Biomedical subjects

Peter Rock

Publications and source records attributed to Peter Rock.

6 recordsLinked to original sources

PubMed2003

The effect of ligation method on friction in sliding mechanics.

During orthodontic tooth movement with the preadjusted edgewise system, friction generated at the bracket/archwire interface tends to impede the desired movement. The method of ligation is an important contributor to this frictional force. This in vitro study investigated the effect of ligation method on friction and evaluated the efficacy of the new slick elastomeric modules from TP Orthodontics (La Porte, Ind), which are claimed to reduce friction at the module/wire interface. Slick modules were compared with regular nonslick modules, stainless steel ligatures, and the SPEED self-ligating bracket system (Strite Industries, Cambridge, Ontario, Canada). The effect of using slick modules with metal-reinforced ceramic (Clarity, 3M Unitek, Monrovia, Calif) and miniature brackets (Minitwin, 3M Unitek) was also examined. Results showed that, when considering tooth movement along a 0.019 x 0.025-in stainless steel archwire, saliva-lubricated slick modules can reduce static friction at the module/archwire interface by up to 60%, regardless of the bracket system. The SPEED brackets produced the lowest friction compared with the 3 other tested bracket systems when regular modules were used. The use of slick modules, however, with all of the ligated bracket types tested significantly reduced friction to below the values recorded in the SPEED groups. Loosely tied stainless steel ligatures were found to generate the least friction.

Analysis of Variance↗

PubMed2002

In vitro activity of Triclisia patens and some bisbenzylisoquinoline alkaloids against Leishmania donovani and Trypanosoma brucei brucei.

In the search for antiprotozoal compounds from natural sources, Triclisia patens displayed activity against L. donovani promastigotes (IC(50) = 1.5 microg/mL) and T. b. brucei blood stream trypomastigote forms (IC(50) = 31.25 microg/mL). In addition, a total of 20 bisbenzylisoquinoline alkaloids were screened for antileishmanial and antitrypanosomal activity in vitro. Fangchinoline (IC(50) = 0.39 microM) was found to be as active as the standard pentamidine against Leishmania donovani promastigotes. Phaeanthine was three-fold more active (IC(50) = 2.41 microM; 1.5 microg/mL) than the standard drug Pentostam against L. donovani amastigotes, but at this concentration was toxic to murine macrophages. In contrast, cocsoline (IC(50) = 12.3 microM; 6.76 microg/mL) was as active as Pentostam, and was not toxic to macrophages at this concentration. Thalisopidine showed the strongest activity (IC(50) = 1.14 microM) against Trypanosoma brucei brucei blood stream form trypomastigotes, but was less active than pentamidine.

Alkaloids↗

PubMed2002

An investigation into the relationship between the cranial base angle and malocclusion.

A number of authors have suggested that there is a relationship between the degree of cranial base flexion and type of malocclusion, with the angle becoming increasingly obtuse from class III through class I to class II subjects. A retrospective cephalometric study was carried out to examine the contribution of cranial base angle in the four groups of malocclusion as classified by the British Standards Institution. Results showed that the cranial base flexure does not play a pivotal role in determining malocclusion. Jaw size, however, was significantly different between the main classes of malocclusion. The maxilla was found to be longer in class II subjects and the mandible longer in class III subjects.

Analysis of Variance↗

PubMed2002

What sample sizes are required for pooling surgical case durations among facilities to decrease the incidence of procedures with little historical data?

BACKGROUND: Better predictions of each case's duration would reduce operating room labor costs and patient waiting times. A barrier to using historical case duration data to predict the duration of future cases is the absence for some cases of previous data for the same scheduled procedure from the same facility. The authors examined sample size requirements for pooling case duration data from several facilities to create a 90% chance of having case duration data for almost all procedures. METHODS: Four academic medical centers provided data, totaling 200,401 cases classified by the scheduled Current Procedural Terminology codes. RESULTS: The 12% of cases in which procedures occurred once or twice accounted for 79% of procedures or combinations of procedures. When a procedure was being performed for the first time at a facility, that same procedure had been performed previously at least once at one or more of the other three facilities only 13-25% of the time. More than 1 million cases would be needed to have a 90% chance of having at least 3 cases for each procedure observed in the original 200,401 cases. However, with N = 200,401 cases in our initial data set, we observed less than one third of the estimated total number of possible procedures. CONCLUSIONS: The lack of historical case duration data for scheduled procedures is an important cause of inaccuracy in predicting case durations. However, millions of cases probably would be required to provide historical case duration data for almost all procedures.

