Evaluating how electronic charting affects resident productivity

Electronic medical records (EMRs) are becoming standard to improve the communication of information and longevity of patient records. Using an EMR in the emergency department (ED) could potentially slow residents evaluating patients. We evaluated how introducing an EMR affected resident productivity in an academic ED. We retrospectively studied first year emergency medicine residents from a large, academic, tertiary care center before-and-after the institution of an EMR on July 1st, 2010. No residents from the 2009–2010 class used the EMR, while all of the 2010–2011 residents used the EMR. We performed univariate and multivariate analyses using productivity, measured in patients per hour (pt/hr), as the primary outcome. A mixed-model multivariate regression, stratified by acuity zone, was created incorporating EMR and other possible confounders: admissions, signouts, daily ED volume, and days after July 1st for each shift. The study was granted IRB waiver of informed. We reviewed 2,405 shifts: 1,259 shifts before and 1,146 shifts after EMR implementation. When using the EMR, the univariate analysis estimated a 0.084 pt/hr increase in the high acuity zone (p = 0.1317) and 0.029 pt/hr decrease (p = 0.7085) in the low acuity zone. The multivariate regression estimated a 0.038 pt/hr increase (p = 0.3413) in the high acuity zone and a 0.009 pt/hr increase (p = 0.9049) in the low acuity zone with the EMR. Despite the expectation that electronic charting is detrimental to resident productivity, our analyses do not suggest a significant relationship between resident productivity and using the EMR.     

Allyl isothiocyanate sensitizes TRPV1 to heat stimulation

The powerful plant-derived irritant allyl isothiocyanate (AITC, aka mustard oil) induces hyperalgesia to heat in rodents and humans through mechanisms that are not yet fully understood. It is generally believed that AITC activates the broadly tuned chemosensory cation channel transient receptor potential cation channel subfamily A member 1 (TRPA1), triggering an inflammatory response that sensitizes the heat sensor transient receptor potential cation channel subfamily V member 1 (TRPV1). In the view of recent data demonstrating that AITC can directly activate TRPV1, we here explored the possibility that this compound sensitizes TRPV1 to heat stimulation in a TRPA1-independent manner. Patch-clamp recordings and intracellular Ca²⁺ imaging experiments in HEK293T cells over-expressing mouse TRPV1 revealed that the increase in channel activation induced by heating is larger in the presence of AITC than in control conditions. The analysis of the effects of AITC and heat on the current–voltage relationship of TRPV1 indicates that the mechanism of sensitization is based on additive shifts of the voltage dependence of activation towards negative voltages. Finally, intracellular Ca²⁺ imaging experiments in mouse sensory neurons isolated from Trpa1 KO mice yielded that AITC enhances the response to heat, specifically in the subpopulation expressing TRPV1. Furthermore, this effect was strongly reduced by the TRPV1 inhibitor capsazepine and virtually absent in neurons isolated from double Trpa1/Trpv1 KO mice. Taken together, these findings demonstrate that TRPV1 is a locus for cross sensitization between AITC and heat in sensory neurons and may help explaining, at least in part, the role of this channel in AITC-induced hyperalgesia to heat.     

Involvement of autophagy in melatonin‐induced cytotoxicity in glioma‐initiating cells

Glioblastoma‐initiating cells (GICs) represent a stem cell‐like subpopulation within malignant glioblastomas responsible for tumor development, progression, therapeutic resistance, and tumor relapse. Thus, eradication of this subpopulation is essential to achieve stable, long‐lasting remission. We have previously reported that melatonin decreases cell proliferation of glioblastoma cells both in vitro and in vivo and synergistically increases effectiveness of drugs in glioblastoma cells and also in GICs. In this study, we evaluated the effect of the indolamine alone in GICs and found that melatonin treatment reduces GICs proliferation and induces a decrease in self‐renewal and clonogenic ability accompanied by a reduction in the expression of stem cell markers. Moreover, our results also indicate that melatonin treatment, by modulating stem cell properties, induces cell death with ultrastructural features of autophagy. Thus, data reported here reinforce the therapeutic potential of melatonin as a treatment of malignant glioblastoma both by inhibiting tumor bulk proliferation or killing GICs, and simultaneously enhancing the effect of chemotherapy.     

Personalized Nutrition and Cardiovascular Disease Prevention: From Framingham to PREDIMED

Diet is considered the cornerstone for the prevention of age-related diseases, and a low-fat diet has been considered for decades as the most suitable alternative to achieve this goal. However, mounting evidence supports the efficacy of other alternatives, such as the Mediterranean diet. Nevertheless, it is well known that people present a dramatic range of responses to similar environmental challenges, and it has been shown that some of this variability is rooted in the genome. In fact, this knowledge is driving the field of nutrigenetics. The finding of interactions between diet and genetic variants has led to intense research and debate about the effectiveness of personalized nutrition as a more suitable tool for the prevention of chronic diseases than the traditional 1-size-fits-all recommendations. Here, we provide some of our own examples that illustrate the progression of nutrigenetics through the years, from the initial studies within the Framingham Heart Study, to the most recent use of large consortia, such as the Cohorts for Heart and Aging Research in Genomic Epidemiology, and ending up with large dietary intervention studies, such as the PREDIMED (Prevención con Dieta Mediterránea) study. These recent approaches are providing more robust and clinically relevant gene–diet interactions. Therefore, although the current evidence level of applying genomic information to tailoring is at its early stages, the prospect of widespread incorporation of nutrigenetics to the clinical practice is encouraging.