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1 nce identity range, the so-called 'BRaliBase Dent'.
2 book, Le Chirurgien Dentiste, ou Traite des Dents (1728), is the discipline's first complete work.
6 temporal endothelial cell density (DenC and DenT), and coefficient of variation in cell area (CVC an
8 uentially transform to nanoporous Cu/Cu2O/Cu dented cubic composites and hollow eightling-like Cu mic
11 hus, we created an animal model for OCRL and Dent Disease 2 tubulopathy by humanizing a modifier para
12 bservation confirms genetic heterogeneity in Dent disease and demonstrates more-extensive phenotypic
15 mal-tubular reabsorption and is decreased in Dent disease because of mutations of the chloride/proton
17 les, phenocopying what has been reported for Dent disease caused by mutations in the gene encoding en
18 s, our studies, which have established human Dent disease ciPTECs that will facilitate studies of mec
20 n occur with the isolated renal phenotype of Dent disease in patients lacking the cataracts, renal tu
22 t with a scenario in which Lowe syndrome and Dent disease result from perturbations at multiple sites
23 ations are responsible for Lowe syndrome and Dent disease, and INPP5B are two similar proteins compri
24 Genetic heterogeneity has been suspected in Dent disease, but no other gene for Dent disease has bee
25 rders oculocerebrorenal syndrome of Lowe and Dent disease, two conditions giving rise to abnormal kid
26 isms in renal reabsorption, demonstrate that Dent disease-causing CLC-5 mutations have differing effe
28 ed to heating process and/or can's damage by denting, exhibited a significant increase in the migrati
29 n the cell cytoskeleton as well as prominent dents in the cell membrane upon induced apoptosis were r
30 t appears that the transient deformation (or dent) in the tube wall may provide a previously unknown
32 ndoreduplication phenotype into a midwestern dent inbred line, a backcross population was generated f
34 idence of selection in the maize Krug Yellow Dent long-term divergent seed-size selection experiment.
38 Hybrid WF9 * 38MS, B73 * Missouri 17, Yellow Dent, Merit, and Great Lakes Hybrid 422) to reinvestigat
40 was observed for eight of nine families with Dent's disease (n = 10) and for the two families with Lo
44 us, CLC-5-deficient mice provide a model for Dent's disease and this will help in elucidating the fun
45 rome and low molecular weight proteinuria in Dent's disease can be explained by disruption of endosom
51 acilitate in vivo investigations of CLC-5 in Dent's disease we generated mice lacking CLC-5 by target
52 rine composition in eight male patients with Dent's disease, ages 6 to 49 yr, all of whom were hyperc
53 jor risk factor promoting stone formation in Dent's disease, also known as X-linked recessive nephrol
54 or are present in the urine of patients with Dent's disease, Lowe's syndrome, or autosomal dominant i
56 disorders of hypercalciuric nephrolithiasis (Dent's disease, X-linked recessive nephrolithiasis (XRN)
61 ssion (probands from the Depression Network [DeNT] study; N=332), and 3) a pharmacogenetic study (the
62 ittle variation was found between midwestern dent types, and high levels of endoreduplication were ob
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