640 resultados para Liaison multipoint
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Review question/objective What are the most effective information sharing strategies used to reduce anxiety in families of patients undergoing elective surgery? This review seeks to synthesize the best available evidence in relation to the most effective information-sharing intervention to reduce anxiety for families waiting for patients undergoing an elective surgical procedure. The specific objectives are to review the effectiveness of evidence of interventions designed to reduce the anxiety of families waiting whilst their loved one undergoes a surgical intervention. A variety of interventions exist and include surgical nurse liaison services, intraoperative reporting either by face-to-face or telephone delivery, informational cards, visual information screens, and intraoperative paging devices for families. Inclusion criteria Types of participants All studies of family members over 18 years of age waiting for patients undergoing an elective surgical procedure will be included, including those waiting for both adult and paediatric patients. Studies of families waiting for other patient populations, eg emergency surgery, chemotherapy or intensive care patients will be excluded. Types of intervention(s)/phenomena of interest All information-sharing Interventions for families of patients undergoing an elective surgical procedure will be included, including but not limited to: surgical nurse liaison services, in-person intraoperative reporting, visual information screens, paging devices, informational cards and telephone delivery of intraoperative progress reports. Interventions that take place during the intraoperative phase of care only will be included in the review. Preadmission information sharing interventions will be excluded. Types of outcomes The outcomes of interest include: Primary outcome: the level of anxiety amongst family members or close relatives whilst waiting for patients undergoing surgery, as measured by a validated instrument (such as the S-Anxiety portion of the State-Trait Anxiety Inventory).4 Secondary outcomes: family satisfaction and other measurements that may be considered indicators of stress and anxiety, such as mean arterial pressure (MAP) and heart rate.
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Harold Pinter's work opens the walls to the relatively closed rooms of domesticity. The room of the love affair, the unpredictable liaison, the cramped cluttered rooms of poverty and the disaffected. This study uses Pinter's rooms to analyse existing ideologies of gender, territory, power and domesticity. Pinter's rooms are more often than not reflections of familiar domestic spaces. This research investigates Pinter's rooms through a case study of a theatre set for one of his plays and textual analysis of selected works, developing an understanding of how Pinter's characters reflect behaviours within the domestic environment, mimicking while subverting domestic ecologies.
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CONTEXT AND OBJECTIVE: Suboptimal vitamin D status can be corrected by vitamin D supplementation, but individual responses to supplementation vary. We aimed to examine genetic and nongenetic determinants of change in serum 25-hydroxyvitamin D (25(OH)D) after supplementation. DESIGN AND PARTICIPANTS: We used data from a pilot randomized controlled trial in which 644 adults aged 60 to 84 years were randomly assigned to monthly doses of placebo, 30 000 IU, or 60 000 IU vitamin D3 for 12 months. Baseline characteristics were obtained from a self-administered questionnaire. Eighty-eight single-nucleotide polymorphisms (SNPs) in 41 candidate genes were genotyped using Sequenom MassArray technology. Serum 25(OH)D levels before and after the intervention were measured using the Diasorin Liaison platform immunoassay. We used linear regression models to examine associations between genetic and nongenetic factors and change in serum 25(OH)D levels. RESULTS: Supplement dose and baseline 25(OH)D level explained 24% of the variability in response to supplementation. Body mass index, self-reported health status, and ambient UV radiation made a small additional contribution. SNPs in CYP2R1, IRF4, MC1R, CYP27B1, VDR, TYRP1, MCM6, and HERC2 were associated with change in 25(OH)D level, although only CYP2R1 was significant after adjustment for multiple testing. Models including SNPs explained a similar proportion of variability in response to supplementation as models that included personal and environmental factors. CONCLUSION: Stepwise regression analyses suggest that genetic variability may be associated with response to supplementation, perhaps suggesting that some people might need higher doses to reach optimal 25(OH)D levels or that there is variability in the physiologically normal level of 25(OH)D.
