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

It has earlier been claimed that clinical improvement of patients with Parkinson's disease is obtained by treatment with NADH. This has to be verified by double-blind, clinical studies and measurement of biochemical effects of the treatment. In a double blind study five patients with clinically moderate Parkinson's disease were treated with NADH, 25 mg, given intravenously once a day for four days. Then they were given 25 mg NADH intramuscularly after 2 and 4 weeks. Disability scores were determined before each treatment and two weeks after the final injection. A control group (n = 4) with the same degree of Parkinson's disease obtained sodium chloride with the same schedule. According to the Unified Parkinson's Disease Rating Scale a tendency to clinical improvement was seen after the iv infusions in both treatment and placebo groups. However, the changes were not statistically significant, and no changes occurred during the following weeks. No changes were found neither in the study nor the control group regarding cerebrospinal fluid concentrations of dynorfin, metenkefalin, somatostatin, hydroxy-methoxy-phenylglycol, homovanillic acid and 5-hydroxyindole acetic acid. The results indicate that no great changes are obtained after short-term treatment of parkinsonian patients with NADH, neither clinically nor biochemically.
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PMID:Treatment of Parkinson's disease with NADH. 788 34

A dispersed culture of cells from the submucous plexus of the human small intestine has been developed to examine the localization, release, and molecular characteristics of somatostatin immunoreactivity. Forty percent of the submucosal neurones per ganglion in tissue sections and 35% of cells per group of cells in culture contained somatostatin immunoreactivity. Acetic acid extracts of culture contained 1990 +/- 809 pg somatostatin immunoreactivity/10(6) cells. Incubation of cultures with phorbol 12-myristate 13-acetate (beta PMA), an activator of protein kinase C, at concentrations up to 10(-6) M for 120 min increased the release of somatostatin immunoreactivity by up to 23 times the basal level, and up to 27 times the basal level when extracellular K+ was increased from 5 to 10 mM. Of the total somatostatin immunoreactivity released in response to beta PMA (10(-6) M, 10 mM K+), 59% was present in the medium after 30 min and 80% after 60 min. Basal release of somatostatin immunoreactivity could be reliably measured only after 120 min. The release of somatostatin immunoreactivity by beta PMA was not due to nonspecific membrane effects, since the inactive 4 alpha-phorbol at the same concentrations did not alter basal release. Greater than 90% of somatostatin immunoreactivity present in acid extracts of cultures and released by beta PMA eluted with the same retention time as synthetic somatostatin-14 on reverse-phase high-performance liquid chromatography.
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PMID:The release of somatostatin-14 from human submucosal ganglia in tissue culture. 790 78

The effects were investigated of cysteamine--a well known somatostatin depletor--on the pain induced by chemical stimuli in mice. Cysteamine injected intraperitoneally 4 h before the test at doses of 50 and 100 mg/kg reduced the second phase of the licking response which was induced by formalin injected into the hind paw. Furthermore, cysteamine administered at the doses of 10, 50 and 100 mg/kg reduced the writhing induced by acetic acid. Naloxone, yohimbine and CGP 35348 administered in cysteamine-pretreated animals were not able to change the cysteamine antinociceptive effects in the formalin test. Intrathecally injected somatostatin was able to revert the cysteamine antinociceptive effects in the second phase of the formalin test and in the writhing test, whereas intracerebroventricularly injected somatostatin reduced the antinociceptive effects induced by cysteamine in the second phase of the formalin test. Intrathecally injected cyclo(7-aminoheptanoyl-Phe-D-Trp-Lys-Thr[Bzl])--a reported somatostatin antagonist--increased cysteamine antinociceptive effects in the second phase of the formalin test and in the writhing test. These results suggest that somatostatin is involved in the effects of cysteamine on the nociceptive threshold.
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PMID:Effects induced by cysteamine on chemically-induced nociception in mice. 790 12

