Interaction of chemical defense clothing and high terrestrial altitudes on lift/carry and marksmanship performance

BACKGROUND: The increased metabolic energy requirement imposed by a chemical defense uniform (CDU) and the lower maximal aerobic capacity associated with increased altitude should produce greater demands on the cardiopulmonary system during the performance of a given work task at increasing altitudes. We hypothesized that: a) relative to sea level, the decrements in physical work performance caused by ascending to high terrestrial altitudes would be greater in a CDU compared with a standard fatigue uniform (U.S. Army, BDU); b) the aversive subjective reactions to the CDU would be accentuated with increasing altitude; and c) that staging at moderate altitude, to induce acclimatization, would restore work performance at higher altitudes to sea level norms. METHODS: The physiological and subjective responses of 8 male soldiers to work (10-min lift-and-carry task and rifle marksmanship) were measured. Subjects wore the BDU and a CDU ensemble (U.S. Army, BDO) at sea level, intermediate (2743 m) and high (4,300 m) altitudes following rapid and staged (3 d at 1,830 m) ascents to the higher altitudes. RESULTS: Lift/carry task performance tended to be lower (p = 0.076) in the CDU vs. the BDU at altitude. The cardiopulmonary responses to the lift/carry task increased at altitude and were greater in the CDU. The subjects' perception of their ability to perform the lift/carry task at altitude was adversely impacted more in the CDU than the BDU. Rapid ascent to intermediate altitude degraded marksmanship in both uniforms. Following staged ascent, lift/carry task and marksmanship performance was restored to sea level norms. CONCLUSIONS: Personnel wearing CDU or equivalent protective clothing at intermediate to high terrestrial elevations should anticipate proportionally larger CDU-induced decrements of work performance and lower tolerance to working in a CDU than experienced near sea level. Staging at moderate altitude is an effective strategy for restoring work performance to sea level norms at higher altitudes.     

Propeller EPI in the other direction.

A new propeller EPI pulse sequence with reduced sensitivity to field inhomogeneities is proposed. Image artifacts such as blurring due to Nyquist ghosting and susceptibility gradients are investigated and compared with those obtained in previous propeller EPI studies. The proposed propeller EPI sequence uses a readout that is played out along the short axis of the propeller blade, orthogonal to the readout used in previous propeller methods. In contrast to long-axis readout propeller EPI, this causes the echo spacing between two consecutive phase-encoding (PE) lines to decrease, which in turn increases the k-space velocity in this direction and hence the pseudo-bandwidth. Long- and short-axis propeller EPI, and standard single-shot EPI sequences were compared on phantoms and a healthy volunteer. Diffusion-weighted imaging (DWI) was also performed on the volunteer. Short-axis propeller EPI produced considerably fewer image artifacts compared to the other two sequences. Further, the oblique blades for the long-axis propeller EPI were also prone to one order of magnitude higher residual ghosting than the proposed short-axis propeller EPI.     

Central sleep apnoea—a clinical review

Central sleep apnoea (CSA) is characterised by recurrent apnoeas during sleep with no associated respiratory effort. It mostly results from withdrawal of the wakefulness drive in sleep leaving ventilation under metabolic control. A detailed physiological understanding of the control of breathing in wakefulness and sleep is essential to the understanding of CSA. It encompasses a diverse group of conditions with differing aetiologies and pathophysiology. Likewise treatment varies according to underlying aetiology. Some of the conditions such as idiopathic (primary) CSA (ICSA) are relatively rare and benign. On the other hand Cheyne-Stokes breathing (CSB) pattern is quite common in patients with heart failure and might be a prognostic indicator of poor outcome. Unfortunately modern medical management of heart failure does not seem to have significantly reduced the prevalence of CSA in this group. Since the adoption of positive airway pressure (PAP) as a common treatment modality of obstructive sleep apnoea (OSA), complex CSA has been increasingly observed either as treatment emergent or persistent CSA. Depending on the particular condition, various treatment strategies have been tried in the past two decades which have included hypnotic therapy, respiratory stimulants, judicious administration of carbon dioxide, oxygen therapy, PAP and bi-level ventilatory support with a backup rate. In the past decade adaptive servo ventilation (ASV) has been introduced with much promise. Various studies have shown its superiority over other treatment modalities. Ongoing long term studies will hopefully shed more light on its impact on cardiovascular morbidity and mortality. Other rare forms are still poorly understood and treatments remain suboptimal.     

