Assessing the accuracy of perceptions of intelligence based on heritable facial features

Perceptions of intelligence based on facial features can have a profound impact on many social situations, but findings have been mixed as to whether these judgements are accurate. Even if such perceptions were accurate, the underlying mechanism is unclear. Several possibilities have been proposed, including evolutionary explanations where certain morphological facial features are associated with fitness-related traits (including cognitive development), or that intelligence judgements are over-generalisation of cues of transitory states that can influence cognition (e.g., tiredness). Here, we attempt to identify the morphological signals that individuals use to make intelligence judgements from facial photographs. In a genetically informative sample of 1660 twins and their siblings, we measured IQ and also perceptions of intelligence based on facial photographs. We found that intelligence judgements were associated with both stable morphological facial traits (face height, interpupillary distance, and nose size) and more transitory facial cues (eyelid openness, and mouth curvature). There was a significant association between perceived intelligence and measured IQ, but of the specific facial attributes only interpupillary distance (i.e., wide-set eyes) significantly mediated this relationship. We also found evidence that perceived intelligence and measured IQ share a familial component, though we could not distinguish between genetic and shared environmental sources

Structural basis of DNA gyrase inhibition by antibacterial QPT-1, anticancer drug etoposide and moxifloxacin

New antibacterials are needed to tackle antibiotic-resistant bacteria. Type IIA topoisomerases (topo2As), the targets of fluoroquinolones, regulate DNA topology by creating transient double-strand DNA breaks. Here we report the first co-crystal structures of the antibacterial QPT-1 and the anticancer drug etoposide with Staphylococcus aureus DNA gyrase, showing binding at the same sites in the cleaved DNA as the fluoroquinolone moxifloxacin. Unlike moxifloxacin, QPT-1 and etoposide interact with conserved GyrB TOPRIM residues rationalizing why QPT-1 can overcome fluoroquinolone resistance. Our data show etoposide’s antibacterial activity is due to DNA gyrase inhibition and suggests other anticancer agents act similarly. Analysis of multiple DNA gyrase co-crystal structures, including asymmetric cleavage complexes, led to a ‘pair of swing-doors’ hypothesis in which the movement of one DNA segment regulates cleavage and religation of the second DNA duplex. This mechanism can explain QPT-1’s bacterial specificity. Structure-based strategies for developing topo2A antibacterials are suggested

Assessing the functional structure of genomic data

Motivation: The availability of genome-scale data has enabled an abundance of novel analysis techniques for investigating a variety of systems-level biological relationships. As thousands of such datasets become available, they provide an opportunity to study high-level associations between cellular pathways and processes. This also allows the exploration of shared functional enrichments between diverse biological datasets, and it serves to direct experimenters to areas of low data coverage or with high probability of new discoveries

B cell antigen receptor signal strength and peripheral B cell development are regulated by a 9-O-acetyl sialic acid esterase

We show that the enzymatic acetylation and deacetylation of a cell surface carbohydrate controls B cell development, signaling, and immunological tolerance. Mice with a mutation in sialate:O-acetyl esterase, an enzyme that specifically removes acetyl moieties from the 9-OH position of α2–6-linked sialic acid, exhibit enhanced B cell receptor (BCR) activation, defects in peripheral B cell development, and spontaneously develop antichromatin autoantibodies and glomerular immune complex deposits. The 9-O-acetylation state of sialic acid regulates the function of CD22, a Siglec that functions in vivo as an inhibitor of BCR signaling. These results describe a novel catalytic regulator of B cell signaling and underscore the crucial role of inhibitory signaling in the maintenance of immunological tolerance in the B lineage

Surrogate/spent fuel sabotage : aerosol ratio test program and Phase 2 test results.

A multinational test program is in progress to quantify the aerosol particulates produced when a high energy density device, HEDD, impacts surrogate material and actual spent fuel test rodlets. This program provides needed data that are relevant to some sabotage scenarios in relation to spent fuel transport and storage casks, and associated risk assessments; the program also provides significant political benefits in international cooperation. We are quantifying the spent fuel ratio, SFR, the ratio of the aerosol particles released from HEDD-impacted actual spent fuel to the aerosol particles produced from surrogate materials, measured under closely matched test conditions. In addition, we are measuring the amounts, nuclide content, size distribution of the released aerosol materials, and enhanced sorption of volatile fission product nuclides onto specific aerosol particle size fractions. These data are crucial for predicting radiological impacts. This document includes a thorough description of the test program, including the current, detailed test plan, concept and design, plus a description of all test components, and requirements for future components and related nuclear facility needs. It also serves as a program status report as of the end of FY 2003. All available test results, observations, and analyses - primarily for surrogate material Phase 2 tests using cerium oxide sintered ceramic pellets are included. This spent fuel sabotage - aerosol test program is coordinated with the international Working Group for Sabotage Concerns of Transport and Storage Casks, WGSTSC, and supported by both the U.S. Department of Energy and Nuclear Regulatory Commission

The Politics of Welfare Exclusion: Immigration and Disparity in Medicaid Coverage

