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)

Whilst the neuropathological correlates of Alzheimer type dementia--cortical neurofibrillary tangles and senile plaques--are well defined, the prevalence of these cortical abnormalities in Parkinson's disease and their relation to dementia is unclear. In a series of 46 consecutive cases of clinically and pathologically established Parkinson's disease the prevalence of mild Alzheimer-type pathology (exceeding the normal but not as extensive as in Alzheimer's disease) was increased 2 to 3 fold compared with an age-matched control group, although there was no obvious relation to the presence or severity of dementia. In a subgroup of Parkinsonian cases (both demented and non-demented), examined neurochemically, there were both similarities (decreased choline acetyltransferase, nicotinic and serotonergic S 1 receptor activities) and distinctions (increased muscarinic receptor binding--particularly to the "L" subtype, and normal serotonergic S 2, somatostatin, and D-aspartate binding together with normal levels of an endogenous nicotine binding inhibitor) compared with a group of cases with Alzheimer's disease. Amongst the various pathological and chemical indices examined, only presynaptic cholinergic markers (including the number of Meynert neurons) and S 1 receptor binding were related to dementia in Parkinson's disease. It is suggested that whilst coincidental classical Alzheimer's disease is infrequent in Parkinson's disease (5% in the present series) Alzheimer's disease itself is distinguished from Parkinson's disease by the formation of numerous neocortical neurofibrillary tangles and a reduction in glutamate uptake, serotonergic S 2 receptors and possibly in endogenous nicotine binding inhibitor.
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PMID:Cortical neuropathological and neurochemical substrates of Alzheimer's and Parkinson's diseases. 282 87

We have investigated in stimulated human pancreatic juice the presence of the following peptides: insulin, glucagon, gastrin, somatostatin, VIP and secretin. Collection of pancreatic juice (3 periods: 20 min each) was completed by endoscopic cannulation of the pancreatic duct during the infusion of secretin (0.5 U/kg/h) and cerulein (75 ng/kg/h) in 6 healthy volunteers. Pure pancreatic juice was recovered in the presence of kallikrein inhibitor (iniprol 8,000 U/ml) in refrigerated collection tubes (4 degrees C). The material was acidified, boiled for 5 min and centrifuged. Radioimmunoassays were performed on the supernatant solutions. The elution profiles on Sephadex G 25 gel filtration of the immunoreactivities were compared with standard samples of hormones, immuno-reactive insulin, glucagon and somatostatin were found in every sample: insulin was present at a constant level (50 microU/ml) during the three periods of collection; glucagon was encountered in large amounts in the first sample and decreased significantly during the subsequent periods; somatostatin which occurred at a low level during the first period was significantly increased in the following periods. Gastrin, VIP and secretin were undetectable or only inconstantly found in very small amounts. These results are in agreement with a two-directional secretion of the human pancreatic endocrine cells. The cellular origin and function of these exocrine secreted peptides need further studies.
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PMID:[Presence of hormonal polypeptides in the pure pancreatic secretion in man under stimulation by cerulein and secretin]. 286 46