Publications

PURPOSE OF REVIEW

Traumatic injury continues to be a significant cause of morbidity and mortality in the year 2011. In addition, the healthcare expenditures and lost years of productivity represent significant economic cost to the affected individuals and their communities. Helicopters have been used to transport trauma patients for the past 40 years, but there are conflicting data on the benefits of helicopter emergency medical service (HEMS) in civilian trauma systems. Debate persists regarding the mortality benefit, cost-effectiveness, and safety of helicopter usage, largely because the studies to date vary widely in design and generalizability to trauma systems serving heterogeneous populations and geography. Strict criteria should be established to determine when HEMS transport is warranted and most likely to positively affect patient outcomes. Individual trauma systems should conduct an assessment of their resources and needs in order to most effectively incorporate helicopter transport into their triage model.

RECENT FINDINGS

Research suggests that HEMS improves mortality in certain subgroups of trauma patients, both after transport from the scene of injury and following interfacility transport. Studies examining the cost-effectiveness of HEMS had mixed results, but the majority found that it is a cost-effective tool. Safety remains an issue of contention with HEMS transport, as helicopters are associated with significant safety risk to the crew and patient. However, this risk may be justified provided there is a substantial mortality benefit to be gained.

SUMMARY

Recent studies suggest that strict criteria should be established to determine when helicopter transport is warranted and most likely to positively affect patient outcomes. Individual trauma systems should conduct an assessment of their resources and needs in order to most effectively incorporate HEMS into their triage model. This will enable regional hospitals to determine if the costs and safety risks associated with HEMS are worthwhile given the potential benefits to patient morbidity and mortality.

The number of women of childbearing age who are active-duty service members or veterans of the US military is increasing. These women may seek reproductive health care at medical facilities operated by the military, in the civilian sector, or through the Department of Veterans Affairs. This article reviews the current data on unintended pregnancy and prevalence of and barriers to contraceptive use among active-duty and veteran women. Active-duty servicewomen have high rates of unintended pregnancy and low contraceptive use, which may be due to official prohibition of sexual activity in the military, logistic difficulties faced by deployed women, and limited patient and provider knowledge of available contraceptives. In comparison, little is known about rates of unintended pregnancy and contraceptive use among women veterans. Based on this review, research recommendations to address these issues are provided.

PURPOSE OF REVIEW

Artemisinin-based combination therapies (ACTs) have been deployed globally with remarkable success for more than 10 years without having lost their malaria treatment efficacy. However, recent reports from the Thai-Cambodian border reveal evidence of emerging resistance to artemisinins. The latest published clinical and molecular findings are summarized herein.

RECENT FINDINGS

Clinical studies have identified delayed parasite clearance time as the most robust marker of artemisinin resistance. Resistance has only been documented from South-east Asia and has been observed in isolates that show no significant decrease in drug susceptibility in vitro. Genetic investigations have yet to uncover robust molecular markers. In-vitro studies have identified parasite quiescence or dormancy mechanisms that protect early 'ring-stage' intra-erythrocytic parasites against short-term artemisinin exposure. This might be achieved by reducing the rate of hemoglobin degradation, important for artemisinin bioactivation.

SUMMARY

Should ACTs fail, no suitable alternatives exist as first-line treatments of P. falciparum malaria. Intensified efforts are essential to monitor the spread of resistance, define therapeutic and operational strategies to counter its impact, and understand its molecular basis. Success in these areas is critical to ensuring that recent gains in reducing the burden of malaria are not lost.

OBJECTIVE

Macrophage recruitment to adipose tissue is a reproducible feature of obesity. However, the events that result in chemokine production and macrophage recruitment to adipose tissue during states of energetic excess are not clear. Sirtuin 1 (SirT1) is an essential nutrient-sensing histone deacetylase, which is increased by caloric restriction and reduced by overfeeding. We discovered that SirT1 depletion causes anorexia by stimulating production of inflammatory factors in white adipose tissue and thus posit that decreases in SirT1 link overnutrition and adipose tissue inflammation.

RESEARCH DESIGN AND METHODS

We used antisense oligonucleotides to reduce SirT1 to levels similar to those seen during overnutrition and studied SirT1-overexpressing transgenic mice and fat-specific SirT1 knockout animals. Finally, we analyzed subcutaneous adipose tissue biopsies from two independent cohorts of human subjects.

RESULTS

We found that inducible or genetic reduction of SirT1 in vivo causes macrophage recruitment to adipose tissue, whereas overexpression of SirT1 prevents adipose tissue macrophage accumulation caused by chronic high-fat feeding. We also found that SirT1 expression in human subcutaneous fat is inversely related to adipose tissue macrophage infiltration.

CONCLUSIONS

Reduction of adipose tissue SirT1 expression, which leads to histone hyperacetylation and ectopic inflammatory gene expression, is identified as a key regulatory component of macrophage influx into adipose tissue during overnutrition in rodents and humans. Our results suggest that SirT1 regulates adipose tissue inflammation by controlling the gain of proinflammatory transcription in response to inducers such as fatty acids, hypoxia, and endoplasmic reticulum stress.