The rapid growth of the immigrant population in the U.S., along with changes in the demographics and the political landscape, has often raised questions for understanding trends of inequality. Important issues that have received little scholarly attention thus far are excluding immigrants’ social rights through decisive policy choices and the distributive consequences of such exclusive policies. In this paper, we examine how immigration and state policies on immigrants’ access to safety net programs together influence social inequality in the context of health care. We analyze the combined effect of immigration population density and state immigrant Medicaid eligibility rules on the gap of Medicaid coverage rates between native- and foreign-born populations. When tracking inequality in Medicaid coverage and critical policy changes in the post-PRWORA era, we find that exclusive state policies widen the native-foreign Medicaid coverage gap. Moreover, the effect of state policies is conditional upon the size of the immigrant population in that state. Our findings suggest immigrants’ formal integration into the welfare system is crucial for understanding social inequality in the U.S. states

Breast cancer patients' clinical outcome measures are associated with Src kinase family member expression

<p>BACKGROUND: This study determined mRNA expression levels for Src kinase family (SFK) members in breast tissue specimens and assessed protein expression levels of prominent SFK members in invasive breast cancer to establish associations with clinical outcome. Ki67 was investigated to determine association between SFK members and proliferation.</p> <p>METHODS: The mRNA expression levels were assessed for eight SFK members by quantitative real-time PCR. Immunohistochemistry was performed for c-Src, Lyn, Lck and Ki67.</p> <p>RESULTS: mRNA expression was quantified in all tissue samples. SRC and LYN were the most highly expressed in malignant tissue. LCK was more highly expressed in oestrogen receptor (ER)-negative, compared with ER-positive tumours. High cytoplasmic Src kinase protein expression was significantly associated with decreased disease-specific survival. Lyn was not associated with survival at any cellular location. High membrane Lck expression was significantly associated with improved survival. Ki67 expression correlated with tumour grade and nuclear c-Src, but was not associated with survival.</p> <p>CONCLUSIONS: All eight SFK members were expressed in different breast tissues. Src kinase was highest expressed in breast cancer and had a negative impact on disease-specific survival. Membrane expression of Lck was associated with improved clinical outcome. High expression of Src kinase correlated with high proliferation.</p&gt

Comparative study of unsupervised dimension reduction techniques for the visualization of microarray gene expression data

<p>Abstract</p> <p>Background</p> <p>Visualization of DNA microarray data in two or three dimensional spaces is an important exploratory analysis step in order to detect quality issues or to generate new hypotheses. Principal Component Analysis (PCA) is a widely used linear method to define the mapping between the high-dimensional data and its low-dimensional representation. During the last decade, many new nonlinear methods for dimension reduction have been proposed, but it is still unclear how well these methods capture the underlying structure of microarray gene expression data. In this study, we assessed the performance of the PCA approach and of six nonlinear dimension reduction methods, namely Kernel PCA, Locally Linear Embedding, Isomap, Diffusion Maps, Laplacian Eigenmaps and Maximum Variance Unfolding, in terms of visualization of microarray data.</p> <p>Results</p> <p>A systematic benchmark, consisting of Support Vector Machine classification, cluster validation and noise evaluations was applied to ten microarray and several simulated datasets. Significant differences between PCA and most of the nonlinear methods were observed in two and three dimensional target spaces. With an increasing number of dimensions and an increasing number of differentially expressed genes, all methods showed similar performance. PCA and Diffusion Maps responded less sensitive to noise than the other nonlinear methods.</p> <p>Conclusions</p> <p>Locally Linear Embedding and Isomap showed a superior performance on all datasets. In very low-dimensional representations and with few differentially expressed genes, these two methods preserve more of the underlying structure of the data than PCA, and thus are favorable alternatives for the visualization of microarray data.</p

Modulation of Integrin Activity is Vital for Morphogenesis

Cells can vary their adhesive properties by modulating the affinity of integrin receptors. The activation and inactivation of integrins by inside-out mechanisms acting on the cytoplasmic domains of the integrin subunits has been demonstrated in platelets, lymphocytes, and keratinocytes. We show that in the embryo, normal morphogenesis requires the α subunit cytoplasmic domain to control integrin adhesion at the right times and places. PS2 integrin (α(PS2)β(PS)) adhesion is normally restricted to the muscle termini, where it is required for attaching the muscles to the ends of other muscles and to specialized epidermal cells. Replacing the wild-type α(PS2) with mutant forms containing cytoplasmic domain deletions results in the rescue of the majority of defects associated with the absence of the α(PS2) subunit, however, the mutant PS2 integrins are excessively active. Muscles containing these mutant integrins make extra muscle attachments at aberrant positions on the muscle surface, disrupting the muscle pattern and causing embryonic lethality. A gain- of-function phenotype is not observed in the visceral mesoderm, showing that regulation of integrin activity is tissue-specific. These results suggest that the α(PS2) subunit cytoplasmic domain is required for inside-out regulation of integrin affinity, as has been seen with the integrin α(IIb)β(3)