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Biomedical subjects

L Levine

Publications and source records attributed to L Levine.

At least 145 records · Page 8Linked to original sources
PubMed1983

Concentrations of arachidonic-acid metabolites in human mixed saliva are independent of flow rate.

Three prostaglandins, PGE2, PGF2 alpha and PGI2 (measured as 6-keto-PGF1 alpha), serologically active 6-sulphidopeptide-containing leukotrienes and hydroxyeicosatetraenoic acids were determined by radioimmunoassay of mixed saliva obtained at several flow rates from 8 healthy volunteers. Flow rates ranged from 0.26 +/- 0.02 ml/min when saliva production was unstimulated to 1.18 +/- 0.14 ml/min (values mean +/- SEM) when maximally stimulated. Concentrations of all compounds tested remained independent of changes in mixed-saliva flow rate.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1983

Inhibitory effect of insulin on prostacyclin production by isolated rat adipocytes.

Physiologic concentrations of insulin completely inhibited the norepinephrine-induced increment in the production of 6-keto-prostaglandin (PG) F1 alpha, the stable derivative of prostacyclin (PGI2), by isolated rat adipocytes. The inhibition of PGI2 production by insulin in isolated rat adipocytes supports the view that the elevated plasma level of 6-keto-PGF1 alpha in rats with non-ketotic diabetes mellitus and diabetic ketoacidosis is derived at least in part from production of PGI2 by the adipocyte cell mass.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Detection of compounds immunologically related to arachidonic acid transformation products in extracts of invertebrates.

Organic extracts of Terpios zeteki, a sponge from the phylum Porifera, Aplysia californica and Helix aspersa, two species from the phylum Mollusca, and Arbacia, the sea urchin, from the phylum Echinodermata, contained compounds that appeared by radioimmunoassays to be HETE, PGE2, PGF2 alpha, and 6-keto-PGF1 alpha, the non-enzymatic hydrolytic product of PGI2. However, lack of coincidence of their retention times on HPLC with authentic oxygenation products of arachidonic acid suggested that most of the immunologically active compounds were derivatives of arachidonic acid metabolites or products derived from polyunsaturated fatty acids other than arachidonic acid.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1983

Inhibition by AA861 of prostaglandin E2 production by activated peritoneal macrophages of rat.

Prostaglandin E2 production by rat peritoneal activated macrophages was inhibited by AA861 which had been reported as a selective inhibitor of 5-lipoxygenase from guinea pig peritoneal leukocytes. At a dose of 3.06 microM, prostaglandin E2 production was decreased to 27% of control. No inhibition of the release of (3H)arachidonic acid from the prelabeled macrophages was observed at the dose.

Animals↗
PubMed1983

Stimulation of arachidonic acid metabolism in rat kidney mesangial cells by bradykinin, antidiuretic hormone, and their analogues.

Kinins, antidiuretic hormone, and several of their analogues stimulated contractile rat kidney mesangial cells growing in culture to produce prostaglandins E2, F2 alpha, and I2. Analogues that are known to be pharmacologically active stimulated arachidonic acid metabolism in these cells, whereas compounds that have little activity were ineffective. Stimulation of arachidonic acid metabolism by these agonists appeared to be receptor-mediated. It is possible that arachidonic acid metabolism is stimulated by contraction of mesangial cells and the released prostaglandins regulate glomerular function.

Animals↗
PubMed1983

Tropicamide-induced mydriasis in densely pigmented eyes.

Clinically effective diameters (CED's) corresponding to illumination intensities used in direct ophthalmoscopy were determined in 30 young adults with densely pigmented irides after instillation of 1 drop of 0.5% tropicamide. All subjects were of Asian, Pacific Island, or Hispanic origin. The maximum CED was attained by 30 min and was maintained without significant change for the next 60 min. Ninety percent of the subjects had maximum CED's of 6.0 mm or more, and 57% had CED's of 7.0 mm or more. These figures correspond to the entrance pupil diameters and are free from the effects of corneal magnification. The average CED's for these densely pigmented eyes did not differ in a statistically significant manner from corresponding mean CED's for 97 less densely pigmented Caucasian eyes during the interval of 30 to 90 min after instillation of tropicamide. Tropicamide at 0.5% concentration appears to be an effective mydriatic for use in these densely pigmented eyes with procedures requiring intensities of illumination similar to those used in direct ophthalmoscopy.

