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Modern Applied Statistics With S

Purpose—The aim of this guideline is to provide a synopsis of best clinical practices in the rehabilitative care of adults recovering from stroke. Methods—Writing group members were nominated by th...

Guidelines for Adult Stroke Rehabilitation and Recovery: A Guideline for Healthcare Professionals from the American Heart Association/American Stroke Association

Hyperglycemia and Adverse Pregnancy Outcomes

Mercury (Hg) is a global pollutant that affects human and ecosystem health. We synthesize understanding of sources, atmosphere-land-ocean Hg dynamics and health effects, and consider the implications of Hg-control policies. Primary anthropogenic Hg emissions greatly exceed natural geogenic sources, resulting in increases in Hg reservoirs and subsequent secondary Hg emissions that facilitate its global distribution. The ultimate fate of emitted Hg is primarily recalcitrant soil pools and deep ocean waters and sediments. Transfers of Hg emissions to largely unavailable reservoirs occur over the time scale of centuries, and are primarily mediated through atmospheric exchanges of wet/dry deposition and evasion from vegetation, soil organic matter and ocean surfaces. A key link between inorganic Hg inputs and exposure of humans and wildlife is the net production of methylmercury, which occurs mainly in reducing zones in freshwater, terrestrial, and coastal environments, and the subsurface ocean. Elevated human exposure to methylmercury primarily results from consumption of estuarine and marine fish. Developing fetuses are most at risk from this neurotoxin but health effects of highly exposed populations and wildlife are also a concern. Integration of Hg science with national and international policy efforts is needed to target efforts and evaluate efficacy.

http://pubs.acs.org/doi/pdf/10.1021/es305071v

Mercury as a Global Pollutant: Sources, Pathways, and Effects

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A User’s Guide

The Publisher of the Journal of Behavioral Medicine and the authors of ‘‘Disentangling Multiple Sclerosis and Depression: An Adjusted Depression Screening Score for Patient-Centered Care’’ (Douglas D. Gunzler, Adam Perzynski, Nathan Morris, Robert Bermel, Steven Lewis & Deborah Miller), published in Volume 38:2, pages 237–250, have come to learn of a registered copyright of the Performance Scales . See Performance Scales, Copyright Registration Number/Date: TXu000743629/1996-0404; assigned to DeltaQuest Foundation, Inc., effective October 1, 2005. U.S. Copyright law governs terms of use. The authors failed to report that Performance Scales is a copyrighted work and is owned by DeltaQuest Foundation. The Performance Scales is a copyrighted work of DeltaQuest Foundation, Inc. that can only be used, amended, adapted, translated, made into a derivative work or published with the explicit permission of and license from DeltaQuest Foundation, Inc. Further, the ‘‘Performance Scales (PS)’’ has been incorrectly referred to as the ‘‘performance scales’’ or ‘‘MS-related fatigue, cognitive, mobility and hand function domains with six ordinal responses’’ throughout the paper. Additionally, the article referenced the original validation paper second rather than first, leading to some confusion as to the authorship of the original validation study which should be Schwartz, C.E., Vollmer, T., and Lee, H. (1999), Reliability and validity of two self-report measures of impairment and disability for MS. Neurology, 52, 63–70, and of the copyrighted work. To address the issue, we are providing this erratum and wish to express our regret for the oversight that resulted in these errors. The online version of the original article can be found under doi:10. 1007/s10865-014-9574-5.