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Background Whilst waiting for patients undergoing surgery, a lack of information regarding the patient’s status and the outcome of surgery, can contribute to the anxiety experienced by family members. Effective strategies for providing information to families are therefore required. Objectives To synthesize the best available evidence in relation to the most effective information-sharing interventions to reduce anxiety for families waiting for patients undergoing an elective surgical procedure. Inclusion criteria Types of participants All studies of family members over 18 years of age waiting for patients undergoing an elective surgical procedure were included, including those waiting for both adult and pediatric patients. Types of intervention All information-sharing interventions for families of patients undergoing an elective surgical procedure were eligible for inclusion in the review. Types of studies All randomized controlled trials (RCTs) quasi-experimental studies, case-controlled and descriptive studies, comparing one information-sharing intervention to another or to usual care were eligible for inclusion in the review. Types of outcomes Primary outcome: The level of anxiety amongst family members or close relatives whilst waiting for patients undergoing surgery, as measured by a validated instrument such as the S-Anxiety portion of the State-Trait Anxiety Inventory (STAI). Secondary outcomes: Family satisfaction and other measurements that may be considered indicators of stress and anxiety, such as mean arterial pressure (MAP) and heart rate. Search strategy A comprehensive search, restricted to English language only, was undertaken of the following databases from 1990 to May 2013: Medline, CINAHL, EMBASE, ProQuest, Web of Science, PsycINFO, Scopus, Dissertation and Theses PQDT (via ProQuest), Current Contents, CENTRAL, Google Scholar, OpenGrey, Clinical Trials, Science.gov, Current Controlled Trials and National Institute for Clinical Studies (NHMRC). Methodological quality Two independent reviewers critically appraised retrieved papers for methodological quality using the standardized critical appraisal instruments for randomized controlled trials and descriptive studies from the Joanna Briggs Institute Meta Analysis of Statistics Assessment and Review Instruments (JBI-MAStARI). Data extraction Two independent reviewers extracted data from included papers using a customized data extraction form. Data synthesis Statistical pooling was not possible, mainly due to issues with data reporting in two of the studies, therefore the results are presented in narrative form. Results Three studies with a total of 357 participants were included in the review. In-person reporting to family members was found to be effective in comparison with usual care in which no reports were provided. Telephone reporting was also found to be effective at reducing anxiety, in comparison with usual care, although not as effective as in-person reporting. The use of paging devices to keep family members informed were found to increase, rather than decrease anxiety. Conclusions Due to the lack of high quality research in this area, the strength of the conclusions are limited. It appears that in-person and telephone reporting to family members decreases anxiety, however the use of paging devices increases anxiety.
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The over-representation of vulnerable populations within the criminal justice system, and the role of police in perpetuating this, has long been a topic of discussion in criminology. What is less discussed is the way in which non-criminal investigations by police, in areas like a death investigation, may similarly disadvantage and discriminate against vulnerable populations. In Australia, as elsewhere, it is police who are responsible for investigating both suspicious and violent deaths like homicide as well as non-suspicious, violent deaths like accidents and suicides. Police are also the agents tasked with investigating deaths which are neither violent nor suspicious but occur outside hospitals and other care facilities. This paper, part of a larger funded Australian research project focusing on the ways in which cultural and religious differences are dealt with during the death investigation process, reports on how police describe – or are described by others – during their role in a non-suspicious death investigation, and the challenges that such investigations raise for police and policing. The employment of police liaison officers is discussed as one response to the difficulty of policing cultural and religious difference with variable results.
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Ankylosing spondylitis (AS) is a common inflammatory arthritis predominantly affecting the axial skeleton. Susceptibility to the disease is thought to be oligogenic. To identify the genes involved, we have performed a genomewide scan in 185 families containing 255 affected sibling pairs. Two-point and multipoint nonparametric linkage analysis was performed. Regions were identified showing "suggestive" or stronger linkage with the disease on chromosomes 1p, 2q, 6p, 9q, 10q, 16q, and 19q. The MHC locus was identified as encoding the greatest component of susceptibility, with an overall LOD score of 15.6. The strongest non-MHC linkage lies on chromosome 16q (overall LOD score 4.7). These results strongly support the presence of non-MHC genetic-susceptibility factors in AS and point to their likely locations.
