On Mathon's construction of maximal arcs in Desarguesian planes. II

In a recent paper [M], Mathon gives a new construction of maximal arcs which generalizes the construction of Denniston. In relation to this construction, Mathon asks the question of determining the largest degree of a non-Denniston maximal arc arising from his new construction. In this paper, we give a nearly complete answer to this problem. Specifically, we prove that when $m\geq 5$ and $m\neq 9$, the largest $d$ of a non-Denniston maximal arc of degree $2^d$ in PG(2,2^m) generated by a {p,1}-map is (\floor {m/2} +1). This confirms our conjecture in [FLX]. For {p,q}-maps, we prove that if $m\geq 7$ and $m\neq 9$, then the largest $d$ of a non-Denniston maximal arc of degree $2^d$ in PG(2,2^m) generated by a {p,q}-map is either \floor {m/2} +1 or \floor{m/2} +2.Comment: 21 page

A new isomer in 125^{125}La

Levels in $^{125}$La have been studied via $\beta ^+$/EC decay of on-line mass-separated $^{125}$Ce using the HIGISOL technique. A new (390 $\pm$ 40) ms isomer is definitely attributed to $^{125}$La by conversion electron measurements of the 107 keV E3 isomeric transition

CD59a deficiency exacerbates influenza-induced lung inflammation through complement-dependent and-independent mechanisms

Influenza-specific immune activity not only promotes virus clearance but also causes immunopathology, thereby underlining the importance of mounting a measured anti-viral immune response. Since complement bridges both the innate and adaptive immune systems and has been implicated in defence against influenza, the role of the complement regulator CD59a in modulating the response to influenza was explored. For this purpose, immune responses to influenza virus, strain E61-13-H17, in mice deficient in the complement regulator protein CD59a (Cd59a–/– mice) were compared to those in wild-type mice. The severity of lung inflammation was significantly enhanced in the lungs of Cd59a–/– mice with increased numbers of infiltrating neutrophils and CD4+ T cells. When complement was inhibited using soluble complement receptor1, the frequency of lung-infiltrating neutrophils in influenza-infected Cd59a–/– mice was much reduced whilst numbers of CD4+ T cells remained unchanged. These results demonstrate that CD59a, previously defined as a complement regulator, modulates both the innate and adaptive immune response to influenza virus by both complement-dependent and-independent mechanisms

Macrophage migration inhibitory factor (MIF) is essential for type 2 effector cell immunity to an intestinal helminth parasite

Immunity to intestinal helminths is known to require both innate and adaptive components of the immune system activated along the Type 2 IL-4R/STAT6-dependent pathway. We have found that macrophage migration inhibitory factor (MIF) is essential for the development of effective immunity to the intestinal helminth Heligmosomoides polygyrus, even following vaccination which induces sterile immunity in wild-type mice. A chemical inhibitor of MIF, 4-IPP, was similarly found to compromise anti-parasite immunity. Cellular analyses found that the adaptive arm of the immune response, including IgG1 antibody responses and Th2-derived cytokines, was intact and that Foxp3+ T regulatory cell responses were unaltered in the absence of MIF. However, MIF was found to be an essential cytokine for innate cells, with ablated eosinophilia and ILC2 responses, and delayed recruitment and activation of macrophages to the M2 phenotype (expressing Arginase 1, Chil3, and RELM-α) upon infection of MIF-deficient mice; a macrophage deficit was also seen in wild-type BALB/c mice exposed to 4-IPP. Gene expression analysis of intestinal and lymph node tissues from MIF-deficient and -sufficient infected mice indicated significantly reduced levels of Arl2bp, encoding a factor involved in nuclear localization of STAT3. We further found that STAT3-deficient macrophages expressed less Arginase-1, and that mice lacking STAT3 in the myeloid compartment (LysMCrexSTAT3fl/fl) were unable to reject a secondary infection with H. polygyrus. We thus conclude that in the context of a Type 2 infection, MIF plays a critical role in polarizing macrophages into the protective alternatively-activated phenotype, and that STAT3 signaling may make a previously unrecognized contribution to immunity to helminths

Micropollutants in Water Recycling: A Case Study of N-Nitrosodimethylamine (NDMA) Exposure from Water versus Food

One of the most concerning xenobiotics currently under discussion by regulators and treatment experts is N-Nitrosodimethylamine (NDMA). NDMA is a carcinogen known to induce cancer in a variety of animals, causing DNA damage at low doses. Human exposure occurs through cigarettes, food, personal care products and drinking water, in addition to endogenous formation in the stomach. The daily tolerable limit for intake has been identified to be 4.0 - 9.3 ng/kg.day (Fitzgerald and Robinson 2007). Water at the WHO proposed guideline value of 100 ng/L would contribute about 2.9 ng/kg.day of this intake, while intake from food varies from 5.7 – 44.2 ng/kg.day. Smoking and workplace are additional exposure routes. This outlines that the exposure is often higher than tolerable limits. In the food and drinks industry this has in recent decades resulted in improved manufacturing processes. Awareness of NDMA in drinking water is a relatively recent issue. NDMA stems from precursors in raw water and can be generated during treatment. Generally removal of precursors is more achievable than the removal of NDMA itself. For example, the potent NDMA precursor dimethylamine is rapidly removed in biological pre-treatment, while many other precursor amines are more persistent. These precursor amines include some ion exchange resins and coagulants, used in water treatment processes, which have been shown to generate NDMA during chlorination. Ozonation has also been shown to produce NDMA in treatment. UV oxidation is the preferred method for removal of NDMA in water treatment, although reverse osmosis membranes are possible alternatives if effective retention can be achieved

The genetic architecture of the human cerebral cortex

The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson's disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder

Early variations in white matter microstructure and depression outcome in adolescents with subthreshold-depression

Objective: White matter microstructure alterations have recently been associated with adolescence depressive episodes, but it is unknown whether they predate depression. We investigated whether subthreshold-depression in adolescence is associated with white matter microstructure variations and whether they relate to depression outcome.Method: Adolescents with subthreshold-depression (n=96) and healthy controls (n=336), drawn from a community-based cohort, were compared using diffusion tensor imaging and whole-brain tractbased spatial statistics (TBSS) at age 14 to assess white matter microstructure. They were followedup at age 16 to assess depression. Probabilistic tractography was used to reconstruct white matter streamlines from the TBSS analysis resulting regions, and along bundles implicated in emotion regulation, the uncinate fasciculus and the cingulum. We searched for mediating effects of white matter microstructure on the relationship between baseline subthreshold-depression and depression at follow-up, and then explored the specificity of the findings.Results: Lower fractional anisotropy (FA) and higher radial diffusivity were found in the anterior corpus callosum in the adolescents with subthreshold-depression. Tractography analysis showed that they also had lower FA in the right cingulum streamlines, along with lower FA and higher mean diffusivity in tracts connecting the corpus callosum to the anterior cingulate cortex. The relation between baseline subthreshold-depression and follow-up depression was mediated by FA values in the latter tracts, and lower FA values in those tracts distinctively predicted higher individual risk for depression.Conclusions: Early FA variations in tracts projecting from the corpus callosum to the anterior cingulate cortex might denote higher risk of transition to depression in adolescents