Syphilis: no longer a historical disease.
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Biomedical subjects
Publications and source records attributed to R F Davis.
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On-axis and vicinal GaN/AlN/6H-SiC structures grown under identical conditions have been studied by x-ray diffraction and transmission electron microscopy to demonstrate the distinctive features of vicinal surface epitaxy (VSE) of nitrides on SiC. In VSE, the epilayers are tilted from the substrate due to the out-of-plane lattice mismatch (Nagai tilts), and the in-plane mismatch strains are more relaxed. The majority of misfit dislocations (MDs) at the vicinal AlN/6H-SiC interface are found to be unpaired partial MDs that are geometrically necessary to correct the stacking sequences from 6H to 2H. This mechanism indicates that it is possible to develop "step-controlled-epitaxy" strategies to control strain relaxation by adjusting the substrate offcut angles.
The relationships between different levels of severity of ambulatory cerebral palsy, defined by the Gross Motor Function Classification System (GMFCS), and several pediatric outcome instruments were examined. Data from the Gross Motor Function Measure (GMFM), Pediatric Orthopaedic Data Collection Instrument (PODCI), temporal-spatial gait parameters, and oxygen cost were collected from six sites. The sample size for each assessment tool ranged from 226 to 1047 participants. There were significant differences among GMFCS levels I, II, and III for many of the outcome tools assessed in this study. Strong correlations were seen between GMFCS level and each of the GMFM sections D and E scores, the PODCI measures of Transfer and Mobility, and Sports and Physical Function, Gait Velocity, and Oxygen Cost. Correlations among tools demonstrated that the GMFM sections D and E scores correlated with the largest number of other tools. Logistic regression showed GMFM section E score to be a significant predictor of GMFCS level. GMFM section E score can be used to predict GMFCS level relatively accurately (76.6%). Study data indicate that the assessed outcome tools can distinguish between children with different GMFCS levels. This study establishes justification for using the GMFCS as a classification system in clinical studies.
Reflected light optical microscopy using a Nomarski prism and a differential interference contrast filter have been employed in concert to achieve a technique that provides an accurate color reference for thickness during the dimpling and ion milling of transparent transmission electron microscopy samples of 6H-SiC(000 1) wafers. The samples had thin films of AIN, GaN, and Au deposited on the SiC substrate. A sequence of variously colored primary and secondary interference bands was observed when the SiC was thinner than 20 microm using an optical microscope. The color bands were correlated with the TEM sample thickness as measured via scanning electron microscopy. The interference contrast was used to provide an indication of the dimpling rate, the ion milling rate, and also the most probable location of perforation, which are useful to reduce sample breakage. The application of pressure during the initial cross-sectional preparation reduced the separation of the two halves of the sample sandwich and resulted in increased shielding of the film surface from ion milling damage.
A model of UV-induced DNA damage in oceanic bacterioplankton was developed and tested against previously published and novel measurements of cyclobutane pyrimidine dimers (CPD) in surface layers of the ocean. The model describes the effects of solar irradiance, wind-forced mixing of bacterioplankton and optical properties of the water on net DNA damage in the water column. The biological part includes the induction of CPD by UV radiation and repair of this damage through photoreactivation and excision. The modeled damage is compared with measured variability of CPD in the ocean: diel variation in natural bacterioplankton communities at the surface and in vertical profiles under different wind conditions (net damage as influenced by repair and mixing); in situ incubation of natural assemblages of bacterioplankton (damage and repair, no mixing); and in situ incubation of DNA solutions (no repair, no mixing). The model predictions are generally consistent with the measurements, showing similar patterns with depth, time and wind speed. A sensitivity analysis assesses the effect on net DNA damage of varying ozone thickness, colored dissolved organic matter concentration, chlorophyll concentration, wind speed and mixed layer depth. Ozone thickness and mixed layer depth are the most important factors affecting net DNA damage in the mixed layer. From the model, the total amplification factor (TAF; a relative measure of the increase of damage associated with a decrease in ozone thickness) for net DNA damage in the euphotic zone is 1.7, as compared with 2.1-2.2 for irradiance weighted for damage to DNA at the surface.
