bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neurochemical alterations in spinocerebellar ataxia type 1 and their correlations with clinical status
Authors: Öz Gülin , Hutter Diane , Tkáč Ivan , Clark H. Brent , Gross Myron D. , Jiang Hong , Eberly Lynn E. , Bushara Khalaf O. , Gomez Christopher M. 
Published: March 2010

AbstractRobust biomarkers of neurodegeneration are critical for testing of neuroprotective therapies. The clinical applicability of such biomarkers requires sufficient sensitivity to detect disease in individuals. Here we tested the sensitivity of high field (4 tesla) proton magnetic resonance spectroscopy (1H MRS) to neurochemical alterations in the cerebellum and brainstem in spinocerebellar ataxia type 1 (SCA1). We measured neurochemical profiles that consisted of 10 to 15 metabolite concentrations in the vermis, cerebellar hemispheres and pons of patients with SCA1 (N = 9) and healthy controls (N = 15). Total NAA (N‐acetylaspartate + N‐acetylaspartylglutamate, tNAA) and glutamate were lower and glutamine, myo‐inositol and total creatine (creatine + phosphocreatine, tCr) were higher in patients relative to controls, consistent with neuronal dysfunction/loss, gliotic activity, and alterations in glutamate–glutamine cycling and energy metabolism. Changes in tNAA, tCr, myo‐inositol, and glutamate levels were discernible in individual spectra and the tNAA/myo‐inositol ratio in the cerebellar hemipheres and pons differentiated the patients from controls with 100% specificity and sensitivity. In addition, tNAA, myo‐inositol, and glutamate levels in the cerebellar hemispheres and the tNAA and myo‐inositol levels in the pons correlated with ataxia scores (Scale for the Assessment and Rating of Ataxia, SARA). Two other biomarkers measured in the cerebrospinal fluid (CSF) of a subset of the volunteers (F2‐isoprostanes asa marker of oxidative stress and glial fibrillary acidic protein (GFAP) as a marker of gliosis) were not different between patients and controls. These data demonstrate that 1H MRS biomarkers can be utilized to noninvasively assess neuronal and glial status in individual ataxia patients. © 2010 Movement Disorder Society
Age of Parkinson's disease onset as a predictor for the development of dyskinesia
Authors: Ku Stephen , Glass Graham A. 
Published: March 2010

AbstractThe risk of developing levodopa‐associated dyskinesia is known to vary inversely with the age of Parkinson's disease onset. This study quantifies dyskinesia risks for different Parkinson's onset ages in a patient population treated at the Parkinson's Disease Research, Education, and Clinical Center at the San Francisco Veterans Affairs Medical Center. Medical records were reviewed to determine age of Parkinson's onset, medication history, and dyskinesia onset. Dyskinesia risks were determined by using Kaplan‐Meier analysis. Cox proportional hazard models were used to compare age groups and to perform multivariate modeling. This study included 109 patients with Parkinson's, 105 of whom had onset of symptoms after 1989. At 5 years of levodopa treatment, the dyskinesia risk for patients with onset age 40–49 was 70%, decreasing to 42% for onset ages 50–59, 33% for onset ages 60–69, and 24% for onset ages 70–79. Pairwise comparisons between the 40–49 age group and the other age groups were statistically significant in time‐to‐event models. After 5 years of levodopa treatment, dyskinesia risks became uniformly high regardless of age of onset. These results suggest it is appropriate to use different baseline dyskinesia risks in clinical decision‐making for patients on the basis of their ages of onset. However, the most significant difference occurs between ages 40–49 and ages 50–79, and if more than 5 years of levodopa therapy are anticipated, dyskinesia risk may have less utility when deciding upon Parkinson's therapy. Drug studies for Parkinson's disease should also take age of Parkinson's onset into account when analyzing dyskinesia outcomes. © 2010 Movement Disorder Society
Effect of histamine H2 receptor antagonism on levodopa–induced dyskinesia in the MPTP‐macaque model of Parkinson's disease
Authors: Johnston Tom H. , van der Meij Anne , Brotchie Jonathan M. , Fox Susan H. 
Published: March 2010

