Products as Affective Modifiers of Identities

© The Author(s) 2015. Are salesclerks seen as better, more powerful, or more active when they drive Mustangs? What about entrepreneurs? What about driving a mid-sized car? Intuitively, we have ideas about these, but much of the research on the affective nature of products is on purchasing, desires, and self-fulfillment. Drawing on symbolic interactionism, we argue that people's association with products has some basis in the impression management of their identity. For this to occur, there must be some cultural consensus about the way that products modify identities. Drawing on affect control theory's (ACT) methodology and equations, we measure the goodness, powerfulness, and activeness of several products, identities, and the associated product-modified identities to explore how products function as affective modifiers of identities. We find consistent effects across several types of technology products, whereby products pull the modified identity in the direction of the products' affective qualities. Support is established for the ACT equations that predict how traits modify identities as also having utility for predicting how products modify identities. This suggests that the opening questions can be answered empirically by measuring cultural-specific sentiments of the identity and the product and by developing equations to predict the identity modification process

Ancestry of the Brazilian TP53 c.1010G>A (p.Arg337His, R337H) founder mutation : clues from haplotyping of short tandem repeats on Chromosome 17p

Rare germline mutations in TP53 (17p13.1) cause a highly penetrant predisposition to a specific spectrum of early cancers, defining the Li-Fraumeni Syndrome (LFS). A germline mutation at codon 337 (p.Arg337His, c1010G>A) is found in about 0.3% of the population of Southern Brazil. This mutation is associated with partially penetrant LFS traits and is found in the germline of patients with early cancers of the LFS spectrum unselected for familial his- tory. To characterize the extended haplotypes carrying the mutation, we have genotyped 9 short tandem repeats on chromosome 17p in 12 trios of Brazilian p.Arg337His carriers. Results confirm that all share a common ancestor haplotype of Caucasian/Portuguese-Ibe- ric origin, distant in about 72–84 generations (2000 years assuming a 25 years intergenera- tional distance) and thus pre-dating European migration to Brazil. So far, the founder p. Arg337His haplotype has not been detected outside Brazil, with the exception of two resi- dents of Portugal, one of them of Brazilian origin. On the other hand, increased meiotic recombination in p.Arg337His carriers may account for higher than expected haplotype diversity. Further studies comparing haplotypes in populations of Brazil and of other areas of Portuguese migration are needed to understand the historical context of this mutation in Brazil.This study was funded by grant # 478430/2012-4 from CNPq (RFA MCT/CNPq - No 14/2012; Universal), Brazil.We would like to thank UFRGS, UFPA, AC Camargo, HC Barretos and University of Minho for their support during this work

2013 ACC/AHA guideline on the assessment of cardiovascular risk: A report of the American College of Cardiology/American heart Association Task Force on Practice Guidelines

1.1. Organization of the Work Group: The Risk Assessment Work Group (Work Group) was composed of 11 members and 5 ex-officio members, including internists, cardiologists, endocrinologists, and experts in cardiovascular epidemiology, biostatistics, healthcare management and economics, and guideline development. 1.2. Document Review and Approval: A formal peer review process, which included 12 expert reviewers and representatives of federal agencies, was initially completed under the auspices of the NHLBI. This document was also reviewed by 3 expert reviewers nominated by the ACC and the AHA when the management of the guideline transitioned to the ACC/AHA. The ACC and AHA Reviewers’ RWI information is published in this document (Appendix 2). This document was approved for publication by the governing bodies of the ACC and AHA and endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation, American Society for Preventive Cardiology, American Society of Hypertension, Association of Black Cardiologists, National Lipid Association, Preventive Cardiovascular Nurses Association, and WomenHeart: The National Coalition for Women With Heart Disease. 1.3. Charge to the Work Group: The Work Group was 1 of 3 work groups appointed by the NHLBI to develop its own recommendations and provide cross-cutting input to 3 Panels for updating guidelines on blood cholesterol, blood pressure (BP), and overweight/obesity. The Work Group was asked to examine the scientific evidence on risk assessment for initial ASCVD events and to develop an approach for quantitative risk assessment that could be used in practice and used or adapted by the risk factor panels (blood cholesterol, hypertension, and obesity) in their guidelines and algorithms. Specifically, the Work Group was charged with 2 tasks: 1) To develop or recommend an approach to quantitative risk assessment that could be used to guide care; and 2) To use systematic review methodology to pose and address a small number of questions judged to be critical to refining and adopting risk assessment in clinical practice