STUDY OBJECTIVE: To describe the perioperative cardiac morbidity in adult patients undergoing retinal surgery using continuous Holter monitoring. DESIGN: Prospective study. SETTING: University hospital. PATIENTS: 56 patients scheduled for elective retinal surgery with local anesthesia. INTERVENTIONS: Patients were monitored continuously for 24 hours using a Holter recorder. Blood samples for creatine phosphokinase (CPK) and serum myocardial creatine phosphokinase (CPK-MB) were taken preoperatively and 24 hours postoperatively. The characteristics of myocardial ischemia were compared according to the number of risk factors for ischemic heart disease. MEASUREMENTS AND MAIN RESULTS: The overall incidence of perioperative myocardial ischemia was high: 26.7% (n = 15). These patients exhibited 41 episodes of ischemia with mean ST segment change from baseline of 2.2+/-0.7 mm. However, almost all (93.3%) ischemic episodes were silent. Patients with two risk factors or more had 77% more episodes of ischemia than patients with one risk factor (p < 0.005), and the duration of ischemia was 47+/-22.5 minutes compared with 34.8+/-27.5 minutes (p = NS). The first episode of ischemia occurred an average of 10 hours after surgery. No patient had intraoperative evidence of ischemia. Half of the ischemic episodes were associated with an increase in heart rate. No patient had evidence of acute myocardial infarction. CONCLUSION: Retinal surgery with local anesthesia is accompanied by a high incidence of postoperative myocardial ischemia. No negative outcome was correlated to the occurrence of postoperative myocardial ischemia. The significance of these findings has yet to be evaluated.
UNLABELLED: We tested the hypothesis that desflurane (DES) and isoflurane (ISO) produce similar effects on systemic and pulmonary hemodynamics and arterial oxygenation before, during, and after one-lung ventilation (OLV) in patients undergoing thoracotomy. After obtaining informed consent, anesthesia was induced with sodium thiopental or thiamylal, fentanyl, and vecuronium in 61 ASA physical status II-IV patients. Patients were randomly assigned to receive either DES (n = 30) or ISO (n = 31) in 100% O2 in separate groups. Hemodynamic data (radial and pulmonary artery [PA] catheters) were recorded, and blood gas values were obtained before and after induction; at selected intervals before, during, and after OLV; and before emergence. DES significantly (P < 0.05) increased heart rate (HR) and decreased mean arterial pressure (MAP) and cardiac output (CO). PA pressures and pulmonary vascular resistance (PVR) increased; systemic vascular resistance (SVR) was unchanged. Increases in HR and CO and decreases in MAP and SVR occurred during OLV and DES. Reductions in PaO2 (411 +/- 88 to 271 +/- 131 mm Hg 5 min after beginning OLV; mean +/- SD) and content (CaO2) and increases in shunt fraction (Qs/Qt; 0.25 +/- 0.12 to 0.40 +/- 0.19 at 5 min after beginning OLV) were also observed. ISO increased HR and PA pressures but did not alter MAP, CO, and PVR, in contrast to the findings with DES. Reductions in MAP and SVR and increases in CO and PA pressures were observed during OLV in the presence of ISO. Similar to the findings during DES, decreases in PaO2 and CaO2 and increases in Qs/Qt occurred during OLV and ISO. We conclude that DES and ISO produce very similar alterations in systemic and pulmonary hemodynamics and arterial oxygenation in patients undergoing OLV during thoracotomy. IMPLICATIONS: Desflurane and isoflurane produce similar cardiovascular and pulmonary effects before, during, and after one-lung ventilation in patients undergoing lung surgery.
OBJECTIVE: The role of the central nervous system in the development of myocardial infarction and ventricular fibrillation in virgin and ischemically preconditioned myocardium was investigated. DESIGN: Infarct size and ventricular arrhythmias were assessed after regional ischemia-reperfusion. Animals were randomly assigned to four groups: (1) preconditioned, central nervous system intact; (2) nonpreconditioned, nervous system intact; (3) preconditioned, nervous system blocked; and (4) nonpreconditioned, nervous system blocked. Differences in hemodynamics and infarct size were assessed with analysis of variance, and differences in ventricular fibrillation were assessed with the Kruskal-Wallis test. SETTING: Experiments were performed in the Anesthesiology Research Laboratory at a medical center. PARTICIPANTS: Anesthetized open-chest New Zealand white rabbits were used for these studies. INTERVENTIONS: Rabbits underwent 30 minutes of coronary artery occlusion and 3 hours of reperfusion. The central nervous system was blocked with total spinal anesthesia. Ischemic preconditioning was elicited with 5 minutes of coronary artery occlusion and 10 minutes of reperfusion. Infarction was assessed with tetrazolium and expressed as a percentage of the risk zone (mean +/- SEM). MEASUREMENTS AND MAIN RESULTS: Preconditioning resulted in infarct size limitation compared with the control (8% +/- 4% v 43% +/- 5%; p < 0.001) and delayed the onset of fibrillation (15.5 minutes v 11 minutes; p = 0.001). Spinal blockade neither altered nonpreconditioned infarct size nor attenuated preconditioning (32% +/- 7% v 8% +/- 3%; p = 0.04), but it was associated with ventricular fibrillation in 24/25 rabbits as compared with 6/14 rabbits without blockade. In blocked animals, preconditioning resulted in a decreased duration of fibrillation (2.5 minutes v 12.5 minutes; p = 0.0004). However, spinal blockade eliminated the preconditioning-induced delay in fibrillation (10 minutes v 12 minutes; p = NS). CONCLUSIONS: It is concluded that (1) activation of efferent sympathetic nerves is not necessary for ischemic preconditioning; (2) preconditioning delays the onset of ventricular arrhythmias; and (3) spinal blockade exacerbates ischemia-induced ventricular arrhythmias.
