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1 dominant disorder consisting of deafness and hypopigmentation.
2 istopathies which display varying degrees of hypopigmentation.
3 evel of protection is compromised in case of hypopigmentation.
4 ardiomyopathy, combined immunodeficiency and hypopigmentation.
5 focal autoimmunity, manifested as autoimmune hypopigmentation.
6  and a small proportion of them develop mild hypopigmentation.
7 ariable microphthalmia and patchy coat color hypopigmentation.
8 -) macrophages did develop antibody-mediated hypopigmentation.
9         All forms of OCA exhibit generalized hypopigmentation.
10 ffects of modifier loci on the patterning of hypopigmentation.
11 nt for the k10(C3H) action on white forelock hypopigmentation.
12 almost all of the genetic variance of dorsal hypopigmentation.
13 responding to immunotherapy who have induced hypopigmentation.
14 ernal behavior in addition to p gene-related hypopigmentation.
15 10.0%) had hyperpigmentation, 43 (13.4%) had hypopigmentation, 249 (77.8%) had small drusen, 250 (78.
16 kin atrophy (17, 28%, vs 5, 8%; p=0.008) and hypopigmentation (27, 45%, vs 9, 15%; p=0.001).
17 e) were fatigue (29 patients), skin and hair hypopigmentation (28), diarrhoea (27), and nausea (27).
18  99%; hyperpigmentation, 11% versus 11%; and hypopigmentation, 4% versus 7%, respectively.
19 es had early AMD (drusen, hyperpigmentation, hypopigmentation), 5 had extrafoveal geographic atrophy,
20 ruption (24 [29%]), pruritus (10 [12%]), and hypopigmentation (7 [8%]).
21                                              Hypopigmentation along Blaschko's lines is a hallmark of
22  a neuroectodermal syndrome combining linear hypopigmentation, alopecia, apparently asymptomatic leuk
23 ates other important disease hallmarks, like hypopigmentation and accumulation of intracellular debri
24 Hermansky-Pudlak syndrome (HPS) is a genetic hypopigmentation and bleeding disorder caused by defecti
25 bentafusp therapy can lead to diffuse fundus hypopigmentation and choroidal thinning, similar to what
26 s, and suggest that other patients with mild hypopigmentation and decreased vision should be examined
27  taken from baseline, the progressive fundus hypopigmentation and depigmentation of the tumour remnan
28 tem and peripheral nervous system as well as hypopigmentation and enteric aganglionosis.
29              Melanoma patients who developed hypopigmentation and had improved survival after polyval
30 me (WS) is a hereditary disorder that causes hypopigmentation and hearing impairment.
31                                   Therefore, hypopigmentation and hearing loss in WS2 are likely to b
32  the DBA/J background and causes generalized hypopigmentation and localized white-spotting in mice, w
33                            Funduscopy showed hypopigmentation and optic disc pallor.
34 s, pekin (pn), also demonstrated generalized hypopigmentation and other defects, including disruption
35 ell as gross morphological defects including hypopigmentation and pericardial oedema.
36 e (HPS), a genetic disorder characterized by hypopigmentation and platelet storage pool deficiency.
37  coat in heterozygotes, but did lead to coat hypopigmentation and reduced copper content in the brain
38  syndrome, a condition characterized by mild hypopigmentation and severe, primary neurological abnorm
39 esented pigmented macules on a background of hypopigmentation and teleangiectasias, resulting in a po
40 e libraries of mutated DNA induce autoimmune hypopigmentation and tumor immunity through cross-recogn
41 ns of all types of OCA include skin and hair hypopigmentation and visual impairment.
42  Here we describe moonlight (mnlt), a second hypopigmentation and white-spotting mutation identified
43 9 years; 273 women), 98 (25.3%) displayed LC hypopigmentation, and 251 (64.7%) exhibited cortical AD
44 e, trichorrhexis nodosa, facial dysmorphism, hypopigmentation, and cardiac defects.
