Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In spite of the development of various antibiotics, management of elderly patients with pneumonia remains an important problem. It is suggested that adult respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC) often occur in elderly patients with pneumonia. Although neutrophils are suggested to be involved in the genesis of these conditions, details remain unknown. We demonstrated that a highly cytotoxic substance, 9,10-epoxy-12-octadecenoate, is biosynthesized from linoleate by human neutrophils, thus it was named leukotoxin. Leukotoxin was detected in lung lavages from patients with ARDS. In these lung lavages, increases in albumin concentration and angiotensin converting enzyme (ACE) activity were also observed. Similar results were observed in lung lavages from rats after exposure to hyperoxia for 60 hours in an experimental model of ARDS. Intravenous administration of leukotoxin (100 mumol/kg) caused lung edema. Albumin concentration and ACE activity were increased in lung lavages of rats receiving leukotoxin. In contrast, these changes were not observed in rats administered with linoleate. Furthermore, administration of leukotoxin (100 mumol/kg) caused coagulation abnormality, i.e., increase in fibrin-fibrinogen degradation products, decrease in fibrinogen, and prolongation of activated partial thromboplastin time and prothrombin time. Administration of linoleate did not induce these changes. It is indicated that O2- was produced by respiratory burst enzyme located in neutrophil plasma membrane, and that hydroxyl radicals derived from O2- by Fenton reaction were responsible for leukotoxin synthesis. From our results, leukotoxin, a product of hydroxyl radicals and linoleate, might be responsible for the genesis of ARDS and DIC.
 ...
PMID:[Leukotoxin and pulmonary injury]. 238 90

Continuous maternal hyperoxygenation treatment (2.5 l/min by means of a nasopharyngeal cannula) was given in four patients presenting with intrauterine growth-retarded (IUGR) fetuses and decelerative fetal heart rate (FHR) patterns at 27-28 weeks of gestation. The effect of maternal hyperoxia was studied longitudinally. Neither the incidence of generalized fetal movements (FGM%) nor the pulsatility index of the internal carotid artery increased under hyperoxia. In fact, both variables decreased progressively. FHR variation was abnormal prior to the start of hyperoxygenation and showed a slight but transient increase. On average, maternal hyperoxygenation 'resulted' in a prolongation of the duration of pregnancy of 9 days. The neonatal mortality was similar in the study group as compared to a control group of IUGR infants. However, hypoglycemia, thrombocytopenia and disseminated intravascular coagulation at birth were found more frequently in the study group. Conversely, blood gas abnormalities were less frequent in the fetuses of mothers that were treated with oxygen. We conclude that positive effects of oxygen therapy in IUGR fetuses remain uncertain and that detrimental effects due to prolongation of intrauterine malnutrition have not as yet been sufficiently excluded.
 ...
PMID:Continuous maternal hyperoxygenation in the treatment of early fetal growth retardation. 1279 38

Heterotrophy is known to stimulate calcification of scleractinian corals, possibly through enhanced organic matrix synthesis and photosynthesis, and increased supply of metabolic DIC. In contrast to the positive long-term effects of heterotrophy, inhibition of calcification has been observed during feeding, which may be explained by a temporal oxygen limitation in coral tissue. To test this hypothesis, we measured the short-term effects of zooplankton feeding on light and dark calcification rates of the scleractinian coral Galaxea fascicularis (n=4) at oxygen saturation levels ranging from 13 to 280%. Significant main and interactive effects of oxygen, heterotrophy and light on calcification rates were found (three-way factorial repeated measures ANOVA, p<0.05). Light and dark calcification rates of unfed corals were severely affected by hypoxia and hyperoxia, with optimal rates at 110% saturation. Light calcification rates of fed corals exhibited a similar trend, with highest rates at 150% saturation. In contrast, dark calcification rates of fed corals were close to zero under all oxygen saturations. We conclude that oxygen exerts a strong control over light and dark calcification rates of corals, and propose that in situ calcification rates are highly dynamic. Nevertheless, the inhibitory effect of heterotrophy on dark calcification appears to be oxygen-independent. We hypothesize that dark calcification is impaired during zooplankton feeding by a temporal decrease of the pH and aragonite saturation state of the calcifying medium, caused by increased respiration rates. This may invoke a transient reallocation of metabolic energy to soft tissue growth and organic matrix synthesis. These insights enhance our understanding of how oxygen and heterotrophy affect coral calcification, both in situ as well as in aquaculture.
 ...
PMID:Oxygen and heterotrophy affect calcification of the scleractinian coral Galaxea fascicularis. 2328 59