ライフサイエンスコーパス: sclerotic

1 Only one patient was classified as sclerotic.

2 Low-risk group (micropapillomas and sclerotic and benign papillomas) was compared with high-

3 Sclerotic and mixed lesion types were more common in bot

4 6.8 times more likely to fracture than were sclerotic and mixed lesions (95% CI, 1.4 to 33.3).

5 allografted facial skin became progressively sclerotic and presented pigmented macules on a backgroun

6 y-three lesions were solid nonsclerotic; 26, sclerotic; and 21, lytic with cystic centers containing

7 himke's Syndrome, 7 of 30 glomeruli globally sclerotic; and one TBMN and early hypertensive changes w

8 d in keloids and dermatofibromas, but not in sclerotic areas of morphea.

9 s, the perivascular dystrophin was absent in sclerotic areas, suggesting that the loss of perivascula

10 Sclerotic bodies have been reported only in association

11 ivided bicellular forms or multiply septated sclerotic bodies in post-log phase, when the G14V-altere

12 Previously, these sclerotic bodies were thought to be pathognomonic for ne

13 ells to a phenotype transition that produces sclerotic bodies while repressing hyphal development.

14 ophilic, collagenous, round or ovoid bodies (sclerotic bodies) in various stages of calcification.

15 ssic hallmarks of osteopetrosis, a family of sclerotic bone diseases.

16 d was 87% for lytic bone lesions and 57% for sclerotic bone lesions (P = .002).

17 Conclusion: The number of sclerotic bone lesions at body CT is of potential value

18 Purpose: To determine if sclerotic bone lesions evident at body computed tomograp

19 among the three patient groups Four or more sclerotic bone lesions were detected in all 25 (100%) of

20 Results: Most commonly the sclerotic bone lesions were round, measured 0.3 cm (rang

21 ed included shape, size, and distribution of sclerotic bone lesions with subsequent calculation of di

22 indeterminate liver lesions, 2 patients with sclerotic bone lesions, 2 patients with breast abnormali

23 megaly, endocrinopathy, skin changes, edema, sclerotic bone lesions, and thrombocytosis.

24 Diagnostic yield is higher in lytic than in sclerotic bone lesions, in larger lesions, and for longe

25 e other 3 major criteria (Castleman disease, sclerotic bone lesions, or elevated VEGF) and at least o

26 papilledema, extravascular volume overload, sclerotic bone lesions, thrombocytosis, elevated VEGF, a

27 atient had a solid renal mass, 1 patient had sclerotic bone metastases (albeit inactive on PET), 1 pa

28 lysis showed nonspecific changes of markedly sclerotic bone with a variable degree of mineralization

29 hich are known to accumulate in the multiple sclerotic brain.

30 emokines were elevated in both lichenoid and sclerotic CGHVD plasma and were linked to CXCR3(+) lymph

31 therapy and resolution in both lichenoid and sclerotic CGVHD patients.

32 trials using imatinib for steroid refractory sclerotic cGVHD,showing response rates of 79%and 50%.

33 Progression of sclerotic change after treatment was identified in 49 pa

34 D is manifested by mucosal, salivary, and/or sclerotic changes that have been linked to pain and poor

35 our knowledge, of the effective treatment of sclerotic chronic cutaneous GVHD with narrowband UV-B (N

36 this therapeutic modality for patients with sclerotic chronic cutaneous GVHD.

37 of NB UV-B phototherapy for the treatment of sclerotic chronic cutaneous GVHD.

38 Sclerotic chronic graft-versus-host disease (GVHD) can r

39 A woman in her 40s presented with sclerotic chronic GVHD of the skin 6 years after HCT for

40 Collagen-rich sclerotic content is increased in restenotic lesions fro

41 ns, the model predicted the hypertrophic and sclerotic features of parenchyma progressing towards end

42 Dermal hyperneury and multiple sclerotic fibromas should be added to the list of cutane

43 ndrome, and 1 relative also showing multiple sclerotic fibromas, a cutaneous manifestation of PTEN (p

44 a chronic lichenoid (clGVHD), and a chronic sclerotic form (csGVHD).

