60 research outputs found
Prevalence of childhood disability and the characteristics and circumstances of disabled children in the UK : secondary analysis of the Family Resources Survey
Background: Robust data on the prevalence of childhood disability and the circumstances and characteristics of
disabled children is crucial to understanding the relationship between impairment and social disadvantage. It is also
crucial for public policy development aimed at reducing the prevalence of childhood disability and providing
appropriate and timely service provision. This paper reports prevalence rates for childhood disability in the United
Kingdom (UK) and describes the social and household circumstances of disabled children, comparing these where
appropriate to those of non-disabled children.
Methods: Data were generated from secondary analysis of the Family Resources Survey, a national UK cross-sectional
survey, (2004/5) which had data on 16,012 children aged 0-18 years. Children were defined as disabled if they met the
Disability Discrimination Act (DDA) definition (1995 and 2005). Frequency distributions and cross-tabulations were run
to establish prevalence estimates, and describe the circumstances of disabled children. To establish the association
between individual social and material factors and childhood disability when other factors were controlled for, logistic
regression models were fitted on the dependent variable 'DDA defined disability'.
Results: 7.3% (CI 6.9, 7.7) of UK children were reported by as disabled according to the DDA definition. Patterns of
disability differed between sexes with boys having a higher rate overall and more likely than girls to experience
difficulties with physical coordination; memory, concentration and learning; communication. Disabled children lived in
different personal situations from their non-disabled counterparts, and were more likely to live with low-income,
deprivation, debt and poor housing. This was particularly the case for disabled children from black/minority ethnic/
mixed parentage groups and lone-parent households. Childhood disability was associated with lone parenthood and
parental disability and these associations persisted when social disadvantage was controlled for.
Conclusion: These analyses suggest that UK disabled children experience higher levels of poverty and personal and
social disadvantage than other children. Further research is required to establish accurate prevalence estimates of
childhood disability among different black and minority ethnic groups and to understand the associations between
childhood disability and lone parenthood and the higher rates of sibling and parental disability in households with
disabled children
Chemical Linkage to Injected Tissues Is a Distinctive Property of Oxidized Avidin
We recently reported that the oxidized avidin, named AvidinOX®, resides for weeks within injected tissues as a consequence of the formation of Schiff's bases between its aldehyde groups and tissue protein amino groups. We also showed, in a mouse pre-clinical model, the usefulness of AvidinOX for the delivery of radiolabeled biotin to inoperable tumors. Taking into account that AvidinOX is the first oxidized glycoprotein known to chemically link to injected tissues, we tested in the mouse a panel of additional oxidized glycoproteins, with the aim of investigating the phenomenon. We produced oxidized ovalbumin and mannosylated streptavidin which share with avidin glycosylation pattern and tetrameric structure, respectively and found that neither of them linked significantly to cells in vitro nor to injected tissues in vivo, despite the presence of functional aldehyde groups. The study, extended to additional oxidized glycoproteins, showed that the in vivo chemical conjugation is a distinctive property of the oxidized avidin. Relevance of the high cationic charge of avidin into the stable linkage of AvidinOX to tissues is demonstrated as the oxidized acetylated avidin lost the property. Plasmon resonance on matrix proteins and cellular impedance analyses showed in vitro that avidin exhibits a peculiar interaction with proteins and cells that allows the formation of highly stable Schiff's bases, after oxidation
Characterization of Granulations of Calcium and Apatite in Serum as Pleomorphic Mineralo-Protein Complexes and as Precursors of Putative Nanobacteria
Calcium and apatite granulations are demonstrated here to form in both human and
fetal bovine serum in response to the simple addition of either calcium or
phosphate, or a combination of both. These granulations are shown to represent
precipitating complexes of protein and hydroxyapatite (HAP) that display marked
pleomorphism, appearing as round, laminated particles, spindles, and films.
