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 sociated with long-term PRO impairment, with sclerotic and combination disease carrying the highest m

4 structures were highly discriminant between sclerotic and healthy glomeruli.

5 Sclerotic and mixed lesion types were more common in bot

6 6.8 times more likely to fracture than were sclerotic and mixed lesions (95% CI, 1.4 to 33.3).

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

8 rticipants (29.0%) had epidermal, 13 (41.9%) sclerotic, and 9 (29.0%) a combination of disease types.

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

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

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

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

13 ges) ranging from isolated foci to confluent sclerotic areas.

14 tinuity of small and large retinal arteries, sclerotic arteries, regions of vascular nonperfusion, co

15 Sclerotic bodies have been reported only in association

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

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

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

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

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

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

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

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

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

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

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

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

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

29 ndrome with use of imaging to assess whether sclerotic bone lesions, effusions, and organomegaly are

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

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

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

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

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

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

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

37 ctory form of cGVHD, and novel therapies for sclerotic cGVHD are critically needed.

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

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

40 an effective treatment option for refractory sclerotic cGVHD.

41 RM, and high FFS in patients with refractory sclerotic cGVHD.

42 b in patients with corticosteroid refractory sclerotic cGVHD.

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

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

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

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

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

48 Sclerotic chronic graft-versus-host disease (cGVHD) repr

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

50 e chronic GVHD (52.5%), followed by 131 with sclerotic chronic GVHD (30.0%), and 76 with combination

51 ter adjusting for confounders, patients with sclerotic chronic GVHD had mean FACT-BMT scores 6.1 poin

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

53 NCA, higher serum creatinine, crescentic and sclerotic classes, and higher Brix score were more frequ

54 s identified by their CT images: (1) biaxial sclerotic condylar SCB with no visible lesions: BS, (2)

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

56 After adjusting for confounders, senile sclerotic discs had the lowest cpCD (37.1% [95% confiden

57 GVHD, purposefully sampled for epidermal and sclerotic disease features, with ongoing sampling until

58 Most cases (77 of 112 [69%]) of sclerotic disease occurred without prior erythema.

59 Sensory innervation of the porous areas of sclerotic endplates in mice was confirmed.

60 and glaucomatous eyes were highest in senile sclerotic eyes (0.928) and lowest in generalized cup enl

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

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

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

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

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

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

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

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

69 Whole-slide features of Sclerotic Glomeruli (GS)%, Arterial Intimal Fibrosis (AI

70 Nephrosclerosis, defined by globally sclerotic glomeruli (GSG) and interstitial fibrosis and

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

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

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

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

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

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

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

78 Sclerotic glomeruli had an additional set of glycans lac

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

80 ed protein N-glycosylation characteristic of sclerotic glomeruli in diabetic kidney disease.

81 ed protein N-glycosylation characteristic of sclerotic glomeruli in DKD.

82 identify N-glycan structures in healthy and sclerotic glomeruli in formalin-fixed paraffin-embedded

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

84 lomerulus, and higher percentage of globally sclerotic glomeruli or IF/TA predicted progressive CKD.

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

86 1 nonsclerotic glomeruli and 16,614 globally sclerotic glomeruli per kidney, which progressively decr

87 Our model identified 96% and 91% of normal/sclerotic glomeruli respectively; 94% of arteries/arteri

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

89 iopsies revealed five N-glycan signatures of sclerotic glomeruli that significantly differed compared

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

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

92 osis (measured as the percentage of globally sclerotic glomeruli) with age, obesity, diabetes, smokin

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

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

95 NN results were used to quantify healthy and sclerotic glomeruli, interstitial fibrosis, tubular atro

96 surface area, greater proteinuria, fewer non-sclerotic glomeruli, larger glomeruli and higher single-

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

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

99 e per glomerulus, and percentage of globally sclerotic glomeruli.

100 istinguish normal versus nonsclerotic versus sclerotic glomeruli.

101 , culminating in reduced podocyte numbers in sclerotic glomeruli.

102 tubular atrophy, and the percentage of renal sclerotic glomeruli.

103 r volume and a higher percentage of globally sclerotic glomeruli.

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

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

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

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

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

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

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

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

112 of SSc, morphea (localized scleroderma), and sclerotic GVHD (SclGVHD) with disease biomarkers.

113 Sclerotic GVHD has clinical and histopathological simila

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

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

116 systemic sclerosis are also associated with sclerotic GVHD.

117 Sclerotic hippocampi contained fewer granule cells, fewe

118 Sclerotic hippocampi displayed proportional losses of sy

119 Sclerotic hippocampi were identified by the loss of Niss

120 boutons per granule cell between control and sclerotic hippocampi.

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

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

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

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

125 Specifically, we applied LFS in the sclerotic hippocampus to study the effects on spontaneou

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

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

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

129 igitally assessed by calculating the average sclerotic index of five random small arterioles in amygd

130 The sclerotic index values, density of collagen IV immunorea

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

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

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

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

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

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

137 , 12-77 years), demonstrating a total of 532 sclerotic lesions of the spine of greater than 0.3 cm(3)

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

139 tion barrier function and the development of sclerotic lesions.

140 helial cells participate in the formation of sclerotic lesions.

141 albuminuria nor in a sustained reduction in sclerotic lesions.

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

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

144 9 dB/year) were faster than in patients with sclerotic (mean -0.14, SD 0.77 dB/year) and diffuse (mea

145 (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

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

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

148 = 60), myopic glaucoma (n = 38), and senile sclerotic (n = 50).

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

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

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

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

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

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

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

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

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

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

159 erating media of leptomeningeal arteries and sclerotic penetrating vessels.

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

161 in cartilage destruction, calcification and sclerotic plate formation and that they remain abundant

162 itionally found in small cavities within the sclerotic plate.

163 sizing fucosylated and branched N-glycans in sclerotic podocytes.

164 used for PV reconstruction in 3 cases due to sclerotic PV.

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

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

167 s, irregular venous caliber with dilated and sclerotic segments, perivenular hemorrhages, and foci of

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

169 Thirty-two patients had severe sclerotic skin and received a median of 5 (range, 2-10)

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

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

172 Sclerotic skin manifestations are especially difficult t

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

174 Therapies to improve sclerotic skin resulting from these diseases are largely

175 Thus, sclerotic skin treated with the anti-EREG therapeutic an

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

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

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

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

180 , 22 myopic glaucomatous (MY), and 67 senile sclerotic (SS).

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

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

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

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

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

186 d young adult (aged <25 years) patients with sclerotic-type cutaneous chronic graft-versus-host disea

187 Sclerotic-type cutaneous chronic graft-versus-host disea

188 Sclerotic-type cutaneous chronic graft-versus-host disea

189 Sclerotic-type cutaneous chronic graft-versus-host disea

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

191 tic tool for detecting either crystalline or sclerotic vessels in BCD.

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

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

194 ages ranging from isolated foci to confluent sclerotic zones which-seemingly-constrain impulse conduc