A novel user interface was designed based on the information needs of intensive care unit providers with a specific goal of development being the reduction of task load and errors of cognition associated with filtering, extracting, and using medical data contained within a comprehensive electronic medical record. The results of this simulated clinical experiment suggest that the configuration of the intensive care unit user interface contributes significantly to the task load, time to task completion, and number of errors of cognition associated with the identification, and subsequent use, of relevant patient data. Task-specific user interfaces, developed from an understanding of provider information requirements, offer advantages over interfaces currently available within a standard electronic medical record.

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This systematic review demonstrated that viruses are strongly associated with AECOPD, with the highest detection rates of viruses being in Europe. The geographical epidemiology of viruses may have important therapeutic implications for management of AECOPD.

Intraperitoneal administration of cadmium acetate (Cd2+, 0.4 mg/kg) to rats daily for 30 days was found to inhibit the activity of superoxide dismutase (SOD), to increase the endogenous levels of lipid peroxides and lipid peroxidation in the liver and the kidney tissues. Addition of varying concentrations of Cd2+ (10-100 microM) in vitro also inhibited SOD in both the tissues. It appears that the inhibition of SOD could be due to direct interaction of Cd2+ with the enzyme molecule. Lipid peroxidation reaction was also increased after addition of Cd2+ to fresh homogenate of these tissues, however, it did not produce any effect in heated homogenates in in vitro experiments. It indicated that Cd-induced elevation in lipid peroxidation may not be only due to the possibility of higher level of superoxide radicals resulting from inhibited superoxide dismutase but could also be as a result of direct action of Cd2+ on the peroxidation reaction. Thus, the possibility of involvement of free radical damage to the membrane structures in Cd toxicity has been demonstrated in these experiments.

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C hest pain is a common presenting complaint in the emergency department that requires efficient risk stratification, timely initiation of treatment in highrisk patients and safe determination of patient disposition. Several studies have been published that stratify the risk of patients in the emergency department with chest pain. [1][2][3][4][5] However, only the Thrombolysis in Myocardial Infarction (TIMI) risk score, which was initially developed for use in patients with unstable angina or non-ST-segment elevation myocardial infarction or both, 6 has been broadly validated in several independent emergency department populations with chest pain and thus constitutes the highest level of evidence available. The TIMI risk score assigns each of seven predictors a value of one point, allowing stratification of patients into one of eight prognostic categories (Box 1). 6 The clinical end points are acute myocardial infarction, coronary revascularization and death from any cause.A robust estimate of the performance of the TIMI risk score obtained from a systematic review may prove useful to both clinicians and researchers. Clinicians would have a reliable quantitative estimate of a patient's short-term risk of a cardiac event. This could be used as an adjunct to clinical acumen and as a tool to communicate risk to patients in a shared decision-making model of care.7 Researchers would also have an estimate of the prognostic accuracy of the TIMI risk score derived from different practice settings and patient populations that represent a wide variety of ethnic backgrounds. This estimate may serve as a useful baseline for comparison as emerging clinical prediction rules and imaging modalities continue to refine our approach to diagnosis and risk stratification in patients in the emergency department with potential acute coronary syndromes.We conducted a comprehensive systematic review and meta-analysis to assess the methodological quality and prognostic performance of studies that had prospectively validated the TIMI risk score in patients in the emergency department. MethodsThis systematic review and meta-analysis adheres to the reporting guidelines of Meta-analysis of Observational Studies in Epidemiology (MOOSE) 8 and the Preferred Reporting Items for Systematic reviews and Meta-analyses (PRISMA) statement as applicable to meta-analyses of observational studies. Background: The Thrombolysis in Myocardial Infarction (TIMI) risk score uses clinical data to predict the short-term risk of acute myocardial infarction, coronary revascularization or death from any cause. It was originally developed for use in patients with unstable angina or non-STelevation myocardial infarction. We sought to expand the clinical application of the TIMI risk score by assessing its prognostic accuracy in patients in the emergency department with potential acute coronary syndromes.

Evidence of moderate quality confirms the high diagnostic performance of EBUS-TBNB for mediastinal and hilar lymphadenopathy, both in malignant and non-malignant conditions. Available evidence also demonstrates the safety of this procedure.

The suitability of liposomes as drug carriers in the treatment of drug-resistant rodent malaria was examined after covalently attaching F(ab) 2 fragments of a mouse monoclonal antibody (MAb), MAb F 10 , raised against the host cell membranes isolated from the Plasmodium berghei-infected mouse erythrocytes, to the liposome surface. The antibody-bearing liposomes thus formed specifically recognized the P. berghei-infected mouse erythrocytes under both in vitro and in vivo conditions. No such specific binding of the liposomes with the infected cells was observed when MAb F 10 was replaced by another mouse monoclonal antibody, MAb D 2 . Upon loading with the antimalarial drug chloroquine, the MAb F 10 -bearing liposomes effectively controlled not only the chloroquine-susceptible but also the chloroquine-resistant P. berghei infections in mice. The chloroquine delivered in these liposomes intravenously at a dosage of 5 mg/kg of body weight per day on days 4 and 6 postinfection completely cured the animals (75 to 90%) of chloroquine-resistant P. berghei infections. These results indicate that selective homing of chloroquine to malaria-infected erythrocytes may help to cure the chloroquine-resistant malarial infections with low doses of chloroquine.