Combat stress casualties in Iraq. Part 2: psychiatric screening prior to aeromedical evacuation

TOPIC: Exposure to combat-related trauma is a leading cause of posttraumatic stress disorder. Deployed military mental health practitioners serve important roles in the assessment, diagnosis, and aeromedical evacuation of psychiatric patients from the combat zone. PURPOSE: To review the role of military mental health professionals working with psychiatric patients at a combat hospital and aeromedical staging facility in Iraq. SOURCE OF INFORMATION: Military operating instructions, existing theoretical and research literature, and personal experiences of the authors while deployed to Iraq. CONCLUSIONS: Psychiatric screening can help reduce risk in potentially unstable mental health patients prior to aeromedical evacuation. Civilian nurse psychotherapists and advanced practice psychiatric nurses will be needed to provide psychiatric follow-up care for the large number of military veterans returning from combat.     

Disparities in Self-Reported Diabetes Mellitus among Arab, Chaldean, and Black Americans in Southeast Michigan

Diabetes mellitus is an important public health problem that disproportionately affects minorities. Using a cross sectional, convenience sample, we estimated the prevalence of self-reported diabetes for Whites (n = 212), Arabs (n = 1,303), Chaldeans (n = 828), and Blacks (n = 789) in southeast Michigan. In addition, using a logistic regression model, we estimated odds ratios and 95% confidence intervals for the association between ethnicity and diabetes before and after adjusting for demographic, socioeconomic status, health care, chronic conditions, and health behavior variables. The overall age- and sex-adjusted prevalence of diabetes was 7.0%. Estimates were highest for Blacks (8.0%) followed by Arabs and Whites (7.0% for each group) and Chaldeans (6.0%). In the fully adjusted model, the association between ethnicity and diabetes was not statistically significant. Future studies should collect more detailed socioeconomic status, acculturation and health behavior information, which are factors that may affect the relationship between race/ethnicity and diabetes.     

