Congenital anomalies of the kidneys and urinary tract (CAKUT) are developmental disorders that commonly cause pediatric chronic kidney disease and mortality. We examine here rare coding variants in 248 CAKUT trios and 1742 singleton CAKUT cases and compare them to 22,258 controls. Diagnostic and candidate diagnostic variants are detected in 14.1% of cases. We find a significant enrichment of rare damaging variants in constrained genes expressed during kidney development and in genes associated with other developmental disorders, suggesting phenotype expansion. Consistent with these data, 18% of CAKUT patients with diagnostic variants have neurodevelopmental or cardiac phenotypes. We identify 40 candidate genes, including CELSR1, SSBP2, XPO1, NR6A1, and ARID3A. Two are confirmed as CAKUT genes: ARID3A and NR6A1. This study suggests that many yet-unidentified syndromes would be discoverable with larger cohorts and cross-phenotype analysis, leading to clarification of the genetic and phenotypic spectrum of developmental disorders.

BACKGROUND:Generative artificial intelligence (AI) tools may soon be integrated into health care practice and research. Nurses in leadership roles, many of whom are doctorally prepared, will need to determine whether and how to integrate them in a safe and useful way. OBJECTIVE:This study aimed to develop and evaluate a brief intervention to increase PhD nursing students' knowledge of appropriate applications for using generative AI tools in health care. METHODS:We created didactic lectures and laboratory-based activities to introduce generative AI to students enrolled in a nursing PhD data science and visualization course. Students were provided with a subscription to Chat Generative Pretrained Transformer (ChatGPT) 4.0, a general-purpose generative AI tool, for use in and outside the class. During the didactic portion, we described generative AI and its current and potential future applications in health care, including examples of appropriate and inappropriate applications. In the laboratory sessions, students were given three tasks representing different use cases of generative AI in health care practice and research (clinical decision support, patient decision support, and scientific communication) and asked to engage with ChatGPT on each. Students (n = 10) independently wrote a brief reflection for each task evaluating safety (accuracy, hallucinations) and usability (ease of use, usefulness, and intention to use in the future). Reflections were analyzed using directed content analysis. RESULTS:Students were able to identify the strengths and limitations of ChatGPT in completing all three tasks and developed opinions on whether they would feel comfortable using ChatGPT for similar tasks in the future. All of them reported increasing their self-rated competency in generative AI by one to two points on a five-point rating scale. CONCLUSION:This brief educational intervention supported doctoral nursing students in understanding the appropriate uses of ChatGPT, which may support their ability to appraise and use these tools in their future work.

Kidney anomalies (KA) are developmental disorders that commonly cause pediatric chronic kidney disease and mortality. We examined rare coding variants in 248 KA trios and 1,742 singleton KA cases and compared them to 22,258 controls. Diagnostic and candidate diagnostic variants were detected in 14.1% of cases. We detected a significant enrichment of rare damaging variants in constrained genes expressed during kidney development and in genes associated with other developmental disorders, suggesting phenotype expansion. Consistent with these data, 18% of KA patients with diagnostic variants had neurodevelopmental or cardiac phenotypes. Extrarenal developmental phenotypes were associated with a higher burden of rare variants. Statistical analyses identified 40 novel candidate genes, 2 of which were confirmed as new KA genes: ARID3A and NR6A1. This study suggests that many yet-unidentified syndromes would be discoverable with larger cohorts and cross-phenotype analysis, leading to clarification the genetic and phenotypic spectrum of developmental disorders. ### Competing Interest Statement A.G. Gharavi receives a research grant from Natera and has served on advisory boards for Natera through a service agreement with Columbia University. A.G. Gharavi has served on advisory boards for Actio Biosciences, Alnylam, Novartis, Calliditas and Travere and has stock options for Actio Biosciences. H.M. Rasouly reports Research Funding: Natera. ### Funding Statement This study was funded by: HMR: the Donald E Wesson Research Fellowship from the ASN Foundation for Kidney Research Three NDDK grants AGG: Genetics of Human Renal HypoDysplasia 5R01DK080099-13 AGG: George M OBrien Center 5U54DK104309-10 HMR: Advancing equitable implementation of genomic medicine in nephrology 5K01DK132495-02 The DDD study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003) This study makes use of DECIPHER funded by Wellcome (grant number WT223718/Z/21/Z) ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: the Institutional Review Board of Columbia University Medical Center, as well as other relevant Ethics Review Boards at collaborating institutions gave ethical approval for this work I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes All data produced in the present study are available upon reasonable request to the authors

