS may regulate TF synthesis and/or release. Circulating TF procoagulant activity (TF-PCA), factor VIIa activity (FVIIa; clotting assays), TF antigen (TF-Ag; ELISA), prothrombin fragment 1.2 (F1.2), thrombin-antithrombin complexes (ELISAs), CD40 ligand expression on platelets, and monocyte-platelet aggregates (flow cytometry) were determined in blood from normal volunteers undergoing 24 h of basal glucose/basal insulin (BG/BI) clamps and high-glucose/high-insulin (HG/HI) clamps with and without SMS. Infusions of SMS under basal conditions (BG/BI) raised TF-PCA 1.8-fold (P < 0.03), TF-Ag 2.3-fold (P < 0.001), and TF expression on monocytes by 36% (P < 0.001) and decreased plasma levels of FVIIa by 30% (P < 0.001). Infusion of SMS reduced the 8.6-fold HG/HI-induced increase in TF-Ag by 26% and the 8.6-fold increase in TF-PCA by 100%. SMS also prevented the 60% increase in TF expression on monocytes, the 2.2-fold increase in F1.2, the 40% increase in CD40L expression on platelets, and the 17% increase in monocyte-platelet aggregates seen during HG/HI. We conclude that SMS completely prevented HG/HI-induced TF activation in normal volunteers and may be of use to reduce the procoagulant state and acute vascular events in hyperinsulinemic insulin-resistant patients with type 2 diabetes.
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PMID:Differential effects of somatostatin on circulating tissue factor procoagulant activity and protein. 1721 71

Tissue factor (TF) is the primary initiator of blood coagulation. Circulating TF procoagulant activity (TF-PCA) is associated with blood cells and microparticles and is elevated in patients with type 2 diabetes mellitus. Combined hyperinsulinemia and hyperglycemia and to a lesser degree selective hyperinsulinemia for 24 hours in healthy volunteers increased circulating TF-PCA, monocyte TF surface expression and mRNA, plasma thrombin generation, and coagulation factors VII and VIII activities, suggesting that the coagulation system had been activated. In addition, platelet CD40L and platelet-monocyte aggregates increased, indicating platelet activation. Somatostatin abolished these changes. We conclude that hyperinsulinemia, but particularly the combination of hyperinsulinemia and hyperglycemia, creates a prothrombotic state and may, in addition, be proinflammatory and proatherogenic by virtue of the actions of CD40L and TF.
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PMID:Effects of hyperglycemia and hyperinsulinemia on the tissue factor pathway of blood coagulation. 1754 39


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