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S Y Tan

Publications and source records attributed to S Y Tan.

At least 19 recordsLinked to original sources

Dengue maculopathy: a case report.

INTRODUCTION: Dengue fever is endemic in many countries of South East Asia. In spite of the occasional epidemics, dengue maculopathy remains a rare entity. CASE HISTORY: A 31-year-old gentleman was admitted with a 6-day history of fever, generalised rash, headache and myalgia after a trip to Malaysia. There were no bleeding manifestations. The lowest platelet count was 71 x 10,000/ml, the haematocrit was 42.7%, and dengue serology was positive. On the 8th day of illness, he complained of bilateral blurred vision. Detailed visual examination showed visual acuity of right eye 6/30 and left eye 6/50. Fundoscopy revealed dilated veins, hyperaemic optic discs, flame and blot haemorrhages, soft exudates and macular ischaemia. After a course of high-dose steroids, the visual acuity as well as colour vision improved markedly. DISCUSSION: The pathology of maculopathy is not obvious in this case, but an immunological reaction is suspected. There is a risk of residual visual impairment, and there is no definitive treatment. The use of high-dose steroids seemed to improve visual acuity and colour vision. However, it is not known whether immunosuppression improves the prognosis. Time for resolution is from 8 weeks to 4 months. Since there is an increase in the incidence of dengue fever in our region, coupled with rising international travel, one could postulate that global incidence of dengue-related maculopathy may become significant. CONCLUSION: Ocular complications associated with dengue fever are rare but may result in permanent visual impairment. Dengue fever should be suspected in travellers, particularly those returning from endemic areas, and they should be systematically screened for maculopathy when visual disturbances arise.

Adult↗

Comparison of oxidative damage in Malaysian end-stage renal disease patients with or without non-insulin-dependent diabetes mellitus.

BACKGROUND: Comparisons of oxidative indices and total antioxidant status between end-stage renal disease (ESRD) patients with or without diabetes is scant, especially in the Asian population. METHOD: The assays were carried out according to known established protocols. RESULT: The present study showed that ESRD patients with or without non-insulin-dependent diabetes mellitus (NIDDM) did not have any significant differences in antioxidant enzyme activities, advanced glycated end products (AGE), advanced oxidized protein products (AOPP) and ferric reducing ability of plasma (FRAP), indicating that hyperglycemia does not exacerbate oxidative damage in ESRD. The regulation of catalase and glutathione peroxidase is also altered in ESRD. Elevated FRAP was observed in both ESRD groups (with and without NIDDM). The dialysis process did not alter the antioxidant enzyme activities but decreased AGEs and FRAP and increased AOPP levels. CONCLUSION: Oxidative stress is present in ESRD but this is not significantly exacerbated by hyperglycemia. The contribution of components in the pathology of renal failure towards oxidative stress exceeds that of hyperglycemia.

Antioxidants↗

Plasmid-electroporated primary hepatocytes acquire quasi-physiological secretion of human insulin and restore euglycemia in diabetic mice.

We describe the durable correction of streptozotocin-induced murine diabetes by in vivo implantation of primary mouse hepatocytes electroporated ex vivo with a human proinsulin cDNA plasmid construct controlled by glucose and zinc regulatory elements. Transfected hepatocytes increased insulin transgene transcription and secretion within 10-20 min of exposure to 25 mM glucose or 60 microM zinc. Insulin release did not occur from secretory granules. Electroporated Rosa26 hepatocytes ( approximately 8 x 10(5) viable cells) were implanted in C57BL/6J diabetic mice in one of three sites: unresected liver, regenerating liver or mesentery. Control diabetic mice were implanted with untransfected hepatocytes. At 30 days after implantation, 8/15 control mice were alive, while 19/19 treated mice were alive. The ratio of body weight on day 30/nadir body weight was significantly higher for all treated groups compared with controls. All eight surviving control mice were hyperglycemic 30 days post-implantation, while 16/19 treated diabetic mice remained normoglycemic. Treated mice had lower mean glucose values (P< or =0.001) without fasting hypoglycemia and better glucose tolerance (P< or =0.0003) than untreated controls. All (6/6) diabetic mice implanted in regenerating liver and 71% (5/7) implanted in unresected liver were alive 77 days after implantation. Engrafted hepatocytes were identified, mainly around central veins, by staining for beta-galactosidase activity and with anti-human insulin antibody.

Animals↗