Shifts in Policy and Power: Calculating the Consequences of Increased Prosecutorial Power and Reduced Judicial Authority in Post 9/11 America

Among many responses to the attacks of September 11, 2001, Congress and the states have shifted to the executive branch certain powers once held by the judicial branch. This article considers the impact of transferring judicial powers to prosecutorial officers, and compares the consequent increased powers of the prosecutor with those powers traditionally held by prosecutors in Japanese criminal courts. It considers the impact of removing from public view and judicial oversight many prosecutorial functions, drawing comparisons between the largely opaque Japanese prosecutorial roles and those roles now assumed in immigration and anti-terrorism laws, noting the need for safeguards not currently in place in U.S. systems but shown to be highly effective in Japanese systems

Short-Interval Cortical Inhibition and Intracortical Facilitation during Submaximal Voluntary Contractions Changes with Fatigue

This study determined whether short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF) change during a sustained submaximal isometric contraction. On 2 days, 12 participants (6 men, 6 women) performed brief (7-s) elbow flexor contractions before and after a 10-min fatiguing contraction; all contractions were performed at the level of integrated electromyographic activity (EMG) which produced 25 % maximal unfatigued torque. During the brief 7-s and 10-min submaximal contractions, single (test) and paired (conditioning–test) transcranial magnetic stimuli were applied over the motor cortex (5 s apart) to elicit motor-evoked potentials (MEPs) in biceps brachii. SICI and ICF were elicited on separate days, with a conditioning–test interstimulus interval of 2.5 and 15 ms, respectively. On both days, integrated EMG remained constant while torque fell during the sustained contraction by ~51.5 % from control contractions, perceived effort increased threefold, and MVC declined by 21–22 %. For SICI, the conditioned MEP during control contractions (74.1 ± 2.5 % of unconditioned MEP) increased (less inhibition) during the sustained contraction (last 2.5 min: 86.0 ± 5.1 %; P \u3c 0.05). It remained elevated in recovery contractions at 2 min (82.0 ± 3.8 %; P \u3c 0.05) and returned toward control at 7-min recovery (76.3 ± 3.2 %). ICF during control contractions (conditioned MEP 129.7 ± 4.8 % of unconditioned MEP) decreased (less facilitation) during the sustained contraction (last 2.5 min: 107.6 ± 6.8 %; P \u3c 0.05) and recovered to 122.8 ± 4.3 % during contractions after 2 min of recovery. Both intracortical inhibitory and facilitatory circuits become less excitable with fatigue when assessed during voluntary activity, but their different time courses of recovery suggest different mechanisms for the fatigue-related changes of SICI and ICF

Cognition and brain iron deposition in whole grey matter regions and hippocampal subfields

ACKNOWLEDGEMENTS We are grateful to the Aberdeen Children of the 1950's (ACONF) subset of Generation Scotland GS:SFHS who took part in the STRADL study, supported and funded by the Wellcome Trust Strategic Award ‘Stratifying Resilience and Depression Longitudinally’ (STRADL) [104036/Z/14/Z]. Generation Scotland received core support from the Chief Scientist Office of the Scottish Government Health Directorates [CZD/16/6] and the Scottish Funding Council [HR03006] and is currently supported by the Wellcome Trust [216767/Z/19/Z]. HS is supported by the Roland Sutton Academic Trust [0076/R/19]. We also thank the STRADL project team. Research Funding Chief Scientist Office. Grant Number: CZD/16/6 Roland Sutton Academic Trust. Grant Number: 0076/R/19 Scottish Funding Council. Grant Number: HR03006 Wellcome Trust. Grant Number: 104036/Z/14/ZPeer reviewedPublisher PD

Orthodontic Treatment Completion and Discontinuation in a Rural Sample from North Central Appalachia in the USA

Background: Orthodontics has inherent demands, requiring regular appointments and active patient engagement, but relatively little is established in regard to rates of completion of treatment and possible factors affecting successful completion. These factors may be particularly important for cultural minority groups, such as those in rural Appalachia, given the environmental, social, and economic complexities affecting access to and utilization of treatment. Design and methods: A naturalistic study design was employed, using retrospective data from a rural outpatient general dental office in July 2012. Chart abstraction yielded 219 (55.3% female) orthodontic patients (M age = 11.0 [3.7]). Chi-square tests for independence were conducted for categorical dependent variables. For continuous variables, t-tests were conducted. A logistic multivariate regression analysis was conducted to predict completion/non-completion of treatment, with age, gender, distance traveled, type of malocclusion, and payment type as predictors. Results: Overall, 49.8% of this sample successfully completed orthodontic treatment. Greater successful conclusion of treatment was found in self-pay patients (i.e., 74%) versus those whose care was funded through Medicaid/Children’s Health Insurance Program (i.e., 34%) or through private insurance (i.e., 36%). Age, gender, and distance to the office from home had no association relative to successful completion of treatment, although average one-way distance to travel for care was considerable (i.e., 38.8 miles). Conclusion: Rate of successful orthodontic treatment completion was low in this rural sample. Treatment outcome was related to the form of payment for services, with self-pay associated with the highest rate of successful completion

Framingham risk prediction equations for incidence of cardiovascular disease using detailed measures for smoking

