Introduction of an assessment toolkit associated with increased rate of DLB diagnosis.

BACKGROUND: Dementia with Lewy bodies (DLB) and dementia in Parkinson's disease (PDD) are recognised to be under-recognised in clinical practice in the UK, with only one third to a half of expected cases diagnosed. We aimed to assess whether clinical diagnostic rates could be increased by the introduction of a structured assessment toolkit for clinicians. METHODS: We established baseline diagnostic rates for DLB and PDD in four memory clinics and three movement disorder/Parkinson's disease (PD) clinics in two separate geographical regions in the UK. An assessment toolkit specifically developed to assist with the recognition and diagnosis of DLB and PDD was then introduced to the same clinical teams and diagnostic rates for DLB and PDD were reassessed. For assessing DLB diagnosis, a total of 3820 case notes were reviewed before the introduction of the toolkit, and 2061 case notes reviewed after its introduction. For PDD diagnosis, a total of 1797 case notes were reviewed before the introduction of the toolkit and 3405 case notes after it. Mean values and proportions were analysed using Student's t test for independent samples and χ2 test, respectively. RESULTS: DLB was diagnosed in 4.6% of dementia cases prior to the introduction of the toolkit, and 6.2% of dementia cases afterwards, an absolute rise of 1.6%, equal to a 35% increase in the number of DLB cases diagnosed when using the toolkit (χ2 = 4.2, P = 0.041). The number of PD patients diagnosed with PDD was not found overall to be significantly different when using the toolkit: 9.6% of PD cases before and 8.2% of cases after its introduction (χ2 = 1.8, P = 0.18), though the ages of PD patients assessed after the toolkit's introduction were lower (73.9 years vs 80.0 years, t = 19.2, p < 0.001). CONCLUSION: Introduction of the assessment toolkit was associated with a significant increase in the rate of DLB diagnosis, suggesting that a structured means of assessing symptoms and clinical features associated with DLB can assist clinicians in recognising cases. The assessment toolkit did not alter the overall rate of PDD diagnosis, suggesting that alternate means may be required to improve the rate of diagnosis of dementia in Parkinson's disease.

Socioeconomic variation in survival from childhood leukaemia in northern England, 1968-2010.

BACKGROUND: Despite marked improvements in childhood leukaemia survival, 20% still die within 5 years of diagnosis. The aim of this study was to evaluate the relationship between socioeconomic status, as assessed by paternal occupation at birth, and survival from childhood leukaemia in children, using data from the Northern Region Young Persons Malignant Disease Registry. METHODS: All 1007 cases of leukaemia in children aged 0-14 years, diagnosed between 1968 and 2010 and registered with the Registry were studied. Paternal occupational social class at the time of the child's birth was obtained and analysed in relation to survival using Cox-proportional regression. RESULTS: Compared with the most advantaged group (I/II), those in the middle group (IIIN/M) had a 68% increased risk of death, while those in the least advantaged group (IV/V) had 86% higher risk for acute lymphoblastic leukaemia. While the survival advantage of children in class I/II was apparent from the time of diagnosis, survival for children in groups IIIN/M and IV/V were comparable until 3-4 years after diagnosis, when they began to minimally diverge. CONCLUSION: The existence of such socioeconomic disparities cannot be attributed to accessibility to health care in the United Kingdom. Further research into the likely factors underlying these disparities is required.

Genetic characterization of the HrpL regulon of the fire blight pathogen Erwinia amylovora reveals novel virulence factors.

The bacterial pathogen Erwinia amylovora is the causal agent of fire blight, an economically significant disease of apple and pear. Disease initiation by E. amylovora requires the translocation of effector proteins into host cells via the hypersensitive response and pathogenicity (hrp) type III secretion system (T3SS). The alternative sigma factor HrpL positively regulates the transcription of structural and translocated components of the T3SS via hrp promoter elements. To characterize genome-wide HrpL-dependent gene expression in E. amylovora Ea1189, wild-type and Ea1189ΔhrpL strains were cultured in hrp-inducing minimal medium, and total RNA was compared using a custom microarray designed to represent the annotated genes of E. amylovora ATCC 49946. The results revealed 24 genes differentially regulated in Ea1189ΔhrpL relative to Ea1189 with fold-change expression ratios greater than 1.5; of these, 19 genes exhibited decreased transcript abundance and five genes showed increased transcript abundance relative to Ea1189. To expand our understanding of the HrpL regulon and to elucidate direct versus indirect HrpL-mediated effects on gene expression, the genome of E. amylovora ATCC 49946 was examined in silico using a hidden Markov model assembled from known Erwinia spp. hrp promoters. This technique identified 15 putative type III novel hrp promoters, seven of which were validated with quantitative polymerase chain reaction based on expression analyses. It was found that HrpL-regulated genes encode all known components of the hrp T3SS, as well as five putative type III effectors. Eight genes displayed apparent indirect HrpL regulation, suggesting that the HrpL regulon is connected to downstream signalling networks. The construction of deletion mutants of three novel HrpL-regulated genes resulted in the identification of additional virulence factors as well as mutants displaying abnormal motility and biofilm phenotypes.

Acquiring new technology and surviving environmental pressures.

CONTEXT: The U.S. health care system faces increased pressures to expand coverage to the elderly, the uninsured and the poor, while maintaining costs and quality of care. Because of the federal budget deficit and continued fiscal uncertainties, resource allocation will become even more scrutinized. OBJECTIVE: How does a health care system allocate limited funds and still provide quality care using innovative technology? METHOD: This article reviews the literature on the acquisition of new technologies from a theoretical perspective, using positron emission tomography (PET) as an example. A unified model, including concepts from the resource dependency theory (RDT) supplemented with organizational survival concepts from the ecological theory, was used to analyze resource acquisition for technological innovation and organizational survival. An attempt was made to evaluate a hospital's profit maximization, recognition as a center of clinical excellence and role as a technological leader of the community with respect to acquisition of PET equipment. CONCLUSION: Organizations acquire new technology for a variety of reasons that can be explained by RDT and ecological theory concepts. In terms of the profit maximization motive, hospitals purchase PET equipment to enhance revenue generation. From the clinical excellence perspective, organizations seek the best available technology to meet the needs of their patients. Finally, hospitals adopt new technology to enhance their image as a technological leader.

The assessment of platelet derived growth factor concentration in post myocardial infarction and stable angina patients.

Platelet derived growth factor (PDGF) has been implicated in the pathogenesis of atherosclerosis. PDGF is released by aggregating platelets and monocytes which gather around sites of arterial injury. In the study reported here the concentration of plasma PDGF was measured in post myocardial infarction (MI) patients (n = 28), angina patients (n = 25), and control subjects (n = 27). Venous blood samples were taken and the concentration of PDGF determined by an enzyme linked immunosorbent assay (ELISA). Plasma PDGF concentrations were significantly higher in the post MI group compared to both the control and angina groups (P < or = 0.05). The increase in PDGF concentration may be due to increased activation of platelets or monocytes since these two cells are major sources of plasma PDGF. High concentrations of PDGF in the circulation could further accelerate the progression of the disease.