Equidistribution of Heegner Points and Ternary Quadratic Forms

We prove new equidistribution results for Galois orbits of Heegner points with respect to reduction maps at inert primes. The arguments are based on two different techniques: primitive representations of integers by quadratic forms and distribution relations for Heegner points. Our results generalize one of the equidistribution theorems established by Cornut and Vatsal in the sense that we allow both the fundamental discriminant and the conductor to grow. Moreover, for fixed fundamental discriminant and variable conductor, we deduce an effective surjectivity theorem for the reduction map from Heegner points to supersingular points at a fixed inert prime. Our results are applicable to the setting considered by Kolyvagin in the construction of the Heegner points Euler system

Multiple guide star tomography demonstration at Palomar observatory

We have built and field tested a multiple guide star tomograph with four Shack-Hartmann wavefront sensors. We predict the wavefront on the fourth sensor channel estimated using wavefront information from the other three channels using synchronously recorded data. This system helps in the design of wavefront sensors for future extremely large telescopes that will use multi conjugate adaptive optics and multi object adaptive optics. Different wavefront prediction algorithms are being tested with the data obtained. We describe the system, its current capabilities and some preliminary results

Plasma ferritin concentrations are not associated with abdominal aortic aneurysm diagnosis, size or growth

Background and aims: Experimental studies using a rodent model have suggested that iron overload may contribute to abdominal aortic aneurysm (AAA) pathogenesis. Methods: We assessed the association of total body iron, as measured by plasma ferritin, with AAA diagnosis, size and growth in 4024 community-dwelling older men screened for AAA, using logistic regression and linear mixed effects models. Results: Plasma ferritin concentrations were similar in men who did (n = 293) and did not (n = 3731) have an AAA (median [inter-quartile range] concentrations 115.4 [63.0–203.1] and 128.5 [66.1–229.1] ng/mL respectively, p = 0.124). There was no association between plasma ferritin concentration and AAA diagnosis in unadjusted logistic regression (odds ratio (OR) for a 1 standard deviation increase: 0.880 [95%CI: 0.764–1.015]; p = 0.078), or when adjusting for AAA risk factors and factors known to influence circulating ferritin (OR for a 1 standard deviation increase: 0.898 [95% CI: 0.778–1.035]; p = 0.138). Iron overload prevalence (plasma ferritin concentrations >200 ng/mL) was lower in men with an AAA (25.3%) than those without (30.8%; p = 0.048), but was not associated with AAA diagnosis after adjusting as above (OR: 0.781 [95% CI:0.589–1.035]; p = 0.086). The association of iron overload with AAA growth was investigated in 265 men with small AAAs who received at least 1 repeat ultrasound scan in the 3 years following screening. We saw no difference in AAA growth between men who did and did not have iron overload (n = 65 and 185 respectively, p = 0.164). Conclusions: Our data suggest that iron overload is unlikely to be important in AAA pathogenesis

Community-based knowledge transfer and exchange: Helping community-based organizations link research to action

<p>Abstract</p> <p>Background</p> <p>Community-based organizations (CBOs) are important stakeholders in health systems and are increasingly called upon to use research evidence to inform their advocacy, program planning, and service delivery efforts. CBOs increasingly turn to community-based research (CBR) given its participatory focus and emphasis on linking research to action. In order to further facilitate the use of research evidence by CBOs, we have developed a strategy for community-based knowledge transfer and exchange (KTE) that helps CBOs more effectively link research evidence to action. We developed the strategy by: outlining the primary characteristics of CBOs and why they are important stakeholders in health systems; describing the concepts and methods for CBR and for KTE; comparing the efforts of CBR to link research evidence to action to those discussed in the KTE literature; and using the comparison to develop a framework for community-based KTE that builds on both the strengths of CBR and existing KTE frameworks.</p> <p>Discussion</p> <p>We find that CBR is particularly effective at fostering a climate for using research evidence and producing research evidence relevant to CBOs through community participation. However, CBOs are not always as engaged in activities to link research evidence to action on a larger scale or to evaluate these efforts. Therefore, our strategy for community-based KTE focuses on: an expanded model of 'linkage and exchange' (<it>i.e</it>., producers and users of researchers engaging in a process of asking and answering questions together); a greater emphasis on both producing and disseminating systematic reviews that address topics of interest to CBOs; developing a large-scale evidence service consisting of both 'push' efforts and efforts to facilitate 'pull' that highlight actionable messages from community relevant systematic reviews in a user-friendly way; and rigorous evaluations of efforts for linking research evidence to action.</p> <p>Summary</p> <p>Through this type of strategy, use of research evidence for CBO advocacy, program planning, and service delivery efforts can be better facilitated and continually refined through ongoing evaluations of its impact.</p

A Cluster-Randomised Trial of Staff Education to Improve the Quality of Life of People with Dementia Living in Residential Care: The DIRECT Study