Given the evolving importance of data science approaches in nursing research, we developed a 3-credit, 15-week course that is integrated into the second year PhD curriculum at Columbia University School of Nursing. As a complement to didactic content, the students address a research question of their choice using a big data source, Jupyter Notebook, and R programming language. The course evolved over time with generative AI tools being added in 2023. Student self-evaluations of their data science competencies improved from baseline. This case study adds to the evolving body of literature on data science and AI competences in nursing.

BackgroundSurvey-driven research is a reliable method for large-scale data collection. Investigators incorporating mixed-mode survey designs report benefits for survey research including greater engagement, improved survey access, and higher response rate. Mix-mode survey designs combine 2 or more modes for data collection including web, phone, face-to-face, and mail. Types of mixed-mode survey designs include simultaneous (ie, concurrent), sequential, delayed concurrent, and adaptive. This paper describes a research protocol using mixed-mode survey designs to explore health IT (HIT) maturity and care environments reported by administrators and nurse practitioners (NPs), respectively, in US nursing homes (NHs). ObjectiveThe aim of this study is to describe a research protocol using mixed-mode survey designs in research using 2 survey tools to explore HIT maturity and NP care environments in US NHs. MethodsWe are conducting a national survey of 1400 NH administrators and NPs. Two data sets (ie, Care Compare and IQVIA) were used to identify eligible facilities at random. The protocol incorporates 2 surveys to explore how HIT maturity (survey 1 collected by administrators) impacts care environments where NPs work (survey 2 collected by NPs). Higher HIT maturity collected by administrators indicates greater IT capabilities, use, and integration in resident care, clinical support, and administrative activities. The NP care environment survey measures relationships, independent practice, resource availability, and visibility. The research team conducted 3 iterative focus groups, including 14 clinicians (NP and NH experts) and recruiters from 2 national survey teams experienced with these populations to achieve consensus on which mixed-mode designs to use. During focus groups we identified the pros and cons of using mixed-mode designs in these settings. We determined that 2 mixed-mode designs with regular follow-up calls (Delayed Concurrent Mode and Sequential Mode) is effective for recruiting NH administrators while a concurrent mixed-mode design is best to recruit NPs. ResultsParticipant recruitment for the project began in June 2023. As of April 22, 2024, a total of 98 HIT maturity surveys and 81 NP surveys have been returned. Recruitment of NH administrators and NPs is anticipated through July 2025. About 71% of the HIT maturity surveys have been submitted using the electronic link and 23% were submitted after a QR code was sent to the administrator. Approximately 95% of the NP surveys were returned with electronic survey links. ConclusionsPros of mixed-mode designs for NH research identified by the team were that delayed concurrent, concurrent, and sequential mixed-mode methods of delivering surveys to potential participants save on recruitment time compared to single mode delivery methods. One disadvantage of single-mode strategies is decreased versatility and adaptability to different organizational capabilities (eg, access to email and firewalls), which could reduce response rates. International Registered Report Identifier (IRRID)DERR1-10.2196/56170

Objective We aimed to evaluate the feasibility of using ChatGPT as programming support for nursing PhD students conducting analyses using the All of Us Researcher Workbench.Materials and Methods 9 students in a PhD-level nursing course were prospectively randomized into 2 groups who used ChatGPT for programming support on alternating assignments in the workbench. Students reported completion time, confidence, and qualitative reflections on barriers, resources used, and the learning process.Results The median completion time was shorter for novices and certain assignments using ChatGPT. In qualitative reflections, students reported ChatGPT helped generate and troubleshoot code and facilitated learning but was occasionally inaccurate.Discussion ChatGPT provided cognitive scaffolding that enabled students to move toward complex programming tasks using the All of Us Researcher Workbench but should be used in combination with other resources.Conclusion Our findings support the feasibility of using ChatGPT to help PhD nursing students use the All of Us Researcher Workbench to pursue novel research directions.

