Էջ 1 սկսած 32 արդյունքներ
Slices and homogenates from rat cerebral cortex were used to study the effect of hypoxia, with or without hypocapnia, on phosphatidylethanolamine synthesis. The incorporation of [1-3H]ethanolamine into the corresponding phospholipid was greatest in slices treated with pure nitrogen, intermediate
By the use of the Langendorff technique, surviving isolated rat hearts were perfused with [1-14 C] palmitate, [1-14C] hexadecanol or [1-14C,1-3H] hexadecanol under normal or anoxic conditions. After perfusion for 30min with either precursor, when oxygenated or in an hypoxic condition, or when
We examined the pulmonary hemodynamics and morphology after injection of a sclerosing solution of 5% ethanolamine oleate (EO) into 24 normal dogs. EO of 0.5 ml/kg (n = 5), 1.0 ml/kg (n = 6), and 3.0 ml/kg (n = 7) was injected through the jugular vein into the right atrium for pathological
Changes in the composition and contents of phospholipids and free fatty acids were observed and compared in three groups: (A) unpreconditoned normal controls, (B) exposure to 1 run of hypoxia and (C) exposure to 4 runs of hypoxia. In group B, the content of phosphatidyl ethanolamine (PE),
Content of lysophospholipids and their diacyl derivatives was astimated in intact and destructed mitochondria of rat spermatic glands in acute hypoxic hypoxia by means of thin-layer chromatography on silica gel. A ratio of phospholipid lysoforms was found to increase with simultaneous decrease in
Tumor hypoxia is a major indicator of treatment resistance to chemotherapeutic drugs, and fluorescence optical tomography has tremendous potential to provide clinically useful, functional information by identifying tumor hypoxia. The synthesis of a 2-nitroimidazole-indocyanine green conjugate using
Exposure of adult rats to hypobaric hypoxia caused hypolipidemia, hypotriglyceridemia and hypophospholipidemia. Hypobaric hypoxia produced an increase in liver triglyceride and cholesterol levels and a decrease in lung triglyceride, total phospholipid and phosphatidyl choline. The proportion of
Tumor hypoxia is associated with the rapid proliferation and growth of malignant tumors, and the ability to detect tumor hypoxia is important for predicting tumor response to anti-cancer treatments. We have developed a class of dye-conjugates that are related to indocyanine green (ICG, ) to target
Patients with disseminated Ewing's family of tumors (ESFT) often experience drug-resistant relapse. We hypothesize that targeting minimal residual disease with the cytotoxic retinoid N-(4-hydroxyphenyl) retinamide (4-HPR; fenretinide) may decrease relapse. We determined the following: (a) 4-HPR
Rats subjected to mild hypoxic and postdecapitative ischemic treatments indicated a decrease (8-16%) in the proportion of polyunsaturated acyl groups of diacyl glycerophosphocholines (diacyl-GPC), diacyl glycerophosphoethanolamines (diacyl-GPE), and alkenylacyl glycerophosphoethanolamines
The mitochondrial fraction obtained from brains of animals submitted to ischemia shows a decrease of phospholipid level, especially plasmalogens in the fraction of ethanolamine phospholipids and choline phospholipids. There appears simultaneously an increase of free radical oxidation processes of
Incubation of mitochondria under hypoxic conditions in hypotonic solution of sucrose containing dinitrophenol as an uncoupler of oxidative phosphorylation led to hydrolysis of mitochondrial phospholipids, with the most pronounced destruction of phosphatidyl ethanolamine and cardiolipin fractions.
In the presence of ATP, Mg and CoA-SH]1-14C]linoleic acid was incorporated into membrane phospholipids (P2 fraction and synaptosomes) prepared from rat brain cortex. The relative order for linoleate incorporation was: phosphatidyl-choline greater than phosphatidylethanolamine greater than
In 34 cirrhotic patients with esophageal varices, a significant but temporary deterioration in pulmonary function tests occurred 24 h after endoscopic injection sclerotherapy using 5% ethanolamine oleate. Included were vital capacity, forced expiratory volume in 1 s, closing volume/vital capacity