bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of Anesthesia Residents Using Mannequin-based Simulation
Authors: Schwid Howard A. , Rooke G. Alec , Carline Jan , Steadman Randolph H. , Murray W. Bosseau , Olympio Michael , Tarver Stephen , Steckner Karen , Wetstone Susan 
Published: August 2004

Background
Anesthesia simulators can generate reproducible, standardized clinical scenarios for instruction and evaluation purposes. Valid and reliable simulated scenarios and grading systems must be developed to use simulation for evaluation of anesthesia residents.

Methods
After obtaining Human Subjects approval at each of the 10 participating institutions, 99 anesthesia residents consented to be videotaped during their management of four simulated scenarios on MedSim or METI mannequin-based anesthesia simulators. Using two different grading forms, two evaluators at each department independently reviewed the videotapes of the subjects from their institution to score the residents' performance. A third evaluator, at an outside institution, reviewed the videotape again. Statistical analysis was performed for construct- and criterion-related validity, internal consistency, interrater reliability, and intersimulator reliability. A single evaluator reviewed all videotapes a fourth time to determine the frequency of certain management errors.

Results
Even advanced anesthesia residents nearing completion of their training made numerous management errors; however, construct-related validity of mannequin-based simulator assessment was supported by an overall improvement in simulator scores from CB and CA-1 to CA-2 and CA-3 levels of training. Subjects rated the simulator scenarios as realistic (3.47 out of possible 4), further supporting construct-related validity. Criterion-related validity was supported by moderate correlation of simulator scores with departmental faculty evaluations (0.37-0.41, P < 0.01), ABA written in-training scores (0.44-0.49, < 0.01), and departmental mock oral board scores (0.44-0.47, P < 0.01). Reliability of the simulator assessment was demonstrated by very good internal consistency (alpha = 0.71-0.76) and excellent interrater reliability (correlation = 0.94-0.96; P < 0.01; kappa = 0.81-0.90). There was no significant difference in METI versus MedSim scores for residents in the same year of training.

Conclusions
Numerous management errors were identified in this study of anesthesia residents from 10 institutions. Further attention to these problems may benefit residency training since advanced residents continued to make these errors. Evaluation of anesthesia residents using mannequin-based simulators shows promise, adding a new dimension to current assessment methods. Further improvements are necessary in the simulation scenarios and grading criteria before mannequin-based simulation is used for accreditation purposes.
Mechanism of Preconditioning by Isoflurane in Rabbits: A Direct Role for Reactive Oxygen Species
Authors: Tanaka Katsuya , Weihrauch Dorothee , Kehl Franz , Ludwig Lynda M. , LaDisa John F. , Kersten Judy R. , Pagel Paul S. , Warltier David C. 
Published: August 2004

Background
Reactive oxygen species (ROS) contribute to myocardial protection during ischemic preconditioning, but the role of the ROS in protection against ischemic injury produced by volatile anesthetics has only recently been explored. We tested the hypothesis that ROS mediate isoflurane-induced preconditioning in vivo.

Methods
Pentobarbital-anesthetized rabbits were instrumented for measurement of hemodynamics and were subjected to a 30 min coronary artery occlusion followed by 3 h reperfusion. Rabbits were randomly assigned to receive vehicle (0.9% saline), or the ROS scavengers N-acetylcysteine (NAC; 150 mg/kg) or N-2-mercaptopropionyl glycine (2-MPG; 1 mg. kg(-1).min(-1)), in the presence or absence of 1.0 minimum alveolar concentration (MAC) isoflurane. Isoflurane was administered for 30 min and then discontinued 15 min before coronary artery occlusion. A fluorescent probe for superoxide anion production (dihydroethidium, 2 mg) was administered in the absence of the volatile anesthetic or 5 min before exposure to isoflurane in 2 additional groups (n = 8). Myocardial infarct size and superoxide anion production were assessed using triphenyltetrazolium staining and confocal fluorescence microscopy, respectively.

