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)

The relationship between neuronal calcium binding protein content (calbindin D28K: CaBP and parvalbumin: PV) and vulnerability to ischemia was studied in different regions of the rat brain using the four vessel occlusion model of complete forebrain ischemia. The areas studied, i.e. the hippocampal formation, neocortex, neostriatum and reticular thalamic nucleus (RTN), show a characteristic pattern of CaBP and PV distribution, and are involved in ischemic damage to different degrees. In the hippocampal formation CaBP is present in dentate granule cells and in a subpopulation of the CA1 pyramidal cells, the latter being the most and the former the least vulnerable to ischemia. Non-pyramidal cells containing CaBP in these regions survive ischemia, whereas PV-containing non-pyramidal cells in the CA1 region are occasionally lost. Hilar somatostatin-containing cells and CA3 pyramidal cells contain neither PV nor CaBP. Nevertheless, the latter are resistant to ischemia and the former is the first population of cells that undergoes degeneration. Supragranular pyramidal neurons containing CaBP are the most vulnerable cell group in the sensory neocortex. In the RTN the degenerating neurons contain both PV and CaBP. In the neostriatum, ischemic damage involves both CaBP-positive and negative medium spiny neurons, although the degeneration always starts in the dorsolateral neostriatum containing relatively few CaBP-positive cells. The giant cholinergic interneurons of the striatum contain neither CaBP nor PV, and they are the most resistant cell type in this area. These examples suggest the lack of a consistent and systematic relationship between neuronal CaBP or PV content and ischemic vulnerability. It appears that some populations of cells containing CaBP or PV are more predisposed to ischemic cell death than neurons lacking these proteins. These neurons may express high levels of calcium binding proteins because their normal activity may involve a high rate of calcium uptake and/or intraneuronal release.
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PMID:Relationship of neuronal vulnerability and calcium binding protein immunoreactivity in ischemia. 207 50

Nineteen combined renal and segmental pancreatic transplantations with enteric exocrine diversion were performed between May 1984 and September 1985. The one year actuarial patient survival rate and pancreatic graft survival rate were 86 and 66 per cent, respectively. Thirteen pancreatic grafts are presently functioning (two to seven months) and all of the recipients are insulin-free. Although graft cold ischemia time was kept low (a mean of 4.6 hours), a moderate graft pancreatitis developed with a peak serum amylase level of 16.8 +/- 2.2 microkatal per liter. Analysis of the fluid drained through an abdominal drain tube placed at the graft site revealed an amylase activity of 280 +/- 110 microkatal per liter on the first postoperative day and rapidly decreasing to a mean of 15 +/- 5 microkatal per liter on day 6. A pancreatic duct catheter was used to divert the exocrine juice to the exterior during the first few postoperative weeks thereby promoting healing of the pancreaticoenteric anastomosis. The volume of pancreatic juice from the ductal catheter was quite low in the first postoperative days but then rose to reach a plateau level of 500 to 600 milliliters. The amylase activity and the lipase concentration in the pancreatic juice was very high (9,100 +/- 2,450 microkatal per liter and 11.1 +/- 4.4 grams per liter, respectively) during the first postoperative day but then gradually decreased to reach a steady level after four to seven days. Intravenous administration of secretin induced a sixfold increase in the flow of pancreatic juice. An intravenous infusion of somatostatin significantly reduced the flow of pancreatic juice and the amylase activity and lipase concentration in the juice but did not abolish the secretin induced increase in pancreatic secretion.
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PMID:Studies on the exocrine secretion of segmental pancreatic grafts in humans. 243 63