2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines

The Expert Panel was charged with using data from randomized controlled trials (RCTs) and systematic reviews and meta-analyses of RCTs to update the clinical practice recommendations for the treatment of blood cholesterol levels to reduce ASCVD risk. For this guideline, ASCVD includes coronary heart disease (CHD), stroke, and peripheral arterial disease, all of presumed atherosclerotic origin. These recommendations are intended to provide a strong, evidence-based foundation for the treatment of cholesterol for the primary and secondary prevention of ASCVD in women and men

ACC/AHA/ACP-ASIM guidelines for the management of patients with chronic stable angina: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients With Chronic Stable Angina)

The ACC/AHA Task Force on Practice Guidelines was formed to make recommendations regarding the diagnosis and treatment of patients with known or suspected cardiovascular disease. Ischemic heart disease is the single leading cause of death in the U.S. The most common manifestation of this disease is chronic stable angina. Recognizing the importance of the management of this common entity and the absence of national clinical practice guidelines in this area, the task force formed the current committee to develop guidelines for the management of patients with stable angina. Because this problem is frequently encountered in the practice of internal medicine, the task force invited the American College of Physicians-American Society of Internal Medicine (ACP-ASIM) to serve as a partner in this effort by naming four general internists to serve on the committee

Exome chip analysis identifies low-frequency and rare variants in MRPL38 for white matter hyperintensities on brain MRI

International audienc

Measurement of the W-boson mass in pp collisions at √s=7 TeV with the ATLAS detector

A measurement of the mass of the W boson is presented based on proton–proton collision data recorded in 2011 at a centre-of-mass energy of 7 TeV with the ATLAS detector at the LHC, and corresponding to 4.6 fb−1 of integrated luminosity. The selected data sample consists of 7.8×106 candidates in the W→μν channel and 5.9×106 candidates in the W→eν channel. The W-boson mass is obtained from template fits to the reconstructed distributions of the charged lepton transverse momentum and of the W boson transverse mass in the electron and muon decay channels, yielding mW=80370±7 (stat.)±11(exp. syst.) ±14(mod. syst.) MeV =80370±19MeV, where the first uncertainty is statistical, the second corresponds to the experimental systematic uncertainty, and the third to the physics-modelling systematic uncertainty. A measurement of the mass difference between the W+ and W−bosons yields mW+−mW−=−29±28 MeV

Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure.

Numerous genetic loci have been associated with systolic blood pressure (SBP) and diastolic blood pressure (DBP) in Europeans. We now report genome-wide association studies of pulse pressure (PP) and mean arterial pressure (MAP). In discovery (N = 74,064) and follow-up studies (N = 48,607), we identified at genome-wide significance (P = 2.7 × 10(-8) to P = 2.3 × 10(-13)) four new PP loci (at 4q12 near CHIC2, 7q22.3 near PIK3CG, 8q24.12 in NOV and 11q24.3 near ADAMTS8), two new MAP loci (3p21.31 in MAP4 and 10q25.3 near ADRB1) and one locus associated with both of these traits (2q24.3 near FIGN) that has also recently been associated with SBP in east Asians. For three of the new PP loci, the estimated effect for SBP was opposite of that for DBP, in contrast to the majority of common SBP- and DBP-associated variants, which show concordant effects on both traits. These findings suggest new genetic pathways underlying blood pressure variation, some of which may differentially influence SBP and DBP