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 authors report the case of a three-month-old infant presenting with hypoglycaemia. The etiology, i.e. nesidioblastosis, was asserted by simultaneous dosage of insulin and glucose and by histologic study of the pancreas. Initial therapy was a combination of diazoxide, continuous enteral alimentation and glucose injections. It's ineffectiveness led to an operative decision and 4/5 ths of the pancreas were removed. After a transitory improvement symptoms recurred. Data provided by studies of baseline levels and response to exogenous somatostatin then allowed to determine the correct dosage for treatment with long-acting somatostatin. The authors also discuss the importance of somatostatin in pathogenesis as well as for diagnosis and therapy of nesidioblasosis.
Sem Hop
PMID:[Somatostatin in a case of nesidioblastosis (author's transl)]. 612 May 72

Somatostatin is a peptide hormone which inhibits the secretion of the growth hormone and certain gastrointestinal hormones. Its main effect is to reduce the gastric acid output and inhibit the exocrine function of the pancreas. It was therefore used as an adjuvant therapy in the conservative treatment of ten patients presenting with fistulas of the small intestine or pancreas. The treatment was successful in eight cases. The short halflife of the hormone makes continuous application of the somatostatin as important as the carrying on of the conservative treatment itself.
Sem Hop 1982 Oct 21
PMID:[Somatostatin in the medical treatment of fistula of the pancreas and the small intestine]. 612 4

The mouse homeodomain protein insulin promoter factor-1 (IPF-1) and the rat homologue somatostatin transactivating factor-1 (STF-1) are involved in early pancreatic development and have been implicated in the cell-specific regulation of insulin- and somatostatin-gene expression in mature islet beta- and delta-cells. The cell specificity of IPF-1/STF-1 expression in mature islets is, however, still unclear. Using antisera against recombinant IPF-1 and STF-1 in combination with antisera against islet hormones we find that all beta-cells in monolayers of newborn rat islet cells express STF-1, as do a fraction of the delta-cells. In adult rat and mouse pancreas we find a similar distribution. IPF-1/STF-1 expression was not detected in glucagon-producing alpha-cells. In islet cell tumour models we found that a glucagon/islet amyloid polypeptide (IAPP)-producing pluripotent rat islet cell line (NHI-6F-GLU) expresses STF-1 in all cells prior to insulin gene activation induced by in vivo culture. In contrast, a mouse alpha-cell line (alpha TC1) exclusively expressed IPF-1 in a small subset of insulin-producing cells while an insulin-negative subclone (alpha TC1.9) was negative for IPF-1. In transfection experiments using alpha TC1.9 cells STF-1 activated a rat insulin 1 reporter gene dependent not only on both STF-1-binding sites, but also on the E1-binding site for the helix-loop-helix factor IEF-1. However, the endogenous mouse insulin genes remained inactive in these cells. These results suggest that the insulin promoter acquires its very high, yet cell-specific, activity at least partly through the action of IPF-1/STF-1. This action is dependent on helix-loop-helix factors bound to the E1 element.
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PMID:The homeodomain protein IPF-1/STF-1 is expressed in a subset of islet cells and promotes rat insulin 1 gene expression dependent on an intact E1 helix-loop-helix factor binding site. 757 38

The mammalian neocortex develops layer organizations with regional differences represented by expression of multiple genes at embryonic stages. These genes could play important roles in the formation of areal cyto-architecture, yet, the number of genes identified so far is not sufficient to explain such intricate processes. Here we collected five regions--the medial, dorsal, lateral, rostral and occipital--from the dissected E16.5 mouse cerebral cortex and performed extensive gene expression analysis using the Affymetrix U74Av2 array with probes for 12,500 genes. After relative quantitative analysis, 34, 33 and 15 genes were selected as highly expressed genes in the medial, dorsal and lateral regions, respectively. The combination of GeneChip system, real-time quantitative reverse transcription polymerase chain reaction and in situ hybridization analyses allowed the successful identification of seven genes from the dorsal region (Neuropeptide Y, Wnt7b, TGF-beta RI, Nrf3, Bcl-6, MT4-MMP and Rptp kappa), three genes from the medial region (Hop-pending, HtrA and Crystallin), and three genes from the lateral region (Somatostatin, Ngef and Fxyd7). Particularly, all seven genes identified in the dorsal region demarcated the future somatosensory and auditory areas in the cortical plate with high rostrolateral-low caudomedial gradation. Their expression patterns were not uniform, but delineated either the superficial or the deep layer in the cortical plate. Furthermore, the regional expression pattern of Neuropeptide Y was shifted rostrally and the layer specificity was disorganized in the Pax6-deficient mice. Our results provide new information about a subclass of regionally expressed genes in the cortical plate at the late embryonic stage, which may help understand the molecular mechanisms of neocortical arealization.
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PMID:Gene expression analysis of the late embryonic mouse cerebral cortex using DNA microarray: identification of several region- and layer-specific genes. 1514 57