45 This study shows that that formation of sclerotic glomerular adhesions is a critical step leadin

46 st genes involved in the pathogenesis of the sclerotic glomerular lesion in HIVAN, representational d

47 s a previously unrecognized component of the sclerotic glomerular lesion that develops in the course

48 rane, and staining was markedly increased in sclerotic glomerular lesions in the transgenic HIVAN mod

49 ors had a significantly higher prevalence of sclerotic glomeruli (P < 0.002), and their nonsclerotic

50 y was 99.2% for distinguishing normal versus sclerotic glomeruli and 96.7 and 97.8% for nonsclerotic

51 nt with atrophy and reabsorption of globally sclerotic glomeruli and hypertrophy of remaining nephron

52 MA had a significantly greater percentage of sclerotic glomeruli and worse tubulointerstitial fibrosi

53 In comparison, the prevalence of sclerotic glomeruli averaged 19 +/- 13%, 4 +/- 7%, and 7

54 i efficiently, including podocytes, but some sclerotic glomeruli contained no detectable Wt1 mutant c

55 rmal baseline Nx tissue and nonsclerotic and sclerotic glomeruli from 12 wk after 5/6 Nx were isolate

56 ed that atubular glomeruli were as common as sclerotic glomeruli in chronic rejection.

57 d by only 16% and the proportion of globally sclerotic glomeruli on biopsy increased by only 15%.

58 per kidney and increased to 141,714 globally sclerotic glomeruli per kidney in donors 70-75 years old

59 1 nonsclerotic glomeruli and 16,614 globally sclerotic glomeruli per kidney, which progressively decr

60 lated proteomic patterns of nonsclerotic and sclerotic glomeruli suggest early activation of proscler

61 However, podocytes in partially sclerotic glomeruli that still expressed WT1 at high lev

62 ly normal-appearing tubules, but enlarged or sclerotic glomeruli were also present.

63 meruli, recipients with a high prevalence of sclerotic glomeruli, and also in four recipients in whom

64 glomerular cellularity, crescent formation, sclerotic glomeruli, and tubulointerstitial injury were

65 ymosin beta4 immunostaining was increased in sclerotic glomeruli, predominantly in endothelial cells.

66 and 97.8% for nonsclerotic versus normal and sclerotic glomeruli, respectively.

67 istinguish normal versus nonsclerotic versus sclerotic glomeruli.

68 , culminating in reduced podocyte numbers in sclerotic glomeruli.

69 ) marked reduction in crescent formation and sclerotic glomeruli; iii) decreased interstitial fibrosi

70 he density of both nonsclerotic and globally sclerotic glomeruli; the total number of glomeruli was e

71 ients as having focal, mixed, crescentic, or sclerotic GN.

72 Sclerotic graft-versus-host disease (GVHD) is a distinct

73 haps through the induction of the potent pro-sclerotic growth factor, transforming growth factor beta

74 T genotype was associated with lower risk of sclerotic GVHD (hazard ratio [HR], 0.43; 95% confidence

75 enotypes were associated with higher risk of sclerotic GVHD (HR, 1.57; 95% CI, 1.13-2.18; P = .007 an

76 enotypes were associated with higher risk of sclerotic GVHD (HR, 2.50; 95% CI, 1.22-5.11; P = .01 and

77 Sclerotic GVHD has clinical and histopathological simila

78 se SNPs are also associated with the risk of sclerotic GVHD.

79 -DP heterodimer were associated with risk of sclerotic GVHD.

80 systemic sclerosis are also associated with sclerotic GVHD.

81 patients, 12 of 15 had abnormally low NAA in sclerotic hippocampi; 3 of these 12 also had abnormally

82 riquidar response was most pronounced in the sclerotic hippocampus (mean 24.5% increase in patients v

83 This suggests that the hyperexcitability of sclerotic hippocampus occurs, at least in part, from the

84 In the non-sclerotic hippocampus of patients with MTS, T2 relaxatio

85 ents with MTS-TLE, T2 relaxation time in the sclerotic hippocampus was prolonged by a mean of 19 ms (

86 terns of tau protein accumulation within the sclerotic hippocampus were noted.

87 ody, and cleft margins appeared increasingly sclerotic in persistently mobile VCFs.

88 The sclerotic index values, density of collagen IV immunorea

89 tal role in the development of the end stage sclerotic lesion characteristic of most forms of chronic

90 plexes can improve the sensitivity to detect sclerotic lesions compared with standard methods.

