Discharge of lubricant from air turbine handpieces.

OBJECTIVE: To demonstrate and quantify the discharge of lubricating oil from high-speed air turbine handpieces whilst running. MATERIALS AND METHODS: Dye-marked oil (Kavospray, KaVo) was used to lubricate four handpieces (Quiet-Air, Midwest) and the air discharged from around the lower bearing was directed at the moving chart paper on a recorder whilst running for 40 minutes. Secondly, seven new handpieces (Quiet-Air, 300SE, Midwest; Topair 796, Topair 795, W+H; VIP-Sigma, Pana-air, NSK; Lares, Lares Research) were cleaned, weighed and then lubricated with unmarked oil (Kavospray, KaVo). Oil discharge was determined gravimetrically over runs of 240 minutes. Data were fitted to the logistic dose response function. RESULT: The dye-marked oil tests showed that oil was discharged for at least 40 minutes in the direction of the bur. The gravimetric tests showed that oil continued to be discharged up to at least 240 minutes, and that the usual practice of removing excess lubricant by running for 1-2 minutes was ineffective in preventing cut-surface contamination. SIGNIFICANCE: Bonding procedures in dentistry may be jeopardised by oil contamination from handpiece lubricants. Decontamination with a detergent is suggested as a means of ensuring effective adhesive dentistry.

Effects of angiotensin subtype 1 and subtype 2 receptor antagonists in normotensive versus hypertensive rats.

The purpose of this study was to examine in vivo the importance of angiotensin subtype 1 (AT1) versus subtype 2 (AT2) receptors in spontaneously hypertensive (hypertensive) versus normotensive Wistar-Kyoto (control) rats. Intravenous infusions of DuP 753, a selective AT1 receptor antagonist, abolished the pressor responses to intravenous infusions of angiotensin II in both strains, and the potency of DuP 753 in this regard was similar in the two strains. DuP 753 also abolished angiotensin II-induced aldosterone release in both strains; however, with respect to inhibiting angiotensin II-induced aldosterone release, DuP 753 was more potent in hypertensive compared with control rats. In hypertensive but not control rats, DuP 753 inhibited angiotensin II-induced aldosterone release at doses lower than required to inhibit angiotensin II-induced pressor responses. Intramesenteric infusions of DuP 753 abolished mesenteric vascular responses to intramesenteric infusions of angiotensin II with a similar potency in both strains. In control but not hypertensive rats, angiotensin II consistently potentiated noradrenergic neurotransmission in the mesenteric vascular bed, and this effect of angiotensin II was abolished by DuP 753. High doses of PD123177, a selective AT2 antagonist, did not influence any of the aforementioned effects of angiotensin II in either strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Human platelet/erythroleukemia cell prostaglandin G/H synthase: cDNA cloning, expression, and gene chromosomal assignment.

Platelets metabolize arachidonic acid to thromboxane A2, a potent platelet aggregator and vasoconstrictor compound. The first step of this transformation is catalyzed by prostaglandin (PG) G/H synthase, a target site for nonsteroidal antiinflammatory drugs. We have isolated the cDNA for both human platelet and human erythroleukemia cell PGG/H synthase using the polymerase chain reaction and conventional screening procedures. The cDNA encoding the full-length protein was expressed in COS-M6 cells. Microsomal fractions from transfected cells produced prostaglandin endoperoxide-derived products which were inhibited by indomethacin and aspirin. Mutagenesis of the serine residue at position 529, the putative aspirin acetylation site, to an asparagine reduced cyclooxygenase activity to barely detectable levels, an effect observed previously with the expressed sheep vesicular gland enzyme. Platelet-derived growth factor and phorbol ester differentially regulated the expression of PGG/H synthase mRNA levels in the megakaryocytic/platelet-like HEL cell line. The PGG/H synthase gene was assigned to chromosome 9 by analysis of a human--hamster somatic hybrid DNA panel. The availability of platelet PGG/H synthase cDNA should enhance our understanding of the important structure/function domains of this protein and its gene regulation.