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)

There is evidence that gastric Helicobacter pylori (Hp) infection promotes duodenal ulceration by releasing gastrin. We therefore asked how Hp releases gastrin. Tumour necrosis factor alpha (TNF-alpha) is up-regulated in Hp gastritis and stimulates hormone release from pituitary cells, so we tested its effect on primary cultures of canine antral G cells and human antral fragments. TNF-alpha pretreatment (100 ng mL-1) of canine G cells significantly increased both basal (by 89%: P < 0.01) and bombesin-stimulated (by 39% P < 0.05) gastrin release. A similar pattern of increase was seen following TNF-alpha (20 ng mL-1) pretreatment of human antral fragments: basal gastrin release was increased by 38% (P < 0.05) and bombesin-stimulated by 26% (P < 0.05). This effect persisted during immunoblockade with anti-somatostatin antibody S6. We propose that TNF-alpha provides the link between Hp infection and gastrin release and thus contributes to duodenal ulceration.
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PMID:Tumour necrosis factor alpha stimulates gastrin release from canine and human antral G cells: possible mechanism of the Helicobacter pylori-gastrin link. 886 24

Biotechnology has enabled greater understanding of the cellular and molecular biology of acute pancreatitis and has offered the possibility of a new generation of biodrugs to treat this disease. The proteases inhibitor gabexate mesilate has proven to be effective for endoscopic retrograde cholangiopancreatography-induced pancreatitis but, given the low incidence of this condition, its cost-effectiveness has to be evaluated. Randomised controlled trials have shown no benefit for somatostatin or its analogue octreotide although some practitioners continue to use it to prevent organ damage and complicated disease. Antioxidant therapy has been thoroughly investigated in animal models but the results of large scale clinical trials are awaited. The use of kinin inhibitors is in its infancy and has not yet reached the clinic. Considerable interest has been engendered in nitric oxide (NO), firstly for its beneficial use in acute lung injury resulting from the multi-organ failure of acute pancreatitis and secondly, the possible benefits of NOS inhibition to prevent pancreatitic necrosis. Tumour necrosis factor antagonism and interleukin- 1 blockade are 2 therapies awaiting clinical trials because there is overwhelming evidence of their benefit in animal models. Interleukin-10, an anticytokine, may have similar benefits and has been shown to be beneficial in animal models when given as pretreatment. The only biodrug that has progressed to phase III clinical trials is the platelet-activating factor antagonist lexipafant. Successful phase II studies have been followed up by a phase III study indicating benefits in reduction of organ failure and pseudocyst formation and reduction in mortality when treatment is given within 48 hours of onset of the disease. Finally, prophylactic therapy with selected antibacterials in patients with predicted severe disease can reduce local complications and possibly mortality.
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PMID:Acute pancreatitis: an overview of emerging pharmacotherapy. 1802 Jun 8