Effect of acetazolamide on leg endurance exercise at sea level and simulated altitude

Acetazolamide can be taken at sea level to prevent acute mountain sickness during subsequent altitude exposure. Acetazolamide causes metabolic acidosis at sea level and altitude, and increases SaO2 (arterial oxygen saturation) at altitude. The aim of the present study was to determine whether acetazolamide impairs muscle endurance at sea level but not simulated altitude (4300 m for <3 h). Six subjects (20+/-1 years of age; mean+/-S.E.M.) performed exhaustive constant work rate one-leg knee-extension exercise (25+/-2 W) once a week for 4 weeks, twice at sea level and twice at altitude. Each week, subjects took either acetazolamide (250 mg) or placebo orally in a double-blind fashion (three times a day) for 2 days. On day 2, all exercise bouts began approx. 2.5 h after the last dose of acetazolamide or placebo. Acetazolamide caused similar acidosis (pH) in all subjects at sea level (7.43+/-0.01 with placebo compared with 7.34+/-0.01 with acetazolamide; P<0.05) and altitude (7.48+/-0.03 with placebo compared with 7.37+/-0.01 with acetazolamide; P<0.05). However, endurance performance was impaired with acetazolamide only at sea level (48+/-4 min with placebo compared with 36+/-5 min with acetazolamide; P<0.05), but not altitude (17+/-2 min with placebo compared with 20+/-3 min with acetazolamide; P = not significant). In conclusion, lack of impairment of endurance performance by acetazolamide compared with placebo at altitude was probably due to off-setting secondary effects resulting from acidosis, e.g. ventilatory induced increase in SaO2 for acetazolamide compared with placebo (89+/-1 compared with 86+/-1% respectively; P<0.05), which resulted in an increased oxygen pressure gradient from capillary to exercising muscle.     

Innate immunity modulates adipokines in humans

CONTEXT: Chronic inflammation converges in type 2 diabetes and atherosclerosis. Modulation of adipokine signaling by innate immunity in humans is of considerable interest given the role of adipokines in insulin resistance and atherosclerosis. OBJECTIVE: The aim of the study was to examine effects of low-grade endotoxemia, a model of human inflammation, on adipokines in vivo. DESIGN/SETTING: An open-label, placebo-controlled, fixed-sequence clinical study was conducted at a General Clinical Research Center. PATIENTS: There were 20 healthy male (50%) and female volunteers aged 18-40 yr. INTERVENTION: Serial blood sampling and adipose biopsies were performed for 24 h before and after iv bolus endotoxin [lipopolysaccharide (LPS), 3 ng/kg]. MAIN OUTCOME MEASURES: We measured plasma leptin, adiponectin, resistin, soluble leptin receptor, cytokines, insulin, and glucose; distribution of adiponectin among multimeric complexes; whole blood, monocyte and adipose mRNA for adipokines and their receptors. RESULTS: LPS induced fever, blood, and adipose TNF and IL-6 and increased homeostasis model assessment of insulin resistance. These were associated with increases in plasma leptin (from 4.1 +/- 1.1 to 6.1 +/- 1.9 ng/ml in men; 21.1 +/- 4.4 to 27.4 +/- 4.7 ng/ml in women; P < 0.005), doubling of the leptin:soluble leptin receptor ratio, and marked induction of whole blood resistin mRNA (13.7 +/- 7.3-fold; P < 0.001) and plasma resistin (8.5 +/- 2.75 to 43.2 +/- 15.3 ng/ml; P < 0.001). Although total adiponectin levels and low and high molecular weight adiponectin complexes were unaltered by LPS treatment, whole blood mRNA for adiponectin receptors 1 (49%; P < 0.005) and 2 (65%; P < 0.001) was suppressed. CONCLUSIONS: Modulation of adipokine signaling may contribute to the insulin resistant, atherogenic state associated with human inflammatory syndromes. Targeting of individual adipokines or their upstream regulation may prove effective in preventing acute and chronic inflammation-related metabolic complications.     