BACKGROUND:Studies have documented AKI with high-grade proteinuria in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In some patients, biopsies have revealed collapsing glomerulopathy, a distinct form of glomerular injury that has been associated with other viruses, including HIV. Previous patient reports have described patients of African ancestry who developed nephrotic-range proteinuria and AKI early in the course of disease.METHODS:In this patient series, we identified six patients with coronavirus disease 2019 (COVID-19), AKI, and nephrotic-range proteinuria. COVID-19 was diagnosed by a positive nasopharyngeal swab RT-PCR for SARS-CoV-2 infection. We examined biopsy specimens from one transplanted kidney and five native kidneys. Three of the six patients underwent genetic analysis of APOL1, the gene encoding the APOL1 protein, from DNA extracted from peripheral blood. In addition, we purified genomic DNA from paraffin-embedded tissue and performed APOL1 genotype analysis of one of the native biopsies and the donor kidney graft.RESULTS:All six patients were of recent African ancestry. They developed COVID-19-associated AKI with podocytopathy, collapsing glomerulopathy, or both. Patients exhibited generally mild respiratory symptoms, and no patient required ventilator support. Genetic testing performed in three patients confirmed high-risk APOL1 genotypes. One APOL1 high-risk patient developed collapsing glomerulopathy in the engrafted kidney, which was transplanted from a donor who carried a low-risk APOL1 genotype; this contradicts current models of APOL1-mediated kidney injury, and suggests that intrinsic renal expression of APOL1 may not be the driver of nephrotoxicity and specifically, of podocyte injury.CONCLUSIONS:Glomerular disease presenting as proteinuria with or without AKI is an important presentation of COVID-19 infection and may be associated with a high-risk APOL1 genotype.

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Individuals with Down syndrome (DS) overexpress many genes on chromosome 21 due to trisomy and have high risk of dementia due to the Alzheimer's disease (AD) neuropathology. However, there is a wide range of phenotypic differences (e.g., age at onset of AD, amyloid β levels) among adults with DS, suggesting the importance of factors that modify risk within this particularly vulnerable population, including genotypic variability. Previous genetic studies in the general population have identified multiple genes that are associated with AD. This study examined the contribution of polymorphisms in these genes to the risk of AD in adults with DS ranging from 30 to 78 years of age at study entry (N = 320). We used multiple logistic regressions to estimate the likelihood of AD using single-nucleotide polymorphisms (SNPs) in candidate genes, adjusting for age, sex, race/ethnicity, level of intellectual disability and APOE genotype. This study identified multiple SNPs in APP and CST3 that were associated with AD at a gene-wise level empirical p-value of 0.05, with odds ratios in the range of 1.5-2. SNPs in MARK4 were marginally associated with AD. CST3 and MARK4 may contribute to our understanding of potential mechanisms where CST3 may contribute to the amyloid pathway by inhibiting plaque formation, and MARK4 may contribute to the regulation of the transition between stable and dynamic microtubules.

Individuals with Down syndrome (DS) overexpress many genes on chromosome 21 due to trisomy and have high risk of dementia due to the Alzheimer's disease (AD) neuropathology. However, there is a wide range of phenotypic differences (e.g., age at onset of AD, amyloid beta- levels) among adults with DS, suggesting the importance of factors that modify risk within this particularly vulnerable population, including genotypic variability. Previous genetic studies in the general population have identified multiple genes that are associated with AD. This study examined the contribution of polymorphisms in these genes to the risk of AD in adults with DS ranging from 30 to 78 years of age at study entry (N = 320). We used multiple logistic regressions to estimate the likelihood of AD using single-nucleotide polymorphisms (SNPs) in candidate genes, adjusting for age, sex, race/ ethnicity, level of intellectual disability and APOE genotype. This study identified multiple SNPs in APP and CST3 that were associated with AD at a gene-wise level empirical p-value of 0.05, with odds ratios in the range of 1.5-2. SNPs in MARK4 were marginally associated with AD. CST3 and MARK4 may contribute to our understanding of potential mechanisms where CST3 may contribute to the amyloid pathway by inhibiting plaque formation, and MARK4 may contribute to the regulation of the transition between stable and dynamic microtubules. (C) 2017 Elsevier Inc. All rights reserved.