AbstractLevodopa‐induced motor complications, including dyskinesia and wearing off, are troublesome side effects of treatment and impair quality of life in Parkinson's disease (PD) patients. The use of nondopaminergic agents as adjuncts to levodopa are potential options for managing these problems. Here, we asses the ability of the clinically available, selective histamine H2 antagonist, famotidine (1, 3, and 30 mg/kg) to treat levodopa‐induced dyskinesia and wearing off in the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐macaque model of PD. Famotidine (3 mg/kg) increased peak activity, enhanced peak anti‐parkinsonian action (1 and 3 mg/kg), and extended duration of action (3 mg/kg, by 38%) of a low dose of levodopa (compared to low dose levodopa alone). Enhancement of anti‐parkinsonian actions of low dose levodopa by famotidine (3 mg/kg) was associated with only mild, nondisabling dystonia. Famotidine had no effect on the anti‐parkinsonian actions of high dose levodopa (compared to high dose levodopa alone). However, famotidine (1, 3, and 30 mg/kg) had a significant effect on chorea, but not dystonia, induced by high dose levodopa (compared to high dose levodopa alone). Famotidine increased high dose levodopa–induced “good quality” on time, i.e., on time not associated with disabling dyskinesia, by up to 28% (compared to high dose levodopa alone). In conclusion, famotidine, a drug currently available for use in the clinic, can enhance the peak‐dose anti‐parkinsonian actions and extend total duration of action of a low dose of levodopa, without producing disabling dyskinesia. Furthermore, in combination with a higher dose of levodopa, famotidine can reduce peak‐dose levodopa‐induced chorea and improve the quality of on‐time. © 2010 Movement Disorder Society
Task force report on scales to assess dyskinesia in Parkinson's disease: Critique and recommendations
Authors: Colosimo Carlo , Martínez‐Martín Pablo , Fabbrini Giovanni , Hauser Robert A. , Merello Marcelo , Miyasaki Janis , Poewe Werner , Sampaio Cristina , Rascol Olivier , Stebbins Glenn T. , Schrag Anette , Goetz Christopher G. 
Published: March 2010

AbstractDrug‐induced dyskinesia is a common phenomenon in Parkinson's disease (PD) and is often socially as well as physically disabling for patients. The Movement Disorders Society commissioned a task force to assess available clinical rating scales, critique their clinimetric properties, and make recommendations regarding their clinical utility. A task force composed six clinical researchers who systematically searched the literature for scales measuring dyskinesia in PD, evaluated the scales' previous use, performance parameters, and quality of validation data (if available). A scale was designated “Recommended” if the scale has been used in clinical studies beyond the group that developed it, has been specifically used in PD reports, and if clinimetric studies have established that it is a valid, reliable, and sensitive. “Suggested” scales met two of the above criteria and those meeting one were “Listed.” Based on the systematic review, eight rating scales for dyskinesia that have either been validated or used in PD were identified. These were the Abnormal Involuntary Movement Scale (AIMS), The Unified Parkinson's Disease Rating Scale (UPDRS) part IV, the Obeso Dyskinesia Rating Scale, the Rush Dyskinesia Rating Scale, the Clinical Dyskinesia Rating Scale (CDRS), the Lang‐Fahn Activities of Daily Living Dyskinesia Scale, the Parkinson Disease Dyskinesia Scale (PDYS‐26), and the Unified Dyskinesia Rating Scale (UDysRS). Based on this review, at present two of the reviewed dyskinesia scales (AIMS and the Rush Dyskinesia Rating Scale) fulfill criteria for Recommended for use in PD populations, albeit weakly so; all of the remaining met criteria to be Suggested. However, the two most recent scales (PDYS‐26 and UDysRS) have excellent clinimetric properties and appear to provide a reliable and valid assessment tool of dyskinesia in PD. If they are used successfully beyond the groups that developed them, both have the potential to be re‐ranked as Recommended. As further testing of these scales in PD is warranted, no new scales are needed until the available scales are fully tested clinimetrically. © 2010 Movement Disorder Society
Association between cognition and function in patients with Parkinson disease with and without dementia
Authors: Rosenthal Emily , Brennan Laura , Xie Sharon , Hurtig Howard , Milber Joshua , Weintraub Daniel , Karlawish Jason , Siderowf Andrew 
Published: March 2010