BACKGROUND: The aim of this study was to determine whether (1) adrenergic activation is cardioprotective, (2) adrenergic cardioprotection occurs via adenosine receptor activation, and (3) ischemic preconditioning requires alpha-adrenergic activation. METHODS: Anesthetised open chest rabbits underwent 30 min coronary occlusion and 3 h reperfusion. Ischemic preconditioning was elicited with 5 min coronary occlusion and 10 min reperfusion. Activation of adrenergic receptors with endogenous norepinephrine was achieved with tyramine (0.28 mg/kg/min intravenously for 5 min). Adenosine receptors were blocked with 8-p-sulfophenyl theophylline (10 mg/kg intravenously), alpha 1-adrenergic receptors were selectively blocked with prazosin (0.1 mg/kg intravenously), and alpha-adrenergic receptors were blocked with phentolamine (4 mg/kg intravenously). RESULTS: Ischemic preconditioning reduced risk-adjusted infarct volume by 79% (P < 0.0005). This protection was attenuated by adenosine receptor blockade. Tyramine infusion resulted in a 1305% change from baseline plasma norepinephrine concentration (P < or = 0.01), and reduced infarct volume by 55% (P = 0.01). Adenosine receptor blockade abolished this protection. Blockade of alpha 1-adrenergic receptors with prazosin failed to abolish ischemic preconditioning (79 versus 89% reduction in infarct volume, without and with prazosin, respectively). Similarly, non-selective blockade of alpha-adrenergic receptors also failed to abolish ischemic preconditioning (79 versus 57% reduction without and with phentolamine, respectively). CONCLUSIONS: We conclude that the cardioprotection of ischemic preconditioning and alpha-adrenergic activation both involve adenosine, but ischemic preconditioning does not require alpha-adrenergic activation.
Dichloroacetate (DCA), an activator of pyruvate dehydrogenase (PDHC), enhances postischemic mechanical recovery of isolated hearts. It is not known whether this is secondary to reduced infarction or preservation of contractile function in viable cardiomyocytes. This study investigated the effect of DCA on myocardial infarct size. Anesthetized open chest rabbits underwent regional coronary occlusion and reperfusion. DCA (300 mg/kg plus 150 mg/kg 1 h later) was administered intravenously either before occlusion (DCA-O; n = 8) or at reperfusion (DCA-R; n = 7). Control rabbits (n = 8) received saline vehicle. Myocardial PDHC activity was measured after administration of 300 mg/kg i.v. DCA in 10 separate rabbits. DCA reduced plasma lactate levels and increased PDHC activity by 76%, from 2.79 +/- .30 mumol/min.g-1 to 4.92 +/- .44 mumol/min.g-1 (p < .005). However, infarct size in DCA-treated animals was not significantly different from Control (60 +/- 5% DCA-O, 57 +/- 6% DCA-R, 58 +/- 7% Control). We conclude that stimulation of pyruvate dehydrogenase does not limit infarct size.
