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)

This review integrates the clinical aspects of systemic sclerosis (SSc; scleroderma) and scleroderma-like conditions with new knowledge of the control of blood vessel tone and the role of anoxia in the activation of connective tissues leading to fibrosis. Serologic tests, high resolution computed tomographic scanning, bronchoalveolar lavage, and physiologic assessment of pulmonary gas diffusion are compared as diagnostic tools and as means of quantitating internal organ involvement. Treatment of Raynaud's disease and phenomenon, management of scleroderma renal crisis, and new means for improving gastrointestinal function with octreotide, the somatostatin analogue, also are discussed. The relationship between idiopathic forms of SSc and eosinophilic fasciitis/eosinophilia-myalgia syndrome caused by L-tryptophan ingestion and the scleroderma-like disease associated with silicone breast implants also is discussed.
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PMID:The many faces of scleroderma. 135 85

This short review examines two examples of studies into the mechanisms of allergic responses which have particular relevance to inflammation research. The first is the ability of human skin mast cells, but not those derived from lung, adenoids, tonsils or intestine, to release histamine in response to stimulation by neuropeptides including substance P, vasoactive intestinal polypeptide (VIP) and somatostatin. The neuropeptide activation site does not appear to be a classical tachykinin receptor but rather a binding site of low affinity and low specificity capable of interacting with neuropeptides and compounds with similar physicochemical characteristics. In contrast to IgE-dependent activation, neuropeptide stimulation of skin mast cells induces a rapid release of histamine with minimal generation of PGD2 and LTC4. This pseudo-allergic reaction is thought to underlie the weal and flare response in the skin and may have a role in urticaria. The second example describes studies to elucidate the mechanisms of the late asthmatic response by use of a guinea-pig model. As in man, both early and late phase responses in the guinea-pig are inhibited by sodium cromoglycate whereas only the early response is inhibited by the beta-adrenoceptor stimulant drug salbutamol. Examination of bronchoalveolar fluid has shown a temporal relationship between an airways neutrophilia and the late response. However, pharmacological manipulation and the use of an anti-neutrophil serum has shown that these events are not interdependent. The role of the airways eosinophilia requires further investigation.
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PMID:Allergy or inflammation? From neuropeptide stimulation of human skin mast cells to studies on the mechanism of the late asthmatic response. 265 5

The factors responsible for in vivo eosinophil recruitment are poorly defined, although T-lymphocytes appear to be involved in the etiology of eosinophilia. In order to clarify this relationship, we studied the modulation of eosinophil mobilization in the rat after immune challenge, by chronic treatment with the PAF-antagonist, BN 52021, the somatostatin analog, BIM 23014 and with Cyclosporin A (CsA). In rats made hypereosinophilic by pretreatment with cyclophosphamide or sephadex, a significant increase of the eosinophil count in blood and peritoneal fluid was induced by anaphylactic reaction. CsA totally abolished both hypereosinophilia and peritoneal eosinophil infiltration. BIM 23014 also, significantly reduced the circulating eosinophils (-68%, p less than 0.001) and cell infiltration (-86%, p less than 0.05). In contrast, BN 52021 decreased peritoneal eosinophil recruitment, while having relatively little effect on circulating cells. CsA and somatostatin are known to affect T-cell proliferation, and as T-cells are involved in the differentiation of hematopoietic cells into eosinophils, these drugs could decrease eosinophil availability for recruitment. In contrast, the PAF antagonist may act by inhibiting PAF-induced eosinophil chemotaxis, providing a more specific inhibition of this process than that exerted by CsA, BIM 23014 and other immunosuppressive agents.
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PMID:Modulation of eosinophil recruitment in the rat by the platelet-activating factor (PAF) antagonist, BN 52021, the somatostatin analog, BIM 23014, and by cyclosporin A. 274 16

The changes of somatostatin (SS)--like immunoreactive cells and morphology were observed in the models of ligation of right MCA and bilateral ligation of CCA respectively. The results showed: (1) a decline of SS immunoreactive nerve cell profiles in right cerebral cortex after 3h ligation of MCA as compared with left cerebral cortex and sham-operated group, while no significant difference was found between RSM-treated and saline-treated groups; (2) selective ischemic cell changes in cerebral cortex, hippocampus and caudate nucleus after 3h ligation of CCA. The changes included shrinkage and condensation of perikaryon, nuclear pyknosis, cytoplasmic eosinophilia in some neurons. The ischemic changes were more severe in saline-treated group than RSM-treated group. The experiments indicated that the selective ischemic cell changes could be improved by RSM, suggesting that treatment to modulate SS metabolism may be indicated after ischemic insults.
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PMID:Evidence for amelioration of cellular damage in ischemic rat brain by radix salviae miltiorrhizae treatment--immunocytochemistry and histopathology studies. 809 33

There are several indications for an involvement of neuroexcitatory mechanisms in ischemic neuron damage. Since we forwarded the hypothesis in 1982 that the transmitter glutamate is playing a key role, several lines of evidence have substantiated this: there is a pronounced transmitter release induced by ischemia and there is uptake of Ca++ via NMDA-operated calcium channels. Under certain circumstances postischemic neuron death can be impaired by administration of either NMDA-antagonists or calcium blockers. Further proof for the induction of harmful excitatory mechanisms by ischemia has been obtained by preischemic denervation of the vulnerable nerve cells. After transient cerebral ischemia in rats or gerbils, there are signs of irreversible damage (eosinophilia) of neurons in the dentate hilus (somatostatin-positive cells) after 2-3 hours and of hippocampal pyramidal neurons after 2-3 days (delayed neuron death). In the first case, removal of the (main) input to hilus cells by degranulation (colchicine selectively eliminates granule cells) protects these. In the case of pyramidal neurons removal of Schaffer collaterals/commisurals or input from the entorhinal cortex have a protective effect. Recently, we have measured glutamate and calcium in CA1 of denervated rats during 10 min of ischemia, and it turns out that there is almost no extracellular glutamate release or lowering of calcium in contrast to ischemic animals with intact innervation. Also in the postischemic period there are indications of a continuation of the damaging processes induced by ischemia. Besides the well known postischemic hypoperfusion, a prolonged release of glutamate has been reported, as well as burst firing in some models.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ischemia as an excitotoxic lesion: protection against hippocampal nerve cell loss by denervation. 838 Jun 75

A pancreaticopleural effusion is a rare complication of chronic pancreatitis. Fasting, a protease inhibitor, and/or a surgical intervention are generally selected for the treatment of the pancreatic effusion. We reported here the case, in which octreotide acetate was effective for resolving pancreatic effusion. A 67-year-old man was admitted with a massive pleural effusion. This effusion contained a high level of amylase. Endoscopic retrograde pancreatography followed by computed tomography revealed a pancreaticopleural fistula. The pleural effusion was not improved by the treatment of the protease inhibitor with total parenteral nutrition and fasting. A pancreatic stent could not be emplaced because the major pancreatic duct was coiled. Administration of octreotide acetate, a long-acting somatostatin analogue, markedly diminished the effusion and closed the pancreaticopleural fistula. Transient eosinophilia of peripheral blood was seen on admission, but the number of eosinophils decreased after the octreotide therapy and normalised when pleural effusion disappeared. Octreotide is one of the effective options for the treatment of pancreatic pleural effusion.
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PMID:Marked effect of octreotide acetate in a case of pancreatic pleural effusion. 1119 Oct 6