BACKGROUND: The Dementia In Residential care: EduCation intervention Trial (DIRECT) was conducted to determine if delivery of education designed to meet the perceived need of GPs and care staff improves the quality of life of participants with dementia living in residential care. METHODOLOGY/PRINCIPAL FINDINGS: This cluster-randomised controlled trial was conducted in 39 residential aged care facilities in the metropolitan area of Perth, Western Australia. 351 care facility residents aged 65 years and older with Mini-Mental State Examination ≤ 24, their GPs and facility staff participated. Flexible education designed to meet the perceived needs of learners was delivered to GPs and care facility staff in intervention groups. The primary outcome of the study was self-rated quality of life of participants with dementia, measured using the QOL-Alzheimer's Disease Scale (QOL-AD) at 4 weeks and 6 months after the conclusion of the intervention. Analysis accounted for the effect of clustering by using multi-level regression analysis. Education of GPs or care facility staff did not affect the primary outcome at either 4 weeks or 6 months. In a post hoc analysis excluding facilities in which fewer than 50% of staff attended an education session, self-rated QOL-AD scores were 6.14 points (adjusted 95%CI 1.14, 11.15) higher at four-week follow-up among residents in facilities randomly assigned to the education intervention. CONCLUSION: The education intervention directed at care facilities or GPs did not improve the quality of life ratings of participants with dementia as a group. This may be explained by the poor adherence to the intervention programme, as participants with dementia living in facilities where staff participated at least minimally seemed to benefit. TRIAL REGISTRATION: ANZCTR.org.au ACTRN12607000417482

Factors Associated with Self and Informant Ratings of the Quality of Life of People with Dementia Living in Care Facilities: A Cross Sectional Study

There is no consensus regarding the optimal approach to assessment of the quality of life of people with dementia. We undertook the present study to describe and determine the factors associated with ratings of the quality of life of a cohort of people with dementia living in a residential care facility.351 people with dementia living in residential care facilities, and their staff and family informants participated in this cross sectional observational study. Quality of life was measured using self (Quality of Life in Alzheimer's Disease [QoL-AD] scale), and informant (QoL-AD and Alzheimer's Disease Related QoL Scale) reports. 226 people (64%) with dementia (median MMSE 17; 12-21) were able to self rate the QoL-AD scale and these subjects' ratings were compared to ratings by staff and family. Both staff and family informant ratings of the QoL-AD underestimated self ratings (mean difference -7.8, 95% CI -8.8, -6.7 for staff rated QoL-AD; and mean difference -7.2, 95% CI -8.5, -6.0 for family rated QoL-AD). Self ratings of QoL were lower among people who were restrained, had fallen or had pain. Informant ratings of the QoL of the participants with dementia were consistently and significantly lower for people with severe cognitive impairment, who had fallen, had presence of neuropsychiatric symptoms, or where care giver distress was present. Documented restraint, reported pain and neuropsychiatric symptoms were independently associated with lower self rating of the QoL-AD in multivariate models. Cognitive impairment, case conferencing, hospitalizations and neuropsychiatric symptoms were found to be independently associated with staff rated ADRQL.The majority of people with dementia living in residential care facilities can rate their own QoL. Informant ratings underestimate self ratings of QoL of people with dementia, and appear to be associated with factors which are not associated with self ratings

Genetic Effects on Bone Loss in Peri- and Postmenopausal Women: A Longitudinal Twin Study

This longitudinal twin study was designed to assess the heritability of bone loss in peri- and postmenopausal women. A sample of 724 female twins was studied. Baseline and repeat BMD measurements were performed. Results of genetic model-fitting analysis indicated genetic effects on bone loss account for similar to 40% of the between-individual variation in bone loss at the lumbar spine, forearm, and whole body. Introduction: BMD and bone loss are important predictors of fracture risk. Although the heritability of peak BMD is well documented, it is not clear whether bone loss is also under genetic regulation. This study was designed to assess the heritability of bone loss in peri- and postmenopausal women. Materials and Methods: A sample of 724 female twins (177 monozygotic [MZ] and 185 dizygotic [DZ] pairs), 45-82 yr of age, was studied. Each individual had baseline BMD measurements at the lumbar spine, hip, forearm, and total body by DXA and at least one repeat measure, on average 4.9 yr later. Change in BMD (Delta BMD) was expressed as percent of gain or loss per year. Intraclass correlation coefficients for ABMD were calculated for MZ and DZ pairs. Genetic model-fitting analysis was conducted to partition the total variance of ABMD into three components: genetic (G), common environment (C), and specific environment, including measurement error (E). The index of heritability was estimated as the ratio of genetic variance over total variance. Results: The mean annual Delta BMD was -0.37 +/- 1.43% (SD) per year at the lumbar spine, -0.27 +/- 1.32% at the total hip, -0.77 +/- 1.66% at the total forearm, -0.36 +/- 56% at the femoral neck, and -0.16 +/- 0.81% at the whole body. Intraclass correlation coefficients were significantly higher in MZ than in DZ twins for all studied parameters, except at the hip sites. Results of genetic model-fitting analysis indicated that the indices of heritability for ABMD were 0.38, 0.49, and 0.44 for the lumbar spine, total forearm, and whole body, respectively. However, the genetic effect on ABMD at all hip sites was not significant. Conclusions: These data suggest that, although genetic effects on bone loss with aging are less pronounced than on peak bone mass, they still account for similar to 40% of the between-individual variation in bone loss for the lumbar spine, total forearm, and whole body in peri- and postmenopausal women. These findings are relevant for studies aimed at identification of genes that are involved in the regulation of bone loss