Academic Medical Centers↗

PubMed2002

Role of nitric-oxide synthase, free radicals, and protein kinase C delta in opioid-induced cardioprotection.

Opioids generate free radicals that mediate protection in isolated cultured cardiomyocytes. We hypothesize that the nature of these radicals is nitric oxide, and that nitric oxide activates the protein kinase C (PKC) delta isoform. Through this signal transduction pathway, opiates protect cardiomyocytes during hypoxia and reoxygenation. Cell viability was quantified in chick embryonic ventricular myocytes with propidium iodide. Oxygen radicals were quantified using a molecular probe, 2',7'-dichlorofluorescin diacetate (DCFH-DA). After a 10-min infusion of the opioid delta receptor agonist BW373U86 (BW; 2 or 20 pM) and a 10-min drug-free period, cells were subjected to hypoxia for 1 h followed by reoxygenation for 3 h. BW produced a concentration-dependent reduction in cardiomyocyte death (2 pM, 35.3 +/- 3.9%, n = 5; 20 pM, 21.5 +/- 4.0%, n = 8, p < 0.05 versus controls) and attenuated oxidant stress compared with controls (43.3 +/- 4.2%, n = 8). The increase in DCFH-DA oxidation with BW before hypoxia was abolished by the specific nitric-oxide synthase inhibitors nitro-L-arginine methyl ester (L-NAME) or N(G)-monomethyl-L-arginine (L-NMMA) (100 microM each). L-NAME or L-NMMA blocked the protective effects of BW. BW selectively increased the activity of PKC delta isoform in the particulate fraction, and its protection was abolished by the selective PKC delta inhibitor rottlerin (1 microM). Similar to BW, infusion with 5 microM of the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP) reduced cardiomyocyte death (24.6 +/- 3.7, n = 8), and this protection was blocked by chelerythrine or rottlerin. Chelerythrine and rottlerin had no effect on BW-generated oxygen radicals before hypoxia, but they abolished the protection of SNAP. The nature of DCFH oxidation produced by opioid delta receptor stimulation is nitric oxide. Nitric oxide mediates cardioprotection via activating PKC delta in isolated myocytes.

Animals↗

PubMed2002

H(2)O(2) opens mitochondrial K(ATP) channels and inhibits GABA receptors via protein kinase C-epsilon in cardiomyocytes.

Oxygen radicals and protein kinase C (PKC) mediate ischemic preconditioning. Using a cultured chick embryonic cardiomyocyte model of hypoxia and reoxygenation, we found that the oxygen radicals generated by ischemic preconditioning were H(2)O(2). Like preconditioning, H(2)O(2) selectively activated the epsilon-isoform of PKC in the particulate compartment and increased cell viability after 1 h of hypoxia and 3 h of reoxygenation. The glutathione peroxidase ebselen (converting H(2)O(2) to H(2)O) and the superoxide dismutase inhibitor diethyldithiocarbamic acid abolished the increased H(2)O(2) and the protection of preconditioning. PKC activation with phorbol 12-myristate 13-acetate increased cell survival; the protection of preconditioning was blocked by epsilonV(1-2), a selective PKC-epsilon antagonist. Similar to preconditioning, the protection of PKC activation was abolished by mitochondrial K(ATP) channel blockade with 5-hydroxydecanoate or by GABA receptor stimulation with midazolam or diazepam. In addition, PKC, mitochondrial ATP-sensitive K(+) (K(ATP)) channels, and GABA receptors had no effects on H(2)O(2) generated by ischemic preconditioning before prolonged hypoxia and reoxygenation. We conclude that H(2)O(2) opens mitochondrial K(ATP) channels and inhibits GABA receptors via activating PKC-epsilon. Through this signal transduction, preconditioning protects ischemic cardiomyocytes.

Animals↗