Results
Isoflurane (P < 0.05) decreased infarct size to 24 +/- 4% (mean +/- SEM; n = 10) of the left ventricular area at risk compared with control experiments (43 +/- 3%; n = 8). NAC (43 +/- 3%; n = 7) and 2-MPG (42 +/- 5%; n = 8) abolished this beneficial effect, but had no effect on myocardial infarct size (47 +/- 3%; n = 8 and 46 +/- 3; n = 7, respectively) when administered alone. Isoflurane increased superoxide anion production as compared with control experiments (28 +/- 12 -6 +/- 9 fluorescence units; P < 0.05).

Conclusions
The results indicate that ROS produced following administration of isoflurane contribute to protection against myocardial infarction in vivo.
Isoflurane-induced Cerebral Hyperemia Is Partially Mediated by Nitric Oxide and Epoxyeicosatrienoic Acids in Mice In Vivo
Authors: Kehl Franz , Shen Hui , Moreno Carol , Farber Neil E. , Roman Richard J. , Kampine John P. , Hudetz Anthony G. 
Published: August 2004

Background
Despite intense investigation, the mechanism of isoflurane-induced cerebral hyperemia is unclear. The current study was designed to determine the contributions of neuronal nitric oxide synthase, prostaglandins, and epoxyeicosatrienoic acids to isoflurane-induced cerebral hyperemia.

Methods
Regional cerebral cortical blood flow was measured with laser Doppler flowmetry during stepwise increases of isoflurane from 0.0 to 1.2, 1.8, and 2.4 vol% end-tidal concentration in alpha-chloralose-urethane-anesthetized, C57BL/6 mice before and 45 min after administration of the neuronal nitric oxide synthase inhibitor 7-nitroindazole (7-NI, 40 mg/kg, intraperitoneal), the cyclooxygenase inhibitor indomethacin (INDO, 10 mg/kg, intravenous), and the cytochrome P450 epoxygenase inhibitor N-methylsulfonyl-6-(2-proparglyoxyphenyl)hexanoic acid (PPOH, 20 mg/kg, intravenous).

Results
Isoflurane increased regional cerebral cortical blood flow by 9 +/- 3, 46 +/- 21, and 101 +/- 26% (SD) at 1.2, 1.8, and 2.4 vol%, respectively. The increases in regional cerebral cortical blood flow were significantly (*P < 0.05) smaller after 7-NI (5 +/- 6, 29 +/- 19*, 68 +/- 15%*) or PPOH (4 +/- 8, 27 +/- 17*, 67 +/- 30%*), but not after administration of INDO (4 +/- 4, 33 +/- 18 [NS], 107 +/- 35% [NS]). The effect of combined treatment with 7-NI, PPOH, and INDO was not additive and was equal to that of either 7-NI or PPOH alone (5 +/- 5, 30 +/- 12*, 76 +/- 24%*). Chronic treatment of mice for 5 days with 7-NI (2 x 40 mg/kg, intraperitoneal) produced similar decreases in regional cerebral cortical blood flow as those seen with acute administration. Neither PPOH nor INDO conferred a significant additional block of the hyperemia in these animals.

Conclusions
Nitric oxide and epoxyeicosatrienoic acids contribute to isoflurane-induced hyperemia. However, only approximately one third of the cerebral hyperemic response to isoflurane is mediated by autacoids. The remaining part of this response appears to be mediated by a direct action of isoflurane on smooth muscle by some yet-unknown mechanism.
Propofol Increases Pulmonary Artery Smooth Muscle Myofilament Calcium Sensitivity
Authors: Tanaka Satoru , Kanaya Noriaki , Homma Yasuyuki , Damron Derek S. , Murray Paul A. 
Published: August 2004

Background
Vascular smooth muscle tone is regulated by changes in intracellular free Ca2+ concentration ([Ca2+]i) and myofilament Ca2+ sensitivity. These cellular mechanisms could serve as targets for anesthetic agents that alter vasomotor tone. This study tested the hypothesis that propofol increases myofilament Ca2+ sensitivity in pulmonary artery smooth muscle (PASM) via the protein kinase C (PKC) signaling pathway.

