Self Reported Incidence and Morbidity of Acute Respiratory Illness among Deployed U.S. Military in Iraq and Afghanistan

Background

Historically, respiratory infections have had a significant impact on U.S. military missions. Deployed troops are particularly at high risk due to close living conditions, stressful work environments and increased exposure to pathogens. To date, there are limited data available on acute respiratory illness (ARI) among troops deployed in support of ongoing military operations, specifically Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF).

Methods

Using self-report data from two sources collected from troops deployed to Iraq, Afghanistan and the surrounding region, we analyzed incidence and risk factors for ARI. Military personnel on mid-deployment Rest & Recuperation (R&R) or during redeployment were eligible to participate in the voluntary self-report survey.

Results

Overall, 39.5% reported having at least one ARI. Of these, 18.5% sought medical care and 33.8% reported having decreased job performance. The rate of self-reported ARI was 15 episodes per 100 person-months among those taking the voluntary survey, and 24.7 episodes per 100 person-months among those taking the clinic health questionnaire. Negative binomial regression analysis found female sex, Navy branch of service and lack of flush toilets to be independently associated with increased rates of ARI. Deployment to OIF, increasing age and higher rank were also positively associated with ARI risk.

Conclusions

The overall percentage of deployed military personnel reporting at least one acute respiratory illness decreased since earlier parts of OIF/OEF. However, the reported effect on job performance increased tremendously. The most important factors associated with increased respiratory infection are female sex, Navy branch of service, lack of improved latrine facilities, deployment to OIF, increasing age and higher rank.     

Localization of a guanylyl cyclase to chemosensory cilia requires the novel ciliary MYND domain protein DAF-25

In harsh conditions, Caenorhabditis elegans arrests development to enter a non-aging, resistant diapause state called the dauer larva. Olfactory sensation modulates the TGF-β and insulin signaling pathways to control this developmental decision. Four mutant alleles of daf-25 (abnormal DAuer Formation) were isolated from screens for mutants exhibiting constitutive dauer formation and found to be defective in olfaction. The daf-25 dauer phenotype is suppressed by daf-10/IFT122 mutations (which disrupt ciliogenesis), but not by daf-6/PTCHD3 mutations (which prevent environmental exposure of sensory cilia), implying that DAF-25 functions in the cilia themselves. daf-25 encodes the C. elegans ortholog of mammalian Ankmy2, a MYND domain protein of unknown function. Disruption of DAF-25, which localizes to sensory cilia, produces no apparent cilia structure anomalies, as determined by light and electron microscopy. Hinting at its potential function, the dauer phenotype, epistatic order, and expression profile of daf-25 are similar to daf-11, which encodes a cilium-localized guanylyl cyclase. Indeed, we demonstrate that DAF-25 is required for proper DAF-11 ciliary localization. Furthermore, the functional interaction is evolutionarily conserved, as mouse Ankmy2 interacts with guanylyl cyclase GC1 from ciliary photoreceptors. The interaction may be specific because daf-25 mutants have normally-localized OSM-9/TRPV4, TAX-4/CNGA1, CHE-2/IFT80, CHE-11/IFT140, CHE-13/IFT57, BBS-8, OSM-5/IFT88, and XBX-1/D2LIC in the cilia. Intraflagellar transport (IFT) (required to build cilia) is not defective in daf-25 mutants, although the ciliary localization of DAF-25 itself is influenced in che-11 mutants, which are defective in retrograde IFT. In summary, we have discovered a novel ciliary protein that plays an important role in cGMP signaling by localizing a guanylyl cyclase to the sensory organelle.     

Paralogous origin of the red- and green-sensitive visual pigment genes in vertebrates

The nucleotide sequence of the red-sensitive visual pigment gene, R007Af, in the fish Astyanax fasciatus, from the initiation codon to the stop codon of this gene, including introns, is 1,592 bp, making it the shortest visual pigment gene known in vertebrates. Analysis of this and other homologous sequence data suggests that vertebrates initially had two duplicate genes and that each ancestor of Astyanax, human, and chicken independently duplicated the gene in the process of developing their red-green color vision. Furthermore, many extant red-green colorblind organisms may be explained simply by the failure of achieving very specific nucleotide substitutions at the three codon positions 180, 277, and 285, rather than by the lack of duplicate loci.      