Adult↗
PubMed1983

Cardiorespiratory responses to exercise distributed between the upper and lower body.

The present study examined the influence that distributing exercise between upper (arm crank exercise) and lower (cycle exercise) body muscle groups had on cardiorespiratory responses to constant power output (PO) exercise. Six male volunteers completed five submaximal exercise bouts of 7-min duration at both 76 and 109 W. The arm PO/total PO (% arm) for these bouts was approximately 0, 20, 40, 60, and 100%. At 76 W, O2 uptake (VO2) did not change (P greater than 0.05) from 0 to approximately 20% arm (approximately 1.30 1 x min-1) but increased with increasing percent arm values up to 100% (1.58 1 x min-1). At 109 W, VO2 increased throughout the range of 0 (1.70 1 x min-1) to 100% arm (2.33 1 x min-1). In general, minute ventilation (VE) and respiratory exchange ratio (R) increased with increased percent arm values at 76 and 109 W. The heart rate (HR) responses remained unchanged from 0 to 60% arm at both 76 and 109 W; however, between 60 and 100% arm, a 26-beats x min-1 increase was observed at 76 W (143 beats x min-1 at 100% arm) and a 45-beats x min-1 increase at 109 W (174 beats x min-1 at 100% arm). These data suggested that during upper body exercise, the increased VO2 associated with increased percent arm values was not accompanied by an elevated HR response when at least 40% of the PO was performed by the lower body. This might be attributed to a facilitated venous return and/or a decreased total peripheral resistance when the lower body was involved in the exercise.

Adult↗
PubMed1983

Fructose and glucose ingestion and muscle glycogen use during submaximal exercise.

Substrate utilization after fructose, glucose, or water ingestion was examined in four male and four female subjects during three treadmill runs at approximately 75% of maximal O2 uptake. Each test was preceded by three days of a carbohydrate-rich diet. The runs were 30 min long and were spaced at least 1 wk apart. Exercise began 45 min after ingestion of 300 ml of randomly assigned 75 g fructose (F), 75 g glucose (G), or control (C). Muscle glycogen depletion determined by pre- and postexercise biopsies (gastrocnemius muscle) was significantly (P less than 0.05) less during the F trial than during C or G. Venous blood samples revealed a significant increase in serum glucose (P less than 0.05) and insulin (P less than 0.01) within 45 min after the G drink, followed by a decrease (P less than 0.05) in serum glucose during the first 15 min of exercise, changes not observed in the C or F trials. Respiratory exchange ratio was higher (P less than 0.05) during the G than C or F trials for the first 5 min of exercise and lower (P less than 0.05) during the C trial compared with G or F for the last 15 min of exercise. These data suggest that fructose ingested before 30 min of submaximal exercise maintains stable blood glucose and insulin concentrations, which may lead to the observed sparing of muscle glycogen.

Administration, Oral↗
PubMed1983

Hypercalcemia in dogs with adenocarcinoma derived from apocrine glands of the anal sac. Biochemical and histomorphometric investigations.

Hypercalcemia, hypercalciuria, and hyperphosphaturia were present in female dogs with adenocarcinomas derived from apocrine glands of the anal sac (CA). Remission of hypercalcemia accompanied tumor excision in all six dogs undergoing surgery, whereas tumor recurrence or growth of metastases was associated with a return of hypercalcemia. Preoperatively, the plasma concentrations of immunoreactive parathyroid hormone in all dogs were undetectable or in the low normal range. Plasma concentrations of 13,14-dihydro-15-keto-prostaglandin E2 (PGE2M) and serum 1,25-dihydroxyvitamin D were not significantly different from control dogs. Urinary cyclic AMP and hydroxyproline were increased in dogs with CA. No immunoreactive parathyroid hormone was detected in extracts from tumor tissue, and parathyroid glands from dogs with CA had ultrastructural characteristics of secretory inactivity. Lumbar vertebrae from hypercalcemic dogs had decreased trabecular bone volume and increased osteoclastic bone resorption compared with age-matched control dogs. After tumor excision, serum total calcium returned to the normal range, whereas immunoreactive parathyroid hormone increased 2- to 20-fold and 1,25-dihydroxyvitamin D decreased 2- to 8-fold. Postoperative hypocalcemia was not observed. These results indicate that CA produces a hypercalcemic factor other than immunoreactive parathyroid hormone or prostaglandin E2 that increases osteoclastic osteolysis distant from the tumor and results in hypercalcemia, hypercalciuria, and hyperphosphaturia.

