Metabolic syndrome is inversely related to cardiorespiratory fitness in male career firefighters

Cardiovascular disease (CVD) accounts for 45% of on-duty fatalities among firefighters, occurring primarily in firefighters with excess CVD risk factors in patterns resembling the metabolic syndrome (MetSyn). Additionally, firefighters have a high prevalence of obesity and sedentary behavior suggesting that MetSyn is also common. Therefore, we assessed the prevalence of MetSyn in firefighters and its association with cardiorespiratory fitness (CRF) in a cross-sectional study of 957 male career firefighters. The CRF was measured by maximal exercise tolerance testing (standard metabolic equivalent [METS]). The MetSyn was defined according to modified criteria from the Joint Scientific Statement. Group differences were compared using χ-test and logistic regression. The prevalence of MetSyn was 28.3%. Firefighters in the lowest fitness category (METS ≤ 10) had a nearly 10-fold higher prevalence of MetSyn (51.2%) compared with colleagues in the highest fitness category (METS > 14) (MetSyn prevalence 5.2%) (p value < 0.0001, adjusted for age). In multivariate regression models, every 1-unit increase in METS decreased the odds of having the MetSyn by 31% (odds ratio 0.69 [95% confidence interval 0.63-0.76] [age adjusted]), whereas age had no significant effect after adjusting for CRF. We found a high prevalence of the MetSyn in this group of career emergency responders expected to be more active, fit, and relatively younger than the general population. Moreover, there is a highly significant inverse, dose-response association with CRF. Firefighters should be given strong incentives to improve their fitness, which would decrease prevalent MetSyn, a likely precursor of on-duty CVD events and contributor to CVD burden in this population.     

The role of IFN-gamma in systemic lupus erythematosus: a challenge to the Th1/Th2 paradigm in autoimmunity

The classification of T helper cells into type 1 (Th1) and type 2 (Th2) led to the hypothesis that Th1 cells and their cytokines (interleukin [IL]-2, interferon [IFN]-γ) are involved in cell-mediated autoimmune diseases, and that Th2 cells and their cytokines (IL-4, IL-5, IL-10, IL-13) are involved in autoantibody(humoral)-mediated autoimmune diseases. However, this paradigm has been refuted by recent studies in several induced and spontaneous mouse models of systemic lupus erythematosus, which showed that IFN-γ is a major effector molecule in this disease. These and additional findings, reviewed here, suggest that these two cross-talking classes of cytokines can exert autoimmune disease-promoting or disease-inhibiting effects without predictability or strict adherence to the Th1-versus-Th2 dualism.     

A Deep Sequencing Approach to Uncover the miRNOME in the Human Heart

MicroRNAs (miRNAs) are a class of non-coding RNAs of ∼22 nucleotides in length, and constitute a novel class of gene regulators by imperfect base-pairing to the 3′UTR of protein encoding messenger RNAs. Growing evidence indicates that miRNAs are implicated in several pathological processes in myocardial disease. The past years, we have witnessed several profiling attempts using high-density oligonucleotide array-based approaches to identify the complete miRNA content (miRNOME) in the healthy and diseased mammalian heart. These efforts have demonstrated that the failing heart displays differential expression of several dozens of miRNAs. While the total number of experimentally validated human miRNAs is roughly two thousand, the number of expressed miRNAs in the human myocardium remains elusive. Our objective was to perform an unbiased assay to identify the miRNOME of the human heart, both under physiological and pathophysiological conditions. We used deep sequencing and bioinformatics to annotate and quantify microRNA expression in healthy and diseased human heart (heart failure secondary to hypertrophic or dilated cardiomyopathy). Our results indicate that the human heart expresses >800 miRNAs, the majority of which not being annotated nor described so far and some of which being unique to primate species. Furthermore, >250 miRNAs show differential and etiology-dependent expression in human dilated cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM). The human cardiac miRNOME still possesses a large number of miRNAs that remain virtually unexplored. The current study provides a starting point for a more comprehensive understanding of the role of miRNAs in regulating human heart disease.     

