Search PubMed⌕ Search

Biomedical subjects

J J Murray

Publications and source records attributed to J J Murray.

At least 163 records · Page 9Linked to original sources
PubMed1990

Prevention of trauma to teeth.

The prevention of disfigurement from loss of or damage to a permanent incisor must be the aim in any caring society. The authors review the options for prevention of trauma, and conclude that the dentist can be of most practical assistance in two ways: by early reduction of pronounced overjets where appropriate, and especially by provision of well-fitting mouthguards for use in sports. The article continues with a critical appraisal of commercial forms of mouthguard, and gives a step-by-step guide to constructing a custom-made mouthguard.

Adolescent↗
PubMed1989

Stimulation of phosphorylcholine turnover and diacylglycerol production in human polymorphonuclear leukocytes. Novel assay for phosphorylcholine.

Receptor-bypassing stimulants of human polymorphonuclear leukocytes (PMNLs), such as ionomycin or phorbol 12-myristate 13-acetate (PMA), generate an increase in diacylglycerol (DAG) which is independent of a phospholipase C specific for phosphatidylinositol 4,5,-bisphosphate (PIP2). Activation of a phospholipase C specific for phosphatidylcholine (PC) has been implicated as a source of DAG in other cells by measuring the release of radiolabelled phosphorylcholine. However, since PMNLs could not be labelled sufficiently with [3H]choline, we developed an h.p.l.c. assay to quantify mass levels of phosphorylcholine after enzymic conversion to [32P]CDP-choline with CTP-phosphorylcholine (choline phosphate) cytidylyltransferase (EC 2.7.7.15). This assay was linear to at least 20 nmol, and was sensitive to 10 pmol of phosphorylcholine. Baseline phosphorylcholine levels in unstimulated PMNLs were 2300 +/- 510 pmol/10(7) cells and were decreased by pretreatment with PMA (166 nM) or ionomycin (1 microM) for 10 min by 360 +/- 130 and 600 +/- 290 pmol/10(7) cells respectively (P less than 0.05). In contrast, baseline DAG levels were 147.6 +/- 11.7 pmol/10(7) cells in unstimulated PMNLs, and were increased by PMA or ionomycin by 1320 +/- 222 and 1891 +/- 264 pmol/10(7) cells respectively (P less than 0.05). Similarly, the chemoattractant fMet-Leu-Phe raised DAG levels by 731 +/- 111 pmol/10(7) cells and decreased phosphorylcholine levels by 180 +/- 60 pmol/10(7) cells. Activation of PMNLs by PMA, ionophore or fMet-Leu-Phe thus leads to the sustained production of DAG accompanied by the disappearance of phosphorylcholine. This suggests that these stimulants enhance PC turnover via a hydrolytic mechanism which is independent of phospholipase C, with activation of a PC-specific phospholipase D being a plausible mechanism.

Choline↗
PubMed1989

The influence of using vacuum-dried poly(alkenoic) acids upon the physical properties of a glass polyalkenoate (ionomer) cement.

Some of the physical characteristics of two glass polyalkenoate cements have been measured. The two cements differ in terms of the presentation of the poly(alkenoic) acid used to form the cement and in the method of mixing of the materials. The 'conventional' cement uses an aqueous solution of poly(acid) and is an encapsulated mechanically mixed material. The alternative material contains a vacuum-dried poly(acid) powder with the ion-leachable glass, and is mixed by hand with a 15 per cent aqueous solution of tartaric acid. There were some minor differences between the two products, including a delay in the onset of the setting reaction for the material containing the vacuum-dried poly(acid) powder. These differences would probably have little significant effect upon the clinical performance of the materials.

Carboxylic Acids↗
PubMed1989

Normal endothelial function and decreased vasoreactivity of experimental arterial grafts.

During autogenous vascular grafting endothelial cell damage inevitably occurs. In this study we examined the functional and morphologic integrity of experimental arterial grafts. The right external iliac artery was grafted into the right carotid artery of 12 male New Zealand white rabbits. The left external iliac artery was used as the control artery. Four weeks after surgery, isometric tension studies were performed on rings of control artery and arterial graft. Control arteries and arterial grafts precontracted with norepinephrine demonstrated endothelium-dependent relaxation of 28.3% +/- 5.6% and 16.1% +/- 1.7%, respectively, in response to acetylcholine (5 x 10(-6) mol/L). Both control arteries and arterial grafts contracted in response to norepinephrine, histamine, and serotonin. The median effective dose (ED50) of norepinephrine was 4.1 +/- 1.3 x 10(-7) mol/L for control arteries and 62.1 +/- 17.9 x 10(-7) mol/L for arterial grafts (p less than 0.005). Similarly, arterial grafts were less sensitive to histamine; the ED50 of histamine for control arteries was 4.6 +/- 1.3 x 10(-7) mol/L and 51.4 +/- 13.0 x -7 mol/L for arterial grafts (p less than 0.005). In contrast, reactivity to serotonin was unaltered. The ED50 was 4.1 +/- 1.3 x 10(-7) mol/L for control arteries and 4.5 +/- 1.3 x 10(-7) mol/L for arterial grafts. Scanning and transmission electron microscopy revealed a largely intact endothelial surface. These data are markedly different from our previous findings with vein grafts in which serotonin supersensitivity was associated with an absence of endothelium-mediated relaxation to acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1989

