DNA barcodes reveal species-specific mercury levels in tuna sushi that pose a health risk to consumers

Excessive ingestion of mercury—a health hazard associated with consuming predatory fishes—damages neurological, sensory-motor and cardiovascular functioning. The mercury levels found in Bigeye Tuna (Thunnus obesus) and bluefin tuna species (Thunnus maccoyii, Thunnus orientalis, and Thunnus thynnus), exceed or approach levels permissible by Canada, the European Union, Japan, the US, and the World Health Organization. We used DNA barcodes to identify tuna sushi samples analysed for mercury and demonstrate that the ability to identify cryptic samples in the market place allows regulatory agencies to more accurately measure the risk faced by fish consumers and enact policies that better safeguard their health.     

Pathogen recognition by Toll-like receptor 2 activates Weibel-Palade body exocytosis in human aortic endothelial cells

The endothelial cell-specific granule Weibel-Palade body releases vasoactive substances capable of modulating vascular inflammation. Although innate recognition of pathogens by Toll-like receptors (TLRs) is thought to play a crucial role in promotion of inflammatory responses, the molecular basis for early-phase responses of endothelial cells to bacterial pathogens has not fully been understood. We here report that human aortic endothelial cells respond to bacterial lipoteichoic acid (LTA) and synthetic bacterial lipopeptides, but not lipopolysaccharide or peptidoglycan, to induce Weibel-Palade body exocytosis, accompanied by release or externalization of the storage components von Willebrand factor and P-selectin. LTA could activate rapid Weibel-Palade body exocytosis through a TLR2- and MyD88-dependent mechanism without de novo protein synthesis. This process was at least mediated through MyD88-dependent phosphorylation and activation of phospholipase Cgamma. Moreover, LTA activated interleukin-1 receptor-associated kinase-1-dependent delayed exocytosis with de novo protein synthesis and phospholipase Cgamma-dependent activation of the NF-kappaB pathway. Increased TLR2 expression by transfection or interferon-gamma treatment increased TLR2-mediated Weibel-Palade body exocytosis, whereas reduced TLR2 expression under laminar flow decreased the response. Thus, we propose a novel role for TLR2 in induction of a primary proinflammatory event in aortic endothelial cells through Weibel-Palade body exocytosis, which may be an important step for linking innate recognition of bacterial pathogens to vascular inflammation.     

Technical developments at the NASA Space Radiation Laboratory

The NASA Space Radiation Laboratory (NSRL) located at Brookhaven National Laboratory (BNL) is a center for space radiation research in both the life and physical sciences. BNL is a multidisciplinary research facility operated for the Office of Science of the US Department of Energy (DOE). The BNL scientific research portfolio supports a large and diverse science and technology program including research in nuclear and high-energy physics, material science, chemistry, biology, medial science, and nuclear safeguards and security. NSRL, in operation since July 2003, is an accelerator-based facility which provides particle beams for radiobiology and physics studies (Lowenstein in Phys Med 17(supplement 1):26–29 2001). The program focus is to measure the risks and to ameliorate the effects of radiation encountered in space, both in low earth orbit and extended missions beyond the earth. The particle beams are produced by the Booster synchrotron, an accelerator that makes up part of the injector sequence of the DOE nuclear physics program’s Relativistic Heavy Ion Collider. Ion species from protons to gold are presently available, at energies ranging from <100 to >1,000 MeV/n. The NSRL facility has recently brought into operation the ability to rapidly switch species and beam energy to supply a varied spectrum onto a given specimen. A summary of past operation performance, plans for future operations and recent and planned hardware upgrades will be described. Work performed under the auspices of the auspices of the US National Aeronautics and Space Administration and the US Department of Energy.     

Aerobic training increases the expression of adiponectin receptor genes in the peripheral blood mononuclear cells of young men

Little is known about the effect of exercise training on the expression of adiponectin receptor genes in peripheral blood mononuclear cells (PBMCs). In this study, we investigated the effects of aerobic training on the expression of AdipoR1 and AidpoR2 mRNAs in PBMCs, whole body insulin sensitivity, and circulating adiponectins in men. Thirty young men were randomly assigned to either a control (n=15) or an exercise (n=15) group. Subjects assigned to the exercise group underwent a 12-week jogging and/or running programme on a motor-driven treadmill at an intensity of 60%-75% of the age-based maximum heart rate with duration of 40 minutes per session and a frequency of 5 days per week. Two-way mixed ANOVA with repeated measures was used to test any significant time-by-group interaction effects for the measured variables at p=0.05. We found significant time-by-group interaction effects for waist circumference (p=0.001), VO_2max (p<0.001), fasting insulin (p=0.016), homeostasis model assessment for insulin resistance (HOMA-IR) (p=0.010), area under the curve (AUC) for insulin response during the 75-g oral glucose tolerance test (p=0.002), high-molecular weight (HMW) adiponectin (p=0.016), and the PBMC mRNA levels of AdipoR1 (p<0.001) and AdipoR2 (p=0.001). The exercise group had significantly increased mRNA levels of AdipoR1 and AdipoR2 in PBMCs, along with increased whole body insulin sensitivity and HMW adiponectin, decreased waist circumference, and increased VO_2max compared with the control group. In summary, the current findings suggest that exercise training modulates the expression of AdipoR1 and AdipoR2 mRNAs in PBMCs, implying that manipulation of the expression of these genes could be a potential surrogate for lifestyle intervention-mediated improvements of whole body insulin sensitivity and glucose homeostasis.     