Assessment of the immune responsiveness of mice irradiated with continuous wave or pulse-modulated 425-MHz radio frequency radiation

Groups of female BALB/C mice were irradiated with 425-MHz radio frequency (RF) radiation either continuous wave (CW) or pulse modulated (PM, 1-ms pulse width, 250 pulses/s). Mice were irradiated in a rectangular strip-transmission line at average forward powers of 78, 17.7, or 5 W for CW and 17.7, 5, or 1.25 W for PM. The mean specific absorption rate, as measured using twin-well calorimetry was 7.7 W/kg for a forward power of 70 W. No differences in the mitogen-stimulated response of lymphocytes or in the primary antibody response to sheep erythrocytes or polyvinylpyrrolidone were observed between irradiated and sham-irradiated mice, nor between mice exposed to either CW or PM 425-MHz RF radiation.     

Development and accumulation of ABA in fluridone-treated and drought-stressed Vicia faba plants under different light conditions

The effects of fluridone on guard cell morphology, chloroplast ultrastructure and accumulation of drought stress-induced abscisic acid (ABA) were studied in Vicia faba L. plants grown under different light conditions. Drought stress was induced by allowing the leaves to lose 12% of their fresh weight. The appearance of defective and undeveloped stomata, and chloroplasts with a destroyed thylakoid membrane system was found in fluridone-treated plants grown at a photosynthetic photon flux (PPF) of 600 μmol m^-2 s^-1. Plants grown at a PPF of 40 μmol m^-2 s^-1 had diminished levels of ABA after imposition of dehydration. Fluridone treatment reduced the level of ABA in both unstressed and dehydrated leaves. Accumulation of ABA in the control plants was considerably reduced when they were exposed to dark periods of 24, 48 and 72 h just before imposition of the stress. Twenty-four hours after the dark treatment dehydration of the leaves resulted in a 3-fold decrease in the level of stress-induced ABA, and 72 h after dark treatment the amount of stress-induced ABA approximated the prestressed values. Fluridone-treated plants failed to accumulate ABA under water stress. In addition to functionally active chloroplasts, well-developed and functional stomata are required for drought stress to elicit a rise in ABA.     

MISC-1/OGC links mitochondrial metabolism, apoptosis and insulin secretion

We identified MISC-1 (Mitochondrial Solute Carrier) as the C. elegans orthologue of mammalian OGC (2-oxoglutarate carrier). OGC was originally identified for its ability to transfer α-ketoglutarate across the inner mitochondrial membrane. However, we found that MISC-1 and OGC are not solely involved in metabolic control. Our data show that these orthologous proteins participate in phylogenetically conserved cellular processes, like control of mitochondrial morphology and induction of apoptosis. We show that MISC-1/OGC is required for proper mitochondrial fusion and fission events in both C. elegans and human cells. Transmission electron microscopy reveals that loss of MISC-1 results in a decreased number of mitochondrial cristae, which have a blebbed appearance. Furthermore, our pull-down experiments show that MISC-1 and OGC interact with the anti-apoptotic proteins CED-9 and Bcl-x(L), respectively, and with the pro-apoptotic protein ANT. Knock-down of misc-1 in C. elegans and OGC in mouse cells induces apoptosis through the caspase cascade. Genetic analysis suggests that MISC-1 controls apoptosis through the physiological pathway mediated by the LIN-35/Rb-like protein. We provide genetic and molecular evidence that absence of MISC-1 increases insulin secretion and enhances germline stem cell proliferation in C. elegans. Our study suggests that the mitochondrial metabolic protein MISC-1/OGC integrates metabolic, apoptotic and insulin secretion functions. We propose a novel mechanism by which mitochondria integrate metabolic and cell survival signals. Our data suggest that MISC-1/OGC functions by sensing the metabolic status of mitochondria and directly activate the apoptotic program when required. Our results suggest that controlling MISC-1/OGC function allows regulation of mitochondrial morphology and cell survival decisions by the metabolic needs of the cell.     

EFFECT OF SEASONAL SEA ICE BREAKOUT ON THE PHOTOSYNTHESIS OF BENTHIC DIATOM MATS AT CASEY,ANTARCTICA1

Photosynthesis of marine benthic diatom mats was examined before and after sea ice breakout at a coastal site in eastern Antarctica (Casey). Before ice breakout the maximum under‐ice irradiance was between 2.5 and 8.2 μmol photons·m^?2·s^?1 and the benthic microalgal community was characterized by low E_k (12.1–32.3 μmol photons·m^?2·s^?1), low relETR_max (9.2–32.9), and high alpha (0.69–1.1). After breakout, 20 days later, the maximum irradiance had increased to between 293 and 840 μmol photons·m^?2·s^?1, E_k had increased by more than an order of magnitude (to 301–395 μmol photons·m^?2·s^?1), relETR_max had increased by more than five times (to 104–251), and alpha decreased by approximately 50% (to 0.42–0.68). During the same time interval the species composition of the mats changed, with a decline in the abundance of Trachyneis aspera (Karsten) Hustedt, Gyrosigma subsalsum Van Heurck, and Thalassiosira gracilis (Karsten) Hustedt and an increase in the abundance of Navicula glaciei Van Heurck. The benthic microalgal mats at Casey showed that species composition and photophysiology changed in response to the sudden natural increase in irradiance. This occurred through both succession shifts in the species composition of the mats and also an ability of individual cells to photoacclimate to the higher irradiances.     

