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Previous Studies Suggesting (previous + studies_suggesting)
Selected AbstractsRisk reduction and real estate portfolio sizeMANAGERIAL AND DECISION ECONOMICS, Issue 7 2001Peter J. Byrne There is remarkably little empirical evidence of the advantages of increased size on risk levels in real estate portfolios based on actual portfolios. This paper improves this by examining the portfolio risk of a large sample of actual real estate data in the UK over the period from 1981 to 1996. The results show that real estate portfolios of larger sizes tend, on average, to have lower risks than smaller sized portfolios and, more importantly, that portfolios with only a few assets can have very high or very low risk. For fund managers to be confident that their portfolio will have a risk level like the average, they need to hold portfolios of a considerably greater size than they might expect, or can sensibly acquire. Previous studies suggesting that only 20,40 properties are needed to reduce the risk of a property portfolio down to the market level are a significant underestimate. The actual figure is likely to be 400,500 properties, well above that of even the largest fund in the UK. Size alone does not necessarily lead to a reduction in portfolio risk. Other factors are of greater importance. Copyright © 2001 John Wiley & Sons, Ltd. [source] Childhood trauma in obsessive-compulsive disorder, trichotillomania, and controlsDEPRESSION AND ANXIETY, Issue 2 2002Christine Lochner M.A. Abstract There is relatively little data on the link between childhood trauma and obsessive-compulsive/putative obsessive-compulsive spectrum disorders. The revised Childhood Trauma Questionnaire (CTQ), which assesses physical, emotional, and sexual abuse as well as physical and emotional neglect, was administered to female patients with obsessive-compulsive disorder (OCD; n = 74; age: 36.1 ± 16.3), TTM (n = 36; age: 31.8 ± 12.3), and a group of normal controls (n = 31; age: 21.5 ± 1.0). The findings showed a significantly greater severity of childhood trauma in general, and emotional neglect specifically, in the patient groups compared to the controls. Although various factors may play a role in the etiology of both OCD and trichotillomania (TTM), this study is consistent with some evidence from previous studies suggesting that childhood trauma may play a role in the development of these disorders. Depression and Anxiety 15:66,68, 2002. © 2002 Wiley-Liss, Inc. [source] Extinction in the developing rat: An examination of renewal effectsDEVELOPMENTAL PSYCHOBIOLOGY, Issue 6 2007Carol S.L. Yap Abstract In the present series of experiments the context-specificity of extinction was examined from a developmental perspective. For postnatal day (PN) 23 rats, renewal of freezing to an aversive odor conditioned stimulus (CS) was observed when rats were conditioned in Context A, extinguished in Context B, and tested in Context A (i.e., ABA renewal). This effect was not observed in PN16 rats, which is consistent with previous studies suggesting that rats <,PN20 are impaired in encoding contextual information [i.e., Carew and Rudy [1991]. Developmental Psychobiology, 24, 191,209]. Subsequent experiments demonstrated that for rats conditioned at PN16 and tested at PN23, contextual regulation of extinction performance depended on the age at which extinction occurred. Specifically, ABA renewal was observed in rats given extinction training at PN22 but not in rats given extinction training at PN17. These latter results show that whether or not context regulates the expression of an ambiguous memory is determined by the animal's age when the memory becomes ambiguous. © 2007 Wiley Periodicals, Inc. Dev Psychobiol 49: 565-575, 2007. [source] Homologous desensitization of guanylyl cyclase A, the receptor for atrial natriuretic peptide, is associated with a complex phosphorylation patternFEBS JOURNAL, Issue 11 2010Juliane Schröter Atrial natriuretic peptide (ANP), via its guanylyl cyclase A (GC-A) receptor and intracellular guanosine 3,,5,-cyclic monophosphate production, is critically involved in the regulation of blood pressure. In patients with chronic heart failure, the plasma levels of ANP are increased, but the cardiovascular actions are severely blunted, indicating a receptor or postreceptor defect. Studies on metabolically labelled GC-A-overexpressing cells have indicated that GC-A is extensively phosphorylated, and that ANP-induced homologous desensitization of GC-A correlates with receptor dephosphorylation, a mechanism which might contribute