To investigate the potential mechanisms by which indigo carmine produces hypertension, we tested the hypothesis that indigo carmine inhibits endothelium-dependent vasodilation and determined the possible site of the inhibition (endothelium versus smooth muscle). Using isolated rat thoracic aortic rings that were precontracted with phenylephrine, we examined vasodilatory responses to acetylcholine, histamine, and Ca2+ ionophore A23187 (in endothelium-intact rings) and sodium nitroprusside and isoproterenol (in endothelium-denuded rings) in the presence and absence of indigo carmine. In addition, the effects of methylene blue on the acetylcholine- and sodium nitroprusside-induced vasodilation were compared with those of indigo carmine. Indigo carmine (10(-6), 10(-5), and 10(-4) mol/L) significantly inhibited receptor- and non-receptor-mediated endothelium-dependent vasorelaxation. Indigo carmine (10(-4) mol/L) also inhibited endothelium-independent vasorelaxation induced by sodium nitroprusside (an activator of vascular smooth muscle soluble guanylyl cyclase), although to a lesser extent than vasodilation from acetylcholine, histamine, and Ca2+ ionophore A23187. In contrast, indigo carmine (10(-4) mol/L) had no effect on the vasodilation induced by isoproterenol (an activator of adenylyl cyclase), indicating that indigo carmine selectively inhibits nitric oxide-mediated responses. Methylene blue, a known inhibitor of soluble guanylyl cyclase, inhibited both acetylcholine- and sodium nitroprusside-induced vasorelaxation. The inhibition was also greater in the acetylcholine- than the sodium nitroprusside-induced vasodilation. These results suggest that indigo carmine, like methylene blue, may inhibit endothelium-dependent relaxation by a mechanism that involves two levels. The major action of indigo carmine appears to be at the level of nitric oxide generation and/or release from the endothelial cell. In addition, indigo carmine appears to inhibit vascular smooth muscle guanylyl cyclase. Thus, indigo carmine may elevate blood pressure by interfering with these nitric oxide-mediated vasodilatory mechanisms.
This study was designed to see whether during ischemia a metabolic advantage results with left-sided ablation of the stellate ganglion (SGA), an available clinical technique. Its effects on hemodynamics and regional metabolism during myocardial ischemia were compared with those of electrical stimulation of the left vagus nerve (VS), a nonclinical technique, and those of a control condition (ischemia without intervention). The left anterior descending coronary artery (LADa) of 30 dogs was constricted to reduce blood flow by 50% and then 75% from that before constriction and after autonomic intervention (baseline). Electrocardiogram, left-ventricular (LV) first-time derivative (dP/dt), and systemic, LADa, and LV end-diastolic pressures were continuously recorded. Before and during each constriction, cardiac output and regional myocardial blood flow (by microspheres), blood gas tensions, pH, hemoglobin O2 saturation, lactate, glucose, sodium, and potassium concentrations were measured. During ischemia, SGA and VS each decreased heart rate, myocardial contractility (dP/dt), and filling pressures, the decrease in each variable being greater with VS. Also during ischemia, myocardial O2 delivery and consumption decreased to the same extent in the ischemic zone with VS, but the O2 delivery/consumption ratio was higher only with SGA. In addition, ischemic lactate production was lower with SGA and VS than with no autonomic intervention. It is concluded that left-sided SGA or VS to a heart rate of 80 to 90 beats per minute similarly mitigated metabolic impairment during myocardial ischemia. Although the study was only designed to compare modification of ischemia by two different techniques, the results suggest that ischemic zone O2 delivery/consumption ratio and hemodynamic stability were better with SGA.
OBJECTIVE: To examine long-term changes in psychological symptomatology from 6 to 24 months after notification of HIV serostatus among male injecting drug users (IDU). DESIGN: Self-report and interview data were collected at 6-month intervals as part of a longitudinal study monitoring HIV infection and risk-associated behaviors among IDU. SETTING: A community-based methadone-maintenance clinic. PARTICIPANTS: Ninety-seven male IDU (81 HIV-seronegative, 16 HIV-seropositive), including both methadone-maintained and out-of-treatment IDU. MAIN OUTCOME MEASURES: Analyses of long-term changes in psychological symptomatology associated with HIV serostatus among male IDU. RESULTS: Analyses of long-term changes in psychological symptomatology between groups revealed no significantly greater levels of overall psychological distress or significant elevations on subscales of the Symptom Checklist-90 for HIV-seropositive compared with HIV-seronegative male IDU. Also, no significantly higher scores on the Beck Depression Inventory or the psychiatric composite score of the Addiction Severity Index were observed between groups. CONCLUSIONS: Our results suggest that HIV-seropositive male IDU do not express greater levels of psychological symptomatology from 6 to 24 months following notification of seropositivity compared with HIV-seronegative male IDU. Several explanations for these findings are considered. Future work should examine why male IDU do not report significant and long-term elevations in symptoms post-notification of HIV seropositivity. Also, studies of changes in psychological symptomatology as a function of HIV serostatus among female IDU need to be conducted to assess implications for treatment interventions among this underserved population.