Methods
Canine PASM strips were denuded of endothelium, loaded with fura-2/AM, and suspended in modified Krebs-Ringer's buffer at 37 degrees C for simultaneous measurement of isometric tension and [Ca2+]i.

Results
The KCl (30 mm) induced monotonic increases in [Ca2+]i and tension. Verapamil, an L-type Ca2+ channel blocker, attenuated KCl-induced increases in [Ca2+]i and tension to an equal extent. In contrast, propofol attenuated KCl-induced increases in [Ca2+]i to a greater extent than concomitant changes in tension and caused an upward shift in the peak tension-[Ca2+]i relation. Increasing extracellular Ca2+ in the presence of 30 mM KCl resulted in similar increases in [Ca2+]i in control and propofol-pretreated strips, whereas concomitant increases in tension were greater during propofol administration. The Ca2+ ionophore, ionomycin (0.1 microm), increased [Ca2+]i to approximately 50% of the value induced by 60 mm KCl. Under these conditions, propofol (10, 100 microm) caused increases in tension equivalent to 11 +/- 2 and 28 +/- 3% of the increases in tension in response to 60 mM KCl, whereas [Ca2+]i was slightly decreased. Similar effects were observed in response to the PKC activator, phorbol 12-myristate 13-acetate (PMA, 1 microm). Specific inhibition of PKC with bisindolylmaleimide I before ionomycin administration decreased the propofol- and PMA-induced increases in tension and abolished the propofol- and PMA-induced decreases in [Ca2+]i. Selective inhibition of Ca2+ -dependent PKC isoforms with Gö 6976 also attenuated propofol-induced increases in tension.

Conclusion
These results suggest that propofol increases myofilament Ca2+ sensitivity in PASM, and this effect involves the PKC signaling pathway.
Effects of Chronic Alcohol Abuse on Alveolar Epithelial Barrier Function and Glutathione Homeostasis
Authors: Burnham Ellen L. , Brown Lou Ann S. , Halls Lynn , Moss Marc 
Published: August 2004

Background: An association between the development and severity of the acute respiratory distress syndrome has been described in individuals who abuse alcohol chronically, possibly through a mechanism involving the deficiency of pulmonary glutathione. In a rodent model of chronic alcohol abuse, this antioxidant contributes to the maintenance of alveolar‐capillary membrane integrity. We postulated that humans who chronically abuse alcohol will have similar alterations in alveolar‐capillary barrier function.Methods: Bronchoalveolar lavage was performed in 18 healthy chronic alcoholics and 18 control subjects; total protein and glutathione concentrations were measured within the epithelial lining fluid. To examine possible protracted effects of alcohol abuse, a subset of 11 chronic alcoholic subjects underwent a second bronchoalveolar lavage after a week of abstinence.Results: Chronic alcoholic subjects had significantly elevated protein concentrations compared with controls (8.64 μg protein/ng immunoglobulin A vs. 5.91 μg protein/ng immunoglobulin A, p= 0.01). After a week of abstinence, no significant increase in either the glutathione levels or normalization of the protein concentrations in the epithelial lining fluid was demonstrable.Conclusions: Increased protein levels in the epithelial lining fluid of individuals who abuse alcohol chronically may signify abnormal alveolar epithelial barrier function that does not appear to readily reverse after a period of abstinence.
Binge Ethanol Treatment Causes Greater Brain Damage in Alcohol‐Preferring P Rats Than in Alcohol‐Nonpreferring NP Rats
Authors: Crews Fulton T. , Braun Christopher J. 
Published: August 2004