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Objective. To localize the regions containing genes that determine susceptibility to ankylosing spondylitis (AS). Methods. One hundred five white British families with 121 affected sibling pairs with AS were recruited, largely from the Royal National Hospital for Rheumatic Diseases AS database. A genome-wide linkage screen was undertaken using 254 highly polymorphic microsatellite markers from the Medical Research Council (UK) (MRC) set. The major histocompatibility complex (MHC) region was studied more intensively using 5 microsatellites lying within the HLA class III region and HLA-DRB1 typing. The Analyze package was used for 2-point analysis, and GeneHunter for multipoint analysis. Results. When only the MRC set was considered, 11 markers in 7 regions achieved a P value of ≤0.01. The maximum logarithm of odds score obtained was 3.8 (P = 1.4 x 10-5) using marker D6S273, which lies in the HLA class III region. A further marker used in mapping of the MHC class III region achieved a LOD score of 8.1 (P = 1 x 10-9). Nine of 118 affected sibling pairs (7.6%) did not share parental haplotypes identical by descent across the MHC, suggesting that only 31% of the susceptibility to AS is coded by genes linked to the MHC. The maximum non-MHC LOD score obtained was 2.6 (P = 0.0003) for marker D16S422. Conclusion. The results of this study confirm the strong linkage of the MHC with AS, and provide suggestive evidence regarding the presence and location of non-MHC genes influencing susceptibility to the disease.
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Objective. To examine whether the T cell receptor (TCR) A or TCRB loci exhibit linkage with disease in multiplex rheumatoid arthritis (RA) families. Methods. A linkage study was performed in 184 RA families from the UK Arthritis and Rheumatism Council Repository, each containing at least 1 affected sibpair. The microsatellites D14S50, TCRA, and D14S64 spanning the TCRA locus and D7S509, Vβ6.7, and D7S688 spanning the TCRB locus were used as DNA markers. The subjects were genotyped using a semiautomated polymerase chain reaction-based method. Two-point and multipoint linkage analyses were performed. Results. Nonparametric single-marker likelihood odds (LOD) scores were 0.49 (P = 0.07) for D14S50, 0.65 (P = 0.04) for TCRA, 0.07 (P = 0.29) for D14S64, 0.01 (P = 0.43) for D7S509, 0.0 (P = 0.50) for Vβ6.7, and 0.0 (P = 0.50) for D7S688. By multipoint analysis, there was no evidence of linkage at TCRB (LOD score 0), and the maximum LOD score at the TCRA locus was 0.37 (at D14S50). The presence of a susceptibility locus (LOD score < -2.0) was excluded, with lambda ≤ 1.8 at TCRA and ≤1.4 at TCRB. Conclusion. These linkage studies provide no significant evidence of a major germline-encoded TCRA or TCRB component of susceptibility to RA.
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Objective. Ankylosing spondylitis (AS) affects 0.25-1.0% of the population, and its etiology is incompletely understood. Susceptibility to this highly familial disease (λ(s) = 58) is primarily genetically determined. There is a significant sex bias in AS, and there are differences in recurrence risk to the offspring of affected mothers and fathers, suggesting that there may be an X-linked recessive effect. We undertook an X- chromosome linkage study to determine any contribution of the X-chromosome to AS susceptibility. Methods. A linkage study of the X-chromosome using 234 affected sibling pairs was performed to investigate this hypothesis. Results. No linkage of the X-chromosome with susceptibility to AS was found. Model- free multipoint linkage analysis strongly excluded any significant genetic contribution (λ ≥1.5) to AS susceptibility encoded on the X-chromosome (logarithm of odds [LOD] <-2.0). Smaller genetic effects (A ≥1.3) were also found to be unlikely (LOD <-1.0). Conclusion. The sex bias in AS is not explained by X-chromosome-encoded genetic effects. The disease model best explaining the sex bias in occurrence and transmission of AS is a polygenic model with a higher susceptibility threshold in females.
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Objective. To undertake a systematic wholegenome screen to identify regions exhibiting genetic linkage to rheumatoid arthritis (RA). Methods. Two hundred fifty-two RA-affected sibling pairs from 182 UK families were genotyped using 365 highly informative microsatellite markers. Microsatellite genotyping was performed using fluorescent polymerase chain reaction primers and semiautomated DNA sequencing technology. Linkage analysis was undertaken using MAPMAKER/SIBS for single-point and multipoint analysis. Results. Significant linkage (maximum logarithm of odds score 4.7 [P = 0.000003] at marker D6S276, 1 cM from HLA-DRB1) was identified around the major histocompatibility complex (MHC) region on chromosome 6. Suggestive linkage (P < 7.4 × 10-4) was identified on chromosome 6q by single- and multipoint analysis. Ten other sites of nominal linkage (P < 0.05) were identified on chromosomes 3p, 4q, 7p, 2 regions of 10q, 2 regions of 14q, 16p, 21q, and Xq by single-point analysis and on 3 sites (1q, 14q, and 14q) by multipoint analysis. Conclusion. Linkage to the MHC region was confirmed. Eleven non-HLA regions demonstrated evidence of suggestive or nominal linkage, but none reached the genome-wide threshold for significant linkage (P = 2.2 × 10-5). Results of previous genome screens have suggested that 6 of these regions may be involved in RA susceptibility.
