Publications by authors named "F Saji"

Background And Aim: Rehabilitation for people with severe mental illness is incomplete without life skills assessment and intervention. The aim of the study was develop a culturally specific performance-based measure assessing life skills of patients with severe mental illness.

Materials And Methods: The items for the Vellore Inventory of Life Skills (VILS) were drawn after consultation with a reference group and from existing standardized scales.

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The detailed ultrastructural changes of uremia-induced hyperplastic parathyroid gland and the effects of current medical treatments for secondary hyperparathyroidism were investigated. Marked enlargement of parathyroid cell with accumulation of mitochondria and lipids and a significant increase in the thickness of the pericapillary area with increased fibrosis and appearance of fibroblast like cells were noted in the hyperplastic gland caused by uremia and phosphate retention. These ultrastructural changes and biochemical findings indicating hyperparathyroidism were significantly suppressed by all of the treatment using phosphate restriction, calcitriol, and cinacalcet.

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Article Synopsis
  • Parathyroid hormone (PTH) from parathyroid glands manages calcium and phosphate balance, and its development begins early in embryonic stages, relying on the transcription factor Gcm2.
  • Genetic loss of Gcm2 leads to parathyroid agenesis, but the role of MafB becomes important later, as it helps with parathyroid cell development and their proper migration.
  • In mice lacking MafB, parathyroid glands remain fused to the thymus, disrupting PTH production and bone mineralization, emphasizing the collaboration between Gcm2 and MafB in parathyroid organogenesis.
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Objective: Although an epidemiological link between the metabolic syndrome and kidney stone formation has been reported, the mechanism by which metabolic syndrome promotes kidney stone formation has yet to be elucidated. We investigated calcium oxalate (CaOx) kidney stone formation in a rat metabolic syndrome model.

Methods: We induced hyperoxaluria in 8-week-old male Otsuka Long-Evans Tokushima fatty (OLETF) rats, and a control strain, Long-Evans Tokushima Otsuka (LETO) rats, by administering 1.

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Fibroblast growth factor 23 (FGF23), which is primarily produced by osteocytes in bone, regulates renal phosphate excretion and 1α,25-dihydroxyvitamin D [1,25(OH)(2)D(3)] metabolism. Patients with chronic kidney disease (CKD) have increased levels of circulating serum FGF23, but the direct effect on circulating FGF23 levels in renal insufficiency is still unclear. To identify the major regulator of FGF23 synthesis in renal insufficiency, we compared the effect of parathyroid hormone (PTH) and 1,25(OH)(2)D(3) on FGF23 synthesis in the calvariae of normal rats with that of uremic rats in vitro.

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