Detailed requirements document for the radiant heat transfer facility post-test data reduction program

The requirements and functional specifications for a program to process test data obtained by the Radiant Heat Data Acquisition System are defined

Affective states contribute to trait reports of affective well-being

Asking people to provide global judgments, or trait reports, of their affective experience is a standard method for assessing trait affective well-being, with countless applications in the social sciences. Trait reports reflect numerous influences that generally go unnoticed. Although state affect is a highly plausible candidate for such influences, this source of unwanted variance does not receive much attention and is usually not controlled for in empirical studies. Using 100-day data from the COGITO study, we provide direct and strong evidence that trait reports of affect depend on how people feel at the time they provide the evaluations (i.e., their affective state). For example, participants experiencing more positive affect on a specific day relative to their individual mean also provide more positive ratings of their global affective experience. Furthermore, we found that current affect influences trait ratings in a surprisingly differentiated way—those particular facets of affect that are more/less prevalent at a certain moment are believed to occur more/less often in general. We stress the need for repeated observations within individuals to estimate state contributions to standard assessments of trait affect, to distinguish between state and trait in psychological assessment, and to achieve good indicators of affective experiences in the social and medical sciences

Toward a unified framework for the study of between-person and within-person structures : Building a bridge between two research paradigms

The vast majority of empirical research in the behavioral sciences is based on the analysis of between-person variation. In contrast, much of applied psychology is concerned with the analysis of variation within individuals. Furthermore, the mechanisms specified by psychological theories generally operate within, rather than across, individuals. This disconnect between research practice, applied demands, and psychological theories constitutes a major threat to the conceptual integrity of the field. Following groundbreaking earlier work, we propose a conceptual framework that distinguishes within-person (WP) and between-person (BP) sources of variation in psychological constructs. By simultaneously considering both sources of variation, it is shown how to identify possible reasons for nonequivalence of BP and WP structures as well as establishing areas of convergence. For this purpose, we first introduce the concept of conditional equivalence as a way to study partial structural equivalence of BP and WP structures in the presence of unconditional nonequivalence. Second, we demonstrate the construction of likelihood planes to explore the causes of structural nonequivalence. Third, we examine 4 common causes for unconditional nonequivalence autoregression, subgroup differences, linear trends, and cyclic trends-and demonstrate how to account for them. Fourth, we provide an empirical example on BP and WP differences in attentiveness

Of Humans and Gerbils— Independent Diversification of Neuroligin-4 Into X- and Y-Specific Genes in Primates and Rodents

The neural cell adhesion protein neuroligin-4 has puzzled neuroscientists and geneticist alike for almost two decades. Its clinical association with autism spectrum disorders (ASD) is well established, however, its diversification into sex chromosome-specific copies, NLGN4X and NLGN4Y, remains uncharted territory. Just recently, the presence of substantial neuroligin-4 sequence differences between humans and laboratory mice, in which Nlgn4 is a pseudoautosomal gene, could be explained as a consequence of dramatic changes affecting the pseudoautosomal region on both sex chromosomes in a subset of rodents, the clade eumuroida. In this study, we describe the presence of sex chromosome-specific copies of neuroligin-4 genes in the Mongolian gerbil (Meriones unguiculatus) marking the first encounter of its kind in rodents. Gerbils are members of the family Muridae and are closely related to mice and rats. Our results have been incorporated into an extended evolutionary analysis covering primates, rodents, lagomorphs, treeshrews and culogos comprising together the mammalian superorder euarchontoglires. We gathered evidence that substantial changes in neuroligin-4 genes have also occurred outside eumuroida in other rodent species as well as in lagomorphs. These changes feature, e.g., a general reduction of its gene size, an increase in its average GC-content as well as in the third position (GC3) of synonymous codons, and the accumulation of repetitive sequences in line with previous observations. We further show conclusively that the diversification of neuroligin-4 in sex chromosome-specific copies has happened multiple times independently during mammal evolution proving that Y-chromosomal NLGN4Y genes do not originate from a single common NLGN4Y ancestor

微細CMOSデバイスの信頼性モデリングの研究

修士論

CAPS-1 and CAPS-2 are essential synaptic vesicle priming proteins

SummaryBefore transmitter-filled synaptic vesicles can fuse with the plasma membrane upon stimulation they have to be primed to fusion competence. The regulation of this priming process controls the strength and plasticity of synaptic transmission between neurons, which in turn determines many complex brain functions. We show that CAPS-1 and CAPS-2 are essential components of the synaptic vesicle priming machinery. CAPS-deficient neurons contain no or very few fusion competent synaptic vesicles, which causes a selective impairment of fast phasic transmitter release. Increases in the intracellular Ca2+ levels can transiently revert this defect. Our findings demonstrate that CAPS proteins generate and maintain a highly fusion competent synaptic vesicle pool that supports phasic Ca2+ triggered release of transmitters

Total arrest of spontaneous and evoked synaptic transmission but normal synaptogenesis in the absence of Munc13-mediated vesicle priming

Synaptic vesicles must be primed to fusion competence before they can fuse with the plasma membrane in response to increased intracellular Ca2+ levels. The presynaptic active zone protein Munc13-1 is essential for priming of glutamatergic synaptic vesicles in hippocampal neurons. However, a small subpopulation of synapses in any given glutamatergic nerve cell as well as all gamma-aminobutyratergic (GABAergic) synapses are largely independent of Munc13-1. We show here that Munc13-2, the only Muncl 3 isoform coexpressed with Munc13-1 in hippocampus, is responsible for vesicle priming in Munc13-1 independent hippocampal synapses. Neurons lacking both Munc13-1 and Munc13- 2 show neither evoked nor spontaneous release events, yet form normal numbers of synapses with typical ultrastructural features. Thus, the two Munc13 isoforms are completely redundant in GABAergic cells whereas glutamatergic neurons form two types of synapses, one of which is solely Munc13-1 dependent and lacks Munc13-2 whereas the other type employs Munc13-2 as priming factor. We conclude that Munc13-mediated vesicle priming is not a transmitter specific phenomenon but rather a general and essential feature of multiple fast neurotransmitter systems, and that synaptogenesis during development is not dependent on synaptic secretory activity

Munc13-1 is a Ca2+-phospholipid-dependent vesicle priming hub that shapes synaptic short-term plasticity and enables sustained neurotransmission

During ongoing presynaptic action potential (AP) firing, transmitter release is limited by the availability of release-ready synaptic vesicles (SVs). The rate of SV recruitment (SVR) to release sites is strongly upregu- lated at high AP frequencies to balance SV consumption. We show that Munc13-1—an essential SV priming protein—regulates SVR via a Ca2+-phospholipid-dependent mechanism. Using knockin mouse lines with point mutations in the Ca2+-phospholipid-binding C2B domain of Munc13-1, we demonstrate that abolishing Ca2+-phospholipid binding increases synaptic depression, slows recovery of synaptic strength after SV pool depletion, and reduces temporal fidelity of synaptic transmission, while increased Ca2+-phospholipid binding has the opposite effects. Thus, Ca2+-phospholipid binding to the Munc13-1-C2B domain accelerates SVR, reduces short-term synaptic depression, and increases the endurance and temporal fidelity of neurotrans- mission, demonstrating that Munc13-1 is a core vesicle priming hub that adjusts SV re-supply to demand