Predictable Patterns Of Disruptive Selection In Stickleback In Postglacial Lakes

Disruptive selection is often assumed to be relatively rare, because it is dynamically unstable and hence should be transient. However, frequency-dependent interactions such as intraspecific competition may stabilize fitness minima and make disruptive selection more common. Such selection helps explain the maintenance of genetic variation and may even contribute to sympatric speciation. There is thus great interest in determining when and where disruptive selection is most likely. Here, we show that there is a general trend toward weak disruptive selection on trophic morphology in three-spine stickleback (Gasterosteus aculeatus) in 14 lakes on Vancouver Island. Selection is inferred from the observation that, within a lake, fish with intermediate gill raker morphology exhibited slower growth than phenotypically extreme individuals. Such selection has previously been shown to arise from intraspecific competition for alternate resources. However, not all environments are equally conducive to disruptive selection, which was strongest in intermediate-sized lakes where both littoral and pelagic prey are roughly balanced. Also, consistent with theory, we find that sexual dimorphism in trophic traits tends to mitigate disruptive selection. These results suggest that it may be possible to anticipate the kinds of environments and populations most likely to experience disruptive selection.Integrative Biolog

Distinguishing permutation isomorphism classes of groups

The ability to distinguish permutation isomorphism classes of groups is an important step in the computation of Galois groups of polynomials over the rationals. In order to distinguish permutation isomorphism classes of groups, it is useful to have an extensive list of their invariants. These invariants include properties such as the order, imprimitivity, parity and shapes, as well as the orbit lengths of sets and sequences. Computing these characteristics can be extremely time consuming. In this thesis, a detailed description of efficient algorithms for solving the problem using the concept of expanding horizon and orbit computation is presented

New Frontier in Hypericin-Mediated Diagnosis of Cancer with Current Optical Technologies

Photosensitizers (PSs) have shown great potentials as molecular contrast agents in photodynamic diagnosis (PDD) of cancer. While the diagnostic values of PSs have been proven previously, little efforts have been put into developing optical imaging and diagnostic algorithms. In this article, we review the recent development of optical probes that have been used in conjunction with a potent PS, hypericin (HY). Various fluorescence techniques such as laser confocal microscopy, fluorescence urine cytology, endoscopy and endomicroscopy are covered. We will also discuss about image processing and classification approaches employed for accurate PDD. We anticipate that continual efforts in these developments could lead to an objective PDD and complete surgical clearance of tumors. Recent advancements in nanotechnology have also opened new horizons for PSs. The use of biocompatible gold nanoparticles as carrier for enhanced targeted delivery of HY has been attained. In addition, plasmonic properties of nanoparticles were harnessed to induce localized hyperthermia and to manage the release of PS molecules, enabling a better therapeutic outcome of a combined photodynamic and photothermal therapy. Finally, we discuss how nanoparticles can be used as contrast agents for other optical techniques such as optical coherence tomography and surface-enhanced Raman scattering imaging

Scientific Opinion on the re-evaluation of Quinoline Yellow (E 104) as a food additive:Question No EFSA-Q-2008-223

The Panel on Food Additives and Nutrient Sources added to Food provides a scientific opinion re-evaluating the safety of Quinoline Yellow (E 104). Quinoline Yellow has been previously evaluated by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) in 1975, 1978 and 1984, and the EU Scientific Committee for Food (SCF) in 1984. Both committees established an Acceptable Daily Intake (ADI) of 0-10 mg/kg body weight (bw). Studies not evaluated by JECFA and the SCF included a chronic toxicity and carcinogenicity study with a reproductive toxicity phase in rats and a study on behaviour in children by McCann et al. from 2007. The latter study concluded that exposure to a mixture of colours including Quinoline Yellow resulted in increased hyperactivity in 8- to 9-years old children. The Panel concurs with the conclusion from a previous EFSA opinion on the McCann et al. study that the findings of the study cannot be used as a basis for altering the ADI. The Panel notes that Quinoline Yellow was negative in in vitro genotoxicity as well as in long term carcinogenicity studies. The Panel concludes that the currently available database on semi-chronic, reproductive, developmental and long-term toxicity of Quinoline Yellow, including a study in rats not apparently taken into consideration by JECFA or the SCF, provides a rationale for re-definition of the ADI. Using the NOAEL of 50 mg/kg bw/day provided by the chronic toxicity and carcinogenicity study with a reproductive toxicity phase carried out in rats and applying an uncertainty factor of 100 to this NOAEL, the Panel establishes an ADI of 0.5 mg/kg bw/day. The Panel notes that at the maximum levels of use of Quinoline Yellow, refined intake estimates are generally well over the ADI of 0.5 mg/kg bw/day

Effect of Hydrogen Peroxide and Superoxide Anions on Cytosolic Ca2+: Comparison of Endothelial Cells from Large-Sized and Small-Sized Arteries