Background: Genetics is a known risk factor for alcoholism, and human alcoholics are known to suffer from a loss of brain function and mass. A 4 day rat binge drinking model is known to cause brain region‐specific damage. To investigate the role of genetics in binge‐drinking‐induced brain damage, we studied bidirectionally selected rat lines, the alcohol‐preferring P and the alcohol‐nonpreferring NP rat lines.Method: P and NP rats were treated with a 4 day binge ethanol protocol. Animals were killed, transcardially perfused, and fixed, and their brains were removed, sectioned, and stained by using the amino cupric silver stain of de Olmos or by using immunohistochemistry for phospho‐extracellular signal regulated kinases and other antigens.Results: Significant brain damage was found in the olfactory bulbs, posterior perirhinal cortex, and entorhinal cortex in both P and NP rats. P rats were found to have significantly greater brain damage, compared with NP rats, in the posterior perirhinal and posterior entorhinal cortexes, 239%± 50% (p < 0.02) and 219%± 46% (p < 0.01), respectively. Phospho‐extracellular signal regulated kinase immunohistochemistry stained prominently in damaged brain areas.Conclusions: The P rat line, a genetic model of alcoholism, shows greater region‐specific brain damage due to binge ethanol treatment than its genetic counterpart, the NP rat line. These findings suggest that genetics contribute to susceptibility for binge‐induced brain damage.
A Comparative Study on Alcohol‐Preferring Rat Lines: Effects of Deprivation and Stress Phases on Voluntary Alcohol Intake
Authors: Vengeliene Valentina , Siegmund Sören , Singer Manfred V. , Sinclair John David , Li Ting‐Kai , Spanagel Rainer 
Published: August 2004

Background: Voluntary alcohol intake in rats can be influenced by alcohol deprivation phases and stress. We investigated the magnitude of the effects of both deprivation and stress (forced swimming in cold water and foot‐shock had been chosen as stressors distinct in their physical and psychological features) on alcohol intake and the influence of these experiences on the time course of alcohol drinking behavior. For the alcohol drinking procedure, a long‐term model of alcohol self‐administration originally developed for heterogeneous Wistar rats was used and was compared with different alcohol‐preferring rat lines.Methods: Adult male Alko alcohol (AA), alcohol‐preferring (P), high‐alcohol‐drinking (HAD), and unselected Wistar rats were given ad libitum access to water, 5%, and 20% alcohol solutions for 6 months. A deprivation phase of 14 days was performed after 8 weeks of access to alcohol. After 16 weeks and 22 weeks of alcohol access, all animals were subjected to forced swimming and foot‐shock, respectively, for 3 consecutive days, while alcohol intake was still being measured.Results: Alcohol deprivation led to a significant increase in alcohol intake in Wistar rats and P rats. No alcohol deprivation effect was observed in HAD and AA rats; after deprivation, however, their preference for the 20% alcohol solution increased, immediately in the HAD rats and gradually over time in the AA rats. Repeated swim stress caused an increase in alcohol intake in Wistar rats but no changes in the alcohol‐preferring rat lines. Foot‐shock stress increased alcohol consumption in all lines of rats, but the most pronounced effects were observed in HAD and P rats.Conclusions: Wistar, HAD, P, and AA rats differentially respond to alcohol deprivation and stress, showing that the genetic background of these different rat lines profoundly affects relapse‐like drinking and stress‐induced drinking.
Alcohol Use and Cognition at Mid‐Life: The Importance of Adjusting for Baseline Cognitive Ability and Educational Attainment
Authors: Krahn Dean , Freese Jeremy , Hauser Robert , Barry Kristen , Goodman Brian 
Published: August 2004

