Accuracy of recording of deaths from asthma in the UK: the false negative rate

BACKGROUND: A study was carried out to determine the extent to which asthma deaths are wrongly attributed to another cause on UK death certificates. METHODS: Deaths from all causes occurring anywhere in the UK were identified amongst 2382 subjects aged 16-64 years within three years of discharge following hospital treatment for asthma (ICD9 493) in hospitals in the South East Thames region. The deaths were reviewed by an expert panel to assess the proportion of asthma deaths identified by the panel which were attributed to another cause of death on the death certificate (false negatives). RESULTS: Eighty five deaths from all causes were identified in a mean follow up period of two years and three months. In 61 cases (72%) there was sufficient information for the expert panel to be confident about the cause of death. The panel identified 22 deaths from asthma, four of which were certified as non-asthma deaths (two as deaths from chronic obstructive pulmonary disease (COPD) and two as deaths from cardiovascular disease). The proportion of false negative death certificates was four of 22 (18%, 95% confidence interval (CI) 5 to 40). CONCLUSIONS: There is evidence that asthma deaths in the UK are wrongly certified as deaths from both chronic obstructive pulmonary disease and diseases of the cardiovascular system.     

Allergen-avoidance measures in homes of house-dust-mite-allergic asthmatic patients: effects of acaricides and mattress encasings

This double-blind, placebo-controlled study investigated whether the application of an acaricide (Acarosan) on mattresses and on textile floor coverings in living rooms and bedrooms can contribute to improvement in lung function and airway hyperresponsiveness in 40 adult asthmatic patients sensitized to house-dust mite. In a second group of 19 patients who refused chemical intervention, the clinical effects of application of allergen-impermeable mattress encasings were studied. In all three treatment groups, Der p 1 levels in mattress dust were statistically significantly decreased after 12 months. However, this decrease was much greater in the group who received mattress encasings (final mean level 430 ng/g) than in groups with acaricide- or placebo-treated mattresses (final mean levels 1730 and 2100 ng/g, respectively). Treatment of textile floors with either Acarosan or placebo chemical caused a statistically significant decrease in the level of the house-dust-mite allergen Der p1 in floor dust. In the group with mattress encasings, no significant changes of floor dust Der p 1 were found. Airway hyperresponsiveness (as measured by the PC20 histamine) improved significantly in the mattress cover group after 6 months. The Acarosan group also showed a small but statistically significant improvement after 12 months.     

Vascular permeability factor/vascular endothelial growth factor-mediated signaling in mouse mesentery vascular endothelium

Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF) is a multifunctional cytokine and growth factor that has important roles in both pathological and physiological angiogenesis. VPF/VEGF induces vascular hyperpermeability, cell division, and other activities by interacting with two specific receptor tyrosine kinases, KDR/Flk-1 and Flt-1, that are selectively expressed on vascular endothelium. The signaling cascade that follows VPF/VEGF interaction with cultured endothelium is only partially understood but is known to result in increased intracellular calcium, activation of protein kinase C, and tyrosine phosphorylations of both receptors, phospholipase C-gamma (PLC-gamma) and phosphatidylinositol 3'-kinase. For many reasons, signaling events elicited in cultured endothelium may not mimic mediator effects on intact normal or tumor-induced microvessels in vivo. Therefore, we developed a system that would allow measurement of VPF/VEGF-induced signaling on intact microvessels. We used mouse mesentery, a tissue whose numerous microvessels are highly responsive to VPF/VEGF and that we found to express Flk-1 and Flt-1 selectively. At intervals after injecting VPF/VEGF i.p., mesenteries were harvested, extracted, and immunoprecipitated. Immunoblots confirmed that VPF/VEGF induced tyrosine phosphorylation of several proteins in mesenteric microvessels as in cultured endothelium: Flk-1; PLC-gamma; and mitogen-activated protein kinase. Similar phosphorylations were observed when mesentery was exposed to VPF/VEGF in vitro, or when mesenteries were harvested from mice bearing the mouse ovarian tumor ascites tumor, which itself secretes abundant VPF/VEGF. Other experiments further elucidated the VPF/VEGF signaling pathway, demonstrating phosphorylation of both PYK2 and focal adhesion kinase, activation of c-jun-NH2-kinase with phosphorylation of c-Jun, and an association between Flk-1 and PLC-gamma. In addition, we demonstrated translocation of mitogen-activated protein kinase to the cell nucleus in cultured endothelium. Taken together, these experiments describe a new model system with the potential for investigating signaling events in response to diverse mediators on intact microvessels in vivo and have further elucidated the VPF/VEGF signaling cascade.     

Direct measurement of differential cognitive deficit in acute schizophrenia.

This is a longitudinal study in which 11 standardized tests of cognitive function were administered to 20,000 normal Ss and at a later point in time readministered to those Ss of the original group (N=15) who became schizophrenic and were hospitalized. The tests were also readministered to part of the original group (N=40) who, at the same point in time, were still normal. The results, which revealed significant differential deficit on 5 of the measures, suggest that lack of motivation to reach out and actively manipulate stimuli or experience new learning produced the differences observed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)