Improving patient safety by modifying provider ordering behavior using alerts (CDSS) in CPOE system.

Medication errors are not unusual in acute care settings. This prospective time series analysis/study evaluates the use of Clinical Decision Support System (CDSS)/alerts in helping providers not to make errors, when putting in orders in a CPOE system. We reviewed electronic health records for all the inpatients coming to 5 community hospitals for a 6 months duration (July 2010 - December 2010). Responses to 9 synchronous alerts (CDSS tools) were studied, that were prompted on computer screens when providers were putting in medication orders in EMR. These alerts guided the providers regarding any drug duplications, interactions, contraindications of the prescribed medicine with patient's clinical condition etc. The CDSS system in place changed the physician behavior & patient therapy 41.75% of the times when medication orders were placed. These alerts substantially decreased the medication error rate/adverse drug events (ADE's) in the patients receiving care at these 5 hospitals.

Neurotrophins modulate the expression of chemokine receptors in the brain.

In the central nervous system, chemokines are primarily mediators of inflammatory processes. Their receptors, in particular, CXCR4 and CCR5, serve as co-factors along with CD4 that permit Human immunodeficiency virus-1 (HIV) infection. Moreover, experimental evidence has shown that CXCR4 and CCR5 mediate the neurotoxic effects of the HIV envelope protein gp120, suggesting that these receptors could also promote the neuropathogenesis observed in HIV-positive individuals. Therefore, a better understanding of the molecular mechanisms governing the expression of chemokine receptors in the brain may lead to improved therapies that reduce HIV neurotoxicity. This study presents evidence that the expression of chemokine receptors in the brain is modulated by two neurotrophins in an area-specific manner. This new evidence suggests that the neurotrophins may be an adjunct therapy to reduce HIV-mediated neuronal injury evoked by chemokine receptor activation.