91 ular crescents in rapidly progressive GN and sclerotic lesions in FSGS.

92 Untreated rats developed sclerotic lesions in glomeruli not connected to normal t

93 system successfully identified and segmented sclerotic lesions in the thoracolumbar spine.

94 re osteopenia accompanied by focal lytic and sclerotic lesions in vertebrae and femur.

95 , 12-77 years), demonstrating a total of 532 sclerotic lesions of the spine of greater than 0.3 cm(3)

96 newly formed woven bone, which together form sclerotic lesions that closely mirror the osteoblastic b

97 helial cells participate in the formation of sclerotic lesions.

98 rn with a well-defined and often extensively sclerotic margin.

99 mixed cortical and nuclear, immature nuclear sclerotic, mature posterior subcapsular, and mature nucl

100 9 dB/year) were faster than in patients with sclerotic (mean -0.14, SD 0.77 dB/year) and diffuse (mea

101 (mean -9.16, SD 14.9 x10(-3) mm(2)/year) and sclerotic (mean -0.45, SD 20.6 x10(-3) mm(2)/year) optic

102 These defects resulted in sclerotic metaphyses with persistence of club-shaped lon

103 s of the target lesions were lytic (n = 33), sclerotic (n = 22), mixed (n = 42), and unclassified (n

104 IgA nephropathy, 5 of 16 glomeruli globally sclerotic; one in a patient with a family history of Sch

105 when compared with patients with diffuse and sclerotic optic disc damage, despite similar IOP reducti

106 Purely sclerotic or mixed (sclerosis and lysis) lesions were fo

107 such as patient's age, type of lesion (lytic/sclerotic or mixed), matrix mineralization, multiplicity

108 Chronic cutaneous GVHD can present with sclerotic or nonsclerotic changes of the skin and often

109 Thus, the sclerotic (Os/+) or normal (+/+) genotype and phenotype

110 with malignancy were benign papilloma (n=1), sclerotic papilloma (n=1), micropapilloma (n=2), and aty

111 papilloma (n=38), atypical papilloma (n=15), sclerotic papilloma (n=6), and micropapilloma (n=4) in 5

112 f four micropapillomas, and one (17%) of six sclerotic papillomas.

113 role of TGF-beta-dependent and -independent sclerotic pathways merit further investigation.

114 erating media of leptomeningeal arteries and sclerotic penetrating vessels.

115 olated from 28-month-old mice retained their sclerotic phenotype in vitro.

116 formation of the PV; eight (23%), a cordlike sclerotic PV; 19 (54%), a splenorenal shunt; 11 (31%), P

117 en to determine whether the intensity of the sclerotic response was modified by the estrogen status i

118 epithelial cells, in vitro and is present in sclerotic skin and diseased lungs of patients suffering

119 sfunction, and (3) limited mouth-opening and sclerotic skin cGVHD.

120 ium exposure (eg, gadodiamide) either in the sclerotic skin in NSF or in GAP.

121 The sclerotic skin manifestations of cGVHD (ScGVHD) result f

122 IL-13+ and CD8+ cells in sclerotic skin were identified by immunohistochemistry.

123 Clinical investigations confirmed sclerotic skin, joint contractures, bone abnormalities,

124 s on the basis of lesion composition (lytic, sclerotic, soft tissue), lesion size (< or = 2, > 2 to 5

125 ed astrocytes were abundantly present in non-sclerotic specimens.

126 ack of enhancement were associated with more sclerotic stroma and older patient age.

127 e nonsclerotic glomeruli was more similar to sclerotic than normal glomeruli (P < 0.0001).

128 The percentage of collagen-rich sclerotic tissue area was larger in restenotic specimens

129 Increased ET-1 immunoreactivity was found in sclerotic tissue compared with control and was associate

130 issue of hypercellular tissue, collagen-rich sclerotic tissue, atheroma and thrombus.

131 dence interval, 1.23 to 2.23) for those with sclerotic valves as compared with those with normal valv

132 ation, subjective lesion attenuation (purely sclerotic vs mixed), central versus peripheral lesion sa

133 ve was normal in 70 percent (3919 subjects), sclerotic without outflow obstruction in 29 percent (161