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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Massive obstetric haemorrhage is a major cause of maternal death and morbidity; abruptio placentae, placenta praevia and postpartum haemorrhage being the main causes. A delay in the correction of hypovolaemia, a delay in the diagnosis and treatment of defective coagulation and a delay in the surgical control of bleeding are the avoidable factors in most maternal deaths caused by haemorrhage. The degree of hypotension is the first guide to the level of blood loss, except in abruptio placentae. A protocol incorporating the guidelines is shown. The rapid correction of hypovolaemia with crystalloids and red cells is the first priority, followed by blood component therapy as indicated by the haematocrit, coagulation tests, platelet count and clinical features. Serial monitoring of the response to treatment is essential. Oxytocin and prostaglandin will correct uterine atony, and appropriate surgical intervention is required for traumatic bleeding. Ligation of the uterine arteries, ovarian arteries and internal iliac arteries will usually control uterine bleeding, arterial embolization also being effective. Hysterectomy should be considered as well. Catastrophic bleeding may also arise in complications such as rupture of the liver and acute fatty liver of pregnancy. These rare complications are best managed by a multidisciplinary team involving the obstetrician, anaesthetist, haematologist, hepatologist and renal physician. The rupture of aneurysms in the splenic artery and in other branches of the aorta can result in massive haemorrhage during pregnancy and following delivery.
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PMID:Massive obstetric haemorrhage. 1078 57

Oxytocin, a protein hormone mainly produced by hypothalamus, has been shown to repress body weight gain in obese animals, in part, by reducing food intake and increasing energy expenditure. Till now, activation of brown fat tissue (BAT) thermogenesis and white adipose tissue (WAT) browning are considered as two main factors for oxytocin-induced energy expenditure. However, the underlying molecular mechanisms are still not understood well. Here, we observed that oxytocin expression in the hypothalamus and its receptor in adipose tissues were induced by cold exposure in mice. In differentiated adipocytes, oxytocin stimulated brown adipocyte specific gene expression by inducing PRDM16. In high fat diet induced obese mice, oxytocin delivery by osmotic minipumps increased body core temperature and decreased body weight gain. Glucose and insulin tolerance were improved by oxytocin. Hyperinsulinemia and fatty liver were ameliorated in oxytocin-treated animals. Moreover, oxytocin treatment induced thermogenic gene expressions in BAT, inguinal WAT (iWAT), and skeletal muscle. Taken together, our findings revealed a new aspect of oxytocin, i.e. oxytocin induces iWAT browning and stimulates thermogenesis in BAT, iWAT and skeletal muscle, through which oxytocin promotes thermogenesis and thus combats obesity and metabolic dysfunctions.
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PMID:The effects of oxytocin to rectify metabolic dysfunction in obese mice are associated with increased thermogenesis. 3253 19