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)

The etiology of Alzheimer's disease (AD) is still unknown, and a definitive diagnosis of the disease can be determined only at autopsy or by brain biopsy. AD can be characterized by various structural changes, including cerebral cortical atrophy, neuronal loss, neuritic plaques, and neurofibrillary tangles. The primary defect involves reduced activity of choline acetyltransferase. Neurotransmitters, such as norepinephrine, serotonin, dopamine, and somatostatin, are also compromised. Treatment of AD requires maintenance of a consistent lifestyle and environment for the patient, as well as counseling and support for the patient's family. Medications, which have been effective in some patients, are primarily used to improve cognitive function and modify behavior. Cognitive medications such as tacrine hydrochloride and physostigmine have proven beneficial in some patients, while behavioral medications have been effective in the treatment of depression, aggression, agitation, and anxiety associated with AD. However, the side effect profile of each medication and its probable overall benefit to the individual patient should be evaluated before beginning therapy. Continued research in patients with AD is required to identify medications that will consistently ameliorate the memory loss associated with the disease.
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PMID:Current concepts in the treatment of Alzheimer's disease. 157 22

The Karolinska Scales of Personality (KSP) and some dimensions of the Bergman scale reflecting social dependency and self-confidence were used in 24 individuals with functional disorders of the gastrointestinal tract. Patients showed higher scores of somatic anxiety, indirect aggression and irritability and lower scores in socialization when compared with a reference group. The levels of gastrointestinal symptoms as well as the levels of some hormones related to vagal nerve activity in this patient group have been reported in a previous publication. When the scores obtained in personality inventories were related to symptom levels, we found significant correlations with intestinal but not abdominal symptoms. Gastrin levels correlated inversely with socialization. Somatostatin levels on the other hand, correlated negatively with social dependency and positively with self-confidence in the Bergman scale. Interestingly, oxytocin levels correlated positively with social dependency and in addition with indirect aggression and verbal aggression. The correlation between hormone levels and scores of personality dimensions will be interpreted and discussed within a physiological context.
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PMID:Personality traits in a group of individuals with functional disorders of the gastrointestinal tract and their correlation with gastrin, somatostatin and oxytocin levels. 168 Oct 96

Administration of 10 and 30 micrograms methionine-enkephalin (MET-ENK)/g bw (n = 10/dose) affected the propensity towards fighting in H. bimaculatus; 10 micrograms increased, while 30 micrograms decreased the aggressive behavior. MET-ENK also affected a number of behavior patterns displayed by the fish. Moreover, the "wet-dog-shakes" observed suggest that MET-ENK acts on opiate-receptors. Treatment with substance P (SP)/g bw (n = 10/dose) induced chafing movements in the fish slightly. It also decreased fighting and increased biting of the air stone, which is evidence that H. bimaculatus is still aggressive, directing its attacks to different objects. When 4, 8, 12 micrograms somatostatin (SRIF)/g bw (n = 10/dose) were injected, H. bimaculatus stopped fighting for several hours after the onset of treatment, depending on the dosage. Somatostatin reduces blood glucose concentration, causing a sudden stop of aggressive behavior, 0.04, 0.1, 0.6, 1.0 and 3.0 IU prolactin (PRL)/g bw (n = 5/dose) eventually decreased fighting and affected a number of behavior patterns displayed by the fish.
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PMID:Effects of MET-ENK, substance P and SRIF on the behavior of Hemichromis bimaculatus. 258 Dec 33

Borna disease (BD) agent is an infectious pathogen that causes progressive central nervous system (CNS) dysfunction in a wide range of vertebrate hosts. The course of BD in adult rats is biphasic. The acute phase is characterized by aggressive behavior and inflammatory cell infiltrates in brain. With chronic infection animals become listless and inflammation resolves. BD antigens are similarly distributed in neurons in hippocampus, neocortex, cerebellum and brainstem in acutely and chronically infected animals. We have recently examined brain levels of neuronal transcripts in rats with acute and chronic BD. Levels for 3 of these mRNAs, cholecystokinin, glutamic acid decarboxylase and somatostatin, were decreased in acutely infected rats and increased toward control values in chronically infected rats. A fourth transcript, MuBr8, correlated in distribution with BD antigen, was persistently decreased throughout the course of infection. These data may have implications for understanding the pathogenesis of neurologic disturbances in BD and other inflammatory CNS diseases.
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PMID:Neurotransmitter abnormalities in Borna disease. 290 25