Fissure sealants: a critique of their cost-effectiveness.

Despite the large number of clinical trials demonstrating the effectiveness of fissure sealants in preventing occlusal caries, it has been suggested that the fundamental principles of cost-effectiveness have not been applied to the use of fissure sealants and there is little in the literature which allows up-to-date judgements to be made. A review of the literature suggests that whilst the limitations in design of some of the earlier fissure sealants studies make it difficult to draw firm conclusions, the results of later studies, particularly those which evaluated fissure sealants as an integral part of routine dental care, are encouraging. A number of factors including durability and tooth selection influence the economic viability of fissure sealants. These factors must be considered and controlled if sealants are to be used cost-effectively.

Child↗
PubMed1989

Effects of a stabilized endothelium-derived relaxing factor on the coronary vasculature in awake dogs.

The effects of a partially purified endothelium-derived relaxing factor (EDRF) stabilized by acidification from cultured bovine aortic endothelial cells stimulated with the calcium ionophore A23187 on coronary and peripheral vasculature were examined in five awake dogs. The dogs were chronically instrumented with miniature arterial dimension crystals and Doppler flow probes. Intracoronary or intra-arterial infusions of this EDRF induced a rapid (less than 15 s) significant increase in the proximal vessel diameter (P less than 0.02). The duration of proximal dilation response to this EDRF persisted up to 6 min, whereas the smaller changes in distal flow were more transient (less than 1 min). Similar but more pronounced changes in the proximal arterial dilation and distal flow occurred with infusion of nitroglycerin (0.4 mg). No vasoactive changes were observed during infusions of the control vehicle. The vasodilatory effects to this EDRF occurred in the absence of changes in aortic and left ventricular pressure, rate of pressure development (dP/dt), and heart rate. These data demonstrate that infusion of this partially purified relaxing factor from cultured endothelial cells causes vasodilation in vivo with a vasoactive profile similar to nitroglycerin. The biological effects of this EDRF persist significantly longer than the extreme lability of EDRF at neutral pH (approximately 6 s), consistent with its in vitro effects. Despite the demonstration of rapid inactivation of EDRF in vitro by hemoglobin, high oxygen tension, and plasma, the study shows that this EDRF can have significant in vivo vasoactive effects.

Animals↗
PubMed1989

Mesangial cell, glomerular and renal vascular responses to endothelin in the rat kidney. Elucidation of signal transduction pathways.

We investigated the actions of endothelin in anesthetized rats and cultured mesangial cells. Intravenous infusion of endothelin (10 pmol/min) decreased renal blood flow by 44% at 20 min without changing arterial pressure, which subsequently rose significantly from 124 +/- 3 to 133 +/- 4 mmHg over 60 min. Micropuncture during the nonhypertensive period revealed increases in afferent (65%) and efferent (82%) arteriolar resistances, thereby reducing nephron plasma flow rate. The glomerular ultrafiltration coefficient (Kf) fell from 0.097 +/- 0.035 to 0.031 +/- 0.011 nl/(s.mmHg) as did single nephron filtration rate (41 +/- 3 to 19 +/- 3 nl/min). Addition of 5 nM endothelin to mesangial cells plated on a silicone rubber substrate increased the intensity and number of tension-generated wrinkles, and caused their reappearance in forskolin prerelaxed cells. 20-30 s following exposure of fura-2 loaded mesangial cells to 10 nM endothelin, single cell intracellular calcium concentration ([Ca]i) increased from a mean baseline value of 66 +/- 11 (SE) to a peak of 684 +/- 250 nM (P less than 0.05) followed by a sustained elevation at 145 +/- 42 nM. Anion exchange HPLC revealed rapid (15 s) and dose-dependent stimulation of inositol 1,4,5-trisphosphate (IP3) generation following exposure of [3H]myoinositol preloaded mesangial cells to 10-100 nM endothelin. Endothelin also led to intracellular alkalinization of 2'7'-bis(2-carboxy-ethyl)-5(and-6)carboxyfluorescein (BCECF)-loaded mesangial cells and its addition was associated with dramatic augmentation of mitogenic activity. Thus, endothelin exerts potent constrictor effects on renal arterioles which precede its systemic hypertensive action. It lowers Kf and contracts mesangial cells, likely through stimulation of IP3 generation and elevation of [Ca]i. It is a potent mesangial cell mitogen. These studies define functional responses and signal transduction pathways for endothelin in the rat kidney and propose a potential role for this peptide in the control of mesangial cell function, glomerular filtration rate, and renal vascular tone.

