Racial prejudice and support by whites for police use of force : A research note

The use of force by police in a democratic society continues to be controversial. Despite the theoretical and practical importance of police use of force, little is known about the sources of public attitudes toward it. Recent research suggests that whites\u27 approval of police use of force may derive partly from racial prejudice against African Americans. In this paper we test this possibility with data from the 1990 General Social Survey and find that negative stereotypes of African Americans contribute to whites\u27 support for police use of excessive force. We also address the theoretical and pragmatic significance of our findings

Gay Movements and Legal Change: Some Aspects of the Dynamics of a Social Problem

This paper examines public opinion and media coverage surrounding four important events which affected the development of homosexual rights in Maine in the 1970s: the birth of a homosexual student group on a University of Maine campus and the conference it organized; the adoption of a gay rights plank in the election platform of the state\u27s Democratic Party; revisions to the state\u27s criminal code which decriminalized homosexual activities; and a second conference organized by the student group. Only the first event aroused major public outcry. We describe these events in detail, examine how the media covered them, and analyze why some were more controversial than others. Our analysis shows how differing levels of control over the media affect the rise and resolution of public issues

Religion and Spiritual Experience: Revisiting Key Assumptions in Sociology

In this paper, we examine the dominant materialist assumption that there is an inherent conflict between sociology, religion, and spirituality. We will suggest that such a conflict is not fundamental and that accepting the possibility that religious experiences might reflect contact with a transcendent reality can enrich the theoretical possibilities of sociology, supplementing rather than replacing existing insights

3D buried utility location using a marching-cross-section algorithm for multi-sensor data fusion

We address the problem of accurately locating buried utility segments by fusing data from multiple sensors using a novel Marching-Cross-Section (MCS) algorithm. Five types of sensors are used in this work: Ground Penetrating Radar (GPR), Passive Magnetic Fields (PMF), Magnetic Gradiometer (MG), Low Frequency Electromagnetic Fields (LFEM) and Vibro-Acoustics (VA). As part of the MCS algorithm, a novel formulation of the extended Kalman Filter (EKF) is proposed for marching existing utility tracks from a scan cross-section (scs) to the next one; novel rules for initializing utilities based on hypothesized detections on the first scs and for associating predicted utility tracks with hypothesized detections in the following scss are introduced. Algorithms are proposed for generating virtual scan lines based on given hypothesized detections when different sensors do not share common scan lines, or when only the coordinates of the hypothesized detections are provided without any information of the actual survey scan lines. The performance of the proposed system is evaluated with both synthetic data and real data. The experimental results in this work demonstrate that the proposed MCS algorithm can locate multiple buried utility segments simultaneously, including both straight and curved utilities, and can separate intersecting segments. By using the probabilities of a hypothesized detection being a pipe or a cable together with its 3D coordinates, the MCS algorithm is able to discriminate a pipe and a cable close to each other. The MCS algorithm can be used for both post-and on-site processing. When it is used on site, the detected tracks on the current scs can help to determine the location and direction of the next scan line. The proposed “multi-utility multi-sensor” system has no limit to the number of buried utilities or the number of sensors, and the more sensor data used, the more buried utility segments can be detected with more accurate location and orientation.</p

Disruption of the Sarcoglycan–Sarcospan Complex in Vascular Smooth Muscle A Novel Mechanism for Cardiomyopathy and Muscular Dystrophy

AbstractTo investigate mechanisms in the pathogenesis of cardiomyopathy associated with mutations of the dystrophin–glycoprotein complex, we analyzed genetically engineered mice deficient for either α-sarcoglycan (Sgca) or δ-sarcoglycan (Sgcd). We found that only Sgcd null mice developed cardiomyopathy with focal areas of necrosis as the histological hallmark in cardiac and skeletal muscle. Absence of the sarcoglycan–sarcospan (SG-SSPN) complex in skeletal and cardiac membranes was observed in both animal models. Loss of vascular smooth muscle SG-SSPN complex was only detected in Sgcd null mice and associated with irregularities of the coronary vasculature. Administration of a vascular smooth muscle relaxant prevented onset of myocardial necrosis. Our data indicate that disruption of the SG-SSPN complex in vascular smooth muscle perturbs vascular function, which initiates cardiomyopathy and exacerbates muscular dystrophy

Ergocalciferol and Microcirculatory Function in Chronic Kidney Disease and Concomitant Vitamin D Deficiency: An Exploratory, Double Blind, Randomised Controlled Trial