Lifelong reduction in complex IV induces tissue‐specific metabolic effects but does not reduce lifespan or healthspan in mice

Loss of SURF1, a Complex IV assembly protein, was reported to increase lifespan in mice despite dramatically lower cytochrome oxidase (COX) activity. Consistent with this, our previous studies found advantageous changes in metabolism (reduced adiposity, increased insulin sensitivity, and mitochondrial biogenesis) in Surf1^?/? mice. The lack of deleterious phenotypes in Surf1^?/? mice is contrary to the hypothesis that mitochondrial dysfunction contributes to aging. We found only a modest (nonsignificant) extension of lifespan (7% median, 16% maximum) and no change in healthspan indices in Surf1^?/? vs. Surf1^+/+ mice despite substantial decreases in COX activity (22%–87% across tissues). Dietary restriction (DR) increased median lifespan in both Surf1^+/+ and Surf1^?/? mice (36% and 19%, respectively). We measured gene expression, metabolites, and targeted expression of key metabolic proteins in adipose tissue, liver, and brain in Surf1^+/+ and Surf1^?/? mice. Gene expression was differentially regulated in a tissue‐specific manner. Many proteins and metabolites are downregulated in Surf1^?/? adipose tissue and reversed by DR, while in brain, most metabolites that changed were elevated in Surf1^?/? mice. Finally, mitochondrial unfolded protein response (UPR^mt)‐associated proteins were not uniformly altered by age or genotype, suggesting the UPR^mt is not a key player in aging or in response to reduced COX activity. While the changes in gene expression and metabolism may represent compensatory responses to mitochondrial stress, the important outcome of this study is that lifespan and healthspan are not compromised in Surf1^?/? mice, suggesting that not all mitochondrial deficiencies are a critical determinant of lifespan.     

Insulin receptor substrate and p55 orthologous adaptor proteins function in the Caenorhabditis elegans daf-2/insulin-like signaling pathway

An insulin-like signaling pathway regulates development and lifespan in Caenorhabditis elegans. Genetic screens that identified many components of the C. elegans insulin pathway did not identify homologs of insulin receptor substrates or the phosphoinositide 3-kinase (PI3K) adaptor/regulatory subunit, which are both required for signaling by mammalian insulin/insulin-like growth factor I pathways. The C. elegans genome contains one homolog of each protein. The C. elegans versions of insulin receptor substrate (IST-1) and PI3K p50/p55 (AAP-1) share moderate sequence similarity with their vertebrate and Drosophila counterparts. Genetic experiments show that ist-1 and aap-1 potentiate C. elegans insulin-like signaling, although they are not required for signaling in the pathway under most conditions. Worms lacking AAP-1 activity because of the mutation aap-1(m889) constitutively arrest development at the dauer larval stage when raised at high temperatures. aap-1 mutants also live longer than wild-type animals, a phenotype observed in other C. elegans mutants with defects in DAF-2 signaling. Interestingly, IST-1 appears to be required for signaling through a pathway that may act in parallel to AGE-1/PI3K.     

A comparison of the short term effects of diesel fuel and lubricant oils on Antarctic benthic microbial communities

The effects of diesel fuel and three lubricating oils on microbial communities in marine sediment were investigated in a field experiment at Casey Station, Antarctica. Sediment from a pristine site in Antarctica was treated with either Special Antarctic Blend (SAB) diesel, a synthetic lubricant (Mobil 0W-40), the same lubricant after use in a vehicle or an equivalent unused biodegradable lubricant (Titan GT1). The sediment was re-deployed in trays on the seabed for 5 weeks during the austral summer. The microbial community structure in the sediment upon collection, deployment and retrieval was investigated using denaturing gradient gel electrophoresis (DGGE), most probable number (MPN) counts and direct microscopic counting. It was found that only minor changes occurred in the microbial communities due to the experimental protocol. After 5 weeks however, there were significant differences between the communities in the SAB and clean and used lubricant (Mobil 0W-40) as compared to the control treatment. There was no significant difference between the control and biodegradable oil (Titan GT1) treatment. These results indicate that SAB and synthetic lubricants have a measurable effect on sediment microbial communities in the short-term. The biodegradable oil did not produce such an effect and we conclude that the use of such an oil could reduce the risks associated with oil spills in the Antarctic environment.