Essential tremor (ET) is one of the most common causes of tremor in humans. Despite its high heritability and prevalence, few susceptibility genes for ET have been identified. To identify ET genes, whole-exome sequencing was performed in 37 early-onset ET families with an autosomal-dominant inheritance pattern. We identified candidate genes for follow-up functional studies in five ET families. In two independent families, we identified variants predicted to affect function in the nitric oxide (NO) synthase 3 gene (NOS3) that cosegregated with disease. NOS3 is highly expressed in the central nervous system (including cerebellum), neurons and endothelial cells, and is one of three enzymes that converts L-arginine to the neurotransmitter NO. In one family, a heterozygous variant, c.46G>A (p.(Gly16Ser)), in NOS3, was identified in three affected ET cases and was absent in an unaffected family member; and in a second family, a heterozygous variant, c.164C>T (p.(Pro55Leu)), was identified in three affected ET cases (dizygotic twins and their mother). Both variants result in amino-acid substitutions of highly conserved amino-acid residues that are predicted to be deleterious and damaging by in silico analysis. In three independent families, variants predicted to affect function were also identified in other genes, including KCNS2 (KV9.2), HAPLN4 (BRAL2) and USP46. These genes are highly expressed in the cerebellum and Purkinje cells, and influence function of the gamma-amino butyric acid (GABA)-ergic system. This is in concordance with recent evidence that the pathophysiological process in ET involves cerebellar dysfunction and possibly cerebellar degeneration with a reduction in Purkinje cells, and a decrease in GABA-ergic tone.

We examined the contribution of candidates genes for Alzheimer's disease (AD) to individual differences in levels of beta amyloid peptides in adults with Down syndrom, a population at high risk for AD. Participants were 254 non-demented adults with Down syndrome, 30-78 years of age. Genomic deoxyribonucleic acid was genotyped using an Illumina GoldenGate custom array. We used linear regression to examine differences in levels of Ab peptides associated with the number of risk alleles, adjusting for age, sex, level of intellectual disability, race and/or ethnicity, and the presence of the APOE epsilon 4 allele. For A beta 42 levels, the strongest gene-wise association was found for a single nucleotide polymorphism (SNP) on CAHLM1; for A beta 40 levels, the strongest gene-wise associations were found for SNPs in IDE and SOD1, while the strongest gene-wise associations with levels of the A beta 42/A beta 40 ratio were found for SNPs in SORCS1. Broadly classified, variants in these genes may influence amyloid precursor protein processing (CALHM1, IDE), vesicular trafficking (SORCS1), and response to oxidative stress (SOD1). (C) 2015 Elsevier Inc. All rights reserved.

Beta amyloid peptides, Aβ40 and Aβ42, are the major species generated by cleavage of the amyloid precursor protein (APP), located on chromosome 21, and play a critical role in the development of Alzheimer's disease (AD). However, there are large individual differences in Aβ peptide levels, and a wide range of age at onset of dementia. We and others have found that high initial levels and subsequent declines in plasma Aβ42 and the Aβ42/Aβ40 ratio are associated with increased risk for AD. Participants were 192 adults with Down syndrome, 40-78 years of age, nondemented at baseline and followed at 18 month intervals for a mean of 4.3 years. Change in Aβ was calculated as the difference between the Aβ level from the first to last assessment. We classified Aβ peptide change into 3 groups based on 0.5 standard deviations of change: 1) no change (+/- 0.5 SD); 2) increasing (> + 0.5 S.D); and 3) decreasing (> - 0.5 SD). We analyzed variants in 43 candidate genes on chromosome 21 and on other chromosomes that have been implicated in AD pathogenesis. Genomic DNA was genotyped using an Illumina GoldenGate custom array. Clustering and genotype calling of SNPs on chromosome 21 was performed using the GenomeStudio genotyping module v1.8 which supports polyploidy loci. We used logistic regression to examine the relation between the number of risk alleles and change group, adjusting for age, sex, level of intellectual disability and the presence of the APOEε4 allele. Mean age of the participants was 50.8 +/- 5.5 years. For decreasing Aβ42 levels, the strongest associations were found for SNPs on CD2AP and GAB2. For decreasing Aβ40 levels, the strongest association was found for a SNP on RUNX1. For decreasing Aβ42/Aβ40 levels the strongest association was found for a SNP on APOC1. Broadly classified, variants in these genes may influence neuritic plaque burden (CD2AP), interactions with APOE (GAB2, APOC1), and neurodevelopmental processes and leukocyte differentiation (RUNX1). AD associated variants influence change in Aβ peptides and can provide insight into pathways active in the pathogenesis of AD in adults with DS.