Human vascular fluid responses to cold stress are not altered by cold acclimation

Repeated cold water immersion can induce the development of an insulative type of cold acclimation in man. This investigation determined if repeated cold water immersion produced changes in vascular fluid responses to cold stress in addition to the previously reported changes in thermoregulation. Seven male subjects performed a standardized cold air and cold water exposure before and again after a cold acclimation program. The cold acclimation program consisted of daily immersion (90 min) in cold water (18 degrees C, stirred) repeated 5 times/wk for 5 consecutive wk. Cold acclimation did not alter the responses of plasma volume or electrolyte concentrations, nor urinary flow or electrolyte excretion during either cold air or cold water exposure. The percent reduction in plasma volume was larger (P less than 0.01) in cold water (-17%) than in cold air (-12%). Cold water immersion resulted in greater (P less than 0.01) diuresis than cold air exposure. Plasma K+ concentration increased (P less than 0.01) during cold (both air and water) exposure, whereas plasma Na+ concentration was unchanged. Calculated renal clearance and urinary excretion rate of both Na+ and K+ increased during cold (both air and water) exposure. The magnitude of plasma volume reduction during cold exposure was not correlated with either the degree of body cooling or diuresis. It is concluded that a) insulative cold acclimation does not influence vascular fluid responses to cold stress, and b) although vascular fluid shifts, body cooling and diuresis are all greater in cold water than in air, a consistent relationship among these parameters could not be established for an individual's response.     

EXAMINING THE LINK BETWEEN CASH FLOW,MARKET VALUE,AND RESEARCH AND DEVELOPMENT INVESTMENT SPENDING IN THE MEDICAL DEVICE INDUSTRY

Unlike the pharmaceutical industry, no empirical research has focused on the factors influencing research and development (R&D) spending in the medical device industry. To fill that gap, this study examines how R&D spending is influenced by prior year cash flow and corporate market value using multiple regression analysis and a panel data set of medical device companies over the period 1962–2008. The empirical findings suggest that the elasticities of R&D spending with respect to cash flow and corporate market value equal 0.58 and 0.31, respectively. Moreover, based upon these estimates, simulations show that the recently enacted excise tax on medical devices, taken alone, will reduce R&D spending by approximately $4 billion and thereby lead to a minimum loss of $20 billion worth of human life years over the first 10 years of its enactment. Copyright © 2012 John Wiley & Sons, Ltd.     

Histochemical and morphological observations on rat myocardium after exercise

Effects of seven levels of chronic physical activity on the metabolic and morphologic characteristics of left ventricular myocardium of adult male albino rats were investigated.Treatments included sedentary control; voluntary running; short-duration, high-intensity running; medium-duration, moderate-intensity running; long-duration, low-intensity running; electric stimulus control; and endurance swimming. Excluding the controls, the animals were trained 5 days per week for 8 consecutive weeks. Food and water were providedad libitum to them. Fifty-six animals comprised the final sample.Histochemical techniques were used to evaluate the relative glycogen, fatty acid, SDH and LDH concentrations in the cardiac fibers. Each stain was measured objectively, using a photometer. A Hematoxylin and Eosin stain was employed to rate morphologic features. These sections were evaluated subjectively on the basis of presence or absence of lesions.Physical training for 8 weeks was sufficient to produce metabolic adaptations in the rats. The trained animals gained 37.4 % less body weight than did the sedentary controls (P < 0.05). However, neither histochemical nor morphological changes had occurred to the hearts of these animals consequent to the 8 weeks training programs. Apparently, the myocardial tissues examined, from the trained animals, contain the enzymes, SDH and LDH, and the substrates, glycogen and fatty acids, in amounts greater than that needed to cope with the exercise stress afforded by these training programs.     

Appetite suppression and weight reduction by a centrally active aminosterol

The rise in obesity and its complications has generated enormous interest in the regulation of feeding and body weight. We show that a spermine metabolite of cholesterol (MSI-1436) decreases body weight, specifically fat, by suppressing feeding and preventing the reduction in energy expenditure, hormonal changes, and patterns of neuropeptide expression normally associated with weight loss. MSI-1436 enters the brain after peripheral injection and is more potent when injected into the cerebral ventricle (intracerebroventricular [ICV]). Systemic or ICV MSI-1436 administration induced similar patterns of Fos immunoreactivity in the brain, especially the paraventricular hypothalamic nucleus (PVN). This brain region integrates neural signals from hypothalamic and brain stem nuclei and regulates feeding behavior, autonomic function, and neuroendocrine function. Microinjection of MSI-1436 into the PVN potently suppressed feeding and reduced body weight for several days. Unlike caloric restriction, MSI-1436 decreased mRNA levels of agouti-related peptide and neuropeptide Y in the hypothalamus. These findings indicate that MSI-1436 acts in the brain to regulate food intake and energy expenditure, likely through suppression of orexigenic hypothalamic pathways.