OBJECTIVES: This study compared simultaneous regional myocardial blood flow (RMBF) measurements using fluorescent microspheres (FM) and radiolabeled microspheres (RM). The utility of an internal standard during processing was also examined. METHODS: Paired FM and RM were injected into the left atrium of 9 anaesthetised rabbits. RMBF was altered by use of either regional ischaemia or (-)-N6-(2-phenylisopropyl)-adenosine. Radioactivity of blood reference and tissue samples was quantitated using standard methods. Samples were then digested with potassium hydroxide and microspheres recovered by vacuum filtration, with an additional label of FM as the internal standard. FM labels were extracted using Carbitol acetate and quantitated using fluorescence spectroscopy. Agreement between the fluorescent and radioactive methods was assessed using both orthogonal regression and difference-against-mean analyses. RESULTS: Using recovery-uncorrected data, the slope of the orthogonal regression of RM and FM-determined RMBF was not statistically different from 1, but the intercept was statistically different from 0 [-0.03(0.01), P = 0.005] and the mean RMBF by each method differed from one another [1.24(0.08) vs. 1.17(0.08) ml.min-1.g-1, P = 0.0002]. The mean +/- 2 s.d. of the differences of RMBF (RM minus FM) was +0.07 +/- 0.30 ml.min-1.g-1. Although recovery of FM from tissue averaged 97.6(1.2)%, use of the internal standard to correct for losses substantially improved the agreement between RM and FM-determined RMBF: the orthogonal regression slope was not statistically different from 1, the intercept was not statistically different from 0, and the means of the flows were not different. The mean +/- 2 s.d. of the differences of RMBF was -0.01 +/- 0.22 ml.min-1.g-1. The internal standard also improved RMBF estimates from samples with simulated large spillage during processing. CONCLUSION: Fluorescent microspheres are an equivalent alternative to radiolabeled microspheres for the estimation of RMBF. Although the overall recovery of microspheres using this technique was high, use of an internal standard is recommended for correction of random losses.
We report the case of a 24-year-old man in whom a clinical syndrome developed while he was on active military duty in Saudi Arabia that was subsequently diagnosed as constrictive pericarditis. Phrenic nerve to phrenic nerve pericardiectomy and posterior pericardial release successfully relieved the ventricular constriction with a resultant increase in the cardiac index from 1.9 to 3.8 L.min-1.m-2. Transesophageal echocardiographic monitoring during the operation disclosed trace mitral regurgitation before median sternotomy. The severity of the regurgitation noticeably increased to the moderate level immediately after pericardial resection. This echocardiographic finding had improved 1 week later, but the regurgitation still was greater than baseline. Mitral valve function had returned to baseline by 4 weeks after the operation. Possible mechanisms of this evolving pattern of perioperative mitral valve dysfunction are discussed.
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OBJECTIVE: The aim was to determine whether three commonly used animal anaesthetics alter the magnitude of infarct limitation achieved with ischaemic preconditioning. METHODS: Eighty four anaesthetised non-preconditioned and preconditioned open chest rabbits underwent a 30 min coronary occlusion followed by 3 h reperfusion. Ischaemic preconditioning was achieved with 5 min coronary occlusion beginning 15 min before the 30 min coronary occlusion. The anaesthetics studied were: pentobarbitone (30 mg.kg-1 intravenously +30-50 mg.kg-1.h-1 intravenously), isoflurane (1.5-2.5% end expiratory), and ketamine/xylazine (cocktail of 67 mg ketamine and 6.7 mg xylazine.ml-1, 1 ml.kg-1 intramuscularly +0.3-1.3 ml.kg-1.h-1 intramuscularly). Area at risk was delineated with ZnCdS particles and infarction assessed with tetrazolium. RESULTS: There were no significant differences in area at risk, heart rate, arterial pressure, and temperature between non-preconditioned and preconditioned hearts. Although infarct size was not significantly different among non-preconditioned hearts for each anaesthetic regimen (p = NS), the magnitude of infarct limitation with preconditioning varied with the anaesthetic employed (decrease in infarct size from control values of 81%, 44%, and 33% for pentobarbitone, isoflurane and ketamine/xylazine, respectively, p = 0.0145 for comparison of the three magnitudes, two factor ANOVA). CONCLUSION: Anaesthetic regimens affect the degree of infarct size limitation seen with ischaemic preconditioning.