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)

To determine the extent of conservation between bovine syntenic group U10, human chromosome 21 (HSA 21), and mouse chromosome 16 (MMU 16), 11 genes were physically mapped by segregation analysis in a bovine-hamster hybrid somatic cell panel. The genes chosen for study span MMU 16 and represent virtually the entire q arm of HSA 21. Because the somatostatin gene (SST), an HSA 3/MMU 16 locus, was previously shown to be in U10, the transferrin gene (TF), an HSA 3/MMU 9 marker, was also mapped to determine whether U10 contains any HSA 3 genes not represented on MMU 16. With the exception of the protamine gene PRM1 (HSA 16/MMU 16), all of the genes studied were syntenic on bovine U10. Thus, all homologous loci from HSA 21 that have been studied in the cow are on a single chromosome. The bovine homolog of HSA 21 also carries several HSA 3 genes, two of which have homologous loci on MMU 16. The syntenic association of genes from the q arm of HSA 3 with HSA 21 genes in two mammalian species, the mouse and the cow, indicates that HSA 21 may have that contained genes now residing on HSA 3. Additionally, the syntenic association of TF with SST in the cow permits the prediction that the rhodopsin gene (RHO) is proximal to TF on HSA 3q.
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PMID:Evidence for the evolutionary origin of human chromosome 21 from comparative gene mapping in the cow and mouse. 198 61

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

A comparative map of human chromosome 3 (HSA 3) and pig chromosome 13 (SSC 13) was constructed using physically assigned pig sequence-tagged sites (STSs). Pig STSs representing 11 HSA 3 genes, including v-Raf-1 murine leukemia viral oncogene homolog 1 (RAF1), retinoic acid beta receptor (RARB), cholecystokinin (CCK), pituitary transcription factor 1 (POU1F1), ceruloplasmin (CP), guanine nucleotide binding protein, alpha-inhibiting polypeptide 2 (GNAI2), sucrase-isomaltase (SI), rhodopsin (RHO), dopamine receptor D3 (DRD3), growth-associated protein 43 (GAP43), and somatostatin (SST), were developed. Ten pig STSs were regionally mapped using a somatic cell hybrid panel (SCHP) to SSC 13 with 80-100% concordance. Large-insert probes were obtained by screening a pig yeast artificial chromosome (YAC) library with primers for each STS. Several YACs were identified for DRD3, GAP43, POU1F1, RHO, SI, and SST for fluorescence in situ hybridization (FISH) mapping. Single gene and bi-color FISH with each pairwise combination were used to further define the gene order on SSC 13. While these data confirm chromosome painting results showing that HSA 3 probes hybridize to a major portion of SSC 13, they also demonstrate extensive gene-order differences between man and pig within this large conserved synteny group. Interestingly, several conserved chromosomal regions have been detected between pig and mouse that are not conserved between man and mouse, suggesting that the SSC 13 gene arrangement may be the closest to that of the ancestral eutherian chromosome.
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PMID:Human chromosome 3 and pig chromosome 13 show complete synteny conservation but extensive gene-order differences. 1044 17

In the differential diagnosis, protein-losing enteropathy (PLE) is a rarely considered explanation of edema. Three such cases are reported in this article. Clinical presentations varied from severe generalized anasarca and respiratory distress to mild pitting edema on the pretibial surface. Hypoalbuminemia (< 35 g/l) was another common finding in addition to edema. The patients were carefully examined to exclude other causes of hypoalbuminemia. Two patients experienced diarrhea. Endoscopic studies (plus biopsies) for any mucosal lesion in the stomach and colon were also performed. PLE was confirmed by the positive radionuclide scanning results after infusing intravenous 99mTc human serum albumin (USA). Investigation for the etiologies showed intestinal lymphangiectasia in 1 patient, Menetrier's disease in another, and no recognizable cause in the third. The severe anasarca of the patient with intestinal lymphangiectasia didn't respond to corticosteroids and albumin supplement plus large doses of furosemide. She died of overwhelming pulmonary infection despite the use of powerful antibiotics (ceftriaxone and amikacin). We planned to treat the Menetrier's disease patient with somatostatin to decrease the exocrine activities of the intestinal tract. The patient with presumable idiopathic PLE had the least severe edema and was not treated with any medication. In addition to the above patients, another 3 patients with hypoalbuminemia and edema were also noted to have positive HSA scan results. However, 2 of these patients had systemic lupus erythromatosus and the third pulmonary tuberculosis and biopsy-proven membranous nephropathy. Treatment of their underlying diseases showed satisfactory remission of edema.
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PMID:Edema due to protein-losing enteropathy--a disorder rarely considered by nephrologists. 1203 1