ObjectiveVariants in GBA are associated with Lewy Body (LB) pathology. We investigated whether variants in other lysosomal storage disorder (LSD) genes also contribute to disease pathogenesis.MethodsWe performed a genetic analysis of four LSD genes including GBA, HEXA, SMPD1, and MCOLN1 in 231 brain autopsies. Brain autopsies included neuropathologically defined LBD without Alzheimer Disease (AD) changes (n = 59), AD without significant LB pathology (n = 71), Alzheimer disease and lewy body variant (ADLBV) (n = 68), and control brains without LB or AD neuropathology (n = 33). Sequencing of HEXA, SMPD1, MCOLN1 and GBA followed by 'gene wise' genetic association analysis was performed. To determine the functional effect, a biochemical analysis of GBA in a subset of brains was also performed. GCase activity was measured in a subset of brain samples (n = 64) that included LBD brains, with or without GBA mutations, and control brains. A lipidomic analysis was also performed in brain autopsies (n = 67) which included LBD (n = 34), ADLBV (n = 3), AD (n = 4), PD (n = 9) and control brains (n = 17), comparing GBA mutation carriers to non-carriers.ResultsIn a 'gene-wise' analysis, variants in GBA, SMPD1 and MCOLN1 were significantly associated with LB pathology (p range: 0.03-4.14 x 10(-5)). Overall, the mean levels of GCase activity were significantly lower in GBA mutation carriers compared to non-carriers (p<0.001). A significant increase and accumulation of several species for the lipid classes, ceramides and sphingolipids, was observed in LBD brains carrying GBA mutations compared to controls (p range: p<0.05-p<0.01).InterpretationOur study indicates that variants in GBA, SMPD1 and MCOLN1 are associated with LB pathology. Biochemical data comparing GBA mutation carrier to non-carriers support these findings, which have important implications for biomarker development and therapeutic strategies.

To date, only one genome-wide study has assessed the contribution of CNVs to Parkinson's Disease (PD). We conducted a genome-wide scan for CNVs in a case-control dataset of Ashkenazi Jewish (AJ) origin (268 PD cases and 178 controls). Using high-confidence CNVs, we examined the global genome wide burden of large (≥100Kb) and rare (≤1% in the dataset) CNVs between cases and controls. A total of 986 such CNVs were observed in our dataset of 432 subjects. Overall global burden analyses did not reveal significant differences between cases and controls in CNV rate, distribution of deletions or duplications or number of genes affected by CNVs. Overall deletions (total CNV size and >2x frequency) were found 1.4 times more often in cases than in controls (p=0.019). The large CNVs (>500kb) were also significantly associated with PD (p=0.046, 1.24-folder higher in cases than in controls). Global burden was elevated for rare CNV regions. Specifically, for OVOS2 on Chr12p11.21, CNVs were observed only in PD cases (n=7) but not in controls (p=0.028) and this was experimentally validated. A total of 81 PD cases carried a rare genic CNV that was absent in controls. Ingenuity pathway analysis (IPA) identified ATXN3, FBXW7, CHCHD3, HSF1, KLC1 and MBD3 in the same disease pathway with known PD genes.

PCDH10 is epigenetically inactivated in multiple tumor types; however, studies in mature lymphoid malignancies are limited. Here, we have investigated the presence of promoter hypermethylation of the PCDH10 gene in a large cohort of well‐characterized subsets of lymphomas. PCDH10 promoter hypermethylation was identified by methylation‐specific PCR in 57 to 100% of both primary B‐ and T‐cell lymphoma specimens and cell lines. These findings were further validated by Sequenom Mass‐array analysis. Promoter hypermethylation was also identified in 28.6% cases of reactive follicular hyperplasia, more commonly occurring in states of immune deregulation and associated with rare presence of clonal karyotypic aberrations, suggesting that PCDH10 methylation occurs early in lymphomagenesis. PCDH10 expression was down regulated via promoter hypermethylation in T‐ and B‐cell lymphoma cell lines. The transcriptional down‐regulation resulting from PCDH10 methylation could be restored by pharmacologic inhibition of DNA methyltransferases in cell lines. Both T‐ and B‐cell lymphoma cell lines harboring methylation‐mediated inactivation of PCDH10 were resistant to doxorubicin treatment, suggesting that hypermethylation of this gene might contribute to chemotherapy response. © 2013 Wiley Periodicals, Inc.

