The current in vitro experiments cannot be directly translated in to in vivo situation in either human or animals. First, the present experiments were conducted in differentiated L6 myotubes and not in fully developed skeletal muscle fibers. Second, the differentiated L6 myotubes were incubated in normal-glucose in the presence of relatively high insulin concentrations in order to elicit maximal effect in an exvivo study. Moreover, the present experiments were conducted in a serum starved state. Therefore, the changes in mRNA transcripts both in the treated and control conditions likely also reflect the effects of progressive serum starvation. The responses may be different in hyperglycemic conditions with lower or higher insulin concentrations. Moreover, insulin is known to reduce protein degradation and amino acid levels Therefore, future in vivo studies are warranted that examine the effect of hyperinsulinemia while maintaining both euglycemia and euaminoacidemia. The present investigation demonstrates a gene array experimental design and methodology for examining temporal changes in gene expression. Using gene array profiling, we identified 12 different temporal patterns of gene expression in response to eight hours of insulin treatment in vitro. These results are likely to help design of Ginkgolide-C in vivo studies to examine the effect of insulin treatment on the temporal regulation of gene expression related to glucose uptake in human and animals. Finally, the insulin treatment affected not only the transcripts involved in glucose metabolism but also stimulated gene transcripts that would promote protein synthesis. design of in vivo studies to examine the effect of insulin treatment on the temporal regulation of gene expression related to glucose uptake in human and animals. Finally, the insulin treatment affected not only the transcripts involved in glucose metabolism but also stimulated gene transcripts that would promote protein synthesis. Genetic and pharmacological evidence has implicated noradrenergic mechanisms in mediating the effects of cocaine and other stimulants. For example, animals which do not express the noradrenergic a1 receptor are insensitive to the locomotor activating effects of cocaine and amphetamine, and treatment with the noradrenergic a1R antagonist prazosin blocks both cocaine-induced locomotor activation and cocaineinduced reinstatement of extinguished cocaine self-administration in rats. Prazosin is the prototypical a1R antagonist. Prazosin has an elimination half-life of 2-3 hours in humans, and this limits Armepavine its potential clinical utility because most patients cannot reliably adhere to dosing regimens that require dosing throughout the day. Doxazosin is a newer a1R antagonist with an elimination half-life of 22 hours in humans, allowing once-daily dosing. Although early reports indicated that doxazosin had poor brain penetration, the side-effects of doxazosin, which include fatigue, dizziness, and somnolence, suggest that doxazosin acts centrally. We assessed the impact of doxazosin treatment on cocaine’s effects using a double-blind, placebo-controlled, within-subjects design in non-treatment-seeking, cocaine-dependent volunteers. We hypothesized that doxazosin treatment would attenuate the subjective effects of cocaine. Most used alcohol and marijuana frequently, though none met criteria for dependence. Most smoked cigarettes and met criteria for nicotine dependence. Doxazosin treatment was well tolerated and no participant was discontinued from the study due to side-effects. No participant spontaneously reported sedation, a known side effect of doxazosin, though we did not rate sedation or query participants. Heart rate and blood pressure were not significantly affected.