Animals↗
PubMed1988

Activation of guanylate cyclase and inhibition of platelet aggregation by endothelium-derived relaxing factor released from cultured cells.

The aggregation of gel-filtered rabbit platelets by 50 microM ADP was inhibited by a labile factor produced by suspensions of cultured bovine pulmonary artery endothelial cells. Inhibition of aggregation occurred when indomethacin-treated endothelial cells (6.10(5) per ml) and rabbit platelets (3.2.10(8) per ml) were incubated together. This anti-aggregatory activity was characterized as similar to endothelium-derived relaxing factor (EDRF) in that it was unstable at neutral pH and by its inhibition by hemoglobin. The activity was unaffected by treatment of the platelets and endothelial cells with the cyclooxygenase inhibitor, indomethacin, and by the lipoxygenase inhibitor, BW755c. In association with the anti-aggregatory activity, the levels of cyclic GMP were elevated 4-fold. The effect of the EDRF-like product on the levels of cyclic nucleotides was mimicked by treatment of platelets with sodium nitroprusside, an activator of soluble guanylate cyclase; sodium nitroprusside had no measurable effect on the levels of cyclic nucleotides of endothelial cells. We conclude that a factor with the properties of EDRF inhibits platelet aggregation, and that this is associated with an activation of guanylate cyclase as in smooth muscle. Thus, EDRF may exert an inhibitory effect on platelets in a manner analogous to its actions on vascular smooth muscle.

Adenosine Diphosphate↗
PubMed1988

Rabbit reticulocyte lipoxygenase catalyzes specific 12(S) and 15(S) oxygenation of arachidonoyl-phosphatidylcholine.

The rabbit reticulocyte lipoxygenase is known to display an unusual facility for oxygenation of esterified polyunsaturated fatty acids, yet the precise structures of the products are not known. With free arachidonate as substrate the enzyme is known to catalyze 15S and 12S oxygenations, and demonstration of a facility for catalysis of these reactions on phospholipids would extend the potential scope of lipoxygenase reactions in cells. We elected to study in detail the reaction of the enzyme with a natural phospholipid, palmitoyl/arachidonoyl-phosphatidylcholine. We determined the nature of the products by initial isolation by RP-HPLC, followed by transesterification and identification of the oxygenated products by HPLC, uv, GC-MS, and steric analysis of hydroxyl configuration by HPLC. The major product was identified as a phosphatidylcholine in which the arachidonate component was converted to the 15(S)-hydroperoxy-eicosatetraenoate. A second oxygenated phospholipid was produced in smaller quantities (2-5% of the latter product) and identified as the 12(S)-oxygenated analog. These products were also identified after reaction of the reticulocyte lipoxygenase with human red cell membranes which were radiolabeled by preincubation with [3H]arachidonic acid. The finding of 12S oxygenation represents the first evidence that a lipoxygenase can control a reaction centered on the 10-carbon of an arachidonoyl phospholipid. This is an important precedent, because hydrogen abstraction from carbon-10 is a critical step in the lipoxygenase-catalyzed synthesis of 8- and 12-hydroperoxy-eicosatetraenoates (HPETEs) and for the conversion of 5- and 15-HPETEs to leukotrienes.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1988

Plasma concentrations of quinidine, its major metabolites, and dihydroquinidine in patients with torsades de pointes.

We examined the hypothesis that excess accumulation of major quinidine metabolites or the commercial impurity dihydroquinidine contributes to the development of polymorphic ventricular tachycardia (torsades de pointes, [TdP]) in patients taking quinidine. Total and free plasma concentrations of these compounds were measured by reverse-phase HPLC with fluorescence detection and equilibrium dialysis in 19 patients with TdP and 38 control patients tolerating quinidine therapy without toxicity. No significant differences were found between the two groups of patients. Ratios of metabolite or dihydroquinidine to quinidine varied up to tenfold among patients but were similarly distributed in the TdP and control groups. Only the metabolite 3-hydroxyquinidine was present at free plasma concentrations that exceeded free concentrations of quinidine. We conclude that although quinidine metabolism is highly variable, there does not appear to be any correlation between the plasma concentrations of quinidine, its metabolites or dihydroquinidine, and the subsequent development of TdP.

Humans↗