ライフサイエンスコーパス: depigmentation

1 mmunity were observed, characterized by coat depigmentation.

2 the incidence of retinal pigment epithelial depigmentation.

3 pigmentation with varying amounts of central depigmentation.

4 ntigen-specific T cells, resulting in patchy depigmentation.

5 disease of the skin characterized by patchy depigmentation.

6 cells and spontaneously developed autoimmune depigmentation.

7 the lack of an assessment method for active depigmentation.

8 ina that progresses to panretinal patches of depigmentation.

9 erse events were diarrhea, fatigue, and hair depigmentation.

10 lative efficacy of these agents in mediating depigmentation.

11 oss of epidermal melanocytes and progressive depigmentation.

12 ed protein 2-derived peptide correlated with depigmentation.

13 econd, unknown locus that causes progressive depigmentation.

14 spotting but show no evidence of progressive depigmentation.

15 ype of HPS with minimal cutaneous and ocular depigmentation.

16 ently experience stress to the skin prior to depigmentation.

17 ctivity in melanocyte cultures, resulting in depigmentation.

18 erall survival, in the absence of autoimmune depigmentation.

19 and is frequently accompanied by autoimmune depigmentation.

20 educed pigment deposition in melanocytes and depigmentation.

21 umor immunity and autoimmunity manifested as depigmentation.

22 ]), generalized pigment dilution and/or hair depigmentation (18 [44%]), xerosis (8 [20%]), scrotal er

23 3.34, 20.08) for retinal pigment epithelium depigmentation, 3.59 (95% CI: 1.71, 7.57) for increased

24 en (51.7%), retinal pigment epithelium (RPE) depigmentation (34.9%), RPE hyperpigmentation (branching

25 Progressive depigmentation accelerates in response to stress.

26 of the cumulative incidence of vitiligo-like depigmentation across studies.

27 al melanocytes is shown to cause progressive depigmentation and autoimmune vitiligo.

28 mally thin ONL co-localizing with severe RPE depigmentation and choroidal thinning.

29 s investigation might be of relevance to the depigmentation and degeneration of neuromelanin-pigmente

30 hogenic Cx31, but not wild-type Cx31, causes depigmentation and degeneration of ommatidia that are re

31 e against TRP-2 peptide, inducing autoimmune depigmentation and further decreasing lung tumor nodules

32 e-transgenic mice developed spontaneous hair depigmentation and had visual defects that progressed wi

33 tion with v-Ha-ras or Ela was accompanied by depigmentation and led to complete loss of msg1 expressi

34 n all transplanted mice, we noted a striking depigmentation and loss of hair follicles.

35 eins (TRP) 1 and TRP-2, we observed striking depigmentation and melanocyte destruction only in the sk

36 ne the cumulative incidence of vitiligo-like depigmentation and the prognostic value of vitiligo deve

37 ng an injection at an outside hospital, iris depigmentation and thinning, iris recession with retinal

38 arnet (Er:YAG) laser techniques for gingival depigmentation and to evaluate their effect on histologi

39 nocytes leads to autonomous growth in vitro, depigmentation, and in the case of the oncogenes, tumori

40 and globules, tan color, irregularly shaped depigmentation, and irregularly distributed and sized do

41 Photoreceptor degeneration, RPE depigmentation, and retinal remodeling follow.

42 such as rickets, abdominal distention, hair depigmentation, and skin lesions and with a maternal his

43 inning, discrete hyperreflective foci, focal depigmentation, and the presence of suprachoroidal hypor

44 ly, porphyrin biosynthesis and light-induced depigmentation are enhanced by starvation, recapitulatin

45 pigment epitelium, defects/pigment mottling, depigmentation area, subretinal haemorrhage, subretinal

46 5% of MT/ret mice develop a vitiligo, a skin depigmentation attributable to the lysis of normal melan

47 ing mouse models of vitiligo consist of hair depigmentation but lack prominent epidermal involvement,

48 Although qualitative SN depigmentation correlated modestly with age (p = 0.02),

49 SN depigmentation correlated with speed of 6- and 50-foot w

50 SN depigmentation, detected neuropathologically, was correl

51 .1(+) cells and Fc receptor gamma-chain, but depigmentation did not require these components.

52 as been shown in vivo that patients with the depigmentation disorder vitiligo accumulate hydrogen per

53 Patients with the depigmentation disorder vitiligo have low catalase expre

54 Vitiligo is the most common cutaneous depigmentation disorder worldwide, yet little is known a

55 king the pathogenesis of alopecia to that of depigmentation disorders.

56 o, and active-specific immunotherapy-induced depigmentation had significant anti-TRP-2 IgG titers.

57 een known for several decades that cutaneous depigmentation, i.e., contact/occupational vitiligo, can

58 ulture, we determined the molecular basis of depigmentation in a mouse melanocyte model system.