45 generation was determined by the presence of hypopigmentation, and cortical AD neuropathology was ass
46 autoimmune disease vitiligo, therapy-induced hypopigmentation, and cutaneous melanoma has not been we
47 opper transporter localization contribute to hypopigmentation, and hence perhaps other systemic defec
48 ts, thickened Bruch's membrane, and atrophy, hypopigmentation, and hyperpigmentation of the retinal p
49 ents such as retarded body growth, cutaneous hypopigmentation, and hypocholesterolemia when compared
50 ve extreme early-onset obesity, hyperphagia, hypopigmentation, and hypocortisolism, resulting from th
51 uch as increased thickness, high resilience, hypopigmentation, and lack of hair follicles.
52 ma, rash, pruritus, hyperpigmentation, pain, hypopigmentation, and oedema) occurred in 943 (93%) of 1
53 imals exhibited growth failure, skin laxity, hypopigmentation, and seizures because of perinatal copp
54 nting with aganglionosis in association with hypopigmentation are classified as Waardenburg syndrome
55 an archetypal rare condition associated with hypopigmentation, as an exemplar for the study of geneti
56 s albinism (OCA) shares cutaneous and ocular hypopigmentation associated with common developmental ab
57 e autosomal recessive disorder, resulting in hypopigmentation, bleeding and immune cell dysfunction.
58 elination and development, organomegaly, and hypopigmentation, but neither had osteopetrosis.
59                     Our results suggest that hypopigmentation can result from a defect in melanosome
60                         Vitiligo (autoimmune hypopigmentation) can be mediated by T cells, FcgammaR+m
61 ipal features (callosal agenesis, cataracts, hypopigmentation, cardiomyopathy, and immune dysfunction
62 ox10(Dom) mice and WS-IV patients consist of hypopigmentation, cochlear neurosensory deafness, and en
63 sative for oculocutaneous albinism type 7, a hypopigmentation disorder accompanied by poor visual acu
64  has provided several significant models for hypopigmentation disorders, including the major forms of
65 rapeutic target to promote repigmentation in hypopigmentation disorders.
66 uction, as occurs in vitiligo and other skin hypopigmentation disorders.
67 ted organelles complex 1 (BLOC-1), result in hypopigmentation due to mistrafficking of cargo to endol
68 oximity to a previously reported modifier of hypopigmentation for the endothelin receptor B mouse mod
69 ssive blood phenylalanine (Phe), musty odor, hypopigmentation, growth retardation, and progressive ne
70               Visual defects associated with hypopigmentation have been studied extensively in Siames
71 PS), an inherited disorder of humans causing hypopigmentation, hemorrhaging and early death due to lu
72 rboring the knock-in Clcn7 variant exhibited hypopigmentation, hepatomegaly resulting from abnormal s
73       Patients exhibit retarded body growth, hypopigmentation, hypocholesterolemia and low levels of
74 s hypopigmentation in 5 (71%), and choroidal hypopigmentation in 5 (71%) patients.
75 nthus in 5 (71%), synophrys in 2 (29%), iris hypopigmentation in 5 (71%), and choroidal hypopigmentat
76                                         Iris hypopigmentation in 8 eyes was sector in 6 (75%) and dif
77                                    Choroidal hypopigmentation in 9 eyes (100%) showed a sector patter
78  phenylalanine concomitant with reversion of hypopigmentation in a dose-dependent manner for more tha
79  (PMH) is a common skin disorder that causes hypopigmentation in a variety of skin types.
80                     Fascin 1 knockout causes hypopigmentation in adult mice owing to migration and ce
81 lver mutation, which is associated with coat hypopigmentation in certain strain backgrounds.
82     However, we also observed an increase in hypopigmentation in conjunction with a C3HeB/FeJLe-a/a l
83 ttranslational processing of tyrosinase, and hypopigmentation in melan-p1 cells is the result of alte
84 tion into the culture medium, explaining the hypopigmentation in OCA-4.
85  development of cutaneous AEs, especially of hypopigmentation in patients with melanoma, could point
86 7]) cause OCA, a disorder that presents with hypopigmentation in skin, eyes, and hair.
87 a null mutation of Gli3 causes the increased hypopigmentation in Sox10(LacZ/+);Gli3(Mos1/)(+) double
88 the homologous mutation, R194C, also exhibit hypopigmentation in the fur and skin, as well as less pi
89  color in Native Americans caused detectable hypopigmentation in the Kalinago.