Background Fetal hemoglobin level is a heritable complex trait that strongly correlates swith the clinical severity of sickle cell disease. Only few genetic loci have been identified as robustly associated with fetal hemoglobin in patients with sickle cell disease, primarily adults. The sole approved pharmacologic therapy for this disease is hydroxyurea, with effects largely attributable to induction of fetal hemoglobin. Methodology/Principal Findings In a multi-site observational analysis of children with sickle cell disease, candidate single nucleotide polymorphisms associated with baseline fetal hemoglobin levels in adult sickle cell disease were examined in children at baseline and induced by hydroxyurea therapy. For baseline levels, single marker analysis demonstrated significant association with BCL11A and the beta and epsilon globin loci (HBB and HBE, respectively), with an additive attributable variance from these loci of 23%. Among a subset of children on hydroxyurea, baseline fetal hemoglobin levels explained 33% of the variance in induced levels. The variant in HBE accounted for an additional 13% of the variance in induced levels, while variants in the HBB and BCL11A loci did not contribute beyond baseline levels. Conclusions/Significance These findings clarify the overlap between baseline and hydroxyurea-induced fetal hemoglobin levels in pediatric disease. Studies assessing influences of specific sequence variants in these and other genetic loci in larger populations and in unusual hydroxyurea responders are needed to further understand the maintenance and therapeutic induction of fetal hemoglobin in pediatric sickle cell disease.