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

In earlier studies performed on a group of women with gastrointestinal symptoms, significant positive correlations between the gastrointestinal hormone gastrin and anxiety, and a negative correlation with socialization were obtained. These and other relationships were tested on 33 healthy women. A comprehensive and concise statistical model was used for the analysis of correlations between, on one hand, the levels of oxytocin and the gastrointestinal hormones gastrin, cholecystokinin, somatostatin and insulin, and, on the other hand, personality traits. Almost all explained variance of the hormone levels could be referred to three personality trait factors, Anxiety, Aggressive non-conformity, and Detachment. The statistical explanation of the gastrin level variance was most successful, the three personality trait factors explaining 48% of this variance. Gastrin "increased" Anxiety while reducing Aggressive non-conformity and Detachment. A similar pattern for insulin was also reliable. Considering general trends, the negative correlations between all hormones and Detachment are interesting. Present data suggest that there is a psychoendocrinological antithesis to the fight-flight individual, characterized by high activity in the sympathoadrenal system: these contrasting persons, with high levels of the gastrointestinal hormones gastrin and insulin, tend to be warm and caring and non-aggressive--but often not free from anxiety. We do not think that the demonstrated associations between hormone levels and personality traits implicate a direct causal relationship. They rather may mirror the activity of centrally acting or hypothalamic control systems which influence both behavioural and endocrine profiles.
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PMID:The relationships between personality traits and plasma gastrin, cholecystokinin, somatostatin, insulin, and oxytocin levels in healthy women. 810 80

The manipulation of the inflammatory and hormonal responses may produce, on one hand, positive effects, and, on the other hand, potentially negative effects. The modification of the neuro-endocrine-humoral pattern may become more important and effective than the supply of nutrients. In this article we bring an up date of the role of insulin, anabolic steroids, blocking the catabolic hormones, phenobarbital, somatostatin, clenbuterol and metaprorenol, growth factors: GH and IGF-1, cytokines, and anti-cytokines sera. The use of GH, IGF-1, and of the epidermal and or colonic growth factors, along with a blocking of the cytokines, the manipulation of the lipidic mediators, and the supply of classical nutrients, specific to the aggression situation, may improve the protein synthesis and tissue repair. It may at the same time both decrease the loss of body proteins as well as promoting and acceleration of the recovery, shortening the hospital stay and reducing the convalescence time. The future seems to point towards molecular and cellular biotechnology and towards "nutritional" pharmacology, which contemplates the effects of growth factors, the recent advances in the field of cytokine modulation, and the manipulation of the binomer nutrient-medication.
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PMID:[Hormones, growth factors, and drugs in metabolism and nutrition]. 851 56

In situ hybridization and immunocytochemistry were applied to investigate changes in the expression of somatostatin, neuropeptide Y, neurokinin B, cholecystokinin, dynorphin, and Met-enkephalin in the rat hippocampus after administration of a single peroral dose of trimethyltin hydroxide (9 mg/kg). Two time intervals were investigated: 5 days after trimethyltin treatment, when CA3 damage becomes manifest and is associated with increased aggression, seizure susceptibility, and memory deficit, and 16 days after trimethyltin, when neuronal damage is almost maximal and seizure susceptibility is declining. Robust but transient increases of neuropeptide Y, neurokinin B, and Met-enkephalin mRNA levels were revealed in the granule cell layer of the dentate gyrus and increased neuropeptide Y and neurokinin B immunoreactivities were found in mossy fibers. In reverse, dynorphin mRNA and immunoreactivity were decreased transiently in the dentate gyrus and mossy fibers, respectively. Strong over-expression of NPY mRNA was also observed in hilar interneurons and in CA1 and CA3 pyramidal cells as well as in the cortex at 5 days postdosing. Cholecystokinin- or neurokinin B-containing basket cells were preserved, while somatostatin-bearing interneurons were damaged by trimethyltin exposure. These neurochemical changes induced by trimethyltin intoxication strikingly parallel to those observed in animal models of temporal lobe epilepsy and may reflect activation of endogenous protective mechanisms. It is also suggested that hilar interneurons respond differently to trimethyltin exposure, for which neuropeptides are valuable markers.
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PMID:Trimethyltin intoxication induces marked changes in neuropeptide expression in the rat hippocampus. 966 Dec 51