Background: The nature of the relationship between cognition and alcohol consumption remains controversial. Studies have reported negative, positive, and nonsignificant effects of alcohol consumption on cognition. Problematic throughout the literature is that baseline cognitive ability has not been adequately controlled in previous studies, and even educational attainment is only sometimes controlled. Because such variables may be associated with both alcohol intake and later‐life cognition, we hypothesize that the observed relationship between alcohol intake and cognition may change when these variables or other conditions in early life have been controlled.Methods: We examined the relationship of alcohol intake and cognition at age 53 using the Wisconsin Longitudinal Study, which has followed Wisconsin high school graduates from 1957 to 1992. Our measures include cognitive ability test scores from the freshman and junior years of high school, educational attainment, an abstract reasoning test score at age 53, alcohol intake at age 53, and other measures.Results: When no controls were used, both men and women with low levels of alcohol consumption at 53 (i.e., 0–1 drink per day) had better scores on the abstract reasoning subtest of the Wechsler Adult Intelligence Scale (WAIS‐R) at age 53 than subjects who never drank or currently did not drink. However, after adjusting for adolescent‐measured cognitive ability and educational attainment, men with low levels of consumption no longer had higher abstract reasoning scores than nondrinking men, but they still did have higher abstract reasoning scores than men who drank more than one drink per day. For women, adjusting for cognitive ability and educational attainment eliminated all significant effects of alcohol on cognition, and reversed the nonsignificant result that women with higher consumption had the highest cognition scores. These results demonstrate the importance of adjusting for baseline cognitive ability when attempting to study the effect of long‐term alcohol use patterns on cognition, and that educational attainment cannot be considered a valid substitute for baseline cognition scores.Conclusions: Much of the apparent benefit of moderate alcohol intake on cognition in our society may well be explained by differential rates of alcohol consumption among subjects with differing baseline cognitive ability scores. Neither is there evidence that moderate alcohol intake reduces cognitive functioning.
Students’ perceptions toward the use of the digital library in weekly web‐based distance learning assignments portion of a hybrid programme
Authors: Koohang Alex 
Published: August 2004

AbstractThis study attempted to investigate students’ perceptions toward the use of the digital library in weekly web‐based distance learning assignments portion of a hybrid instructional programme. Attention was given to three variables—age, gender, and prior experience with the Internet. A Likert‐type instrument consisting of 10 items was designed to collect information about students’ perceptions toward the use of digital library. The subjects of this study were 154 students enrolled in an undergraduate hybrid programme in management at a medium‐sized university in the Midwest, USA. Collected data were analysed using ANOVA. The overall results suggest that students had positive perceptions toward the use of the digital library. Age was found to be an insignificant factor. However, gender and prior experience with the Internet were found to be significant factors. Males had significantly higher positive perceptions toward using the digital library. Students who had more prior experience with the Internet had significantly higher positive perceptions toward using the digital library. Implications for practice are discussed and recommendations are made for future research.
Prevention of erosive oesophagitis relapse with pantoprazole
Authors: Richter J. E. , Fraga P. , Mack M. , Sabesin S. M. , Bochenek W. ,   The Pantoprazole US GERD Study Group
Published: August 2004

SummaryAim : To compare the safety and efficacy of pantoprazole and ranitidine in maintaining erosive oesophagitis healing.Methods : Gastro‐oesophageal reflux disease patients (349) with endoscopically documented healed erosive oesophagitis (grade 0 or 1) were randomly assigned to receive pantoprazole (10, 20 or 40 mg/q.d.s.) or ranitidine (150 mg/b.d.). Erosive oesophagitis status was assessed endoscopically at months 1, 3, 6 and 12 or when relapse symptoms appeared (relapse = reappearance of erosive oesophagitis grade 2 within 12 months). Symptom‐free days were also assessed.Results : Pantoprazole 20‐ and 40‐mg were significantly more effective than ranitidine in maintaining healing regardless of initial erosive oesophagitis grade. Response was dose‐related. After 12 months 78, 55, 46 and 21% of patients remained healed (40‐, 20‐, 10‐mg pantoprazole and ranitidine). Pantoprazole 40‐mg produced significantly more symptom‐free days (83%) than ranitidine (58%). Heartburn‐free days/nights were significantly higher with pantoprazole 40‐mg (92 and 93%) than ranitidine (73 and 77%). The most frequent reason for discontinuation, unsatisfactory efficacy, occurred most often with ranitidine (P < 0.001).Conclusion : Once‐daily pantoprazole therapy prevented relapse of healed erosive oesophagitis more effectively than ranitidine and with fewer heartburn days. Response to pantoprazole was dose‐related. Pantoprazole 40‐mg was the most effective regimen and consistent in maintaining erosive oesophagitis healing with a good safety and tolerability profile.
Phagocytic Activation Induces Formation of Platelet‐Activating Factor in Human Monocyte‐Derived Macrophages and in Macrophage‐Derived foam Cells
Authors: Dentan Christine , Lesnik Philippe , Chapman M. John , Ninio Ewa 
Published: August 2004