Excitatory amino acids have been implicated in ischemic neuronal injury. To test this hypothesis in neonatal hypoxia-ischemia, lesions of the cortex and striatum were induced in 7-day-old rats by unilaterally ligating their carotid arteries and subjecting them to hypoxic conditions for 2 hours. Brains examined 1 week later demonstrated, within the regions of ischemic damage, a striking preservation of neurons that stained histochemically for nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) activity. Concentrations of the neuropeptides somatostatin and neuropeptide Y, which colocalize in neurons containing NADPH-d, were unaffected in the areas of ischemic damage. The same pattern of injury with sparing of NADPH-d-reactive neurons was reproduced by focal microinfusion of the excitotoxin quinolinic acid, an endogenous N-methyl-d-aspartate (NMDA) agonist, into the striatum. These results support the hypothesis that neonatal hypoxic-ischemic injury is mediated through excitatory transmitters acting at the NMDA receptor and that the NADPH-d-reactive neurons in the neonate are resistant to excitotoxic damage. This pattern of cell vulnerability is unique to the developing striatum and may relate to the distinct pathological appearance of the basal ganglia that follows neonatal asphyxia.
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PMID:Selective sparing of NADPH-diaphorase neurons in neonatal hypoxia-ischemia. 290 92

The prevalence of severe dementia in the United States is about 1.3 million cases, of which at least 50 to 60% are of the Alzheimer type. Severe dementia of the Alzheimer type is found rarely in a clearly dominant pattern, although often one or more relatives are affected. Down's syndrome in adults is often associated with Alzheimer changes. The diagnosis is a clinicopathological one; there is a considerable error rate in the clinical diagnosis early in the course of the disease, especially in regard to dementia in depression. The differential diagnosis involves a great many disorders, including multi-infarct dementia, tumors, subdural hematomas, and others. Physiological aspects of Alzheimer's disease include a diffusely slow electroencephalogram, reduced cerebral blood flow, and particular patterns noted on positron emission tomographic scanning. The latter technique has also demonstrated that oxygen extraction is normal in Alzheimer's disease, thus excluding ischemia from possible pathogenetic factors. Morphological changes, that is, the presence of plaques and tangles, are widely distributed in neocortex, paleocortex, and many deep gray areas down through the pontine tegmentum, but largely exclude the basal ganglia, thalamus, and substantia nigra. Numerous plaques without neocortical tangles are found in many demented persons older than 75 years. A severe loss of large neocortical neurons is characteristic of the disease. The chemical nature of the paired helical filaments that make up the neurofibrillary tangle has not yet been ascertained. Neurons are markedly deficient in the basal forebrain nuclei, and this deficiency may account for the severe diminution of choline acetyltransferase and acetylcholine in the neocortex and paleocortex. Muscarinic cholinergic receptors are present in normal amounts. Norepinephrine is reduced in some cases, and somatostatin in most. Substance P is low in severe cases. The etiology of the disorder is unknown and the role of aluminum is disputed. Management of patients with Alzheimer's disease is difficult, and neuroleptics are to be used with great caution because of their side effects. Substrate therapy has not been effective; physostigmine improves memory but is not suitable for general use. Trophic factors, gangliosides, and aluminum chelation are being investigated for use in pharmacological intervention.
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PMID:Senile dementia of the Alzheimer type. 613 75

The aim of this paper is to elucidate the cause of death after 90 min of normothermic partial (2/3) ischemia of the liver and to examine the effects of glucagon, somatostatin, insulin, prednisolone and oral administration of polymyxin B (PB). The animals 24 hr after partial ischemia for 90 min were divided into two groups; namely, animals with normal appearance and those with moribund state. There were no significant differences in the plasma level of S-GOT, S-GPT, amino acids, NH3 or insulin, or in morphometrically estimated volume ratio of necrotic hepatocytes between the two groups of rats. The blood glucose level, however, was significantly decreased (31 +/- 28 mg/100 ml, n = 6) in the moribund rats with a higher incidence of positive Limulus gelation tests as compared with the rats with normal appearance (149 +/- 19, n = 5). The 1-day and 1-week survival rates of the animals were 42/62 (69%) and 32/61 (53%), respectively. A glucagon injection (1.5 mg/kg, after ischemia) was effective to elevate the 1-day survival rate (14/14), but failed to increase the 1-week survival rate (11/14). On the other hand, a somatostatin injection (100 micrograms/kg, after ischemia) or PB treatment (15 mg/kg/day x 5-9, before ischemia) succeeded to increase the 1-week survival rate (20/22 p less than 0.01 and 17/17 p less than 0.01, respectively), although no significant amelioration in transaminase levels or volume ratio of necrosis was demonstrated. It could be seen that a moribund state after partial ischemia was accompanied by severe hypoglycemic shock, and that the injection of somatostatin after ischemia or the annihilation of gram-negative bacteria by means of oral administration of polymyxin B before ischemia prevented the occurrence of the hypoglycemic shock.
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PMID:Postischemic liver damage in rats: effect of some therapeutic interventions on survival rate. 629 17

