“
“This study aimed to determine the optimal model for explaining the aggressive behavior of schizophrenic patients in relation to certain behavioral variables including anger, schizophrenic symptoms, and cognitive function. Schizophrenic patients were evaluated with the Modified Overt Aggression Scale BMS-777607 datasheet (MOAS) for aggressive behaviors, with irritability and resentment; with the Buss-Durkee Hostility Inventory (BDHI) for anger; with the Wisconsin Card Sorting Test (WCST) and the Grooved Pegboard Test
for cognitive function; and with the Positive and Negative Syndrome Scale (PANSS) for schizophrenic symptoms. The structural equation model (SEM) in AMOS 7 for the score of “”aggressive behavior in the last week”" in the MOAS, was used for statistical analysis. For the SEM, two factors (irritability and resentment) were selected from the BDHI and constituted the anger construct. Through factor analysis, two factors (executive function And motor function) were selected from the cognitive function measurements to constitute the cognitive function construct. Two factors (positive and negative symptoms) in the PANSS constituted the symptom construct. The best model for aggressive behavior (MOAS) with three constructs revealed a direct, significant path of “”anger emotion to aggressive behavior”". This result suggests that the aggressive
behavior of schizophrenic patients is directly related to anger. Schizophrenic symptoms and cognitive function were indirectly related to aggressive GSK461364 behavior through the relationship between the emotion of anger and aggressive behavior. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“BACKGROUND
Some patients with asthma have frequent
exacerbations and persistent airflow obstruction despite treatment with inhaled glucocorticoids and long-acting beta-agonists (LABAs).
METHODS
In two replicate, randomized, controlled trials involving 912 patients with asthma who were receiving inhaled glucocorticoids and LABAs, we compared the effect on MEK162 lung function and exacerbations of adding tiotropium (a total dose of 5 mu g) or placebo, both delivered by a soft-mist inhaler once daily for 48 weeks. All the patients were symptomatic, had a post-bronchodilator forced expiratory volume in 1 second (FEV1) of 80% or less of the predicted value, and had a history of at least one severe exacerbation in the previous year.
RESULTS
The patients had a mean baseline FEV1 of 62% of the predicted value; the mean age was 53 years. At 24 weeks, the mean (+/- SE) change in the peak FEV1 from baseline was greater with tiotropium than with placebo in the two trials: a difference of 86 +/- 34 ml in trial 1 (P=0.01) and 154 +/- 32 ml in trial 2 (P<0.001). The predose (trough) FEV1 also improved in trials 1 and 2 with tiotropium, as compared with placebo: a difference of 88 +/- 31 ml (P=0.01) and 111 +/- 30 ml (P<0.001), respectively.