59 egional magnetic resonance (MR) quantifiable depigmentation in association with PD severity and (b) t

60 herapy also induced tumor rejection and skin depigmentation in B cell-deficient and in CD4(+) T cell-

61 sed the regression of established tumors and depigmentation in lymphopenic hosts.

62 egeneration, attenuated retinal vessels, and depigmentation in mice lacking Sema4A.

63 that simvastatin both prevented and reversed depigmentation in our mouse model of vitiligo, and reduc

64 tical for the progression and maintenance of depigmentation in our mouse model of vitiligo.

65 Vitiligo-like depigmentation in patients with melanoma may be associat

66 Depigmentation in PD follows a distinct spatial pattern,

67 ed metastatic melanomas and developed patchy depigmentation in their coats.

68 f the 14 known missense mutations that cause depigmentation in these species map to the tyrosine kina

69 that the coexistence of parkinsonism and SN depigmentation in this birth cohort may have resulted fr

70 ocol significantly increased and accelerated depigmentation in this model, accompanied by the inducti

71 gly support a role for HSP70i in progressive depigmentation in vivo.

72 , size, and type; retinal pigment epithelium depigmentation; increased pigment; geographic atrophy; a

73 The cutaneous depigmentation induced by phenolic derivatives results f

74 donetwork, multiple blue-gray dots, scarlike depigmentation, irregularly distributed and sized brown

75 Depigmentation is accompanied by accumulation of autorea

76 Clinical repigmentation after gingival depigmentation is an outcome of histologic changes in th

77 , occurring in a kindred with more extensive depigmentation, is a novel four-base insertion in exon 2

78 retinal pigment, retinal pigment epithelial depigmentation, neovascular lesions, and geographic atro

79 retinal pigment, retinal pigment epithelial depigmentation, neovascular lesions, and geographic atro

80 However, loss of Rb resulted in severe depigmentation of hair follicles.

81 iameter with drusen area >/=196350 mum2) and depigmentation of retinal pigment epithelium (slope of -

82 ch the presence of bilateral soft drusen and depigmentation of retinal pigment epithelium was associa

83 by melanocyte loss, which results in patchy depigmentation of skin and hair, and is associated with

84 autoimmune disease in which acquired patchy depigmentation of skin, hair, and mucous membranes resul

85 and induced long term antitumor immunity and depigmentation of skin.

86 ratinocyte-melanocyte contact and results in depigmentation of the dark skinned Yucatan swine, sugges

87 sease of the skin causing disfiguring patchy depigmentation of the epidermis and, less commonly, hair

88 Depigmentation of the substantia nigra and other brainst

89 The prognostic value of vitiligo-like depigmentation on survival outcome was assessed using ra

90 no reduction in the severity or kinetics of depigmentation or long-lived protection against melanoma

91 5.6); presence of retinal pigment epithelial depigmentation (OR, 9.0; 95% CI, 4.1-19.8); or hyperpigm

92 stically significant values for Er:YAG laser depigmentation (P = 0.001).

93 al drusen (P<0.001) and mottled FAF with RPE depigmentation (P<0.001).

94 gaging anti-CD25 antibody fully restored the depigmentation phenotype in h3TA2-IFN-gamma(-/-) mice, m

95 Gingival melanin depigmentation procedures are commonly associated with r

96 Surgical stripping for gingival depigmentation remains the gold standard; however, Er:YA

97 go (GV) is a complex disease in which patchy depigmentation results from autoimmune loss of melanocyt

98 combination treatment, 56% (38/68) developed depigmentation, starting at the site of vaccination or c

99 d kindred characterized by unusually limited depigmentation, substitutes a threonine for an alanine a

100 body prevents CD8(+) T-cell accumulation and depigmentation, suggesting a therapeutic potential for t

101 peripheral nerve remyelination and focal fur depigmentation; surviving weak mice had persistent expre

102 d Drug Administration approved drug used for depigmentation therapy of advanced vitiligo.

103 TRP) 1, are relevant to both autoimmune skin depigmentation (vitiligo) and tumor immunity, because th

104 SN depigmentation was detected in 57 (13.2%) of the cohort.

105 of Treg abundance in preventing progressive depigmentation was evaluated by adoptively transferring

106 Depigmentation was found to occur in CD4-depleted mice,

107 In this model, depigmentation was introduced by gene gun vaccination wi

108 Depigmentation was significantly impaired only in IFN-ga

109 ciated with retinal pigment epithelium (RPE) depigmentation, was followed by disorganization and furt

110 Quantitative measures of SN depigmentation were increased in this birth cohort compa

111 Qualitative indices of substantia nigra (SN) depigmentation were verified in a subset of 40 randomly

112 ulating S100B levels in patients with active depigmentation which were strongly correlated with the e

113 ing offers a fully reversible model for hair depigmentation, which might be used for the studies of h

114 Treatment produced a skin depigmentation, which was associated with prolonged surv

115 es the human condition by inducing epidermal depigmentation while sparing the hair.

116 nknown origin, is the most frequent cause of depigmentation worldwide, with an estimated prevalence o