to a loss of function in vivo. In this study, tandem MS analysis of the GC-A receptor, expressed in the human embryonic kidney cell line HEK293, revealed unambiguously that the intracellular domain of the receptor is phosphorylated at multiple residues: Ser487, Ser497, Thr500, Ser502, Ser506, Ser510 and Thr513. MS quantification based on multiple reaction monitoring demonstrated that ANP-provoked desensitization was accompanied by a complex pattern of receptor phosphorylation and dephosphorylation. The population of completely phosphorylated GC-A was diminished. However, intriguingly, the phosphorylation of GC-A at Ser487 was selectively enhanced after exposure to ANP. The functional relevance of this observation was analysed by site-directed mutagenesis. The substitution of Ser487 by glutamate (which mimics phosphorylation) blunted the activation of the GC-A receptor by ANP, but prevented further desensitization. Our data corroborate previous studies suggesting that the responsiveness of GC-A to ANP is regulated by phosphorylation. However, in addition to the dephosphorylation of the previously postulated sites (Ser497, Thr500, Ser502, Ser506, Ser510), homologous desensitization seems to involve the phosphorylation of GC-A at Ser487, a newly identified site of phosphorylation. The identification and further characterization of the specific mechanisms involved in the downregulation of GC-A responsiveness to ANP may have important pathophysiological implications. Structured digital abstract ,,MINT-7713870, MINT-7713887: PMCA (uniprotkb:P20020) and GC-A (uniprotkb:P18910) colocalize (MI:0403) by fluorescence microscopy (MI:0416) [source] Effects of body mass, climate, geography, and census area on population density of terrestrial mammalsGLOBAL ECOLOGY, Issue 5 2001Marina Silva Abstract Aim The aim of this study was to investigate the effects of climate, geography, census area and the distribution of body mass on the mass : density relationship in terrestrial mammal populations. Location The areas covered include most major terrestrial biomes including the tropics, savannas, and temperate forests. Method Data on population density and body mass from 827 populations belonging to 330 different terrestrial mammal species were derived from a review of the literature. Results LOWESS and polynomial regression analysis indicated that the overall mass : density relationship on log-log scales was not linear and that the slope of this relationship behaves differently across the range of body mass. Body mass explained between 37 and 67% of the variability in population density depending upon the dietary category or the biome group. We also developed two multivariate models that can explain up to 65% of the variability in population density in terrestrial mammals. We also tested for a confounding effect of census area on the mass : density relationship on log-log scales in terrestrial mammals. Conclusions Our findings support previous studies suggesting that body mass is a major predictor of the variance in population density in terrestrial mammals. We suggest that the non-linearity of the mass : density relationship may result from the fact that the overall distribution of body mass is a mixture of distributions across dietary groups and biomes. In contrast to body mass, our results indicate that climatic and geographical factors have a minor effect on population density. Although census area was closely correlated with body mass, body mass was generally a better predictor of population density than was census area. [source] Haplotype Analysis Confirms the Association Between the HCRTR2 Gene and Cluster HeadacheHEADACHE, Issue 7 2008Innocenzo Rainero MD Background., Several studies suggested that genetic factors play a role in cluster headache (CH) susceptibility. We found a significant association between the 1246 G>A polymorphism of the hypocretin receptor-2 (HCRTR2) gene and the disease. This association was confirmed in a large study from Germany but was not replicated in a dataset of CH patients from Northern Europe. Objective., The purpose of this study was to further evaluate the association between CH and the HCRTR2 gene using new polymorphisms, estimating the frequency of different gene haplotypes, searching for gene mutations, and evaluating the effects of the examined polymorphisms on hypocretin binding sites. Methods., We genotyped 109 CH patients and 211 healthy controls for 5 new polymorphisms of the HCRTR2 gene and we inferred different gene haplotypes. Complete HCRTR2 sequencing was undertaken for 11 independent CH patients, 5 of whom had