Somatostatin receptors type 2 (sst2) have been frequently detected in neuroendocrine tumors and bind somatostatin analogues, such as octreotide, with high affinity. Receptor autoradiography, specific mRNA detection and, more recently, antisst2 polyclonal antibodies are currently employed to reveal sst2. The aim of the present study was to investigate by three different techniques the presence of sst2 in a series of 26 neuroendocrine tumors of the lung in which fresh frozen tissue and paraffin sections were available. It was possible, therefore, to compare, in individual cases, RNA analysis studied by reverse transcriptase polymerase chain reaction (RT-PCR), in situ hybridization (ISH), and immunohistochemistry. A series of 20 nonneuroendocrine lung carcinoma samples served as controls. RT-PCR was positive for sst2 in 22 of 26 samples, including 15 of 15 typical carcinoids, 5 of 6 atypical carcinoids, and 2 of 5 small-cell carcinomas. The sst2 mRNA signal obtained by RT-PCR was strong in the majority (87%) of typical carcinoids and of variable intensity in atypical carcinoids and small-cell carcinomas. A weakly positive signal was observed in 5 of 20 control samples. In immunohistochemistry, two different antibodies (anti-sst2) were employed, including a monoclonal antibody, generated in the Department of Pathology, University of Turin. In the majority of samples a good correlation between sst2 mRNA (as detected by RT-PCR) and sst2 protein expression (as detected by immunohistochemistry) was observed. However, one atypical carcinoid and one small-cell carcinoma had focal immunostaining but no RT-PCR signal. ISH performed in selected samples paralleled the results obtained with the other techniques. A low sst2 expression was associated with high grade neuroendocrine tumors and with aggressive behavior. It is concluded that 1) neuroendocrine tumors of the lung express sst2, and there is a correlation between the mRNA amount and the degree of differentiation; 2) immunohistochemistry and ISH are reliable tools to demonstrate sst2 in these tumors; and 3) sst2 identification in tissue sections may provide information on the diagnostic or therapeutic usefulness of somatostatin analogues in individual patients with neuroendocrine tumors.
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PMID:Correlative immunohistochemical and reverse transcriptase polymerase chain reaction analysis of somatostatin receptor type 2 in neuroendocrine tumors of the lung. 1071 13

Trimethyltin (TMT) is an organic metal known to induce neuronal degeneration in the hippocampus, and abnormal behavior characterized by seizures, increased aggression and memory deficits. We administered TMT to rats and studied the changes of neuropeptide Y (NPY) and somatostatin (SOM) in the hippocampus. Phenobarbital (PB) was administered as an anticonvulsant to assess the effect of seizures on neuropeptide expressions in both dorsal and ventral hippocampus. Histochemically, NPY-immunoreactivity increased 4 days after TMT treatment in the hilus of the hippocampus, then progressively decreased and dropped to a level below control 16 days after TMT treatment. Detection of NPY mRNA by in situ hybridization preceded the detection of NPY by immunohistochemistry. NPY mRNA signals increased in the hilus 2 days after TMT treatment. SOM-immunoreactivity also increased in the hilus of the hippocampus 2 days after TMT treatment, then decreased rapidly to a normal level. Similar changes in SOM mRNA were demonstrated by in situ hybridization. PB treatment significantly inhibited changes of NPY in terms of both immunoreactivity and mRNA expression; however, the same treatment failed to affect changes in SOM expression. This suggests that NPY and SOM act by different mechanisms in TMT-induced neurodegeneration.
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PMID:Neuropeptide Y and somatostatin participate differently in the seizure-generating mechanisms following trimethyltin-induced hippocampal damage. 1241 52


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