A 28-year-old man with a thyroid stimulating hormone/prolactin (TSH/PRL)-secreting pituitary macroadenoma is discussed in relation to dopamine D2 and somatostatin receptor single-photon emission tomography (SPET). The patient presented with decreased vision in the left eye as a result of a temporal visual field defect and with mild hyperthyroidism. Medical therapy was tried. A test dose of both octreotide and bromocriptine resulted in an acute reduction in serum levels of TSH, alpha-subunits and PRL, whereas there was no response to TRIAC. Somatostatin and dopamine D2 receptors were present on the tumour as visualised by SPET with the ligands indium-111 diethylene triamine penta-acetic acid (DTPA)-octreotide (111In-SMS) and iodine-123 iodobenzamide (123I-IBZM), respectively. Therefore, treatment with octreotide 150 micrograms t.i.d. subcutaneously and bromocriptine 10 mg b.i.d. orally was given for > 12 and > 6 weeks, respectively. Following this treatment the visual defects disappeared, although tumour size, as measured by CT scanning, and serum TSH levels did not decrease. SPET with 111In-SMS and 123I-IBZM after therapy revealed no change or a possible increase in somatostatin receptor binding potential and a possible decrease in dopamine D2 receptor binding potential. The lack of long-term effects of the medical treatment is discussed. It is concluded that a high somatostatin and dopamine D2 receptor binding potential in vivo in a TSH/PRL-producing adenoma does not necessarily predict a successful outcome of medical treatment.
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PMID:Imaging of dopamine D2 and somatostatin receptors in vivo using single-photon emission tomography in a patient with a TSH/PRL-producing pituitary macroadenoma. 833 37

Anesthetic management of a 75-year-old female with carcinoid syndrome is reported. She had a tumor on the ileum and multiple metastatic tumors in the both lobes of the liver. Levels of both plasma serotonin and urinary 5-hydroxyindole acetic acid (5-HIAA) were significantly elevated before the operation. Although she was treated with somatostatin-analogue percutaneously, the levels of these hormones did not decrease significantly. The partial resection of the small intestine was scheduled under general anesthesia. Before induction of general anesthesia, hydrocortisone and ulinastatin were administered intravenously to prevent the release of chemical mediators. Anesthesia was induced with ketamine, diazepam, and vecuronium, and maintained with nitrous oxide, oxygen and enflurane. There was mild bronchospasm at the beginning of the surgery and the blood pressure was unstable during the operation, but anesthetic course was relatively uneventful. Although the patient recovered from anesthesia smoothly, she developed respiratory acidosis 45 minutes after extubation. She was intubated again and ventilated artificially with pressure support ventilation whose support level was 15 cmH2O for only three hours. We conclude that we should pay much attention not only during anesthesia but also after surgery, especially to respiratory system in patients with carcinoid syndrome.
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PMID:[Anesthetic management of a patient with carcinoid syndrome]. 835 Apr 72

The effect of octreotide, a synthetic analogue of somatostatin, on the modulation of the acetic acid model of experimental colitis was examined. Colitis was induced by intracolonic administration of 2 ml of 5% acetic acid. The inflammatory response elicited by the acetic acid resulted in increased colonic synthesis of platelet activating factor, leukotriene B4 and decreased mucosal somatostatin levels. Subcutaneous administration of octreotide (10 micrograms/rat) 1 hour before or immediately after damage induction, as well as 1 and 23 hours after acetic acid application, resulted in a significant reduction in mucosal damage. The protective effect was accompanied by a significant reduction in platelet activating factor activity, leukotriene B4, and vasoactive intestinal peptide concentrations. There were no significant changes in mucosal leukotriene C4 and calcitonin gene related peptide levels. This study shows that acetic acid induced colitis is pharmacologically manipulated by octreotide. The mechanism of action of octreotide has not yet been fully determined. The potential use of octreotide in treating active inflammatory bowel disease remains to be evaluated.
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PMID:Octreotide effectively decreases mucosal damage in experimental colitis. 838 60

In adult gastric epithelium, gastrin and somatostatin regulate parietal cell acid secretion; however, their expression and function in the fetus are largely unknown. We defined the developmental expression of gastrin and somatostatin in the fetal rabbit stomach and determined their effects on fetal acid secretion. To define peptide expression, fetuses from 12 time-mated New Zealand white rabbit does were analyzed at successive ages during the third trimester (term is 31 days). Peptides were extracted from fetal gastric tissue by boiling in water and then in acetic acid. Amidated gastrin and somatostatin levels were measured by radioimmunoassay using antisera 1296 for gastrin and 8402 for somatostatin. To determine the effects of gastrin and somatostatin, pentagastrin (64 microg/kg/hr) or octreotide (35 microg/kg/hr) were infused intravenously in conscious pregnant rabbits at 28 days of gestation for 3 hr. Fetuses (n = 45) were harvested and gastric acid was titrated with 0.02 N NaOH. Gastrin and somatostatin tissue content were 12 +/- 3 and 51 +/- 6 pmol/g at gestational day 20, respectively, and increased to 146 +/- 10 and 162 +/- 5 pmole/g by day 30 (P < 0.05). Between days 24 and 26, when gastric acid was first detectable, the molar ratio of somatostatin to gastrin decreased from 5.0 +/- 1.0 to 1.1 +/- 0.1 (P < 0.05). Fetal gastric acid content (micromole) was 28.5 +/- 1.7 in controls, 27.5 +/- 1.9 with pentagastrin treatment, and 15.8 +/- 1.4 micromole with octreotide (P < 0.05). In summary, 1) In fetal gastric tissue, gastrin increased 12-fold and somatostatin increased 3-fold between days 20 and 30 of gestation. 2) The decreased ratio of somatostatin to gastrin between days 24 and 26 of gestation coincides with the onset of fetal gastric acid secretion in the fetal rabbit. 3) Maternal administration of octreotide inhibited fetal gastric acid content; however, pentagastrin had no effect. We conclude that, in the fetal rabbit stomach, the relative expression of gastrin and somatostatin may regulate the onset of parietal cell acid secretion.
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PMID:Roles of gastrin and somatostatin in the regulation of gastric acid secretion in the fetal rabbit. 866 Dec 27