a positive family history. The effects of the 1246 G>A polymorphism on the hypocretin binding sites were evaluated using different computer-assisted analyses. Results., Three new polymorphisms of the HCRTR2 gene resulted significantly associated with CH. The GTAAGG haplotype resulted more frequent in cases than in controls (OR: 3.68; 95% CI: 1.85-7.67). No point mutation of the HCRTR2 gene was found. Binding analyses showed that the 1246 G>A polymorphism (substitution of valine at position 308 by isoleucine) has no effect on the hypocretin binding sites but could influence the dimerization process of the receptor. Conclusion., Our data confirm previous studies suggesting that the HCRTR2 gene or a linked locus significantly modulates the risk for CH. In addition, we suggest that the V308I substitution of the HCRTR2 may interfere with the dimerization process of the receptor, thereby influencing its functional activity. [source] Phasic muscle activity in sleep and clinical features of Parkinson diseaseANNALS OF NEUROLOGY, Issue 3 2010Donald L. Bliwise PhD Objective: The absence of atonia during rapid eye movement (REM) sleep and dream-enactment behavior (REM sleep behavior disorder [RBD]) are common features of sleep in the alpha-synucleinopathies. This study examined this phenomenon quantitatively, using the phasic electromyographic metric (PEM), in relation to clinical features of idiopathic Parkinson disease (PD). Based on previous studies suggesting that RBD may be prognostic for the development of later parkinsonism, we hypothesized that clinical indicators of disease severity and more rapid progression would be related to PEM. Methods: A cross-sectional convenience sample of 55 idiopathic PD patients from a movement disorders clinic in a tertiary care medical center underwent overnight polysomnography. PEM, the percentage of 2.5-second intervals containing phasic muscle activity, was quantified separately for REM and non-REM (NREM) sleep from 5 different electrode sites. Results: Higher PEM rates were seen in patients with symmetric disease, as well as in akinetic-rigid versus tremor-predominant patients. Men had higher PEM relative to women. Results occurred in all muscle groups in both REM and NREM sleep. Interpretation: Although our data were cross-sectional, phasic muscle activity during sleep suggests disinhibition of descending motor projections in PD broadly reflective of more advanced and/or progressive disease. Elevated PEM during sleep may represent a functional window into brainstem modulation of spinal cord activity and is broadly consistent with the early pathologic involvement of non-nigral brainstem regions in PD, as described by Braak. ANN NEUROL 2010 [source] Oxidation of carotenoids by heat and tobacco smokeBIOFACTORS, Issue 1 2004John S. Hurst Abstract The stability to autoxidation of the polar carotenoids, lutein and zeaxanthin, was compared to that of the less polar carotenoids, ,-carotene and lycopene at physiologically or pathophysiologically relevant concentrations of 2 and 6 ,M, after exposure to heat or cigarette smoke. Three methodological approaches were used: 1) Carotenoids dissolved in solvents with different polarities were incubated at 37 and 80°C for different times. 2) Human plasma samples were subjected to the same temperature conditions. 3) Methanolic carotenoid solutions and plasma were also exposed to whole tobacco smoke from 1,5 unfiltered cigarettes. The concentrations of individual carotenoids in different solvents were determined spectrophotometrically. Carotenoids from plasma were extracted and analyzed using high performance liquid chromatography. Carotenoids were generally more stable at 37 than at 80°C. In methanol and dichloromethane the thermal degradation of ,-carotene and lycopene was faster than that of lutein and zeaxanthin. However, in tetrahydrofuran ,-carotene and zeaxanthin degraded faster than lycopene and lutein. Plasma carotenoid levels at 37°C did not change, but decreased at 80°C. The decrease of ,-carotene and lycopene levels was higher than those for lutein and zeaxanthin. Also in the tobacco smoke experiments the highest autoxidation rates were found for ,-carotene and lycopene at 2 ,M, but at 6 ,M lutein and zeaxanthin depleted to the same extent as ,-carotene. These data support our previous studies suggesting that oxidative stress degrade ,-carotene and lycopene faster than lutein and zeaxanthin. The only exception was the thermal degradation of carotenoids solubilized in tetrahydrofuran, which favors faster breakdown of ,-carotene and zeaxanthin. [source] | |||||||||||||