The pancreases of 17 patients who had cystic fibrosis with and without diabetes mellitus were evaluated at autopsy by routine staining and immunohistochemical methods for insulin, glucagon, somatostatin, and pancreatic polypeptide. Qualitative assessment of the number of islets of Langerhans and the degrees of exocrine pancreatic atrophy, fibrosis, and fat replacement was made for each pancreas. Quantitative assessment of islet composition was performed in 15 of the 17 based on the immunochemical reactivity of each cell type. Nondiabetic patients with cystic fibrosis in the latter part of the first decade of life have classic fibrocystic changes of the pancreas, with some persisting exocrine tissue, islets that appear normal, and prominent nesidioblastosis. The latter process may protect these patients from glucose intolerance. Young adult diabetic patients with cystic fibrosis have total loss of exocrine pancreas with fat replacement, lack of nesidioblastosis, a qualitative decrease in the number of islets, fibrosis of and amyloid deposits in islets, decreased numbers of insulin-containing cells in each islet, and atrophy of islet cells, probably resulting from progressive ischemia. Although the potential exists for an increasing incidence of diabetes mellitus in patients with cystic fibrosis as their life spans increase, individual variation occurs in this disease.
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PMID:Endocrine pancreas in cystic fibrosis: an immunohistochemical study. 636 38

The process of bacterial translocation (BT) after ischemia/reperfusion (I/R) injury is reported to be mediated by local mucosal factors, the effects of pancreatic enzymes, epithelial disruption, and by dysfunctional intestinal motility. Octreotide (OCT), a somatostatin analog, has been postulated to protect against BT by influencing one or more of these factors. Twenty-two formula-fed piglets (weight, 3.5 +/- 0.5 kg; age, 20 +/- 5 days) were divided into four groups: control (no drug given; no I/R; n = 6), I/R (no drug given; n = 5), I/R plus low-dose OCT (LD OCT, 0.08 microgram/kg; n = 6), and I/R plus high-dose OCT (HD OCT, 8 micrograms/kg; n = 5). All experimental subjects had nonocclusive mesenteric ischemia induced by reversible pericardial tamponade with mesenteric flow decreased to 25 +/- 5% of baseline for 5 hours followed by 15 +/- 5 hours of reperfusion. Mesenteric lymph nodes (MLN), liver, spleen, blood, and peritoneum were harvested for blind microbial analysis. None of the animals in the control group experienced translocation to the tissues tested. All of the animals in the I/R group experienced BT to the MLN. The subjects in the LD OCT and HD OCT groups experienced BT to the MLN 66% and 80% of the time, respectively. Despite the reported clinical evidence that OCT can protect the intestinal mucosa from injury and increase the clearance of bacteria from the gastrointestinal tract, in this study in which variables other than I/R known to promote bacterial translocation were eliminated, OCT failed to modify or prevent the occurrence of translocation to the MLN after I/R injury.
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PMID:Octreotide does not prevent bacterial translocation in an infant piglet model of intestinal ischemia-reperfusion. 747 54