Excess cholesterol induces mouse egg activation and may cause female infertility

The HDL receptor scavenger receptor, class B type I (SR-BI) controls the structure and fate of plasma HDL. Female SR-BI KO mice are infertile, apparently because of their abnormal cholesterol-enriched HDL particles. We examined the growth and meiotic progression of SR-BI KO oocytes and found that they underwent normal germinal vesicle breakdown; however, SR-BI KO eggs, which had accumulated excess cholesterol in vivo, spontaneously activated, and they escaped metaphase II (MII) arrest and progressed to pronuclear, MIII, and anaphase/telophase III stages. Eggs from fertile WT mice were activated when loaded in vitro with excess cholesterol by a cholesterol/methyl-β-cyclodextrin complex, phenocopying SR-BI KO oocytes. In vitro cholesterol loading of eggs induced reduction in maturation promoting factor and MAPK activities, elevation of intracellular calcium, extrusion of a second polar body, and progression to meiotic stages beyond MII. These results suggest that the infertility of SR-BI KO females is caused, at least in part, by excess cholesterol in eggs inducing premature activation and that cholesterol can activate WT mouse eggs to escape from MII arrest. Analysis of SR-BI KO female infertility raises the possibility that abnormalities in cholesterol metabolism might underlie some cases of human female infertility of unknown etiology.Scavenger receptor, class B type I (SR-BI) is an HDL receptor that transports unesterified cholesterol (UC) and its esters between lipoproteins and cells (1–3) and functions as a signaling receptor (4). SR-BI controls the structure and composition of plasma HDL and the amounts and fates of HDL cholesterol (2, 3, 5, 6). Homozygous null SR-BI knockout (KO) mice exhibit hypercholesterolemia with unusually large and UC-enriched HDL particles [abnormally high UC to total cholesterol (TC) ratio] (5, 7, 8). This unusual hypercholesterolemia apparently induces a deleterious accumulation of UC in RBCs and platelets that influences their maturation, lifetime in the bloodstream, structure, and/or function (7–13).Female but not male SR-BI KO mice exhibit fully penetrant infertility, despite their essentially normal ovarian histology (6, 14). Several lines of surgical transplantation, genetic, histologic, and pharmacologic evidence indicate that the abnormal structure and composition of circulating HDL in SR-BI KO mice contribute to their female infertility (Discussion). This infertility can be effectively corrected by altering (through a variety of approaches) the structure and abundance of the circulating HDL to which the ovaries are exposed (7, 14, 15). This evidence also suggests that the infertility is likely caused by defects in oocytes/eggs manifested during the periovulatory period without affecting the primordial follicle pool. Indeed, ∼19% of the ovulated eggs harvested ∼16 h after hormone-induced superovulation are dead (6, 14) (see below). The remaining oocytes are unable to be fertilized or develop into viable pups. Here, we examined SR-BI KO oocyte growth and progression through the peri- and postovulatory stages of meiosis (Fig. 1) and investigated the possibility that high levels of UC in HDL might result in excess cholesterol deposition in oocytes or eggs that might influence their growth, meiotic progression, and/or viability.Open in a separate windowFig. 1.Meiotic resumption and egg activation in the mouse. Schematic representation of meiotic resumption and egg activation by either fertilization or chemical agents. The stages at which primary (prophase I) and secondary (MII) arrest occur are indicated. Oocytes initiate meiosis during fetal development and enter primary arrest at the diplotene stage of prophase I around the time of birth (not illustrated here). Prophase I arrest is maintained during oocyte growth and differentiation. Prior to ovulation, meiosis resumes, the nuclear envelope of the germinal vesicle (GV) dissassembles [GV breakdown (GVBD)], and chromosomes condense and align on the first metaphase plate. During the first division, homologous chromosomes segregate and the first polar body (PB) is extruded (first PB in anaphase/telophase I). The remaining chromosomes realign on the second metaphase plate (MII) followed by secondary arrest. During MII arrest, the first PB often degrades. Eggs that are ovulated can exit MII arrest and complete meiosis when activated by a fertilizing sperm (upper right) or chemical agents, such as SrCl₂ or ethanol (lower right), which induce a spike (ethanol) or oscillations (sperm and SrCl₂) in cytoplasmic Ca²⁺ levels and suppress MAPK and MPF activities. On activation, sister chromatids segregate, and the second PB is extruded (second PB in anaphase/telophase II). The activated egg then progresses to pronuclear stage as the nuclear envelope reforms. On chemical activation, the egg can alternatively progress to metaphase III, segregate the remaining chromatids randomly during anaphase III, and extrude a third PB (anaphase/telophase III).Normally, after the luteinizing hormone surge of the estrous cycle and just before ovulation, mammalian oocytes complete the first meiotic division [meiosis I (MI)] and immediately thereafter proceed to metaphase II (MII), a stage at which they arrest (Fig. 1). A complex network of proteins and intracellular signals establishes and maintains MII arrest [e.g., elevated MAPK and maturation promoting factor (MPF; or cdk1/cyclin B) kinase activities] (16, 17) and subsequently permits exit from this stage after fertilization (e.g., reduction in MAPK and MPF activities) (16, 17). Productive fertilization of MII-arrested eggs leads to inositol triphosphate-induced oscillations in intracellular calcium concentration ([Ca²⁺]_i) that activate the eggs [exit from MII arrest, second polar body (PB) extrusion, formation of pronuclei, etc.] (Fig. 1) (18, 19). Fertilization-induced changes in intracellular zinc levels also may influence activation (19). The parthenogenetic stimulant SrCl₂ activates normal eggs (20) by inducing oscillations in [Ca²⁺]_i (21, 22) and suppressing MAPK and MPF kinase activities (23) that mimic those that occur after fertilization (21, 22). Brief exposure to ethanol induces a single spike in [Ca²⁺]_i and activates eggs (24, 25). Unlike fertilized eggs, which receive the paternal chromosome complement from the sperm, SrCl₂- or ethanol-activated eggs are haploid (Fig. 1) and cannot support proper embryogenesis (22).Here, we found that, within follicles of hormone-treated SR-BI KO females, oocytes apparently resumed meiosis normally. However, these cells spontaneously escaped MII arrest, exhibited reduced MPF and MAPK activities, and aberrantly progressed to haploid pronuclear, metaphase III, and anaphase/telophase III stages, similar to normal ovulated eggs after chemical (e.g., SrCl₂) (22, 25) activation (Fig. 1). Compared with control eggs, the eggs of SR-BI KO females accumulated excess cholesterol. Strikingly, we could recapitulate the apparently spontaneous activation of ovulated SR-BI KO eggs in eggs ovulated from fertile control mice (WT or SR-BI^+/−) by treating those eggs with a cholesterol/methyl-β-cyclodextrin (MβCD) complex to load them with excess cholesterol (26). In addition, cholesterol loading induced a single spike in [Ca²⁺]_i reminiscent of that seen in ethanol-activated eggs (24, 25). These results establish that excess cholesterol loading provides a new approach to activating mammalian MII-arrested eggs and suggest that the infertility of SR-BI KO females is caused, at least in part, by excess cholesterol acting directly on the egg to induce premature activation. Analysis of SR-BI KO female infertility also raises the possibility that abnormalities in cholesterol metabolism might underlie some forms of human female infertility of unknown etiology.     