AbstractPatients with Parkinson's disease (PD) often have cognitive deficits from the time of diagnosis. Except in patients with dementia, the impact of cognitive symptoms on daily function is not well documented. This study had two objectives: (1) to determine the functional significance of cognitive deficits in nondemented patients with PD and (2) to assess the sensitivity of two measures of global cognitive abilities to identify individuals with impaired ADL function. One hundred eleven subjects with PD and a range of cognitive abilities were included. Of these, 20 were diagnosed with PDD. All subjects were assessed with the Mattis Dementia Rating Scale to two (DRS‐2) and the Mini‐Mental State Examination (MMSE). ADL function was reported by an informant using the Alzheimer's Disease Cooperative Study Activities of Daily Living Inventory (ADCS‐ADL). The ability of the DRS‐2 and MMSE to capture the impact of cognitive impairment on ADL function was assessed in the entire cohort and in subsets of nondemented individuals. After adjustment for covariates, cognition as measured by the DRS‐2 was strongly related to ADL function in the entire cohort (partial correlation coefficient = 0.55, P < 0.001). The association remained strong when only nondemented subjects were included (r = 0.42, P < 0.001). The DRS‐2 was significantly more accurate than the MMSE, particularly for detecting milder degrees of ADL impairment (ROC area = 0.87 vs. 0.75, P = 0.0008). Cognition is associated with impairment in ADL function, even in nondemented patients with PD. However, sensitive cognitive assessment measures may be needed to identify these functionally relevant impairments. © 2010 Movement Disorder Society
Depression and the subsequent risk of Parkinson's disease in the NIH‐AARP Diet and Health Study
Authors: Fang Fang , Xu Qun , Park Yikyung , Huang Xuemei , Hollenbeck Albert , Blair Aaron , Schatzkin Arthur , Kamel Freya , Chen Honglei 
Published: March 2010

AbstractWe conducted a case‐control study to examine the association between depression and Parkinson's disease (PD). Participants included 992 PD cases diagnosed after 2,000 and 279,958 individuals without PD from the NIH‐AARP Diet and Health Study follow‐up survey. Physician‐diagnosed depression and PD were self‐reported with information on the year of diagnosis in the following categories: before 1985, 1985–1994, 1995–1999, and 2000–present. Only PD cases diagnosed after 2000 were included in the analysis. Odds ratios (ORs) and 95% confidence intervals (CIs) were derived from logistic regression models, adjusted for age, gender, educational level, marital status, smoking, and coffee drinking. Individuals with depression diagnosed after 2000 were more likely to report a concurrent diagnosis of PD than those without depression (OR = 4.7, 95% CI = 3.9, 5.7). Depression diagnosed before 2000 was also associated with higher odds of PD diagnosed after 2000 (OR = 2.0, 95% CI = 1.6, 2.4). This association was stronger for depression diagnosed in 1995–1999 (OR = 2.7, 95% CI = 2.0, 3.6), but was also noted for depression diagnosed in 1985–1994 (OR = 1.6, 95% CI = 1.1, 2.3) or even before 1985 (OR = 1.7, 95% CI = 1.3, 2.3). This association was not modified by other factors and persisted in an analysis excluding participants who reported poor health status. The results suggest that depression may either be a very early symptom of PD or share common etiological factors with PD. © 2010 Movement Disorder Society
Bladder symptoms assessed with overactive bladder questionnaire in Parkinson's disease
Authors: Iacovelli Elisa , Gilio Francesca , Meco Giuseppe , Fattapposta Francesco , Vanacore Nicola , Brusa Livia , Giacomelli Elena , Gabriele Maria , Rubino Alfonso , Locuratolo Nicoletta , Iani Cesare , Pichiorri Floriana , Colosimo Carlo , Carbone Antonio , Palleschi Giovanni , Inghilleri Maurizio 
Published: March 2010