Current prediction models for risk of cardiovascular disease (CVD) incidence incorporate smoking as a dichotomous yes/no measure. However, the risk of CVD associated with smoking also varies with the intensity and duration of smoking and there is a strong association between time since quitting and the risk of disease onset. This study aims to develop improved risk prediction equations for CVD incidence incorporating intensity and duration of smoking and time since quitting. The risk of developing a first CVD event was evaluated using a Cox’s model for participants in the Framingham offspring cohort who attended the fourth examination (1988–92) between the ages of 30 and 74 years and were free of CVD (n=3751). The full models based on the smoking variables and other risk factors, and reduced models based on the smoking variables and non-laboratory risk factors demonstrated good discrimination, calibration and global fit. The incorporation of both time since quitting among past smokers and pack-years among current smokers resulted in better predictive performance as compared to a dichotomous current/non-smoker measure and a current/quitter/never smoker measure. Compared to never smokers, the risk of CVD incidence increased with pack-years. Risk among those quitting more than five years prior to the baseline exam and within five years prior to the baseline exam were similar and twice as high as that of never smokers. A CVD risk equation incorporating the effects of pack-years and time since quitting provides an improved tool to quantify risk and guide preventive care

Structural brain complexity and cognitive decline in late life : A longitudinal study in the Aberdeen 1936 Birth Cohort

Copyright © 2014 Elsevier Inc. All rights reserved.Peer reviewedPostprin

Framingham risk prediction equations for incidence of cardiovascular disease using detailed measures for smoking



Abstract
Current prediction models for risk of cardiovascular disease (CVD) incidence incorporate smoking as a dichotomous yes/no measure. However, the risk of CVD associated with smoking also varies with the intensity and duration of smoking and there is a strong association between time since quitting and the risk of disease onset. This study aims to develop improved risk prediction equations for CVD incidence incorporating intensity and duration of smoking and time since quitting.
The risk of developing a first CVD event was evaluated using a Cox's model for participants in the Framingham offspring cohort who attended the fourth examination (1988-92) between the ages of 30 and 74 years and were free of CVD (n=3751). The full models based on the smoking variables and other risk factors, and reduced models based on the smoking variables and non-laboratory risk factors demonstrated good discrimination, calibration and global fit. The incorporation of both time since quitting among past smokers and packyears among current smokers resulted in better predictive performance as compared to a dichotomous current/non-smoker measure and a current/quitter/never smoker measure. Compared to never smokers, the risk of CVD incidence increased with pack-years. Risk among those quitting more than five years prior to the baseline exam and within five years prior to the baseline exam were similar and twice as high as that of never smokers. A CVD risk equation incorporating the effects of pack-years and time since quitting provides an improved tool to quantify risk and guide preventive care

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Validation and comparison of two automated methods to quantify brain white matter hyperintensities of presumed vascular origin

Funding Data collection was funded by grants from the Alzheimer’s Research Trust (now Alzheimer’s Research UK, grant reference: ART/SPG2003B), Alzheimer’s Research UK (grant reference: ARUK-SB2012B-2), the University of Aberdeen Development Trust (grant reference RGB3109) and NHS Grampian and the Chief Scientist’s Office (grant reference: CAF/08/08). JMJW is funded by the University of Aberdeen Development Trust and TauRx Therapeutics Ltd. CP is funded by Royal Surrey County Hospital NHS Foundation Trust. CJM, ADM, and GDW are funded by the Scottish Funding Council.Peer reviewedPublisher PD

Differential effects of nutritional folic acid deficiency and moderate hyperhomocysteinemia on aortic plaque formation and genome-wide DNA methylation in vascular tissue from ApoE-/- mice

Low folate intake is associated with vascular disease. Causality has been attributed to hyperhomocysteinemia. However, human intervention trials have failed to show the benefit of homocysteine-lowering therapies. Alternatively, low folate may promote vascular disease by deregulating DNA methylation. We investigated whether folate could alter DNA methylation and atherosclerosis in ApoE null mice. Mice were fed one of six diets (n = 20 per group) for 16 weeks. Basal diets were either control (C; 4% lard) or high fat (HF; 21% lard and cholesterol, 0.15%) with different B-vitamin compositions: (1) folic acid and B-vitamin replete, (2) folic acid deficient (−F), (3) folic acid, B6 and B12 deficient (−F−B). −F diets decreased plasma (up to 85%; P < 0.05), whole blood (up to 70%; P < 0.05), and liver folate (up to 65%; P < 0.05) and hepatic SAM/SAH (up to 80%; P < 0.05). −F−B diets reduced plasma (up to 76%; P < 0.05), whole blood (up to 72%; P < 0.05), and liver B12 (up to 39%; P < 0.05) and hepatic SAM/SAH (up to 90%; P < 0.05). −F increased homocysteine 2-fold, while −F−B increased homocysteine 3.6- and 6.8-fold in the C and HF groups (P < 0.05). Plaque formation was increased 2-fold (P < 0.0001) in mice fed a HF diet. Feeding a HF–F diet increased lesion formation by 17% (P < 0.05). There was no change in 5-methyldeoxycytidine in liver or vascular tissue (aorta, periadventitial tissue and heart). These data suggest that atherogenesis is not associated with genome-wide epigenetic changes in this animal model