/pdf/erratum-to-disentangling-multiple-sclerosis-and-depression-2xa49f470x.pdf

Erratum to: Disentangling Multiple Sclerosis and depression: an adjusted depression screening score for patient-centered care (J Behav Med, (2015), 38, (237–250), 10.1007/s10865-014-9574-5)

Structural Equation Modeling with Longitudinal Data

Model Identifiability and Equivalence

Measurement Models for Patient-Reported Outcomes and Other Health-Related Outcomes

<h3>Objective:</h3> To conduct the first genome-wide association study (GWAS) of pain in persons with Parkinson’s disease (PWP). <h3>Background:</h3> Pain is a common and complex non-motor symptom experienced by ~60% of PWP. Little is known about the genetic and non-genetic determinants of pain in PWP. <h3>Design/Methods:</h3> Using data spanning ~4.5 years from 8,612 PWP who are early in their disease course (&lt;3 years), and available through the Fox Insight Data Exploration Network, we empirically discerned 5 subgroups of PWP with similar longitudinal patterns of pain using latent class growth analysis. 4,411 PWP were also genotyped across two customized Illumina platforms that had significant overlap. Quality control criteria (minor allele frequency &lt;1%, Hardy Weinberg Equilibrium p&lt;5×10<sup>−5</sup>) were imposed prior imputation using the TOPMed reference panel. After post-imputation quality control (same as above + imputation R<sup>2</sup>&gt;70%), there were 7.7×10<sup>6</sup> genetic variants. We retained 4,159 PWP who self-identified as White and who genetically clustered with other European samples. For this analysis, we focused on a GWAS of the most severe pain subgroup (N=97) to the least impaired subgroup (N=934). Gene-based and pathway enrichment analyses were also conducted. <h3>Results:</h3> For the GWAS of extreme pain phenotypes, top genic SNP association were <i>MAPK8</i>-rs72794357 (OR=4.6; p=1×10<sup>−6</sup>) and <i>VLDLR-</i>rs4741753 (OR=2.2; p=1.5×10<sup>−6</sup>) and top gene-based results included <i>CTNNB1</i> (p=3.5×10<sup>−5</sup>) and <i>KLK7</i> (p=7.7×10<sup>−5</sup>). These results are intriguing since <i>MAPK8</i> is involved in opioid receptor pathways, <i>VLDLR</i> is a ApoE receptor involved in brain development through Reelin signaling, <i>CTNNB1</i> promotes neurogenesis and de novo mutations have been associated with polyneuropathy in lower limbs, and <i>KLK7</i> is an astrocyte-derived amyloid-β degrading enzyme. Overall there was an enrichment of genes associated with oxytocin signaling (p=0.14), opioid signaling (p=0.045), and Wnt signaling pathway (p=0.021). <h3>Conclusions:</h3> The findings are consistent with known neuropathic mechanisms, thus therapeutic targets for these mechanisms may be relevant for PWP. <b>Disclosure:</b> The institution of Miss Liu has received research support from NIH/NIGMS. The institution of Miss Liu has received research support from Diana Jacobs Kalman/AFAR Scholarships for Research in the Biology of Aging The Program. The institution of Miss Liu has received research support from Michael J. Fox Foundation. Doug Gunzler has nothing to disclose. Dr. Gunzler has received research support from NIH/NINDS. The institution of Dr. Gunzler has received research support from Biogen. The institution of Dr. Gunzler has received research support from Amneal. Dr. Gunzler has received research support from Michael J Fox Foundation. Dr. Crawford has received personal compensation in the range of $5,000-$9,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Frontiers in Genetics. The institution of Dr. Crawford has received research support from NIH/NIDDK. The institution of Dr. Crawford has received research support from NIH/NCATS. The institution of Dr. Crawford has received research support from VA. The institution of Dr. Crawford has received research support from NIH/NIGMS. The institution of Dr. Crawford has received research support from NHGRI. The institution of Dr. Crawford has received research support from NIH/NIA. Dr. Crawford has received personal compensation in the range of $500-$4,999 for serving as a Member with NIH Study Section. The institution of Prof. Briggs has received research support from NIH. The institution of Prof. Briggs has received research support from Michael J. Fox Foundation. 

Data-Driven Genome-Wide Association Study of Pain Trajectories in Persons with Parkinson’s Disease (P7-11.012)

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Douglas D. Gunzler

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