Population Seroprevalence Study after a West Nile Virus Lineage 2 Epidemic,Greece, 2010

Introduction

During summer 2010, 262 human cases including 35 deaths from West Nile virus (WNV) infection were reported from Central Macedonia, Greece. Evidence from mosquitoes, birds and blood donors demonstrated that the epidemic was caused by WNV lineage 2, which until recently was considered of low virulence. We conducted a household seroprevalence study to estimate the spread of infection in the population during the epidemic, ascertain the relationship of infection to clinical disease, and identify risk factors for infection.

Methods

We used a two-stage cluster design to select a random sample of residents aged ≥18 years in the outbreak epicentre. We collected demographic, medical, and risk factor data using standard questionnaires and environmental checklists, and tested serum samples for presence of WNV IgG and IgM antibodies using ELISA.

Results

Overall, 723 individuals participated in the study, and 644 blood samples were available. Weighted seropositivity for IgG antibodies was 5.8% (95% CI: 3.8–8.6; n=41). We estimated that about 1 in 130 (1:141 to 1:124) infected individuals developed WNV neuroinvasive disease, and approximately 18% had clinical manifestations attributable to their infection. Risk factors for infection reflected high exposure to mosquitoes; rural residents were particularly at risk (prevalence ratio: 8.2, 95% CI: 1.1–58.7).

Discussion

This study adds to the evidence that WNV lineage 2 strains can cause significant illness, demonstrating ratios of infection to clinical disease similar to those found previously for WNV lineage 1.     

Minimal model of plasma membrane heterogeneity requires coupling cortical actin to criticality

We present a minimal model of plasma membrane heterogeneity that combines criticality with connectivity to cortical cytoskeleton. The development of this model was motivated by recent observations of micron-sized critical fluctuations in plasma membrane vesicles that are detached from their cortical cytoskeleton. We incorporate criticality using a conserved order parameter Ising model coupled to a simple actin cytoskeleton interacting through point-like pinning sites. Using this minimal model, we recapitulate several experimental observations of plasma membrane raft heterogeneity. Small (r ∼ 20 nm) and dynamic fluctuations at physiological temperatures arise from criticality. Including connectivity to the cortical cytoskeleton disrupts large fluctuations, prevents macroscopic phase separation at low temperatures (T ≤ 22°C), and provides a template for long-lived fluctuations at physiological temperature (T = 37°C). Cytoskeleton-stabilized fluctuations produce significant barriers to the diffusion of some membrane components in a manner that is weakly dependent on the number of pinning sites and strongly dependent on criticality. More generally, we demonstrate that critical fluctuations provide a physical mechanism for organizing and spatially segregating membrane components by providing channels for interaction over large distances.     

The response to fire by two eusocial bee species

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A convenient assay for detection of soluble interferon receptors

The most common problem that must be overcome in purification of plasma membrane receptors from a cell line or a tissue is the loss of activity after solubilization with a detergent. This paper describes a simple dot blot assay with 32P-labeled human interferon gamma (Hu-IFN-gamma) for the detection of a functionally active Hu-IFN-gamma receptor from soluble plasma membranes prepared from human placenta.     

Human complement factor I glycosylation: structural and functional characterisation of the N-linked oligosaccharides

Factor I (fI) is a key serine protease that modulates the complement cascade by regulating the levels of C3 convertases. Human fI circulates in plasma as a heavily N-glycosylated (25-27% w/w) heterodimer composed of two disulphide linked chains, each carrying three N-linked oligosaccharide chains. It had been suggested that the oligosaccharides may have both structural and functional roles in the interactions with the natural substrate and the cofactor during a catalysis. The N-linked glycans of each fI chain were characterised in detail and the analysis revealed a similar composition of the glycan pools with both chains heavily sialylated. Disialylated structures were in excess over monosialylated ones: 55% over 40% for the heavy chain and 62% over 35% for the light chain. The dominant type of glycan identified on both chains was A(2)G(2)S(2), a biantennary structure with chains terminating in sialic acid linked to galactose. The glycan characterisation facilitated a strategy for the partial deglycosylation of the enzyme. Assessment of the proteolytic activities of the native and partially deglycosylated forms of fI showed that both forms of the enzyme have very similar proteolytic activities against C3(NH(3)) indicating that the charged glycans of fI do not influence the fI-cofactor-substrate interactions.