This report concerns two patients with severe protein losing enteropathy and refractory diarrhea due to AA amyloidosis who were successfully treated with corticosteroid and octreotide. In these patients, biopsied tissues from the gastrointestinal (GI) tract showed extensive deposition of AA amyloid, which was caused by rheumatoid arthritis in one case and was of unidentified etiology in the other. Both patients manifested severe diarrhea unresponsive to conventional treatment with hypoproteinemia, and protein leakage from the small intestine to the ascending colon was confirmed by 99mTc-diethylene triamine pentaacetic acid human serum albumin (HSA-D) scintigraphy. Soon after starting a long-acting somatostatin analogue, octreotide, with co-administration of oral prednisolone, their general status improved in parallel with a rapid decrease in the volume of watery diarrhea and an increase in serum levels of albumin and IgG. Also on 99mTc-HSA-D scintigraphy protein leakage from the GI tract was apparently decreased in both patients. Combination therapy with a somatostatin analogue and corticosteroid may be effective for protein losing enteropathy with intractable diarrhea ascribable to GI amyloidosis. Because of the lack of specific therapies in this serious clinical situation, the described therapy should actively be considered as a therapeutic option not only in AA amyloidosis, but also in other types of systemic amyloidosis.
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PMID:Severe protein losing enteropathy with intractable diarrhea due to systemic AA amyloidosis, successfully treated with corticosteroid and octreotide. 1607 11

Vapreotide (RC-160), an octapeptide analog of somatostatin, has a high affinity for somatostatin receptor subtypes SSTR2 and SSTR5. Vapreotide binds differently to the tumors of the breast, ovary, exocrine pancreas, prostate and colon, than octreotide another octapeptide analog of somatostatin. Vapreotide was labeled with Tc-99m, a radionuclide highly suitable for scintigraphic imaging. The labeling procedure was simple, produced >70% yields and could be applicable to label other peptides containing a cystine bridge. HPLC analysis showed that the tracer was stable when Tc-99m-RC-160 was challenged with 100 fold molar excess DTPA (diethylenetriaminepentaacetic acid), HSA (human serum albumin) or cysteine and incubated at 37 degrees C for 4 h. HPLC analysis of urine samples obtained from mice that received Tc-99m-RC-160 showed that the preparation was stable in vivo. Rat brain cortex membrane receptor displacement assays showed that the Kd values for Tc-99m-RC-160 (71x10(-9) M) and Tc-99m-octreotide (86x10(-9) M) (Sandostatin(R)) were in nM range, and were similar to that for I-125-RC-160 (46x10(-9) M). High binding affinity of Tc-99m-RC-160 for human breast tumor cells SKBR-3 was also observed. These results suggest that Tc-99m-RC-160 is worthy of evaluation as an agent for scintigraphic imaging of tumors rich in somatostatin receptor subtypes SSTR2 and SSTR5.
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PMID:Vapreotide labeled with Tc-99m for imaging tumors. 2154 33

Somatostatin, a natural inhibitor of growth hormone (GH), and its analogs have been used in clinical settings for the treatment of acromegaly, gigantism, thyrotropinoma, and other carcinoid syndromes. However, natural somatostatin is limited for clinical usage because of its short half-life in vivo. Albumin fusion technology was used to construct long-acting fusion proteins and Pichia pastoris was used as an expression system. Three fusion proteins (SS28)(2)-HSA, (SS28)(3)-HSA, and HSA-(SS28)(2), were constructed with different fusion copies of somatostatin-28 and fusion orientations. The expression level of (SS28)(3)-HSA was much lower than (SS28)(2)-HSA and HSA-(SS28)(2) due to the additional fusion of the somatostatin-28 molecule. MALDI-TOF mass spectrometry revealed that severe degradation occurred in the fermentation process. Similar to the standard, somatostatin-14, all three fusion proteins were able to inhibit GH secretion in blood, with (SS28)(2)-HSA being the most effective one. A pharmacokinetics study showed that (SS28)(2)-HSA had a prolonged half-life of 2 h. These results showed that increasing the number of small protein copies fused to HSA may not be a suitable method for improving protein bioactivity.
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PMID:The effect of albumin fusion structure on the production and bioactivity of the somatostatin-28 fusion protein in Pichia pastoris. 2475 60