PurposeWe evaluated whether orally administered astaxanthin (AST) protects against oxidative damage in the ocular tissues of streptozotocin (STZ)-induced diabetic rats.Methods and ResultsFifty 6-week-old female Wistar rats were randomly assigned to receive an injection of STZ to induce diabetes (n = 40) or to remain uninduced (n = 10). The diabetic rats were randomly selected into four groups and they were separately administered normal saline, 0.6 mg/kg AST, 3 mg/kg AST, or 0.5 mg/kg lutein daily for eight weeks. Retinal functions of each group were evaluated by electroretinography. The expression of oxidative stress and inflammatory mediators in the ocular tissues was then assessed by immunohistochemistry, western blot analysis, ELISA, RT-PCR, and electrophoretic mobility shift assay (EMSA). Retinal functions were preserved by AST and lutein in different levels. Ocular tissues from AST- and lutein-treated rats had significantly reduced levels of oxidative stress mediators (8-hydroxy-2'-deoxyguanosine, nitrotyrosine, and acrolein) and inflammatory mediators (intercellular adhesion molecule-1, monocyte chemoattractant protein-1, and fractalkine), increased levels of antioxidant enzymes (heme oxygenase-1 and peroxiredoxin), and reduced activity of the transcription factor nuclear factor-kappaB (NF-κB).ConclusionThe xanthophyll carotenoids AST and lutein have neuroprotective effects and reduce ocular oxidative stress, and inflammation in the STZ diabetic rat model, which may be mediated by downregulation of NF-κB activity.

For the salvage of thrombosed AV fistulas, a device using rotational mechanism is more time-saving with a higher immediate success rate and secondary patency rate. However, the long-term patency results were not different.

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Growth impairment has been described in patients with juvenile rheumatoid arthritis (JRA). Both the direct action of underlying disease and prolonged corticosteroid usage for disease management may contribute to growth impairment. The purpose of this retrospective study was to evaluate the effect of systemic corticosteroid treatment on attained adult height in patients with JRA. We reviewed patients who first visited our hospital from 1973 to 1995 with a diagnosis of JRA. Adult height (AH) and the reported parental heights of these patients were recorded. Target height (TH) is estimated according to midparental height. Patients who never had or had only transient (less than 1 week) systemic corticosteroid therapy were classified as group 1. Group 2 included patients who had corticosteroid therapy for more than 1 week but never continuously for more than 12 months, and group 3 included patients on long-term steroid treatment (continuously for more than 1 year). Height data were analysed using adult height and the difference between adult height and target height (AH minus TH). Thirty-three patients fulfilling the diagnostic criteria for JRA were reviewed. Fourteen belonged to group 1, 13 to group 2 and six to group 3. The difference between adult height and target height in group 1 was 2.96 +/- 4.54 cm, in group 2 0.71 +/- 6.08 cm (group 1 vs. group 2, P = 0.28), and in group 3 -11.65 +/- 10.71 cm (group 1 vs. group 3, P<0.05). In 15 patients who never received corticosteroid therapy continuously for more than 1 year, AH-TH was statistically correlated neither with the cumulative corticosteroid exposure dose nor with cumulative corticosteroid exposure period by linear regression ( P = 0.408, P = 0.278, respectively). We concluded that continuous systemic corticosteroid usage for less than 1 year does not affect attained adult height in JRA patients; however, prolonged corticosteroid treatment for more than 1 year can lead to irreversible growth impairment.