Cluster Lenses

Clusters of galaxies are the most recently assembled, massive, bound structures in the Universe. As predicted by General Relativity, given their masses, clusters strongly deform space-time in their vicinity. Clusters act as some of the most powerful gravitational lenses in the Universe. Light rays traversing through clusters from distant sources are hence deflected, and the resulting images of these distant objects therefore appear distorted and magnified. Lensing by clusters occurs in two regimes, each with unique observational signatures. The strong lensing regime is characterized by effects readily seen by eye, namely, the production of giant arcs, multiple-images, and arclets. The weak lensing regime is characterized by small deformations in the shapes of background galaxies only detectable statistically. Cluster lenses have been exploited successfully to address several important current questions in cosmology: (i) the study of the lens(es) - understanding cluster mass distributions and issues pertaining to cluster formation and evolution, as well as constraining the nature of dark matter; (ii) the study of the lensed objects - probing the properties of the background lensed galaxy population - which is statistically at higher redshifts and of lower intrinsic luminosity thus enabling the probing of galaxy formation at the earliest times right up to the Dark Ages; and (iii) the study of the geometry of the Universe - as the strength of lensing depends on the ratios of angular diameter distances between the lens, source and observer, lens deflections are sensitive to the value of cosmological parameters and offer a powerful geometric tool to probe Dark Energy. In this review, we present the basics of cluster lensing and provide a current status report of the field.Comment: About 120 pages - Published in Open Access at: http://www.springerlink.com/content/j183018170485723/ . arXiv admin note: text overlap with arXiv:astro-ph/0504478 and arXiv:1003.3674 by other author

Gender differences in Parkinson\u27s disease

We examined data from 630 patients entered into the University of Kansas Medical Center\u27s Parkinson\u27s Disease (PD) Registry to determine if gender differences exist in terms of both cognitive and motor symptoms of PD. An analysis of the Mini-Mental State Examination scores indicated slightly higher scores for women relative to men. Although women had significantly better scores than did men on the motor section of the Unified Parkinson\u27s Disease Rating Scale (UPDRS), they had a significantly greater prevalence of dyskinesias compared with men. These motor differences were significant only in patients with PD of greater than 5 years duration. There were no gender differences for age of diagnosis, Hoehn and Yahr Staging, Schwab and England Scale, or the mentation and activities of daily living sections of the UPDRS. We conclude that as PD progresses, gender differences emerge, with men exhibiting more severe parkinsonian motor features and women experiencing more levodopa-induced dyskinesia

Differentiation of the Dementias of Alzheimer\u27s and Parkinson\u27s Disease with the Dementia Rating Scale

The Mattis Dementia Rating Scale (DRS) was used to distinguish between 50 dementia of the Alzheimer\u27s type (DAT) and 50 Parkinson\u27s disease (PD) subjects matched for age, education, and DRS total score. Despite a similar level of overall cognitive impairment, the DAT group earned significantly lower scores than did the PD group on the Memory subscale, while the PD group displayed lower scores than did the DAT subjects on the Construction subscale. A jackknifed, stepwise, linear discriminant function using the five DRS subscales revealed that the Memory, Construction, and Initiation subtests significantly distinguished the groups. These results suggest qualitative differences in the dementias of DAT and PD patients and reveal that such differences can emerge on brief mental status examinations. © 1995, SAGE Publications. All rights reserved

Apolipoprotein E genotypes in Parkinson\u27s disease with and without dementia

The apolipoprotein E gene (Apo E) type 4 allele is a genetic risk factor influencing the development and age of onset of Alzheimer\u27s disease. Because Parkinson\u27s disease shares many characteristics of Alzheimer\u27s disease, we studied the frequencies of Apo E genotypes in a cohort of 52 Parkinson\u27s disease patients with dementia and 61 patients without dementia. Dementia was determined per National Institute of Neurological and Communicative Disorders and Stroke criteria and Mattis Dementia Rating Scale (DRS) \u3c 126. Normal cognition was defined as DRS \u3e 132. Apo E genotype and allele frequencies did not differ between demented and nondemented parkinsonian patients. Neither group\u27s genotype and allele frequencies differed from that of a nondemented population of 78 controls. We conclude that the Apo E ε4 allele influences neither the development of Parkinson\u27s disease nor the dementia associated with Parkinson\u27s disease nor the dementia associated with Parkinson\u27s disease. Copyright © 1995 American Neurological Associatio

PARK3 Influences Age at Onset in Parkinson Disease: A Genome Scan in the GenePD Study

Parkinson disease (PD) is a late-onset neurodegenerative disorder. The mean age at onset is 61 years, but the disease can range from juvenile cases to cases in the 8th or 9th decade of life. The parkin gene on chromosome 6q and loci on chromosome 1p35-36 and 1p36 are responsible for some cases of autosomal recessive early-onset parkinsonism, but they do not appear to influence susceptibility or variability of age at onset for idiopathic PD. We have performed a genomewide linkage analysis using variance-component methodology to identify genes influencing age at onset of PD in a population of affected relatives (mainly affected sibling pairs) participating in the GenePD study. Four chromosomal loci showed suggestive evidence of linkage: chromosome 2p (maximum multipoint LOD [MaxLOD] = 2.08), chromosome 9q (MaxLOD = 2.00), chromosome 20 (MaxLOD = 1.82), and chromosome 21 (MaxLOD = 2.21). The 2p and 9q locations that we report here have previously been reported as loci influencing PD affection status. Association between PD age at onset and allele 174 of marker D2S1394, located on 2p13, was observed in the GenePD sample (P=.02). This 174 allele is common to the PD haplotype observed in two families that show linkage to PARK3 and have autosomal dominant PD, which suggests that this allele may be in linkage disequilibrium with a mutation influencing PD susceptibility or age at onset of PD

Mitochondrial Polymorphisms Significantly Reduce the Risk of Parkinson Disease

Mitochondrial (mt) impairment, particularly within complex I of the electron transport system, has been implicated in the pathogenesis of Parkinson disease (PD). More than half of mitochondrially encoded polypeptides form part of the reduced nicotinamide adenine dinucleotide dehydrogenase (NADH) complex I enzyme. To test the hypothesis that mtDNA variation contributes to PD expression, we genotyped 10 single-nucleotide polymorphisms (SNPs) that define the European mtDNA haplogroups in 609 white patients with PD and 340 unaffected white control subjects. Overall, individuals classified as haplogroup J (odds ratio [OR] 0.55; 95% confidence interval [CI] 0.34–0.91; P=.02) or K (OR 0.52; 95% CI 0.30–0.90; P=.02) demonstrated a significant decrease in risk of PD versus individuals carrying the most common haplogroup, H. Furthermore, a specific SNP that defines these two haplogroups, 10398G, is strongly associated with this protective effect (OR 0.53; 95% CI 0.39–0.73; P=.0001). SNP 10398G causes a nonconservative amino acid change from threonine to alanine within the NADH dehydrogenase 3 (ND3) of complex I. After stratification by sex, this decrease in risk appeared stronger in women than in men (OR 0.43; 95% CI 0.27–0.71; P=.0009). In addition, SNP 9055A of ATP6 demonstrated a protective effect for women (OR 0.45; 95% CI 0.22–0.93; P=.03). Our results suggest that ND3 is an important factor in PD susceptibility among white individuals and could help explain the role of complex I in PD expression