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2 votal factor in the cell injury mechanism of nephropathic cystinosis and provide evidence linking cel
3 dysfunction and progressive renal failure in nephropathic cystinosis are largely unclear, and increas
12 agement of primary hyperoxalurias as well as nephropathic cystinosis provide important general inform
16 mutations in the CTNS gene, is a hallmark of nephropathic cystinosis, but the role of these crystals
18 In kidney biopsy samples from patients with nephropathic cystinosis, clusterin protein expression wa
19 te, an antioxidant therapy for patients with nephropathic cystinosis, in a mouse model of unilateral
20 hogenic mutations in patients with infantile nephropathic cystinosis, including a common, approximate
21 s study, we screened patients with infantile nephropathic cystinosis, those with late-onset cystinosi
22 e of pathogenic and adaptation mechanisms of nephropathic cystinosis, we defined the onset of Fanconi
23 molecular and cellular mechanisms underlying nephropathic cystinosis, which exhibits generalized prox
24 functional evidence of abnormal mitophagy in nephropathic cystinosis, which may contribute to the ren
31 It is here reported that in both normal and nephropathic cystinotic fibroblasts and cultured renal p
32 thdrawal causes an apoptotic rate of 8.7% in nephropathic cystinotic fibroblasts, compared with 6.1%
33 sure induced apoptosis in 18.1% and 17.4% of nephropathic cystinotic fibroblasts, respectively, versu
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