Search PubMed⌕ Search

Biomedical subjects

R Rajendram

Publications and source records attributed to R Rajendram.

4 recordsLinked to original sources
PubMed2001

Eclipse retinopathy.

PURPOSE: Solar retinopathy is a well-recognised clinical entity of macular damage caused by viewing the sun, induced by a photochemical process. The term 'eclipse retinopathy' is frequently employed when the condition is sustained as a result of viewing a solar eclipse. Considerable public excitement had been raised in anticipation of the full solar eclipse on 11 August 1999. Whilst experience has shown that visual morbidity is likely to be temporary, current evidence is anecdotal and restricted to isolated case reports and series. This study was conducted to establish the true visual morbidity associated with a solar eclipse, and whether it was temporary or permanent. METHODS: A 3 month active case ascertainment study was carried out from July to September 1999 to record cases presenting to ophthalmologists with visual symptoms arising from solar viewing. Further information about the cases was sought using a short questionnaire. A follow-up questionnaire requesting outcome data at 6 months was also employed. RESULTS: There were 70 reported cases of visual loss. The average age was 29.5 +/- 12.9 years. Half the cases presented to an ophthalmologist within 2 days of the eclipse. An abnormal macular appearance was reported in 84% of patients at presentation. There have been no reported cases of continued visual loss or symptoms at 6 months. CONCLUSIONS: This is the largest nationwide study of the visual effects of a solar eclipse ever undertaken. There were no recorded cases of permanent visual loss, which corroborates the previous evidence that visual morbidity is likely to be temporary. It would appear probable that public health education was most effective in reducing visual morbidity and hence keeping the consequent burden on the NHS to a minimum.

Adolescent↗
PubMed2001

Alcoholic skeletal muscle myopathy: definitions, features, contribution of neuropathy, impact and diagnosis.

Alcohol misusers frequently have difficulties in gait, and various muscle symptoms such as cramps, local pain and reduced muscle mass. These symptoms are common in alcoholic patients and have previously been ascribed as neuropathological in origin. However, biochemical lesions and/or the presence of a defined myopathy occur in alcoholics as a direct consequence of alcohol misuse. The myopathy occurs independently of peripheral neuropathy, malnutrition and overt liver disease. Chronic alcoholic myopathy is characterized by selective atrophy of Type II fibres and the entire muscle mass may be reduced by up to 30%. This myopathy is arguably the most prevalent skeletal muscle disorder in the Western Hemisphere and occurs in approximately 50% of alcohol misusers. Alcohol and acetaldehyde are potent inhibitors of muscle protein synthesis, and both contractile and non-contractile proteins are affected by acute and chronic alcohol dosage. Muscle RNA is also reduced by mechanisms involving increased RNase activities. In general, muscle protease activities are either reduced or unaltered, although markers of muscle membrane damage are increased which may be related to injury by reactive oxygen species. This supposition is supported by the observation that in the UK, alpha-tocopherol status is poor in myopathic alcoholics. Reduced alpha-tocopherol may pre-dispose the muscle to metabolic injury. However, experimental alpha-tocopherol supplementation is ineffective in preventing ethanol-induced lesions in muscle as defined by reduced rates of protein synthesis and in Spanish alcoholics with myopathy, there is no evidence of impaired alpha-tocopherol status. In conclusion, by a complex series of mechanisms, alcohol adversely affects skeletal muscle. In addition to the mechanical changes to muscle, there are important metabolic consequences, by virtue of the fact that skeletal muscle is 40% of body mass and an important contributor to whole-body protein turnover.

Alcoholic Neuropathy↗
PubMed2001

Heart 7-hydroperoxycholesterol and oxysterols are elevated in chronically ethanol-fed rats.

Recently, cholesterol hydroperoxides have been shown to be sensitive pathogenic markers of reactive oxygen species (ROS)-mediated damage though they have never been measured in heart tissue. We hypothesized that cholesterol hydroperoxides and oxysterols, putative cardiotoxic products of cholesterol oxidation, are elevated in the hearts of alcoholics as a consequence of ROS-mediated reactions. To test this, we measured 7alpha- and 7beta-hydroperoxycholest-5-en-3beta-ol (7alpha-OOH and 7beta-OOH) by HPLC with postcolumn chemiluminescence as well as 7alpha- and 7beta-hydroxycholesterol (7alpha-OH and 7beta-OH) and 3beta-hydroxycholest-5-en-7-one (also termed 7-ketocholesterol; 7-keto) by HPLC-UV in cardiac muscle of alcohol-fed rats. Alcohol feeding was carried out using a pair-feeding protocol with 35% of total dietary energy as ethanol; controls were pair-fed isocaloric glucose. After 6-7 wk treatment with alcohol, heart 7alpha-OOH, 7beta-OOH and 7beta-OH were significantly greater than in controls. Levels of heart phospholipid 16:0 and 18:1 were lower than in controls, while 18:0 and 18:2 were greater. This is the first report of the presence of 7alpha-OOH, 7beta-OOH and 7alpha-OH in cardiac tissue. The elevations in 7alpha-OOH and 7beta-OOH as well as 7beta-OH are evidence of increased oxidative stress and possible membrane changes. Alterations in the proportions of 16:0, 18:1, 18:2 and 18:0 in heart phospholipids provide further evidence of an altered membrane domain.

Administration, Oral↗