74 research outputs found

    The “Unwelcome Obligation”: Why Neither State nor Federal Courts Should Draw District Lines

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    In recent years, the judiciary’s inability to hold state legislatures accountable for partisan gerrymanders has encouraged state governments to draw legislative and congressional district lines with high partisan advantage, thereby allowing a political party to acquire seats in numbers disproportionate to their popular support. In 2017, the U.S. Supreme Court granted certiorari on two partisan gerrymandering cases: Gill v. Whitford and Benisek v. Lamone. Although the Court might articulate a judicially manageable standard to determine when a districting plan is politically fair, other methods to prevent federal courts from creating district maps that perpetuate partisan bias exist. This Note examines and critiques current debates regarding the judiciary’s role in redistricting and adjudicating partisan gerrymandering claims. It argues that independent redistricting commissions—enacted through state voter initiatives or referendums—should replace federal courts’ authority to develop redistricting plans

    Obesity-related cardiovascular risk factors after weight loss: a clinical trial comparing gastric bypass surgery and intensive lifestyle intervention

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    Objective: Weight reduction improves several obesity-related health conditions. We aimed to compare the effect of bariatric surgery and comprehensive lifestyle intervention on type 2 diabetes and obesityrelated cardiovascular risk factors. Design: One-year controlled clinical trial (ClinicalTrials.gov identifier NCT00273104). Methods: Morbidly obese subjects (19–66 years, mean (S.D.) body mass index 45.1 kg/m2 (5.6), 103 women) were treated with either Roux-en-Y gastric bypass surgery (nZ80) or intensive lifestyle intervention at a rehabilitation centre (nZ66). The dropout rate within both groups was 5%. Results: Among the 76 completers in the surgery group and the 63 completers in the lifestyle group, mean (S.D.) 1-year weight loss was 30% (8) and 8% (9) respectively. Beneficial effects on glucose metabolism, blood pressure, lipids and low-grade inflammation were observed in both groups. Remission rates of type 2 diabetes and hypertension were significantly higher in the surgery group than the lifestyle intervention group; 70 vs 33%, PZ0.027, and 49 vs 23%, PZ0.016. The improvements in glycaemic control and blood pressure were mediated by weight reduction. The surgery group experienced a significantly greater reduction in the prevalence of metabolic syndrome, albuminuria and electrocardiographic left ventricular hypertrophy than the lifestyle group. Gastrointestinal symptoms and symptomatic postprandial hypoglycaemia developed more frequently after gastric bypass surgery than after lifestyle intervention. There were no deaths. Conclusions: Type 2 diabetes and obesity-related cardiovascular risk factors were improved after both treatment strategies. However, the improvements were greatest in those patients treated with gastric bypass surgery

    Do national resources have to be centrally managed? Vested interests and institutional reform in Norwegian fisheries governance

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    Corporatism -with its privileged access, restricted participation and centralized structures - has a long history in Norwegian fisheries governance. Co-management – understood as a decentralized, bottom-up and more inclusive form of fisheries governance - has not been considered a relevant alternative.. Why does corporatism still prevail in a context where stakeholder status in fisheries governance globally – both in principle and practice - has been awarded environmental organizations, municipal authorities and even consumer advocacy groups? Why then have alternatives to the corporatist system of centralized consultation and state governance never been seriously considered in Norway, in spite of the growing emphasis on fish as a public resource and fisheries management as human intervention in geographically confined and complex ecosystems? We suggest that thismay have to do with the fundamental assumptions behind Norwegian fisheries governance that since fish is a national resource, it must be centrally managed. We argue that this is an assumption that may be contested

    Low serum creatinine is associated with type 2 diabetes in morbidly obese women and men: a cross-sectional study

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    <p>Abstract</p> <p>Background</p> <p>Low skeletal muscle mass is associated with insulin resistance and metabolic syndrome. Serum creatinine may serve as a surrogate marker of muscle mass, and a possible relationship between low serum creatinine and type 2 diabetes has recently been demonstrated. We aimed to validate this finding in a population of Caucasian morbidly obese subjects.</p> <p>Methods</p> <p>Cross-sectional study of 1,017 consecutive morbidly obese patients with an estimated glomerular filtration rate >60 ml/min/1.73 m<sup>2</sup>. Logistic regression (univariate and multiple) was used to assess the association between serum creatinine and prevalent type 2 diabetes, including statistically testing for the possibility of non-linearity in the relationship by implementation of Generalized Additive Models (GAM) and piecewise linear regression. Possible confounding variables such as age, family history of diabetes, waist-to-hip ratio, hypertension, current smoking, serum magnesium, albuminuria and insulin resistance (log HOMA-IR) were adjusted for in three separate multiple logistic regression models.</p> <p>Results</p> <p>The unadjusted GAM analysis suggested a piecewise linear relationship between serum creatinine and diabetes. Each 1 μmol/l increase in serum creatinine was associated with 6% (95% CI; 3%-8%) and 7% (95% CI; 2%-13%) lower odds of diabetes below serum creatinine levels of 69 and 72 μmol/l in women and men, respectively. Above these breakpoints the serum creatinine concentrations did not reduce the odds further. Adjustments for non-modifiable and modifiable risk factors left the piecewise effect for both women and men largely unchanged. In the fully adjusted model, which includes serum magnesium, albuminuria and log HOMA-IR, the piecewise effect for men was statistically non-significant, but it remained present for women. Patients with creatinine levels below median had approximately 50% (women) and 75% (men) increased odds of diabetes.</p> <p>Conclusions</p> <p>Low serum creatinine is a predictor of type 2 diabetes in Caucasian morbidly obese patients, independent of age, gender, family history of diabetes, anthropometric measures, hypertension, and current smoking. Longitudinal studies of both obese and non-obese populations are needed to investigate whether serum creatinine may be causally linked with type 2 diabetes, and if so, precisely how they are linked.</p