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Objective The ank/ank mouse develops a phenotype similar to ankylosing spondylitis (AS) in humans. ANKH, the human homolog of the mutated gene in the ank/ank mouse, has been implicated in familial autosomal-dominant chondrocalcinosis and autosomal-dominant craniometaphyseal dysplasia. This study was undertaken to investigate the role of ANKH in susceptibility to and clinical manifestations of AS. Methods Sequence variants were identified by genomic sequencing of the 12 ANKH exons and their flanking splice sites in 48 AS patients; variants were then screened in 233 patients and 478 controls. Linkage to the ANKH locus was assessed in 185 affected-sibling-pair families. Results Five single-nucleotide polymorphisms were identified within the coding region and flanking splice sites. No association between either susceptibility to AS or its clinical manifestations and these novel polymorphisms, or between disease susceptibility and 3 known promoter variants, was seen. No linkage between the ANKH locus and AS was observed. Multipoint exclusion mapping rejected the hypothesis of a locus of a magnitude λ≥1.4 (logarithm of odds score <-2) (equivalent to a genetic contribution of >10% to the AS sibling recurrence risk ratio) within this area contributing to AS. Conclusion These findings indicate that ANKH is not significantly involved in susceptibility to or clinical manifestations of AS.
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At Purdue University, the Libraries participate in a provost-initiated, campus-wide course redesign program called Instruction Matters: Purdue Academic Course Transformation (IMPACT). This initiative aims to bring active-learning to foundational courses traditionally taught through lectures. Purdue librarians recognized the IMPACT initiative as one way to enter the conversations blooming on our campus about the nature of learning, curriculum design, and how space design impacts potential learning. This article presents three perspectives: 1) the information literacy coordinator, 2) a libraries’ administrator with a gift for space planning, and; 3) an in-the-trenches liaison to course redesign projects. Each discusses the IMPACT initiative from his or her unique perspective and view of its impact on librarian roles. Collectively, the article explains why we think it is essential that this kind of campus effort is supported by libraries.
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Primary microcephaly (MCPH) is an autosomal-recessive congenital disorder characterized by smaller-than-normal brain size and mental retardation. MCPH is genetically heterogeneous with six known loci: MCPH1-MCPH6. We report mapping of a novel locus, MCPH7, to chromosome 1p32.3-p33 between markers D1S2797 and D1S417, corresponding to a physical distance of 8.39 Mb. Heterogeneity analysis of 24 families previously excluded from linkage to the six known MCPH loci suggested linkage of five families (20.83%) to the MCPH7 locus. In addition, four families were excluded from linkage to the MCPH7 locus as well as all of the six previously known loci, whereas the remaining 15 families could not be conclusively excluded or included. The combined maximum two-point LOD score for the linked families was 5.96 at marker D1S386 at theta = 0.0. The combined multipoint LOD score was 6.97 between markers D1S2797 and D1S417. Previously, mutations in four genes, MCPH1, CDK5RAP2, ASPM, and CENPJ, that code for centrosomal proteins have been shown to cause this disorder. Three different homozygous mutations in STIL, which codes for a pericentriolar and centrosomal protein, were identified in patients from three of the five families linked to the MCPH7 locus; all are predicted to truncate the STIL protein. Further, another recently ascertained family was homozygous for the same mutation as one of the original families. There was no evidence for a common haplotype. These results suggest that the centrosome and its associated structures are important in the control of neurogenesis in the developing human brain.
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Research Services Librarian, JCU and Paula Callan, Scholarly communications Librarian, QUT. Presented 16 September via Blackboard Collaborate as part of the QULOC Research Support for Library Liaison webinar series. This work is licensed under a Creative Commons
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“Predatory vs Quality journals,” presented by Paula Callan, Scholarly communications Librarian, QUT and Stephanie Bradbury, Research Support Coordinator, QUT. Presented 5 August via Blackboard Collaborate as part of the QULOC Research Support for Library Liaison webinar series. This work is licensed under a Creative Commons Attribution 4.0 International License