During the last decade, evidence increased that microcirculatory disorders play a pivotal role in the development of mucosal injury, and, hence, formation of gastric ulcer. Mucosal microcirculation is altered at least by two distinct mechanisms: Stimulation of acid secretion leads to a rise of blood flow in the acid-secreting areas, and, concomitantly, due to a steal-phenomenon to a decrease of mucosal capillary perfusion of the antrum, which results in temporary ischemia. In addition, surface noxae-induced release of potent mediators, such as histamine, leukotrienes, thromboxane, platelet-activating factor and reactive oxygen metabolites cause vasoconstriction, capillary stasis and increase of microvascular permeability (loss of endothelial integrity), which aggravate mucosal injury. Therefore, therapeutic strategies should consider leukotriene-synthesis inhibitors, histamine-, thromboxane- and platelet-activating factor receptor antagonists, oxygen radical scavengers, as well as counteracting mediators and hormones, such as prostaglandins and somatostatin, inasmuch as these compounds have been shown to additionally prevent mucosal microvascular injury, in particular capillary perfusion failure and loss of endothelial integrity, during gastric ulcer formation.
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PMID:[Microcirculation of gastric mucosa in pathogenesis of stomach ulcer]. 751 63

The distribution of somatostatin in both the human and rat brain suggests that it is involved in numerous functions, including endocrine regulation, cognition and memory, autonomic regulation and motor activity. We have examined the regulation of somatostatin mRNA in the striatum, a brain region involved in motor and cognitive behaviour. Somatostatin and its mRNA are expressed in this region in interneurons which are resistant to ischaemia, excitotoxicity and Huntington's disease, possibly because they express high levels of superoxide dismutase. Striatal somatostatin mRNA is increased by stimulation of NMDA (N-methyl-D-aspartate) receptors. Ischaemia-induced cortical lesions also increase somatostatin gene expression in the striatum. In contrast, the levels of striatal somatostatin mRNA decrease after treatment with haloperidol, an antipsychotic agent that produces extrapyramidal symptoms, but not clozapine, which does not. Further evidence for a role for striatal somatostatin in extrapyramidal symptoms includes the observation that somatostatin mRNA levels decrease in the striatum after lesions are made in the dopaminergic pathway, a feature of Parkinson's disease. The largest change in somatostatin gene expression after dopaminergic lesions is the increase in somatostatin mRNA level sin neurons of the internal pallidum and lateral hypothalamus projecting to the lateral habenula. The results suggest that changes in brain somatostatin gene expression occur in pathological conditions and may be related to their symptoms.
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PMID:Anatomical localization and regulation of somatostatin gene expression in the basal ganglia and its clinical implications. 758 52

Repeated episodes of cerebral hypoxia-ischemia can cause primarily striatal neuronal loss in the developing brain. We investigated the effect of repeated episodes of asphyxia on specific neuronal sub-populations of the basal ganglia in late-gestation fetal sheep. Asphyxia was induced in 10 fetal sheep (118-126 days gestation) by occluding the umbilical cord for 5 min. This procedure was repeated four times at 30 min intervals and the brains were fixed 3 days later for histopathology. Immunohistochemical markers were used to identify various populations of neurons in the striatum. Antibodies to calbindin were used to stain the GABAergic medium-sized striatal projection neurons and antibodies to somatostatin and parvalbumin to identify striatal interneurons. Striatal projection neurons to the globus pallidus were recognized by enkephalin immunoreactivity, while the striatonigral terminals were identified in the substantia nigra pars reticulata by substance P immunohistochemical labelling. The results showed a marked loss of calbindin staining in the striatum, evident by both reduced cell numbers and a decrease in neuropil staining. The number of parvalbumin immunoreactive cells was also reduced in the striatum, while somatostatin interneurons were selectively preserved. In addition, immunostaining for enkephalin in the globus pallidus and for substance P in the substantia nigra was markedly reduced. These results show that the stiatal GABAergic medium-sized projection neurons are severely affected by recurrent episodes of asphyxia. These findings are confirmed and extended by the results demonstrating that both the enkephalin/GABA striatopallidal and the substance P/GABA stiatonigral pathways are affected. The results of this study therefore suggest that the efferent striatal projections to the globus pallidus and to the substantia nigra may be involved in asphyxial episodes resulting in cerebral palsy.
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PMID:Repeated asphyxia causes loss of striatal projection neurons in the fetal sheep brain. 760 81


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