Environmental exposure assessment of pesticides in farmworker homes

Farmworkers and their families are exposed to pesticides both at work and in their homes. Environmental exposure assessment provides a means to evaluate pesticides in the environment and human contact with these chemicals through identification of sources and routes of exposure. To date, a variety of methods have been used to assess pesticide exposure among farmworker families, mostly focusing on dust and handwipe samples. While many of the methods are similar, differences in the collection, chemical analysis, and statistical analysis, can limit the comparability of results from farmworker studies. This mini-monograph discusses the strategies used to assess pesticide exposures, presents limitations in the available data for farmworkers, and suggests research needs for future studies of pesticide exposure among farmworker families.     

Atherosclerotic risk genotypes and recurrent coronary events after myocardial infarction

The association of a group of prespecified atherosclerotic risk genotypes with recurrent coronary events (coronary-related death, nonfatal myocardial infarction, or unstable angina) was investigated in a cohort of 1,008 patients after infarction during an average follow-up of 28 months. We used a carrier-ship approach with time-dependent survivorship analysis to evaluate the average risk of each carried genotype. Contrary to expectation, the hazard ratio for recurrent coronary events per carried versus noncarried genotype was 0.89 (95% confidence interval 0.80 to 0.99, p = 0.03) after adjustment for relevant genetic, clinical, and environmental covariates. This hazard ratio, derived from the 7 prespecified genotypes, indicated an average 11% reduction in the risk of recurrent coronary events per carried versus noncarried genotype. At 1 year after hospital discharge, the cumulative probability of recurrent coronary events was 26% in those who carried < or =1, 20% for those with 2 to 4, and 13% for those with > or =5 of these genotypes (p = 0.02). This unexpected risk reversal is a likely consequence of changes in the mix of risk factors in pre- and postinfarction populations. In conclusion, this under appreciated, population-based, risk-reversal phenomenon may explain the inconsistent associations of genetic risk factors with outcome events in previous reports involving coronary populations with different risk attributes.     

A european, multicenter, observational study to assess the value of gastric-to-end tidal PCO2 difference in predicting postoperative complications

Automated online tonometry displays a rapid, semicontinuous measurement of gastric-to-endtidal carbon dioxide (Pr-etCO2) as an index of gastrointestinal perfusion during surgery. Its use to predict postoperative outcome has not been studied in general surgery patients. We, therefore, studied ASA physical status III-IV patients operated on for elective surgery under general anesthesia and a planned duration of >2 h in a European, multicenter study. As each center was equipped with only 1 tonometric monitor, a randomization was performed if more than one patient was eligible the same day. Patients not monitored with tonometry were assessed only for follow-up. The main outcome measure was the assessment of postoperative functional recovery delay (FRD) on day 8. Among the 290 patients studied, 34% had FRD associated with a longer hospital stay. The most common FRDs were gastrointestinal (45%), infection (39%), and respiratory (35%). In those monitored with tonometry (n = 179), maximum Pr-etCO2 proved to be the best predictor increasing the probability of FRD from 34% for all patients to 65% at a cut-off of 21 mm Hg (2.8kPa) (sensitivity 0.27, specificity 0.92, positive predictive value 64%, negative predictive value 70%). We conclude that intraoperative Pr-etCO2 measurement may be a useful prognostic index of postoperative morbidity.