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[Falls in PaO2 owing to prostaglandin E1 infusion in an obese patient undergoing laparoscopic cholecystectomy--detection by intra-arterial blood gas monitoring].

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We monitored the changes of arterial blood gas tensions using a continuous blood gas monitor (Paratrend-7) in an obese patient who underwent laparoscopic cholecystectomy. We could observe continuous changes in PaO2 caused by prostaglandin E1 (PGE1) infusion. Suppression in hypoxic pulmonary

Prostaglandin E2-mediated impairment of innate immune response to A(H1N1)pdm09 infection in diet-induced obese mice could be restored by paracetamol.

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UNASSIGNED To investigate why obesity leads to increased severity of influenza infection. UNASSIGNED We employed a mouse model with diet-induced obesity (DIO) to study the innate immune responses induced by influenza virus. UNASSIGNED The lungs of DIO mice were heavily affected by obesity-associated

Evidence for abnormal prostaglandin synthesis in obese Zucker rat adipose cell cultures.

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Prostaglandin E2 (PGE2) is synthesized in adipose tissue and acts locally to inhibit lipolysis. This study examined PGE2 synthesis by presumptive and mature adipocytes isolated from lean and obese Zucker rats. Isoproterenol-stimulated lipolysis was greater in short-term incubations of mature

Plasma prostaglandin levels in fed and starved lean, normal and obese women.

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The plasma obtained from fed and starved lean, normal and obese women was estimated, by a radio-immunoassay method, for prostaglandins, owing to their implication in the regulation of adipose tissue lipolysis and the development of obesity. No significant differences were found due to nutritional

Prostaglandin synthesis and membrane fatty acid composition in the heart of obese Zucker rats.

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Genetically obese Zucker rats share several abnormalities with obese patients: inheritance of the obesity, hyperinsulinemia, hypertriglyceridemia. Because alterations in membrane fatty acid composition and in prostaglandin synthesis can be involved in the genesis of the cardiovascular complications

Treatment of obesity and pulmonary arterial hypertension with inhibitors of the prostaglandin transporter: evaluation of patent WO2014/204895A1.

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Prostaglandins display a wide array of pharmacological effects and prostaglandin analogs are already used in the treatment of pulmonary arterial hypertension (PAH). After synthesis and release from cells, prostaglandins undergo reuptake by the prostaglandin transporter (PGT). WO2014/204895 claims

Dose-dependent reduction of hereditary obesity in the non-diabetic mouse by polymeric prostaglandin PGBx.

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Mice genetically obese but not diabetic show large reductions of excessive body weight and excessive food intake when treated with polymeric prostaglandin PGBx. Larger doses of PGBx produce greater reduction of both body weight and food consumption, in agreement with dose-dependent effects of PGBx

Stimulation of leptin release by arachidonic acid and prostaglandin E(2) in adipose tissue from obese humans.

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The purpose of this study was to examine the effect of arachidonic acid and its metabolites on leptin formation by explants of human adipose tissue over a 48-hour incubation in primary culture. We found that arachidonic acid or prostaglandin E(2) (PGE(2)) stimulated leptin release by explants of

Suppression of insulitis in non-obese diabetic (NOD) mice by oral insulin administration is associated with selective expression of interleukin-4 and -10, transforming growth factor-beta, and prostaglandin-E.

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Oral administration of autoantigens suppresses development of autoimmunity in several animal models, and is being tested in clinical trials in patients with autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. Non-obese diabetic (NOD) mice spontaneously develop insulin-dependent

Antilipolytic effects of N6-phenylisopropyladenosine and prostaglandin E2 in fat-cells of obese volunteers before and during energy restriction.

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The antilipolytic effects of N6-phenylisopropyladenosine and of prostaglandin E2 were studied with adipocytes of obese volunteers before and after 4 weeks of severe energy restriction [1250 kJ (300 cal)/day] in the presence and absence of adenosine deaminase (1.6 micrograms/ml, corresponding to 320

Prostaglandins and obesity.

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In metabolic obesity energy in triglyceride stores is not readily accessible, and lipolysis to free fatty acid and glycerol seems to be somehow restrained. In the normal situation, there is a balance between a forward reaction via cyclic A.M.P. ending in lipolysis and a negative-feedback mechanism

Defective renal prostaglandin synthesis in hypertensive patients with morbid obesity.

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Renal prostaglandin synthesis in 36 obese hypertensive patients was estimated from measurements of 24-hour urinary prostaglandin E2 (PGE2) excretion rates. PGE2 was measured by radioimmunoassay using Dray antiserum prior to and 1 week after starting a fast supplemented by 320 cal derived from 30 g

Prostaglandin E2 action and binding in human adipocytes: effects of sex, age, and obesity.

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The antilipolytic effect of prostaglandin E2 (PGE2) was studied in subcutaneous human adipocytes. The influence of sex, age, and obesity on the PGE2 effect was investigated. The antilipolytic effects of PGE2 were related to the PGE2 binding data obtained in the same adipocytes. The maximal

NSAID use reduces breast cancer recurrence in overweight and obese women: role of prostaglandin-aromatase interactions.

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Obesity is associated with a worse breast cancer prognosis and elevated levels of inflammation, including greater cyclooxygenase-2 (COX-2) expression and activity in adipose-infiltrating macrophages. The product of this enzyme, the proinflammatory eicosanoid prostaglandin E2 (PGE2), stimulates

Importance of adipocyte cyclooxygenase-2 and prostaglandin E2-prostaglandin E receptor 3 signaling in the development of obesity-induced adipose tissue inflammation and insulin resistance.

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We examined the involvement of adipocyte cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2)-prostaglandin E receptor (EP)3-mediated signaling during hypertrophy and hypoxia in the development of obesity-associated adipose tissue (AT) inflammation and insulin resistance. The experiments were

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