Quantum dots coordinated with conjugated organic ligands: new nanomaterials with novel photophysics

CdSe quantum dots functionalized with oligo-(phenylene vinylene) (OPV) ligands (CdSe-OPV nanostructures) represent a new class of composite nanomaterials with significantly modified photophysics relative to bulk blends or isolated components. Single-molecule spectroscopy on these species have revealed novel photophysics such as enhanced energy transfer, spectral stability, and strongly modified excited state lifetimes and blinking statistics. Here, we review the role of ligands in quantum dot applications and summarize some of our recent efforts probing energy and charge transfer in hybrid CdSe-OPV composite nanostructures

The genetic architecture of the human cerebral cortex

INTRODUCTION The cerebral cortex underlies our complex cognitive capabilities. Variations in human cortical surface area and thickness are associated with neurological, psychological, and behavioral traits and can be measured in vivo by magnetic resonance imaging (MRI). Studies in model organisms have identified genes that influence cortical structure, but little is known about common genetic variants that affect human cortical structure. RATIONALE To identify genetic variants associated with human cortical structure at both global and regional levels, we conducted a genome-wide association meta-analysis of brain MRI data from 51,665 individuals across 60 cohorts. We analyzed the surface area and average thickness of the whole cortex and 34 cortical regions with known functional specializations. RESULTS We identified 306 nominally genome-wide significant loci (P < 5 × 10−8) associated with cortical structure in a discovery sample of 33,992 participants of European ancestry. Of the 299 loci for which replication data were available, 241 loci influencing surface area and 14 influencing thickness remained significant after replication, with 199 loci passing multiple testing correction (P < 8.3 × 10−10; 187 influencing surface area and 12 influencing thickness). Common genetic variants explained 34% (SE = 3%) of the variation in total surface area and 26% (SE = 2%) in average thickness; surface area and thickness showed a negative genetic correlation (rG = −0.32, SE = 0.05, P = 6.5 × 10−12), which suggests that genetic influences have opposing effects on surface area and thickness. Bioinformatic analyses showed that total surface area is influenced by genetic variants that alter gene regulatory activity in neural progenitor cells during fetal development. By contrast, average thickness is influenced by active regulatory elements in adult brain samples, which may reflect processes that occur after mid-fetal development, such as myelination, branching, or pruning. When considered together, these results support the radial unit hypothesis that different developmental mechanisms promote surface area expansion and increases in thickness. To identify specific genetic influences on individual cortical regions, we controlled for global measures (total surface area or average thickness) in the regional analyses. After multiple testing correction, we identified 175 loci that influence regional surface area and 10 that influence regional thickness. Loci that affect regional surface area cluster near genes involved in the Wnt signaling pathway, which is known to influence areal identity. We observed significant positive genetic correlations and evidence of bidirectional causation of total surface area with both general cognitive functioning and educational attainment. We found additional positive genetic correlations between total surface area and Parkinson’s disease but did not find evidence of causation. Negative genetic correlations were evident between total surface area and insomnia, attention deficit hyperactivity disorder, depressive symptoms, major depressive disorder, and neuroticism. CONCLUSION This large-scale collaborative work enhances our understanding of the genetic architecture of the human cerebral cortex and its regional patterning. The highly polygenic architecture of the cortex suggests that distinct genes are involved in the development of specific cortical areas. Moreover, we find evidence that brain structure is a key phenotype along the causal pathway that leads from genetic variation to differences in general cognitive function

Untersuchungen zum Strahlenrisiko in der fruehen Schwangerschaft der Maus -Fehlbildungen, zytogenetische Veraenderungen und Mechanismen

In dem Forschungsvorhaben, ueber das hier abschliessend berichtet wird, wurde die Strahlenempfindlichkeit von Praeimplantationsembryonen der Maus mit verschiedenen biologischen Endpunkten untersucht. Es wurden folgende Ergebnisse erzielt: Die Radiotoxizitaet von Tritium haengt sehr stark von der Lokalisation der zerfallenden Tritiumnuklide in der Zelle ab. Bei Maeusestaemmen mit einer genetischen Praedisposition fuer bestimmte Fehlbildungen werden diese entgegen frueheren Regeln auch durch eine Bestrahlung der Embryonen in der Praeimplantationsphase verursacht. Es treten auch Veraenderungen in der Expression von Proteinenin der Leber der missgebildeten Foeten auf. Durch Rueckkreuzungsexperimente wurde festgestellt, dass drei Gen-Loci an der Auspraegung der Gastroschisis beteiligt sind. Eine Bestrahlung im 1-Zell-Stadium gibt die Moeglichkeit, Chromosomenaberrationen in der1., 2. und 3. Mitose nach Bestrahlung zu bestimmen. Die Embryonen verfuegen ueber eine sehr differenzierte Reparatur von DNA-Schaeden nach Bestrahlung. Der G2-Block ist offensichtlich eine Reaktion der Zelle, um die DNA-Reparatur zu bewerkstelligen. Es konnte kein ''adaptive response'' durch eine niedrige Strahlendosis beobachtet werden. (orig./MG)The project research work summarized in this concluding report was to investigate the radiosensitivity of pre-implantation mouse embryos with regard to various biological development stages. The results are: The radiotoxicity of tritium very strongly depends on the localisation of decaying nuclides in the cell. In mouse strains with a genetic predisposition for certain malformations, these have been found to be induced also by irradiation of pre-implantation embryos, which contradicts earlier statements. The malformations may also be accompanied by modifications in the expression of proteins in the liver of the damaged fetuses. By way of backcrossing experiments it was found that three gene loci are involved in the expression of gastroschisis. Irradiation of one-cell embryos allows determination of chromosome aberrations at the 1., second, and 3. post-irradiation mitotic division. The embryos revealed a very differentiated mechanism of DNA repair after irradiation. The G2 block obviously is a reaction of the cell for achieving DNA repair. No 'adaptive response' was found upon low-dose irradiation. (MG/CB)SIGLEAvailable from TIB Hannover: RO 3190(518) / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekDEGerman

Potential causes and life-history consequences of sexual size dimorphism in mammals

1. Male-biased sexual size dimorphism (SSD) in mammals has been explained by sexual selection favouring large, competitive males. However, new research has identified other potential factors leading to SSD. The aim of this review is to evaluate current research on the causes of SSD in mammals and to investigate some consequences of SSD, including costs to the larger sex and sexual segregation. 2. While larger males appear to gain reproductive benefits from their size, studies have also identified alternative mating strategies, unexpected variance in mating success and found no clear relationship between degree of polygyny and dimorphism. This implies that sexual selection is unlikely to be the single selective force directing SSD. 3. Latitude seems to influence SSD primarily through variation in overall body size and seasonal food availability, which affect potential for polygyny. Likewise, population density influences resource availability and evidence suggests that food scarcity differentially constrains the growth of the sexes. Diverging growth patterns between the sexes appear to be the primary physiological mechanism leading to SSD. 4. Female-biased dimorphism is most adequately explained by reduced male–male competition resulting in a decrease in male size. Female–female competition for dominance and resources, including mates, may also select for increased female size. 5. Most studies found that sexual segregation arises through asynchrony of activity budgets between the sexes. The larger sex can suffer sex-biased mortality through increased parasite load, selective predation and the difficulty associated with sustaining a larger body size under conditions of resource scarcity. 6. None of the variables considered here appears to contribute a disproportionate amount to SSD in mammals. Several promising avenues of research are currently overlooked and long-term studies, which have previously been biased toward ungulates, should be carried out on a variety of taxa