RESUMEN
Industry funds nearly two-thirds of US healthcare research, and industry-sponsorship may produce more favorable research results and conclusions. Medical students report feeling inadequately prepared to avoid negative industry influence. Research of educational interventions that educate students on the potential effects of industry influence is lacking, and no interventions have demonstrated long-term benefit. Surveying and assessing student opinions of the relationship between industry and research may help improve future educational interventions. We surveyed preclinical and clinical students at seven US medical schools regarding their attitudes towards industry conflicts of interest (COIs) in medical research. A total of 466 medical students including 232 preclinical and 234 clinical students completed the survey. Of those who had research experience, clinical students were more likely than preclinical students to look for COIs (62.0% v 45.9%, p = .014) and to consider whether author COIs are pertinent to the article (68.1% v 54.1%, p = .023). Many disagreed that they felt adequately educated on the issue of COIs (42.7%), but most agreed that medical school should take a role in guiding student interactions with industry (65.0%). Students responded that all listed financial relationships between industry and investigator, except for providing food and/or beverage, would likely bias the investigator's research. Many students feel inadequately educated on industry issues in biomedical research, and most believe medical schools should help guide interactions with industry. Our findings support further development of educational interventions that prepare students to navigate the relationship between industry and medical research during and after medical school.
RESUMEN
Ethanol is one of the most commonly used substances in the world. Behavioral effects of alcohol are well described, however, cellular mechanisms of its action are poorly understood. There is an apparent contradiction between measurable behavioral changes produced by low concentrations of ethanol, and lack of evidence of synaptic changes at these concentrations. Furthermore, effects of ethanol on synaptic transmission in the neocortex are poorly understood. Here, we set to determine effects of ethanol on excitatory synaptic transmission in the neocortex. We show that 1-50 mm ethanol suppresses excitatory synaptic transmission to layer 2/3 pyramidal neurons in rat visual cortex in a concentration-dependent manner. To the best of our knowledge, this is the first demonstration of the effects of very low concentrations of ethanol (from 1 mm) on synaptic transmission in the neocortex. We further show that a selective antagonist of A1 adenosine receptors, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), blocks effects of 1-10 mm ethanol on synaptic transmission. However, the reduction in excitatory postsynaptic potential amplitude by 50 mm ethanol was not affected by DPCPX. We propose that ethanol depresses excitatory synaptic transmission in the neocortex by at least two mechanisms, engaged at different concentrations: low concentrations of ethanol reduce synaptic transmission via A1 R-dependent mechanism and involve presynaptic changes, while higher concentrations activate additional, adenosine-independent mechanisms with predominantly postsynaptic action. Involvement of adenosine signaling in mediating effects of low concentrations of ethanol may have important implications for understanding alcohol's effects on brain function, and provide a mechanistic explanation to the interaction between alcohol and caffeine.