Monocyte‐derived macrophages and macrophage‐derived foam cells in arterial tissue may undergo phagocytic activation and thereby contribute to an inflammatory reaction. We have investigated the effect of phagocytic activation on the formation of platelet‐activating factor (1‐O‐alkyl‐2–acetyl‐sn‐glycero‐3‐phosphocholine, PAF‐acether, PAF), a proinflammatory phospholipid, in human monocyte‐derived macrophages (macrophages) and in cholesterol‐loaded macrophage foam cells (foam cells). Adherent human monocyte‐derived macrophages were transformed into foam cells upon incubation with acetylated low‐density lipoproteins (Ac‐LDL). Such foam cells characteristically displayed a markedly increased content of cholesteryl esters compared with macrophages (4.3±1.3 μg/μg DNA and 0.2±0.3 μg/μg DNA, n= 5, respectively). After phagocytic stimulation with serum‐opsonized zymosan (OPZ), both macrophages and foam cells synthesized PAF transiently with maximal production (0.5–1.1 pmol PAF/μg DNA, n= 5, corresponding to 4.0–8.8 pmol PAF/106 cells, as assessed by bioassay) occurring approximately 15 min after stimulation. A major fraction of the synthesized PAF remained cell‐associated; such PAF was composed mainly of the hexadecyl (16:0 PAF, ∼ 75%) and the octadecenyl (18:1 PAF) species and of trace amounts of octadecyl (18:0 PAF), as assessed by reverse‐phase liquid chromatography. Addition of exogenous 16:0 lyso‐PAF alone triggered PAF formation (0.9–1.7 pmol PAF/μg DNA, after 15 min of cellular stimulation); simultaneous cellular stimulation with OPZ and 16:0 lyso‐PAF increased PAF formation in an additive manner.Acetyltransferase, the enzyme which acetylates the precursor lyso‐PAF and transforms it into PAF, displayed elevated activity both in macrophages and in foam cells, attaining 83–240 pmol PAF formed · min−1· mg DNA−1 (n= 4); such elevated activity was not increased by OPZ‐stimulation. The activity of acetylhydrolase, the PAF‐degrading enzyme, was similar in macrophages and in foam cells, and varied between 120 pmol and 320 pmol PAF degraded · min−1· mg DNA−1 (n= 5). Cell‐associated acetylhydrolase activity was increased significantly by 40±15% (P < 0.003, n= 5) after 15–30 min of activation with OPZ compared with non‐stimulated cells and may account for the rapid decrease in cellular PAF content observed approximately 30 min after stimulation. These studies have established that metabolism of PAF in foam cells closely resembles that in macrophages, and thus PAF metabolism is largely independent of cellular cholesterol content. Moreover our data are consistent with the hypothesis that both macrophages and macrophage‐derived foam cells upon phagocytic‐activation constitute a significant transient source of PAF at inflammatory sites in the arterial intima where this phospholipidic mediator may exert potent proatherogenic and prothrombotic effects.