Adenocarcinoma↗
PubMed1983

Hypercalcemia in dogs with lymphosarcoma. Biochemical, ultrastructural, and histomorphometric investigations.

Dogs with lymphosarcoma and hypercalcemia had decreased trabecular bone volume and increased osteoclastic osteolysis, whereas dogs with lymphosarcoma that were normocalcemic did not have increased bone resorption. Increased osteoclastic resorption was present only in bone from hypercalcemic dogs that contained neoplastic tissue but not in bone free of tumors, suggesting that the factor(s) responsible for stimulating bone resorption were elaborated locally by the tumor tissue. Hypercalcemic dogs with lymphosarcoma had decreased concentrations of plasma immunoreactive parathyroid hormone and serum 1,25-(OH)2D compared with normocalcemic dogs with lymphosarcoma and control dogs with and without other neoplasms. Immunoreactive parathyroid hormone was not detected in lymphosarcoma tissue. The plasma concentration of 13,14-dihydro-15-keto-prostaglandin E2 (PGE2M) was increased approximately 2-fold in hypercalcemic dogs with lymphosarcoma as compared with other groups. Urine excretion of calcium, phosphorus, and hydroxyproline were increased in hypercalcemic dogs with lymphosarcoma. Ultrastructurally, lymphosarcomas were composed of tumor cells with large nuclei and a paucity of cytoplasmic organelles. Light and electron microscopic examination of parathyroid glands revealed inactive or atrophic chief cells in dogs with lymphosarcoma and hypercalcemia. The increased osteoclastic bone resorption in hypercalcemic dogs with lymphosarcoma was not mediated by increased circulating levels of immunoreactive parathyroid hormone and 1,25-(OH)2D but was dependent upon infiltration of bone marrow by neoplastic cells and, presumably, the local production of a bone resorption-stimulating factor.

Animals↗
PubMed1983

Requirements for protein synthesis and calcium for stimulation of prostaglandin synthesis in cultured rat liver cells by tumor promoters.

The tumor promoters, 12-O-tetradecanoylphorbol-13-acetate (TPA), phorbol-12,13-didecanoate, teleocidin, and dihydroteleocidin, at nM levels, but not the non-tumor-promoting 4 alpha-phorbol-12,13-didecanoate even at microM concentrations, stimulated arachidonic acid metabolism in cultured rat liver cells. These liver cells synthesize primarily prostaglandin I2 [measured as its nonenzymatic hydrolytic product, 6-keto-prostaglandin F1 alpha (PGF1 alpha)]. The production of 6-keto-PGF1 alpha increased with time of incubation with TPA and was essentially complete in 4 hr. Cycloheximide, at nM levels, blocked the TPA-stimulated 6-keto-PGF1 alpha production in a dose-dependent manner; this inhibition was related to inhibition of protein synthesis. Chelation of Ca2+ by ethyleneglycol-bis(beta-aminoethyl ether)-N,N'-tetraacetic acid, treatment of the cells with the Ca2+ channel blocker, nifedipine, or inhibition of intracellular Ca2+ mobilization by 8-(diethylamine)octyl-3,4, 5-trimethoxybenzoate hydrochloride also inhibited TPA-stimulated 6-keto-PGF1 alpha production. The steroidal antiinflammatory drug, dexamethasone, a potent in vivo inhibitor of tumor promotion, was an inhibitor of 6-keto-PGF1 alpha stimulation by TPA.

Alkaloids↗
PubMed1982

Prostaglandin production by homogeneous cultures of rat glomerular epithelial and mesangial cells.

Prostaglandin production was measured in homogeneous cultures that had been characterized as glomerular epithelial and mesangial cells. Glomerular epithelial cells produced ten times more cyclooxygenase products than mesangial cells; 88 to 95% of its products were prostacyclin. Mesangial cells produced predominantly prostaglandin E2 (57 to 66%); only 14 to 15% of the prostaglandins produced by mesangial cells was PGI2. Cultured glomerular epithelial and mesangial cells produced little prostaglandin D2, thromboxane, 12-L-hydroxyeicosatetraenoic acid, or 6-sulfido-peptide-containing leukotrienes.

Angiotensin II↗