Seasonal Trends for Environmental Illness Incidence in the U.S. Army.

INTRODUCTION: The incidence of and risk factors for exertional heat illness (EHI) and cold weather injury (CWI) in the U.S. Army have been well documented. The "heat season", when the risk of EHI is highest and application of risk mitigation procedures is mandatory, has been arbitrarily defined as May 1 through September 30, while the "cold season" is understood to occur from October 1 to April 30 each year. The proportions of EHI and CWI that occur outside of the traditional heat and cold seasons are unknown. Additionally, it is unknown if either of the seasonal definitions are appropriate. The primary purpose of this study was to determine the proportion of EHI and of CWI that occur within the commonly accepted seasonal definitions. We also report the location-specific variability, seasonal definitions, and the demographic characteristics of the populations. METHODS: The U.S. Army installations with the highest frequency of EHI and of CWI from 2008 to 2013 were identified and used for analysis. In total there were 15 installations included in the study, with five installations used for analysis in both the EHI and CWI projects. In- and out-patient EHI and CWI data (ICD-9-CM codes 992.0 to 992.9 and ICD codes 991.0 to 991.9, respectively) were obtained from the Defense Medical Surveillance System. Installation-specific denominator data were obtained from the Defense Manpower Data Center, and incidence rates were calculated by week, for each installation. Segmental (piecewise) regression analysis was used to determine the start and end of the heat and cold seasons. RESULTS: Our analysis indicates that the heat season starts around April 22 and ends around September 9. The cold season starts on October 3 and ends on March 24. The majority (n = 6,445, 82.3%) of EHIs were diagnosed during the "heat season" of May 1 to September 30, while 10.3% occurred before the heat season started (January1 to April 30) and 7.3% occurred after the heat season ended (October 1 to December 31). Similar to EHI, 90.5% of all CWIs occurred within the traditionally defined cold season, while 5.7% occurred before and 3.8% occurred after the cold season. The locations with the greatest EHI frequency were Ft Bragg (n = 2,129), Ft Benning (n = 1,560), and Ft Jackson (n = 1,538). The bases with the largest proportion of CWI in this sample were Ft Bragg (17.8%), Ft Wainwright (17.2%), and Ft Jackson (12.7%). There were considerable inter-installation differences for the start and end dates of the respective seasons. CONCLUSIONS: The present study indicates that the traditional heat season definition should be revised to begin ∼3 weeks earlier than the current date of May 1; our data indicate that the current cold season definition is appropriate. Inter-installation variability in the start of the cold season was much larger than that for the heat season. Exertional heat illnesses are a year-round problem, with ∼17% of all cases occurring during non-summer months, when environmental heat strain and vigilance are lower. This suggests that EHI mitigation policies and procedures require greater year-round emphasis, particularly at certain locations.

Iminobiotin binding induces large fluorescent enhancements in avidin and streptavidin fluorescent conjugates and exhibits diverging pH-dependent binding affinities.

The pH-dependent binding affinity of either avidin or streptavidin for iminobiotin has been utilized in studies ranging from affinity binding chromatography to dynamic force spectroscopy. Regardless of which protein is used, the logarithmic dependence of the equilibrium dissociation constant (K(d)) on pH is assumed conserved. However a discrepancy has emerged from a number of studies which have shown the binding affinity of streptavidin for iminobiotin in solution to be unexpectedly low, with the K(d) at values usually associated with non-specific binding even at strongly basic pH levels. In this work we have utilized a Bodipy fluorescent conjugate of avidin and an Oregon Green fluorescent conjugate of streptavidin to determine the K(d) of the complexes in solution in the pH range of 7.0 to 10.7. The study was made possible by the remarkable fluorescent enhancement of the two fluorescent conjugates (greater than 10 fold) upon saturation with iminobiotin. The streptavidin-iminobiotin interaction exhibited almost no pH dependence over the range studied, with K(d) consistently on the order of 10(-5) M. In contrast, under identical experimental conditions the avidin-iminobiotin interaction exhibited the expected logarithmic dependence on pH. We discuss the possible origins for why these two closely related proteins would diverge in their binding affinities for iminobiotin as a function of pH.