    The relationship between various measures of obesity and arterial stiffness in morbidly obese patients

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    <p>Abstract</p> <p>Background</p> <p>Obesity is associated with increased risk of cardiovascular disease. Arterial stiffness assessed by carotid femoral pulse wave velocity (PWV) is an independent predictor of cardiovascular morbidity and mortality. We aimed to investigate how various measures of body composition affect arterial stiffness.</p> <p>Methods</p> <p>This is an analysis of cross-sectional baseline data from a controlled clinical trial addressing changes in arterial stiffness after either surgery or lifestyle intervention in a population of morbidly obese patients. High-fidelity applanation tonometry (Millar<sup>®</sup>, Sphygmocor<sup>®</sup>) was used to measure pulse wave velocity (PWV). Carotid femoral PWV is a direct measure of arterial stiffness and is considered to be the gold standard method. The Inbody 720 Body Composition Analyzer was used for bioelectrical impedance analysis (BIA). Spearman's correlation, independent samples <it>t</it>-test, chi-square tests, Fisher's exact test and multiple linear regression analyses were used as statistical methods.</p> <p>Results</p> <p>A total of 133 patients (79 women), with a mean (SD) age of 43 (11) years were included in the study. Men had a significantly higher prevalence of obesity related comorbidities and significantly higher PWV, 9.1 (2.0) m/s vs. 8.1 (1.8) m/s, p = 0.003, than women. In the female group, PWV was positively correlated with WC, WHtR, BMI and visceral fat area. In the male group, PWV was negatively correlated with BMI. Multiple linear regression analysis showed that increasing BMI, WC, WHtR, visceral fat area and fat mass were independently associated with higher PWV in women, but not in men, after adjustment for age, hypertension and type 2 diabetes.</p> <p>Conclusion</p> <p>Most measures of general and abdominal obesity were predictors of arterial stiffness in female morbidly obese patients.</p> <p>Trial registration</p> <p>ClinicalTrials.gov Identifier <a href="http://www.clinicaltrials.gov/ct2/show/NCT00626964">NCT00626964</a></p

    DNA methylation on N6-adenine in mammalian embryonic stem cells

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    It has been widely accepted that 5-methylcytosine is the only form of DNA methylation in mammalian genomes. Here we identify N6-methyladenine as another form of DNA modification in mouse embryonic stem cells. Alkbh1 encodes a demethylase for N6-methyladenine. An increase of N6-methyladenine levels in Alkbh1-deficient cells leads to transcriptional silencing. N6-methyladenine deposition is inversely correlated with the evolutionary age of LINE-1 transposons; its deposition is strongly enriched at young (6 million years old) L1 elements. The deposition of N6-methyladenine correlates with epigenetic silencing of such LINE-1 transposons, together with their neighbouring enhancers and genes, thereby resisting the gene activation signals during embryonic stem cell differentiation. As young full-length LINE-1 transposons are strongly enriched on the X chromosome, genes located on the X chromosome are also silenced. Thus, N6-methyladenine developed a new role in epigenetic silencing in mammalian evolution distinct from its role in gene activation in other organisms. Our results demonstrate that N6-methyladenine constitutes a crucial component of the epigenetic regulation repertoire in mammalian genomes

    Genome Sequence of a Lancefield Group C Streptococcus zooepidemicus Strain Causing Epidemic Nephritis: New Information about an Old Disease

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    Outbreaks of disease attributable to human error or natural causes can provide unique opportunities to gain new information about host-pathogen interactions and new leads for pathogenesis research. Poststreptococcal glomerulonephritis (PSGN), a sequela of infection with pathogenic streptococci, is a common cause of preventable kidney disease worldwide. Although PSGN usually occurs after infection with group A streptococci, organisms of Lancefield group C and G also can be responsible. Despite decades of study, the molecular pathogenesis of PSGN is poorly understood. As a first step toward gaining new information about PSGN pathogenesis, we sequenced the genome of Streptococcus equi subsp. zooepidemicus strain MGCS10565, a group C organism that caused a very large and unusually severe epidemic of nephritis in Brazil. The genome is a circular chromosome of 2,024,171 bp. The genome shares extensive gene content, including many virulence factors, with genetically related group A streptococci, but unexpectedly lacks prophages. The genome contains many apparently foreign genes interspersed around the chromosome, consistent with the presence of a full array of genes required for natural competence. An inordinately large family of genes encodes secreted extracellular collagen-like proteins with multiple integrin-binding motifs. The absence of a gene related to speB rules out the long-held belief that streptococcal pyrogenic exotoxin B or antibodies reacting with it singularly cause PSGN. Many proteins previously implicated in GAS PSGN, such as streptokinase, are either highly divergent in strain MGCS10565 or are not more closely related between these species than to orthologs present in other streptococci that do not commonly cause PSGN. Our analysis provides a comparative genomics framework for renewed appraisal of molecular events underlying APSGN pathogenesis
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