90 ecessive mutation in the mouse, mhyp (mosaic hypopigmentation), in a screen for novel proviral integr
91 ice exhibit variability of aganglionosis and hypopigmentation influenced by genetic background simila
92                                              Hypopigmentation is a consistent clinical feature in PKD
93 udlak Syndrome (HPS), whose symptoms include hypopigmentation, lysosomal abnormalities, and prolonged
94                 Linkage analysis localized a hypopigmentation modifier of the Dom phenotype to mouse
95                                    The mouse hypopigmentation mutant pearl is an established model fo
96 let-dense granules are abnormal in the mouse hypopigmentation mutant pearl.
97 d the varied expressivity of white spotting (hypopigmentation) observed in intrasubspecific crosses o
98                                              Hypopigmentation occurred in mice deficient in activatin
99 n of tebentafusp, fundoscopy revealed marked hypopigmentation of both fundi and depigmentation of the
100 ested as congenital hearing loss (~ 70%) and hypopigmentation of skin, hair and eyes.
101 lanosome production was evident in increased hypopigmentation of the coat together with dramatic quan
102 hain 3 beta (LC3), in MCs and induced slight hypopigmentation of the epidermis in mice.
103 als within a single pedigree exhibiting both hypopigmentation of the fur and diminished T cell-indepe
104               Waardenburg syndrome manifests hypopigmentation of the iris and choroid with imaging fe
105        Fundus examination disclosed punctate hypopigmentation of the retinal pigment epithelium mainl
106 on characterized by a bleeding diathesis and hypopigmentation of the skin, hair, and eyes.
107  group of genetic disorders characterized by hypopigmentation of the skin, hair, and eyes.
108 features associated with albinism, including hypopigmentation of the skin, hair, and eyes; optic trac
109  which include drusen of >= 1 disc area, any hypopigmentation or hyperpigmentation in zones 2 or 3, o
110 utosomal recessive disorder characterized by hypopigmentation or oculocutaneous albinism and severe i
111 causes widespread severe lysosome pathology (hypopigmentation, organomegaly, and delayed myelination
112    Chronic IFN-gamma signaling shows a clear hypopigmentation phenotype in both mouse and human skin.
113 and inactivation of mouse Vps33a causes buff hypopigmentation phenotype.
114 endent step, and likely explain the distinct hypopigmentation phenotypes associated with BLOC-1 and B
115 derwhite locus confer one of the most severe hypopigmentation phenotypes, similar to mutations at the
116                                The fact that hypopigmentation profoundly alleviates the D2 disease in
117 ients with Griscelli syndrome, presents with hypopigmentation, prolonged bleeding times, and platelet
118                                Patients show hypopigmentation, recurrent infections, mild coagulation
119  with developmental delay, organomegaly, and hypopigmentation resulting from lysosomal hyperacidity,
120                             In contrast, the hypopigmentation seen in the gunmetal strain is due to t
121 hree cellular mechanisms contributing to the hypopigmentation seen in the Hermansky-Pudlak syndrome:
122 utosomal recessive disorder characterized by hypopigmentation, severe immunologic deficiency with neu
123  the Fig4(Sac3) gene that results in tremor, hypopigmentation, spongiform degeneration of the brain,
124 n no skin/fur color change in a 13-day mouse hypopigmentation study and demonstrated robust and susta
125 both Fc gamma R gamma and C3 did not develop hypopigmentation, suggesting that complement and Fc gamm
126 ortin receptor 1 locus exhibited more severe hypopigmentation than either mutation alone, suggesting
127 phy, hippocampal atrophy and locus coeruleus hypopigmentation, than controls.
128  (TYRP-1) of melanocytes leads to autoimmune hypopigmentation (vitiligo) in mice.
129 ral/hippocampal atrophy) and locus coeruleus hypopigmentation were comparable among the groups.
130 athology, lobar atrophy and substantia nigra hypopigmentation were comparable among the three groups.
131                               Patches of RPE hypopigmentation were noted clinically in 57% of Rab38(c
132                 All 7 patients who developed hypopigmentation were treated for melanoma.
133 pigmentation with varying degrees of central hypopigmentation without exposure of underlying choroida
134                    The progressive choroidal hypopigmentation, without evidence of associated intraoc

 
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