Contemporary Africa through the theory of Louis Dumont

Abstract This article responds to a trend in recent anthropological scholarship in Africa that has overemphasized a lack of social organization following the advancement of neoliberal reforms across the continent. Using a theoretical framework informed by the theory of Louis Dumont, I show that social organization remains an important analytical topic in times of crisis, and that this is best apprehended through an analysis of values. The ethnographic focus of this article is Pentecostal Christianity as it is practiced on the Zambian Copperbelt. In this particular African context, Pentecostalism is animated by an overarching value that I call "moving," which is in turn made up to two sub-values: charisma and prosperity. By exploring how Pentecostal believers navigate the hierarchical relationship between these two sub-values, we are given a clear picture of the social world that Pentecostal adherence makes possible

Acute Exercise-Induced Response of Platelet-Monocyte Complexes in Obese, Postmenopausal Women

Inactivity-related diseases such as cardiovascular disease (CVD) are linked to chronic low-grade, systemic inflammation. Platelet-monocyte complexes (PMCs) are markers of in vivo platelet activation and atherosclerosis, and may be early indicators of subclinical inflammation. PURPOSE: To examine the effects of an exercise bout on PMCs in those at risk for CVD. METHODS: Twenty-five overweight-obese (BMI 32.7 ± 5.2 kg×m-2, 55-75 yr) women were randomly assigned to either the exercise (EX, n=13) or non-exercise control (CON, n=12) group. EX performed 2 sets of 8 resistance exercises and a 25-min treadmill walk at 70-80% HRR. Blood was obtained pre-exercise (PR), post- (PO), 1-hour and 2 hours post-exercise (1HR and 2HR). Blood was obtained at the same time points in CON. PMCs were identified via flow cytometry and analyzed in each monocyte phenotype. Monocyte phenotypes were defined as: Mon1 (CD14+CD16−CCR2+), Mon2 (CD14+CD16+CCR2+), and Mon3 (CD14+CD16+CCR2−). All events positive for both CD14 and CD42a (marker for platelets) were considered PMCs. RESULTS: A main effect for time revealed an increase in PMC number at PO (p=0.036) which appears to have been driven by EX (EX = 61.5%; CON = 33.8% increase). PMCs formed with Mon1 and Mon2 followed a similar response. A significant group x time interaction for Mon3 PMC number (p=0.002) indicated an increase from PR to PO (PR = 5218±1170, PO = 8195±1152 cells·ml-1), and a decrease from PO to 1HR and 2HR (1HR = 3767±820 cells·ml-1 2HR = 3818±814 cells·ml-1) in EX. PMC number remained constant for CON at all timepoints. Estimated VO2max was negatively correlated with CD42a MFI (a marker of platelet density per monocyte) (r = -0.583, p = 0.003). Systolic blood pressure (SBP) positively correlated with percent PMC (% CD42a positive monocytes; r = 0.458, p = 0.042). CONCLUSION: Aerobic fitness appears to reduce platelet activation indicated by the negative relationship between VO2max and CD42a MFI. Chronic elevations in resting SBP are linked to PMC percentage, possibly due to sheer stress-induced platelet activation. It is possible that PMC elevation at PO is at least partially driven by exercise-induced increases in BP. These results support previous literature, indicating that PMCs are a CVD risk marker and may elucidate one mechanism by which physical fitness reduces risk for CVD

Risk of major cardiovascular events in patients with psoriatic arthritis, psoriasis and rheumatoid arthritis: a population-based cohort study.

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Files. This article is open access.We aimed to quantify the risk of major adverse cardiovascular events (MACE) among patients with psoriatic arthritis (PsA), rheumatoid arthritis (RA) and psoriasis without known PsA compared with the general population after adjusting for traditional cardiovascular risk factors.A population-based longitudinal cohort study from 1994 to 2010 was performed in The Health Improvement Network (THIN), a primary care medical record database in the UK. Patients aged 18-89 years of age with PsA, RA or psoriasis were included. Up to 10 unexposed controls matched on practice and index date were selected for each patient with PsA. Outcomes included cardiovascular death, myocardial infarction, cerebrovascular accidents and the composite outcome (MACE). Cox proportional hazards models were used to calculate the HRs for each outcome adjusted for traditional risk factors. A priori, we hypothesised an interaction between disease status and disease-modifying antirheumatic drug (DMARD) use.Patients with PsA (N=8706), RA (N=41 752), psoriasis (N=138 424) and unexposed controls (N=81 573) were identified. After adjustment for traditional risk factors, the risk of MACE was higher in patients with PsA not prescribed a DMARD (HR 1.24, 95% CI 1.03 to 1.49), patients with RA (No DMARD: HR 1.39, 95% CI 1.28 to 1.50, DMARD: HR 1.58, 95% CI 1.46 to 1.70), patients with psoriasis not prescribed a DMARD (HR 1.08, 95% CI 1.02 to 1.15) and patients with severe psoriasis (DMARD users: HR 1.42, 95% CI 1.17 to 1.73).Cardiovascular risk should be addressed with all patients affected by psoriasis, PsA or RA.American College of Rheumatology R01HL089744 K24AR064310 Clinical and Translational Science Award at the University of Pennsylvania from the National Center for Research Resources 8UL1TR000003 American College of Rheumatology Research and Education Foundation NIH K23AR063764 Doris Duke Charitable Foundation Center for Clinical Epidemiology and Biostatistics Icelandic Research Fund 120433021 R01AG025152 K23HL097151-0

