PubMed · 12568640
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
2003. MT 100.. https://doi.org/10.2165/00126839-200304010-00011
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
In clinical trials or drug development studies, researchers are often interested in identifying which treatments or dosages are more effective than the standard one. Recently, several multiple testing procedures based on weighted logrank tests have been proposed to compare several treatments with a control in a one-way layout where survival data are subject to random right-censorship. However, weighted logrank tests are based on ranks, and these tests might not be sensitive to the magnitude of the difference in survival times against a specific alternative. Therefore, it is desirable to develop a more robust and powerful multiple testing procedure. This paper proposes multiple testing procedures based on two-sample weighted Kaplan-Meier statistics, each comparing an individual treatment with the control, to determine which treatments are more effective than the control. The comparative results from a simulation study are presented and the implementation of these methods to the prostate cancer clinical trial and the renal carcinoma tumour study are presented.
The dopamine (DA) precursor, L-DOPA (500 microg), was injected into living crickets, which were ingested (one each) by adult male Anolis carolinensis. This method of delivery elevated plasma L-DOPA and DA concentrations by approximately 1000-fold. In contrast, plasma epinephrine (Epi) and norepinephrine (NE) were not influenced by L-DOPA treatment, although they were elevated following the consumption of the cricket. Lizards that ingested L-DOPA treated crickets had elevated L-DOPA in all brain regions measured, with DA and/or DOPAC also increased significantly in most brain regions studied. Despite increased DA levels in the striatum and nucleus accumbens as a response to L-DOPA, the treatment had no influence on general motor activity. Central serotonin, NE, and Epi systems were not affected in any brain region by oral L-DOPA treatment. In addition, aggression was inhibited by this dose of L-DOPA, even though there was no effect on serotonergic systems. This is surprising because controlling aggressive behavior is usually considered the province of serotonergic activity. Aggression was measured before and after treatment, and while saline-treated lizards retained the full vigor of aggressive activity, those fed a cricket injected with L-DOPA were only one-third as aggressive after treatment. As L-DOPA treatment did not affect general motor activity, the effect appears to be directly associated with aggression. This is supported by the observation that L-DOPA treatment delayed latency to eyespot darkening, which predicts the latency to aggression.
OBJECTIVES: To test the effects of clonidine in comparison with active placebo on premenstrual symptoms, mood scores and norepinephrine (NE) concentration, in women with premenstrual dysphoric disorder (PMDD). METHODS: Twelve women with prospectively confirmed PMDD were randomly assigned to oral 0.3 mg/day clonidine, as an active treatment, or 10 mg/day loratadine, as an active placebo, for 2 months each using a double-blind, cross-over design. NE concentration, premenstrual symptom ratings and mood scales were measured on three occasions: at pretreatment, after clonidine treatment and after placebo treatment. All patients were free of current psychiatric co-morbidity and medication use. RESULTS: There were no significant differences between clonidine and placebo for mood scales or premenstrual symptom ratings, though clonidine significantly suppressed NE concentration and produced more side effects in comparison with placebo. CONCLUSION: Compared with an active placebo clonidine demonstrated no beneficial changes in mood and premenstrual symptoms in women with PMDD.