Vitamin D deficiency and endothelial dysfunction are non-traditional risk factors for cardiovascular events in chronic kidney disease. Previous studies in chronic kidney disease have failed to demonstrate a beneficial effect of vitamin D on arterial stiffness, left ventricular mass and inflammation but none have assessed the effect of vitamin D on microcirculatory endothelial function.We conducted a randomised controlled trial of 38 patients with non diabetic chronic kidney disease stage 3-4 and concomitant vitamin D deficiency (<16 ng/dl) who received oral ergocalciferol (50,000 IU weekly for one month followed by 50,000 IU monthly) or placebo over 6 months. The primary outcome was change in microcirculatory function measured by laser Doppler flowmetry after iontophoresis of acetylcholine. Secondary endpoints were tissue advanced glycation end products, sublingual functional capillary density and flow index as well as macrovascular parameters. Parallel in vitro experiments were conducted to determine the effect of ergocalciferol on cultured human endothelial cells.Twenty patients received ergocalciferol and 18 patients received placebo. After 6 months, there was a significant improvement in the ergocalciferol group in both endothelium dependent microcirculatory vasodilatation after iontophoresis of acetylcholine (p = 0.03) and a reduction in tissue advanced glycation end products (p = 0.03). There were no changes in sublingual microcirculatory parameters. Pulse pressure (p = 0.01) but not aortic pulse wave velocity was reduced. There were no significant changes in bone mineral parameters, blood pressure or left ventricular mass index suggesting that ergocalciferol improved endothelial function independently of these parameters. In parallel experiments, expression of endothelial nitric oxide synthase and activity were increased in human endothelial cells in a dose dependent manner.Ergocalciferol improved microcirculatory endothelial function in patients with chronic kidney disease and concomitant vitamin D deficiency. This process may be mediated through enhanced expression and activity of endothelial nitric oxide synthase.Clinical trials.gov NCT00882401

Mutations in Protein-Binding Hot-Spots on the Hub Protein Smad3 Differentially Affect Its Protein Interactions and Smad3-Regulated Gene Expression

Hub proteins are connected through binding interactions to many other proteins. Smad3, a mediator of signal transduction induced by transforming growth factor beta (TGF-β), serves as a hub protein for over 50 protein-protein interactions. Different cellular responses mediated by Smad3 are the product of cell-type and context dependent Smad3-nucleated protein complexes acting in concert. Our hypothesis is that perturbation of this spectrum of protein complexes by mutation of single protein-binding hot-spots on Smad3 will have distinct consequences on Smad3-mediated responses.We mutated 28 amino acids on the surface of the Smad3 MH2 domain and identified 22 Smad3 variants with reduced binding to subsets of 17 Smad3-binding proteins including Smad4, SARA, Ski, Smurf2 and SIP1. Mutations defective in binding to Smad4, e.g., D408H, or defective in nucleocytoplasmic shuttling, e.g., W406A, were compromised in modulating the expression levels of a Smad3-dependent reporter gene or six endogenous Smad3-responsive genes: Mmp9, IL11, Tnfaip6, Fermt1, Olfm2 and Wnt11. However, the Smad3 mutants Y226A, Y297A, W326A, K341A, and E267A had distinct differences on TGF-β signaling. For example, K341A and Y226A both reduced the Smad3-mediated activation of the reporter gene by ∼50% but K341A only reduced the TGF-β inducibilty of Olfm2 in contrast to Y226A which reduced the TGF-β inducibility of all six endogenous genes as severely as the W406A mutation. E267A had increased protein binding but reduced TGF-β inducibility because it caused higher basal levels of expression. Y297A had increased TGF-β inducibility because it caused lower Smad3-induced basal levels of gene expression.Mutations in protein binding hot-spots on Smad3 reduced the binding to different subsets of interacting proteins and caused a range of quantitative changes in the expression of genes induced by Smad3. This approach should be useful for unraveling which Smad3 protein complexes are critical for specific biological responses

In Support of a Patient-Driven Initiative and Petition to Lower the High Price of Cancer Drugs

Comment in Lowering the High Cost of Cancer Drugs--III. [Mayo Clin Proc. 2016] Lowering the High Cost of Cancer Drugs--I. [Mayo Clin Proc. 2016] Lowering the High Cost of Cancer Drugs--IV. [Mayo Clin Proc. 2016] In Reply--Lowering the High Cost of Cancer Drugs. [Mayo Clin Proc. 2016] US oncologists call for government regulation to curb drug price rises. [BMJ. 2015

Genome-Wide Association Study in BRCA1 Mutation Carriers Identifies Novel Loci Associated with Breast and Ovarian Cancer Risk

BRCA1-associated breast and ovarian cancer risks can be modified by common genetic variants. To identify further cancer risk-modifying loci, we performed a multi-stage GWAS of 11,705 BRCA1 carriers (of whom 5,920 were diagnosed with breast and 1,839 were diagnosed with ovarian cancer), with a further replication in an additional sample of 2,646 BRCA1 carriers. We identified a novel breast cancer risk modifier locus at 1q32 for BRCA1 carriers (rs2290854, P = 2.7×10-8, HR = 1.14, 95% CI: 1.09-1.20). In addition, we identified two novel ovarian cancer risk modifier loci: 17q21.31 (rs17631303, P = 1.4×10-8, HR = 1.27, 95% CI: 1.17-1.38) and 4q32.3 (rs4691139, P = 3.4×10-8, HR = 1.20, 95% CI: 1.17-1.38). The 4q32.3 locus was not associated with ovarian cancer risk in the general population or BRCA2 carriers, suggesting a BRCA1-specific associat

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead