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Biomedical subjects

J S Day

Publications and source records attributed to J S Day.

30 records · Page 2Linked to original sources
PubMed1988

Dose-dependent down-regulation of beta-adrenergic receptors after chronic intravenous infusion of antidepressants.

1. The effects of intravenous infusion of desipramine (1, 3, 10, and 60 mg/kg/day), amitriptyline, zimelidine, iprindole (3, 10, 30, 60, and 100 mg/kg/day each), imipramine (10, 30, and 100 mg/kg/day), or U-48753E (1, 3, 10, and 30 mg/kg/day) on the density of central beta-adrenergic receptors (beta-AR) were investigated in female Sprague-Dawley rats. 2. Desipramine, amitriptyline, zimelidine, iprindole, imipramine, and U-48753E dose-dependently reduced the density of beta-AR in the cerebral cortex. 3. The time of onset of down-regulation of beta-AR was negatively correlated with the doses of drugs. 4. At equipotent doses, antidepressants seem to have a similar profile for the time of onset of reduction in the density of beta-AR. 5. The results indicate that down-regulation of beta-AR may be involved in mediating the therapeutic effects of antidepressants, and this effect can be rapidly achieved by intravenous infusion of drugs.

Amitriptyline↗
PubMed1988

A new 21-aminosteroid antioxidant lacking glucocorticoid activity stimulates adrenocorticotropin secretion and blocks arachidonic acid release from mouse pituitary tumor (AtT-20) cells.

The compound U74006F (21-[4-(2,6-di-1-pyrrolidinyl-4-pyrimidinyl)-1-piperazinyl]-16 alpha-methyl- pregna-1,4,9(11)-triene-3,20-dione) is one of a novel series of 21-aminosteroids that are potent inhibitors of iron-dependent lipid peroxidation. Chronic (4-6 days) dosing of mice or rats with high doses of U74006F (30-200 mg/kg/day) has indicated that the compound is devoid of both glucocorticoid and mineralocorticoid activity. Although the compound is not a glucocorticoid antagonist, it markedly stimulated secretion of adrenocorticotropin by the murine pituitary tumor (AtT-20) cell. The enhanced secretion of adrenocorticotropin was not associated with an increased incorporation of [3H]thymidine or [14C]leucine into DNA or protein, respectively. Although not a glucocorticoid, U74006F also blocked the release of [14C]arachidonic acid from AtT-20 cells damaged by either Fe++ or the metabolic poison, iodoacetate. U74006F represents a novel class of antioxidant which displays cytoprotective activity and may uniquely affect cell growth or function in culture systems.

Adrenocorticotropic Hormone↗
PubMed1986

The effect of proadifen on the metabolism of adinazolam.

Binding affinities of adinazolam and its metabolite mono-N-demethyladinazolam, U-42352, to the brain tissue are not altered by the presence of proadifen (SKF-525A) in [3H]flunitrazepam [( 3H]FNZ) binding assays in-vitro. Pretreatment of mice with proadifen significantly blocked the ability of intravenously administered adinazolam to inhibit [3H]FNZ binding in the studies ex-vivo. The binding profile of [3H]FNZ to the brain tissue was not significantly different when animals were treated with U-42352 or proadifen with U-42352. These results suggest that proadifen may block the conversion of adinazolam to its active metabolite U-42352.

Animals↗
PubMed1986

Rapid changes in central beta-adrenergic receptors after chronic intravenous infusion of antidepressants.

The effects of intravenous infusion of desipramine (1, 3, 10, and 60 mg/kg/24 hr), amitriptyline, zimelidine, iprindole (3, 10, 30, 60, and 100 mg/kg/24 hr each), imipramine (10, 30, and 100 mg/kg/24 hr), or U-48,753E (1, 3, 10, and 30 mg/kg/24 hr) on the density of central beta-adrenergic receptors were investigated in Sprague-Dawley rats. A comparative study with oral desipramine (3 mg/kg/24 hr) for 74 hrs was also carried out. Desipramine, amitriptyline, zimelidine, iprindole, imipramine, and U-48,753E reduced the density of beta-adrenergic receptors in the cerebral cortex, and the effect seems to be dose-dependent. In the oral study, desipramine failed to down-regulate beta-adrenergic receptors. These results indicate that down-regulation of beta-adrenergic receptors can be rapidly achieved by intravenous infusion of drugs.

Administration, Oral↗
PubMed1983

Immunochemical evidence for the involvement of prostaglandin H synthase in hydroperoxide-dependent oxidations by ram seminal vesicle microsomes.

Monoclonal antibodies against prostaglandin H (PGH) synthase have been used to precipitate cyclooxygenase and peroxidase activities from detergent-solubilized preparations of ram seminal vesicle microsomes. Approximately 85% of the solubilized cyclooxygenase activity was precipitated using an excess of anti-PGH synthase antibody; under similar conditions, immunoprecipitation of 60% of the diphenylisobenzofuran peroxidase, 75% of the phenylbutazone peroxidase, and 50% of the epinephrine peroxidase activities occurred. In contrast, less than 10% of the cyclooxygenase or peroxidase activities could be precipitated with nonimmune, control antibody preparations. These data indicate that the hydroperoxidase activity of PGH synthase is the major peroxidase activity catalyzing the co-oxidation of xenobiotics in ram seminal vesicle microsomes.

Animals↗
PubMed1983

Concentrations of prostaglandin endoperoxide synthase and prostaglandin I2 synthase in the endothelium and smooth muscle of bovine aorta.

Platelets adhere to the subendothelial layer of newly deendothelialized arteries. Attachment can be reduced with exogenous prostacyclin (PGI2). Thus, the subendothelium may be unable to produce sufficient PGI2 to prevent platelet adherence and subsequent platelet-platelet interaction. Consistent with this explanation are data from an earlier report (1977. Moncada S., A. G. Herman, E. A. Higgs, and J. R. Vane. Thromb. Res. 11:323-344) indicating that the smooth muscle layer of aorta has only 10-15% of the capacity of endothelial cells to synthesize PGI2. We have measured the concentrations of PGI2 synthase and prostaglandin endoperoxide (PGH) synthase in bovine aorta and obtained results quite different from those described in this earlier report. Tandem immunoradiometric assays for PGI2 synthase and PGH synthase antigens were used to quantitate these proteins in detergent-solubilized homogenates of endothelial cells and smooth muscle tissue prepared from 10 different bovine aorta. The concentrations of PGI2 synthase in endothelial cells and smooth muscle were found to be the same. However, the concentration of PGH synthase in endothelial cells averaged greater than 20 times that of smooth muscle. Results similar to those determined by immunoradiometric assay were also obtained when PGH synthase and PGI2 synthase catalytic activities were measured in preparations of endothelial and smooth muscle cells. Furthermore, when bovine aorta and renal arteries were subjected to immunocytofluorescence staining using monoclonal antibodies to PGI2 synthase, fluorescence staining of equivalent intensity was detected in both the endothelial cells and the smooth muscle. Moreover, the intensity of fluorescence was similar throughout cross-sections of vascular smooth muscle, indicating that there is no gradient in PGI2 synthase concentrations between the endothelium and adventitia. Our results indicate that the propensity of platelets to adhere to the subendothelium of deendothelialized arteries and form aggregates cannot be attributed simply to an inability of the denuded vasculature to produce PGI2 from PGH2, but may be a consequence of the low PGH synthase activity of smooth muscle. Consistent with this concept are the results of Eldor et al. (1981. J. Clin. Invest. 67:735-741) who reported that increases in PGH synthase activity are associated with formation of a nonthrombogenic neointima.

Animals↗
PubMedDate not supplied

Epidemiology and prevention of blood and body fluid exposures among emergency department staff.

Emergency Department (ED) staff are vulnerable to occupational exposure to infectious blood and body fluids (BBF). Universal precautions are often ignored in the ED setting. Identification of body locations at high risk of BBF exposure may allow development of site specific protective garments that minimize risk and inconvenience. All permanent staff (92) in a 58,000 visit public university hospital ED with potential for BBF exposure were surveyed. Respondents estimated the number of BBF contacts sustained during the past year, describing their most recent contact in detail. Seventy-eight of 91 (85%) responded, reporting average rates of 54.1 intact skin, 1.5 nonintact skin, and .87 mucous membrane BBF contacts per full-time employee per year. Of the most recent incidents, 94% involved blood, 22% involved vomit or urine, and 11% involved saliva. Eighty-eight percent of BBF contacts were to unprotected skin or mucous membranes, either when no barrier was worn or at the gap between gloves and sleeves. Most (66%) were distal to the elbow; 13% involved the face. Use of long gloves or another continuous protective barrier from the fingers to the elbow, in addition to increased use of face masks or shields, would markedly reduce the rate of ED BBF contacts with a minimum of inconvenience.

Blood-Borne Pathogens↗
PubMedDate not supplied

Quantification of subchondral bone changes in a murine osteoarthritis model using micro-CT.

In the past few years there has been a considerable interest in the role of bone in osteoarthritis. Despite the increasing evidence of the involvement of bone in osteoarthritis, it remains very difficult to attribute the cause or effect of changes in subchondral bone to the process of osteoarthritis. Although osteoarthritis in mice provides a useful model to study changes in the subchondral bone, detailed quantification of these changes is lacking. Therefore, the goal of this study was to quantify subchondral bone changes in a murine osteoarthritis model by use of micro-computed tomography (micro-CT). We induced osteoarthritis-like characteristics in the knee joints of mice using collagenase injections, and after four weeks we calculated various 3D morphometric parameters in the epiphysis of the proximal tibia. The collagenase injections caused cartilage damage, visible in histological sections, particularly on the medial tibial plateau. Micro-CT analysis revealed that the thickness of the subchondral bone plate was decreased both at the lateral and the medial side. The trabecular compartment demonstrated a small but significant reduction in bone volume fraction compared to the contralateral control joints. Trabeculae in the collagenase-injected joints were thinner but their shape remained rod-like. Furthermore, the connectivity between trabeculae was reduced and the trabecular spacing was increased. In conclusion, four weeks after induction of osteoarthritis in the murine knee subtle but significant changes in subchondral bone architecture could be detected and quantified in 3D with micro-CT analysis.

Animals↗