Radiolabeling of the somatostatin analog octreotide was attempted with p-[18F]fluorophenacyl bromide ([18F]FPB). Following these unsuccessful trials, the reactivity of FPB was studied using benzyl mercaptan, phenyl acetic acid, benzyl alcohol, and benzyl amine as model compounds for amino acid functional groups. Structure and purity of products, relative reactivity of FPB in competition reactions, and radiolabeling experiments are described. In addition, improvement in labeling efficiency of HSA using [18F]FPB was achieved by pretreatment with 2-iminothiolane.
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PMID:Reactivity of p-[18F]fluorophenacyl bromide for radiolabeling of proteins and peptides. 937 25

[Tyr0]-somatostatin-14 (SST-14) was converted to the corresponding radiolabeled 125I-[Tyr0]-SST-14 derivative by use of the chloramine-T technique. After solid-phase extraction (SPE) of the crude radiopeptide with microfine silica gel and desorption with acetone-water-acetic acid 39:40:1, the label was subjected to size exclusion chromatography (SEC) on Sephadex G-25 fine. Fractions attributable to the target compound were collected and investigated with respect to their specific as well as non-specific binding to a specific anti-somatostatin antibody. All fractions exhibiting an optimum ratio of specific versus non-specific binding were pooled and lyophilized for their further use in both radioimmunoassay (RIA) measurements of somatostatin like immunoreactivity (SLI) and receptor-binding experiments. A specific activity of approx. 1.6 x 10(6) Ci/M was calculated for the radiolabel prepared in this manner. Approximately 85-90% of radioactivity attributable to labeled [Tyr0]-SST species was incorporated into the desired mono-iodinated component. When 125I-[Tyr0]-SST-14 was purified by reversed-phase high performance liquid chromatography (RP-HPLC) using isocratic elution with 0.1 M triethylammonium formate (TEAF) buffer of pH 2.2 in 22% acetonitrile after prior SPE, specific binding decreases to about 80% compared with the value obtained for the radiopeptide subjected to SEC. Nevertheless, RP-HPLC proves as an efficient tool for rapid purity control of 125I-[Tyr0]-somatostatin-14 samples at different storage time intervals.
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PMID:Preparation and chromatographic purification of 125I-[Tyr0]-somatostatin-14 for the use in radioimmunoassay and receptor-binding experiments. 971 Aug 95

Activation of neurons in the inferior mesenteric ganglion (IMG) was assessed using c-fos, JunB, and c-Jun expression in the guinea pig IMG and colonic myenteric plexus during mechanosensory stimulation and acute colitis in normal and capsaicin-treated animals. Intracolonic saline or 2% acetic acid was administered, and mechanosensory stimulation was performed by passage of a small (0.5 cm) balloon either 4 or 24 hr later. Lower doses of capsaicin or vehicle were used to activate primary afferent fibers during balloon passage. c-Jun did not respond to any of the stimuli in the study. c-fos and JunB were absent from the IMG and myenteric plexus of untreated and saline-treated animals. Acetic acid induced acute colitis by 4 hr, which persisted for 24 hr, but c-fos was found only in enteric glia in the myenteric plexus and was absent from the IMG. Balloon passage induced c-fos and JunB in only a small subset of IMG neurons and no myenteric neurons. However, balloon passage induced c-fos and JunB in IMG neurons (notably those containing somatostatin) and the myenteric plexus of acetic acid-treated animals. After capsaicin treatment, c-fos and JunB induction by balloon passage was inhibited in the IMG, but there was enhanced c-fos expression in the myenteric plexus. c-fos and JunB induction by balloon stimulation was also mimicked by acute activation of capsaicin-sensitive nerves. These data suggest that colitis enhances reflex activity of the IMG by a mechanism that involves activation of both primary afferent fibers and the myenteric plexus.
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PMID:Immediate-early gene expression in the inferior mesenteric ganglion and colonic myenteric plexus of the guinea pig. 1008 87


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