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1 f melanocytes and the clinical appearance of white spots.
2 ease of the skin that results in disfiguring white spots.
3 atches of depigmentation that are visible as white spots.
4 of me(v)/me(v) mice revealed numerous, small white spots.
5 abs were demineralized to produce artificial white spots.
6 he retinal pigment epithelium (89.3%), small white spots (80.2%), and optic nerve atrophy (76.9%) wer
8 ption, and was marked by the appearance of a white spot and a dark ring, coincident with entry into m
10 f esophagitis including oedema, granularity, white spots, and furrowing, while histology revealed oed
11 mature leaves suffered from burnt edges and white spots as well as a reduction in photosynthetic pig
12 ed a naive vNAR phage display library from a white-spotted bamboo shark (Chiloscyllium plagiosum), wi
13 ith progressive piebaldism, exhibit dominant white spotting but show no evidence of progressive depig
14 ents with TSC develop hypomelanotic macules (white spots), but the molecular mechanisms underlying th
15 the survival of these cells in vivo, because white spotting (c-kit(W/W)) mice, carrying a natural ina
17 cassava orthologous gene resulting in yellow-white spots characteristic of the inhibition of su expre
18 mestic cattle, the variants underpinning the white-spotted coat pattern of Holstein-Friesian and rela
19 caries-free subjects (SRS), (3) plaque from "white spot" coronal lesions and sound coronal surfaces o
22 virus susceptibility gene 2 (Fv2), dominant white spotting gene (W), and Steel gene (Sl), regulate t
23 normal a-wave and b-wave activity, yellowish-white spots, hyperfluorescence, and reduced retinal thic
25 n, which are defined clinically as yellowish white spots in the outer retina, are cardinal features o
26 biochemical evidence that hydrocephalus and white spotting in B3glct mutants resulted from loss of A
27 s generalized hypopigmentation and localized white-spotting in mice, with a lack of pigment on the be
28 es that differentiate this entity from other white spots, including acute placoid multifocal pigment
29 moderate certainty) and in the incidence of white spot lesions (risk ratio, 0.48; 95% CI, 0.35 to 0.
34 estigating mice with mutations affecting the white spotting locus (which encodes KIT) or the steel lo
35 e have a naturally occurring mutation in the white spotting locus that causes reduced c-Kit receptor
37 nlight (mnlt), a second hypopigmentation and white-spotting mutation identified on the C57BL/6J backg
39 descriptions of a dilution of coat color and white spotting of the belly and extremities, suggesting
40 vitiligo and persist to maintain disease, as white spots often recur rapidly after discontinuing ther
41 stage caries lesions typically present as a white spot on a white background, resulting in many lesi
42 he silencing phenotype ranged from scattered white spots on the normal purple background to entirely
43 ommon autoimmune conditions characterized by white spots on the skin (vitiligo) and bald spots on the
46 e report that a point mutation, the dominant white spotting oncogene allele, Kit(W-42J), exacerbates
47 a pronounced forehead blaze, with additional white spots over the cervical region, as well as a very
49 Transgene induction in skin resulted in a white spotting phenotype due to somatic ORFeus-mediated
50 us that were exclusively present in white or white-spotted pigs, carrying the Dominant white, Patch,
51 traits with mendelian inheritance: the major white spotting (S) locus and the hair ridge in Rhodesian
61 susceptibility of this nephrocomplex to both white spot syndrome virus and Vibrio infection compared
63 includes vertebrates, nonvertebrates, shrimp white spot syndrome virus, Streptococcus equi, and Bacil
64 d, accurate, single copy detection assay for White Spot Syndrome Virus, the most devastating virus im
65 retinal vasculitis, a characteristic retinal white spot syndrome, Bartonella retinitis, branch retina
66 diseases of the posterior fundus, including white spot syndromes and autoimmune, hereditary, paraneo
68 estruction of epidermal melanocytes produces white spots that can be repigmented by melanocyte precur
69 varian cancer risk using germ cell-deficient white-spotting variant (Wv) mice, incorporating oncogeni
70 us (IHHNV), a single-stranded DNA virus, and white spot virus (WSV), a double-stranded DNA (dsDNA) vi
71 clones from a hepatopancreas cDNA library of white spot virus (WSV)-infected shrimp provided a partia
72 lacking a SCF-responsive population of HPC [White spotted (W/WV) and Steel (SI/SId)] are unresponsiv
77 rtile mouse strains, Steel (Sl) and dominant white spotting (W), to determine if stem cells from an i
80 nary night blindness characterized by yellow-white spots, which were classically described as subreti