AbstractIn Parkinson's disease (PD) the urinary dysfunction manifests primarily with symptoms of overactive bladder (OAB). The OAB questionnaire (OAB‐q) is a measure designed to assess the impact of OAB symptoms on health‐related quality of life. In this study, we quantified the urinary symptoms in a large cohort of PD patients by using the OAB‐q short form. Possible correlations between the OAB‐q and clinical features were tested. Three hundred and two PD patients were enrolled in the study. Correlations between the OAB‐q and sex, age, Unified Parkinson's Disease Rating Scale part III (UPDRS‐III), Hoehn‐Yahr (H‐Y) staging, disease duration, and treatment were analyzed. Data were compared with a large cohort of 303 age‐matched healthy subjects. The OAB‐q yielded significantly higher scores in PD patients than in healthy subjects. In the group of PD patients, all the variables tested were similar between men and women. Pearson's coefficient showed a significant correlation between mean age, disease duration, mean OAB‐q scores, UPDRS‐III scores, and H‐Y staging. A multiple linear regression analysis showed that OAB‐q values were significantly influenced by age and UPDRS‐III. No statistical correlations were found between OAB‐q scores and drug therapy or the equivalent levodopa dose, whilst the items relating to the nocturia symptoms were significantly associated with the equivalent levodopa dose. Our findings suggest that bladder dysfunction assessed by OAB‐q mainly correlates with UPDRS‐III scores for severity of motor impairment, possibly reflecting the known role of the decline in nigrostriatal dopaminergic function in bladder dysfunction associated with PD and patients' age. Our study also suggests that the OAB‐q is a simple, easily administered test that can objectively evaluate bladder function in patients with PD. © 2010 Movement Disorder Society
Changes in occurrences of temperature extremes in continental Portugal: a stochastic approach
Authors: Lucio P. S. , Silva A. M. , Serrano A. I. 
Published: March 2010

AbstractIn this paper the tail regions of the air‐surface temperature are modelled explicitly, using the recent developments of extreme value theory. The tails are estimated by fitting a Generalized Pareto Distribution to the observations disregarding certain thresholds (lying beyond) that mark the beginning of the tail regions. There are different approaches to characterize the spatial behaviour of climatological phenomena, and a particularly elegant formulation is derived from the theory of point process governing peaks‐over‐threshold. The aim of this study is to verify whether extreme values related to weather attributes from Continental Portugal (regional scale) show any structural alteration, which can reflect global changes during the last century. For this purpose, daily extremes of air‐surface temperatures, as well as the clustering of extreme temperatures defined by the peaks‐over‐random‐threshold (PORT) methodology, are strongly indicated to detect signals concerning global change. The analysis of meteorologically extreme events in Continental Portugal indicates that there has been a sizable change in their frequency. Even the experimental design, as presented here, does not allow an assessment of the reasons for these changes in frequency of temperature extremes, suggesting that natural variability in the climate system could be the cause of the recent changes, besides anthropogenic forcing due to the increase of greenhouse gas concentrations in the atmosphere. These findings can be linked to studies which have attempted to determine causing mechanisms, analysing large‐scale natural oscillations such as the North Atlantic Oscillation (NAO). Copyright © 2010 Royal Meteorological Society
Race, Ethnicity, Ancestry, and Pharmacogenetics
Authors: Urban Thomas J. 
Published: March 2010

AbstractPharmacogenetics is the study of how genetic variation influences the response to drugs. The concepts of race, ethnicity, and ancestry have long had a strong influence on pharmacogenetic discovery and on our understanding of population‐level differences in drug response. The primary goal of pharmacogenetics, however, is to identify the individual genetic determinants of drug activity so that therapy can be tailored to the individual patient. This article describes the relationship between the concepts of race, ethnicity, and ancestry and how these concepts have been applied to pharmacogenetics, and it provides examples of the benefits and pitfalls associated with the use of racial or ethnic labels in genetic studies. The future of pharmacogenetics, including the study of rare genetic variation and what this means for racial or ethnic disparities in pharmacogenetic discovery, is also discussed. Mt Sinai J Med 77:133–139, 2010. © 2010 Mount Sinai School of Medicine
Genetic and Environmental Contributions to Racial Disparities in Preterm Birth
Authors: Dolan Siobhan M. 
Published: March 2010