We compared the Ca2+ responses to reactive oxygen species (ROS) between mouse endothelial cells derived from large-sized arteries, aortas (aortic ECs), and small-sized arteries, mesenteric arteries (MAECs). Application of hydrogen peroxide (H2O2) caused an increase in cytosolic Ca2+ levels ([Ca2+]i) in both cell types. The [Ca2+]i rises diminished in the presence of U73122, a phospholipase C inhibitor, or Xestospongin C (XeC), an inhibitor for inositol-1,4,5-trisphosphate (IP3) receptors. Removal of Ca2+ from the bath also decreased the [Ca2+]i rises in response to H2O2. In addition, treatment of endothelial cells with H2O2 reduced the [Ca2+]i responses to subsequent challenge of ATP. The decreased [Ca2+]i responses to ATP were resulted from a pre-depletion of intracellular Ca2+ stores by H2O2. Interestingly, we also found that Ca2+ store depletion was more sensitive to H2O2 treatment in endothelial cells of mesenteric arteries than those of aortas. Hypoxanthine-xanthine oxidase (HX-XO) was also found to induce [Ca2+]i rises in both types of endothelial cells, the effect of which was mediated by superoxide anions and H2O2 but not by hydroxyl radical. H2O2 contribution in HX-XO-induced [Ca2+]i rises were more significant in endothelial cells from mesenteric arteries than those from aortas. In summary, H2O2 could induce store Ca2+ release via phospholipase C-IP3 pathway in endothelial cells. Resultant emptying of intracellular Ca2+ stores contributed to the reduced [Ca2+]i responses to subsequent ATP challenge. The [Ca2+]i responses were more sensitive to H2O2 in endothelial cells of small-sized arteries than those of large-sized arteries

Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells

<p>Abstract</p> <p>Background</p> <p>The SARS outbreak in 2003 provides a unique opportunity for the study of human responses to a novel virus. We have previously reported that dendritic cells (DCs) might be involved in the immune escape mechanisms for SARS-CoV. In this study, we focussed on the gene expression of toll-like receptors (TLRs), chemokine receptors (CCRs) and death receptor ligands in SARS-CoV infected DCs. We also compared adult and cord blood (CB) DCs to find a possible explanation for the age-dependent severity of SARS.</p> <p>Results</p> <p>Our results demonstrates that SARS-CoV did not modulate TLR-1 to TLR-10 gene expression but significantly induced the expression of CCR-1, CCR-3, and CCR-5. There was also strong induction of TNF-related apoptosis-inducing ligand (TRAIL), but not Fas ligand gene expression in SARS-CoV infected DCs. Interestingly, the expressions of most genes studied were higher in CB DCs than adult DCs.</p> <p>Conclusion</p> <p>The upregulation of chemokines and CCRs may facilitate DC migration from the infection site to the lymph nodes, whereas the increase of TRAIL may induce lymphocyte apoptosis. These findings may explain the increased lung infiltrations and lymphoid depletion in SARS patients. Further explorations of the biological significance of these findings are warranted.</p

Cardioprotective Effects of Selective Mitochondrial-Targeted Antioxidants in Myocardial Ischemia/Reperfusion (I/R) Injury

During myocardial ischemia, coronary blood flow interruption deprives cardiomyocytes of oxygen, glucose and fatty acids. Ischemic damage is exacerbated by a burst of reactive oxygen species (ROS) generated at reperfusion when oxygen interacts with damaged mitochondrial electron transport chains (ETC), especially uncoupled complexes I and III (Fig. 1,2). Nicotinamide adenine dinucleotide phosphate oxidase (Nox) activity can also release ROS, inducing additional tissue/organ damage. Surgical intervention or thrombolytic treatments can restore coronary blood flow. However, as blood flow reestablishes, oxidative stress leads to I/R injury. Clinical treatment remains a challenge as no pharmaceutical agents effectively limit I/R-induced damage. Mitochondria are implicated in I/R as a major source of ROS3,4,5. Excess ROS leads to mitochondrial and cardiac contractile dysfunction6. Conventional antioxidants have limited efficacy in myocardial I/R because they are not targeted selectively to where most I/R damage occurs, in mitochondria (Fig. 3)3,4,5. Mitoquinone (mitoQ, MW=600 g/mol), a coenzyme Q analog, easily crosses phospholipid bilayers and is driven by the large electrochemical membrane potential to concentrate mitoQ several hundred-fold within mitochondria. The respiratory chain reduces mitoQ to its active ubiquinol antioxidant form to limit myocardial I/R injury5. The SS-31 (Szeto-Schiller) peptide ((D-Arg)-Dmt-Lys-Phe-Amide, MW=640 g/mol, Genemed Synthesis, Inc., San Antonio, TX) is also of interest since it is cellpermeable, specifically targeted to inner mitochondrial membranes based on its alternating cationic aromatic residue sequence, with an antioxidant dimethyltyrosine moeity. SS peptides scavenge ROS in I/R models. Although mitochondrial-targeted antioxidant pretreatment can effectively limit I/R injury, pretreatment is not always possible in cases of myocardial infarction. Therefore, evaluating cardioprotective efficacy of mitochondrialtargeted antioxidants when given at reperfusion is of high significanc

TRPC5 channels participate in pressure-sensing in aortic baroreceptors

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