Objective: We describe all Juvenile Parkinson9s Disease (JPD) probands who were recruited through the CORE-PD study. Background JPD is exceptionally rare, seldom reported, and defined as disease age at onset (AAO) Design/Methods: Eleven hundred and three individuals with early-onset PD (defined as AAO SNCA , PRKN , PINK1 , DJ1 , LRRK2 and GBA . Results: Twenty probands (1.8%) reported AAO PRKN carriers, two were PRKN heterozygotes, two carried heterozygous GBA mutations (one L444P and one N370S) and one carried the LRRK2 G2019S mutation. Only four (20%) reported a family history of PD in a first degree relative, all of whom carried PRKN mutations (two compound heterozygotes and two heterozygotes). Of these four probands, two had a family history of JPD in siblings (one heterozygote with AAO=16 and one compound heterozygote with AAO=12), each with a similar genotype to proband. None of the 66 PRKN mutation carriers with disease onset>20 had a sibling with JPD. Conclusions: JPD is extremely rare among EOPD. While identifiable genetic risk factors are common, first degree family history of PD is present in a minority. Supported by: Funded by NIH NS36630, UL1 RR024156 (K.S.M.), NS050487, NS060113 (L.N.C.), the Parkinson9s Disease Foundation (K.S.M., S.F., and L.N.C.), P50 NS039764 (W.K.S) and NS36960 (H.P). RNA is a Brookdale Foundation Leadership in Aging Fellow. Disclosure: Dr. Alcalay has nothing to disclose. Dr. Rosado has nothing to disclose. Dr. Mejia-Santana has nothing to disclose. Dr. Orbe-Reilly has nothing to disclose. Dr. Caccappolo has nothing to disclose. Dr. Tang has nothing to disclose. Dr. Ruiz has nothing to disclose. Dr. Ross has nothing to disclose. Dr. Verbitsky has nothing to disclose. Dr. Kisselev has nothing to disclose. Dr. Louis has nothing to disclose. Dr. Comella has received personal compensation for activities with Ipsen, Merz Pharma, Allergan, Inc., and NuPathe. Dr. Comella has received research support from Ipsen, Merz Pharma, Allergan, Inc., the National Institutes of Health, and the Dystonia Study Group. Dr. Colcher has nothing to disclose. Dr. Jennings has received personal compensation for activities with Lundbeck Research USA as a speaker. Dr. Nance has received research support from Medivation, Santhera, Juvantia, Neurosearch Sweden, Pfizer Inc, Neuraltus, Impax, and Schwarz Biosciences. Dr. Bressman has received license fee payments from Beth Israel/Mount Sinai/Athena. Dr. Scott has nothing to disclose. Dr. Tanner has received personal compensation for activities with Impax Pharmaceuticals, Allergan, Inc. & Genentech, Inc. as a consultant. Dr. Tanner has received research support from Michael J. Fox Foundation, Department of Defense, Parkinson9s Disease Foundation, Parkinson9s Institute, Unity Walk and Brin Foundation. Dr. Andrews has nothing to disclose. Dr. Waters has received personal compensation for activities with Boehringer Ingelheim Pharmaceuticals, Inc., Novartis, and Teva Neuroscience as a speaker. Dr. Fahn has received personal compensation for activities with Intec Pharma, Merz Pharma, Oxford Biomedica, RJG Foundation, IMPAX Pharmaceuticals, and Lundbeck as a consultant. Dr. Fahn has received personal compensation in an editorial capacity for Elsevier and Springer. Dr. Cote has nothing to disclose. Dr. Frucht has received personal compensation for activities with UCB Pharma. Dr. Ford has received personal compensation for activities with Novartis and Medtronic, Inc. Dr. Rezak has received personal compensation for activities with Medtronic, Teva, Novartis, Allergan, Smih-Klein, Boehringer-Ingleheim, and UBC as a speaker. Dr. Novak has nothing to disclose. Dr. Friedman has received personal compensation for activities with Teva Neuroscience, Boehringer Ingelheim Pharmaceuticals, Inc., Genzyme Corporation, Adix, Roche Diagnostics Corporation. Dr. Friedman has received research support from Teva Neuroscience, Merck & Co., Inc., EMD Serono, Schering-Plough Corporation, National Institutes of Health, Michael J. Fox Foundation, GE Healthcare and Acadia. Dr. Pfeiffer has received personal compensation for activities with UCB Pharmaceuticals, Teva Neurosciences, Novartis, Glaxo-Smith-Kline, and Boehringer Ingelheim.Dr. Pfeiffer has received personal compensation in an editorial capacity for Parkinsonism and Related Disorders.Dr. Pfeiffer has received (royalty or license fee or contractual rights) payments from Butterworth Heinemann, Elsevier, CRC Press, Taylor & Francis, and Humana Press.Dr. Pfeiffer has received research support from Boehringer Ingelheim, UCB Pharmaceuticals, and Schwarz Biosciences. Dr. Marsh has received research support from Eli Lilly & Company, Forest Pharmaceuticals, Acadia, Ovation, and National Institutes of Health. Dr. Hiner has received personal compensation for activities with Teva Neuroscience. Dr. Siderowf has received personal compensation for activities with Teva Neuroscience, Supernus Pharmaceuticals, Schering-Plough, and Merck Serono. Dr. Siderowf has received research support from the NINDS, the Department of Health of the Commonwealth of Pennsylvania, and Avid Radiopharmaceuticals. Dr. Payami has nothing to disclose. Dr. Molho has received personal compensation for activities with Allergan, Teva, Merz, Ipsen, and Boehringer Ingelheim. Dr. Molho has received research support from Teva, Allergan, Merz, IPsen, Parkinson9s Study Group, and Huntington9s Study Group. Dr. Nutt has received personal compensation for activities with XenPort, Impax Laboratories, Neurogen, Synosia, Neuroderm, Merck, Lily/Medtronic, Elan Pharmaceuticals, Lundbeck, Merz Pharmaceuticals, Synagile, and the National Parkinson Foundation. Dr. Nutt has received research support from Merck. Dr. Factor has received personal compensation for activities with Merz and Ipsen as a consultant. Dr. Factor has received personal compensation in an editorial capacity for Current Neurology and Neuroscience. Dr. Factor has received research support from Ceregene, Teva Neuroscience, Ipsen, and EMD Serono. Dr. Ottman has received personal compensation for activities with Ortho-McNeil Janssen Scientific Affairs, LLC. Dr. Clark has nothing to disclose. Dr. Marder has received personal compensation in an editorial capacity for Current Neuroscience. Dr. Marder has received research support from the NIH, Michael J. Fox Parkinson Disease Foundation, CHDI, and the Huntington9s Disease Society of America.