TLR4 Asp299Gly and Thr399Ile Polymorphisms: No Impact on Human Immune Responsiveness to LPS or Respiratory Syncytial Virus

A broad variety of natural environmental stimuli, genotypic influences and timing all contribute to expression of protective versus maladaptive immune responses and the resulting clinical outcomes in humans. The role of commonly co-segregating Toll-like receptor 4 (TLR4) non-synonymous single nucleotide polymorphisms Asp299Gly and Thr399Ile in this process remains highly controversial. Moreover, what differential impact these polymorphisms might have in at risk populations with respiratory dysfunction, such as current asthma or a history of infantile bronchiolitis, has never been examined. Here we determine the importance of these polymorphisms in modulating LPS and respiratory syncytial virus (RSV)--driven cytokine responses. We focus on both healthy children and those with clinically relevant respiratory dysfunction.To elucidate the impact of TLR4 Asp299Gly and Thr399Ile on cytokine production, we assessed multiple immune parameters in over 200 pediatric subjects aged 7-9. Genotyping was followed by quantification of pro- and anti-inflammatory cytokine responses by fresh peripheral blood mononuclear cells upon acute exposure to LPS or RSV.In contrast to early reports, neither SNP influenced immune responses evoked by LPS exposure or RSV infection, as measured by the intermediate phenotype of pro- and anti-inflammatory cytokine responses to these ubiquitous agents. There is no evidence of altered sensitivity in populations with "at risk" clinical phenotypes.Genomic medicine seeks to inform clinical practice. Determination of the TLR4 Asp299Gly/Thr399Ile haplotype is of no clinical benefit in predicting the nature or intensity of cytokine production in children whether currently healthy or among specific at-risk groups characterized by prior infantile broncholitis or current asthma

Associations of iron metabolism genes with blood manganese levels: a population-based study with validation data from animal models

<p>Abstract</p> <p>Background</p> <p>Given mounting evidence for adverse effects from excess manganese exposure, it is critical to understand host factors, such as genetics, that affect manganese metabolism.</p> <p>Methods</p> <p>Archived blood samples, collected from 332 Mexican women at delivery, were analyzed for manganese. We evaluated associations of manganese with functional variants in three candidate iron metabolism genes: <it>HFE </it>[hemochromatosis], <it>TF </it>[transferrin], and <it>ALAD </it>[δ-aminolevulinic acid dehydratase]. We used a knockout mouse model to parallel our significant results as a novel method of validating the observed associations between genotype and blood manganese in our epidemiologic data.</p> <p>Results</p> <p>Percentage of participants carrying at least one copy of <it>HFE C282Y</it>, <it>HFE H63D</it>, <it>TF P570S</it>, and <it>ALAD K59N </it>variant alleles was 2.4%, 17.7%, 20.1%, and 6.4%, respectively. Percentage carrying at least one copy of either <it>C282Y </it>or <it>H63D </it>allele in <it>HFE </it>gene was 19.6%. Geometric mean (geometric standard deviation) manganese concentrations were 17.0 (1.5) μg/l. Women with any <it>HFE </it>variant allele had 12% lower blood manganese concentrations than women with no variant alleles (β = -0.12 [95% CI = -0.23 to -0.01]). <it>TF </it>and <it>ALAD </it>variants were not significant predictors of blood manganese. In animal models, <it>Hfe</it>^-/-mice displayed a significant reduction in blood manganese compared with <it>Hfe</it>^+/+mice, replicating the altered manganese metabolism found in our human research.</p> <p>Conclusions</p> <p>Our study suggests that genetic variants in iron metabolism genes may contribute to variability in manganese exposure by affecting manganese absorption, distribution, or excretion. Genetic background may be critical to consider in studies that rely on environmental manganese measurements.</p

The Fifteenth Data Release of the Sloan Digital Sky Surveys: First Release of MaNGA-derived Quantities, Data Visualization Tools, and Stellar Library

Twenty years have passed since first light for the Sloan Digital Sky Survey (SDSS). Here, we release data taken by the fourth phase of SDSS (SDSS-IV) across its first three years of operation (2014 July–2017 July). This is the third data release for SDSS-IV, and the 15th from SDSS (Data Release Fifteen; DR15). New data come from MaNGA—we release 4824 data cubes, as well as the first stellar spectra in the MaNGA Stellar Library (MaStar), the first set of survey-supported analysis products (e.g., stellar and gas kinematics, emission-line and other maps) from the MaNGA Data Analysis Pipeline, and a new data visualization and access tool we call "Marvin." The next data release, DR16, will include new data from both APOGEE-2 and eBOSS; those surveys release no new data here, but we document updates and corrections to their data processing pipelines. The release is cumulative; it also includes the most recent reductions and calibrations of all data taken by SDSS since first light. In this paper, we describe the location and format of the data and tools and cite technical references describing how it was obtained and processed. The SDSS website (www.sdss.org) has also been updated, providing links to data downloads, tutorials, and examples of data use. Although SDSS-IV will continue to collect astronomical data until 2020, and will be followed by SDSS-V (2020–2025), we end this paper by describing plans to ensure the sustainability of the SDSS data archive for many years beyond the collection of data