These same complexes can be found in normal untreated serum, albeit at much
lower amounts, and appear to result from the progressive binding of serum
proteins with apatite until reaching saturation, upon which the mineralo-protein
complexes precipitate. Chemically and morphologically, these complexes are
virtually identical to the so-called nanobacteria (NB) implicated in numerous
diseases and considered unusual for their small size, pleomorphism, and the
presence of HAP. Like NB, serum granulations can seed particles upon transfer to
serum-free medium, and their main protein constituents include albumin,
complement components 3 and 4A, fetuin-A, and apolipoproteins A1 and B100, as
well as other calcium and apatite binding proteins found in the serum. However,
these serum mineralo-protein complexes are formed from the direct chemical
binding of inorganic and organic phases, bypassing the need for any biological
processes, including the long cultivation in cell culture conditions deemed
necessary for the demonstration of NB. Thus, these serum granulations may result
from physiologically inherent processes that become amplified with calcium
phosphate loading or when subjected to culturing in medium. They may be viewed
as simple mineralo-protein complexes formed from the deployment of
calcification-inhibitory pathways used by the body to cope with excess calcium
phosphate so as to prevent unwarranted calcification. Rather than representing
novel pathophysiological mechanisms or exotic lifeforms, these results indicate
that the entities described earlier as NB most likely originate from calcium and
apatite binding factors in the serum, presumably calcification inhibitors, that
upon saturation, form seeds for HAP deposition and growth. These calcium
granulations are similar to those found in organisms throughout nature and may
represent the products of more general calcium regulation pathways involved in
the control of calcium storage, retrieval, tissue deposition, and disposal
Update on hypertrophic cardiomyopathy and a guide to the guidelines
Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular disorder, affecting 1 in 500 individuals worldwide. Existing epidemiological studies might have underestimated the prevalence of HCM, however, owing to limited inclusion of individuals with early, incomplete phenotypic expression. Clinical manifestations of HCM include diastolic dysfunction, left ventricular outflow tract obstruction, ischaemia, atrial fibrillation, abnormal vascular responses and, in 5% of patients, progression to a 'burnt-out' phase characterized by systolic impairment. Disease-related mortality is most often attributable to sudden cardiac death, heart failure, and embolic stroke. The majority of individuals with HCM, however, have normal or near-normal life expectancy, owing in part to contemporary management strategies including family screening, risk stratification, thromboembolic prophylaxis, and implantation of cardioverter-defibrillators. The clinical guidelines for HCM issued by the ACC Foundation/AHA and the ESC facilitate evaluation and management of the disease. In this Review, we aim to assist clinicians in navigating the guidelines by highlighting important updates, current gaps in knowledge, differences in the recommendations, and challenges in implementing them, including aids and pitfalls in clinical and pathological evaluation. We also discuss the advances in genetics, imaging, and molecular research that will underpin future developments in diagnosis and therapy for HCM
Genetically elevated high-density lipoprotein cholesterol through the cholesteryl ester transfer protein gene does not associate with risk of Alzheimer's disease
Introduction: There is conflicting evidence whether high-density lipoprotein cholesterol (HDL-C) is a risk factor for Alzheimer's disease (AD) and dementia. Genetic variation in the cholesteryl ester transfer protein (CETP) locus is associated with altered HDL-C. We aimed to assess AD risk by genetically predicted HDL-C.
Methods: Ten single nucleotide polymorphisms within the CETP locus predicting HDL-C were applied to the International Genomics of Alzheimer's Project (IGAP) exome chip stage 1 results in up 16,097 late onset AD cases and 18,077 cognitively normal elderly controls. We performed instrumental variables analysis using inverse variance weighting, weighted median, and MR-Egger.
Results: Based on 10 single nucleotide polymorphisms distinctly predicting HDL-C in the CETP locus, we found that HDL-C was not associated with risk of AD (P > .7).
Discussion: Our study does not support the role of HDL-C on risk of AD through HDL-C altered by CETP. This study does not rule out other mechanisms by which HDL-C affects risk of AD
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