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Biomedical subjects

K Raza

Publications and source records attributed to K Raza.

23 records · Page 2Linked to original sources
PubMed1997

Juvenile onset ankylosing spondylitis--more girls than we thought?

OBJECTIVE: To define the sex ratio of juvenile onset ankylosing spondylitis (AS) among a large population. METHODS: Using a standard questionnaire, data were collected from 3362 subjects, members of the National Ankylosing Spondylitis Society and patients at a tertiary referral center. RESULTS: Of 3362 patients, 2461 (73%) were male; male:female sex ratio was 2.7:1. Of the total, 379 (11%) had disease onset between the ages of 5 and 16 years. Of these, 278 were boys and 101 girls, giving an overall male:female ratio, in juvenile AS, of 2.6:1. For those with onset ages 5-13 years there was a ratio of 2.1:1, while for those aged over 14 years at onset, the ratio was 3.2:1. CONCLUSION: Older published ratios, ranging from 4.5:1 to 6:1, used smaller samples, focusing only on subjects who were juveniles at the time of the study. Our data collection method, which recruits from 2 sources and includes adults with juvenile onset, attempts to avoid these methodological problems. The data suggest a higher incidence of juvenile AS among females than previously described.

Adolescent↗
PubMed1993

Role of magnetic resonance imaging in the assessment of spinal injuries.

Magnetic Resonance Imaging (MRI) examination was carried out on 44 patients who had spinal injuries with neurological involvement. The technique provided valuable information about the nature of the injuries and, in particular, about the state of the spinal cord. The appearances of the cord on MRI ranged from normal, to oedema, to more severe damage such as cord haemorrhage or transection or, in later cases, myelomalacia. The appearance of the cord on MRI correlated strongly with both the severity of the neurological deficit and also the degree of subsequent recovery. In the assessment of the acute spinal injury, MRI has been shown to be a good prognostic indicator; it may also help to identify which patients are likely to benefit from early decompression.

Acute Disease↗
PubMed1991

Non-enzymic modification of lens proteins by glucose and fructose: effects of ibuprofen.

Cataract is the major cause of blindness worldwide. Non-enzymic modification of lens proteins leading to a disruption of their short range order is an important route to cataract formation. A reaction between lens proteins and a compound found in the lens indicates a potential role for that compound in cataract formation. The reactions of glucose and fructose with lens protein in vitro were investigated. Fructose bound to lens protein at pH 6.9 in a time-dependent fashion over a period of 20 days. The reactions of both glucose and fructose with lens proteins and bovine serum albumin led to the formation of coloured and fluorescent compounds. The formation of such compounds was greater with fructose than with glucose. The kinetics of the reactions of lens proteins and bovine serum albumin with fructose as measured by the formation of the above compounds were not identical. This point must be appreciated when attempting to extrapolate from results obtained with bovine serum albumin as to the reactions of lens proteins. The incubation of lens proteins with fructose led to an enhancement of protein aggregation. The implications of the reactions between lens proteins and fructose for the formation of cataract in diabetics are discussed. Ibuprofen intake is associated with protection against cataract. At relatively high concentrations (10-20 mM) ibuprofen decreased the binding of fructose to lens protein: this decrease was statistically significant at selected times (Student's t-test, P less than 0.05). The formation of fluorescent compounds in the presence of fructose was also decreased by ibuprofen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

The role of endothelial cell dysfunction in the cardiovascular mortality of RA.

Rheumatoid patients present clinically with chronic inflammatory immune arthritis but die of the same cardiovascular (CVS) disease as the normal population. Recent studies emphasize the increased frequency and earlier development of CVS involvement in RA. The mechanisms of this accelerated atherosclerosis are the subject of active research. The hypothesis that rheumatoid vasculitis is a major factor has been pursued through studies in primary systemic vasculitis. These reveal diffuse endothelial dysfunction occurring across a spectrum of vasculitis and involving more than one vascular bed. This may relate to cytokines such as TNF alpha that are both prominent in rheumatoid inflammation and important in the upregulation of endothelium in innate immune responses. Endothelial injury or dysfunction is widely accepted as the initial factor in atheroma. Its occurrence in vasculitis leads us to propose a model for RA where this dysfunction is the essential first step on which other factors, ranging from adverse lipid profiles to specific T-cell subsets, may build accelerated atherogenesis related to the rheumatoid inflammation.

Arteriosclerosis↗