Evolution and Conservation of Central African Biodiversity: Priorities for Future Research and Education in the Congo Basin and Gulf of Guinea

The tropical forests of the Congo Basin and Gulf of Guinea harbor some of the greatest terrestrial and aquatic biological diversity in the world. However, our knowledge of the rich biological diversity of this region and the evolutionary processes that have shaped it remains limited, as is our understanding of the capacity for species to adapt or otherwise respond to current and projected environmental change. In this regard, research efforts are needed to increase current scientific knowledge of this region's biodiversity, identify the drivers of past diversification, evaluate the potential for species to adapt to environmental change and identify key populations for future conservation. Moreover, when evolutionary research is combined with ongoing environmental monitoring efforts, it can also provide an important set of tools for assessing and mitigating the impacts of development activities. Building on a set of recommendations developed at an international workshop held in Gabon in 2011, we highlight major areas for future evolutionary research that could be directly tied to conservation priorities for the region. These research priorities are centered around five disciplinary themes: (1) documenting and discovering biodiversity; (2) identifying drivers of evolutionary diversification; (3) monitoring environmental change; (4) understanding community and ecosystem level processes; (5) investigating the ecology and epidemiology of disease from an evolutionary perspective (evolutionary epidemiology). Furthermore, we also provide an overview of the needs and priorities for biodiversity education and training in Central Africa.     

Immunological thresholds in neurological gene therapy: highly efficient elimination of transduced cells might be related to the specific formation of immunological synapses between T cells and virus-infected brain cells

First-generation adenovirus can be engineered with powerful promoters to drive expression of therapeutic transgenes. Numerous clinical trials for glioblastoma multiforme using first generation adenoviral vectors have either been performed or are ongoing, including an ongoing, Phase III, multicenter trial in Europe and Israel (Ark Therapeutics, Inc.). Although in the absence of anti-adenovirus immune responses expression in the brain lasts 6-18 months, systemic infection with adenovirus induces immune responses that inhibit dramatically therapeutic transgene expression from first generation adenoviral vectors, thus, potentially compromising therapeutic efficacy. Here, we show evidence of an immunization threshold for the dose that generates an immune response strong enough to eliminate transgene expression from the CNS. For the systemic immunization to eliminate transgene expression from the brain, > or = 1 x 10(7) infectious units (iu) of adenovirus need to be used as immunogen. Furthermore, this immune response eliminates >90% of transgene expression from 1 x 10(7)-1 x 10(3) iu of vector injected into the striatum 60 days earlier. Importantly, elimination of transgene expression is independent of the nature of the promoter that drives transgene expression and is accompanied by brain infiltration of CD8(+) T cells and macrophages. In conclusion, once the threshold for systemic immunization (i.e. 1 x 10(7) iu) is crossed, the immune response eliminates transgene expression by >90% even from brains that receive as little as 1000 iu of adenoviral vectors, independently of the type of promoter that drives expression.     

Osteoclasts activation by bacterial endotoxins during periodontal diseases

During periodontal infections, bacterial lipopolysaccharides (LPS) from Gram negative bacteria, along with other bacterial products, drive alveolar bone destruction. Tissue destruction occurs through both direct and indirect pathways. In the indirect pathway, LPS induce the secretion of proinflammatory cytokines, which in turn provokes a cascade of reactions leading to osteoclasts activation. In the direct pathway, LPS stimulate osteoblasts, osteoclasts precursors and osteoclasts, with an inflammatory cytokines independent manner. In this paper, the mechanisms involved in these two pathways are reviewed.     

N-ethylmaleimide-sensitive factor: a redox sensor in exocytosis

Vascular injury triggers endothelial exocytosis of granules, releasing pro-inflammatory and pro-thrombotic mediators into the blood. Nitric oxide (NO) and reactive oxygen species (ROS) limit vascular inflammation and thrombosis by inhibiting endothelial exocytosis. NO decreases exocytosis by regulating the activity of the N-ethylmaleimide-sensitive factor (NSF), a central component of the exocytic machinery. NO nitrosylates specific cysteine residues of NSF, thereby inhibiting NSF disassembly of the soluble NSF attachment protein receptor (SNARE). NO also modulates exocytosis of other cells; for example, NO regulates platelet activation by inhibiting alpha-granule secretion from platelets. Other radicals besides NO can regulate exocytosis as well. For example, H(2)O(2) inhibits exocytosis by oxidizing NSF. Using site-directed mutagenesis, we have defined the critical cysteine residues of NSF, and found that one particular cysteine residue, C264, renders NSF sensitive to oxidative stress. Since radicals such as NO and H(2)O(2) inhibit NSF and decrease exocytosis, NSF may act as a redox sensor, modulating exocytosis in response to changes in oxidative stress.