AbstractThe preterm birth rate exceeds 12% in the United States, and preterm birth continues to be a clinical and public health challenge globally. Even though preterm birth is a major contributor to infant mortality and lifelong morbidity, there are few effective strategies to predict preterm birth and few clinical interventions to prevent it. Genomic research approaches that identify risk factors at the intersection of genetics and the environment will likely provide insights. Both genetic and environmental factors are known to contribute to the racial disparity seen in preterm birth. Through the identification of relevant gene‐environment interactions that contribute to preterm birth and may underlie the racial disparity in preterm birth, research that will translate to clinical practice and ultimately prevent a number of preterm births is possible. Mt Sinai J Med 77:160–165, 2010. © 2010 Mount Sinai School of Medicine
Is There a Genetic Basis for Health Disparities in Human Immunodeficiency Virus Disease?
Authors: Winkler Cheryl 
Published: March 2010

AbstractThe highest global prevalence rates for human immunodeficiency virus and acquired immune deficiency syndrome have been recorded in southern Africa; in the United States, individuals of African descent are disproportionately affected by human immunodeficiency virus infection. Human immunodeficiency virus–infected individuals with African ancestry are also estimated to have a 17‐fold or greater risk for developing human immunodeficiency virus–associated nephropathy in comparison with their counterparts of non‐African descent. Several recent studies have implicated genetic alleles that are more frequent in populations of African descent and increase the risk of human immunodeficiency virus infection and the risk of human immunodeficiency virus–associated neuropathy (HIVAN). The supposition that persons of African descent are more susceptible to human immunodeficiency virus infection because of an underlying genetic predisposition is not supported by available evidence. However, strong, replicated data show that the increased risk for human immunodeficiency virus–associated nephropathy, as well as other major forms of kidney disease in individuals of African descent, is due in part to MYH9 (myosin, heavy chain 9, non‐muscle) renal disease susceptibility alleles that are very frequent throughout sub‐Saharan Africa but are infrequent or absent in non‐Africans. Selection, drift, and demographic events shape the allelic architecture of the human genome: it is expected that these events will be reflected in geographic‐specific differentiation in allele frequencies for a small subset of alleles that may be associated with either increased or reduced risk for complex and infectious diseases. Mt Sinai J Med 77:149–159, 2010. © 2010 Mount Sinai School of Medicine
Environmental Justice and the Health of Children
Authors: Landrigan Philip J. , Rauh Virginia A. , Galvez Maida P. 
Published: March 2010

AbstractEnvironmental injustice is the inequitable and disproportionately heavy exposure of poor, minority, and disenfranchised populations to toxic chemicals and other environmental hazards. Environmental injustice contributes to disparities in health status across populations of differing ethnicity, race, and socioeconomic status. Infants and children, because of their unique biological vulnerabilities and age‐related patterns of exposure, are especially vulnerable to the health impacts of environmental injustice. These impacts are illustrated by sharp disparities across children of different racial and ethnic backgrounds in the prevalence of 3 common diseases caused in part by environmental factors: asthma, lead poisoning, and obesity. Documentation of linkages between health disparities and environmental injustice is an important step toward achieving environmental justice. Mt Sinai J Med 77:178–187, 2010. © 2010 Mount Sinai School of Medicine
Colonoscopy Versus Computed Tomography Colonography for Colorectal Cancer Screening
Authors: Akhtar Reza , Lee Michelle , Itzkowitz Steven H. 
Published: March 2010

AbstractColorectal cancer is second only to lung cancer as the leading cause of death among North Americans of both sexes. Although screening rates for colorectal cancer in the United States have increased over the past decade, these rates (in the range of 45%−60%) are still lower than the screening rates for breast cancer (approximately 80%). Optical colonoscopy has been recognized as the preferred method for colorectal cancer screening in the United States, but computed tomography colonography has recently been gaining favor. This article compares the 2 methods with respect to both advantages and disadvantages. Mt Sinai J Med 77:214–224, 2010. © 2010 Mount Sinai School of Medicine