ライフサイエンスコーパス: affected tissue

1 affected by diverticulitis and adjacent non-affected tissue.

2 mulation of lymphocytes and monocytes in the affected tissue.

3 mited T cell populations are concentrated in affected tissue.

4 le in the scavenging of apoptotic cells from affected tissue.

5 ammation requires their recruitment into the affected tissue.

6 at facilitated leukocyte infiltration to the affected tissue.

7 allele frequencies ranged from 6% to 19% in affected tissue.

8 he growth, survival, and general behavior of affected tissue.

9 ve B-cell and plasma cell infiltrates in the affected tissue.

10 g a slight reduction in the thickness of the affected tissue.

11 ces inflammation and oxidative stress in the affected tissue.

12 d activities of respiratory chain enzymes in affected tissues.

13 TCR analysis was applied to biopsies of GVHD-affected tissues.

14 accumulation of multiple mtDNA deletions in affected tissues.

15 rofiling and immunohistochemical analysis of affected tissues.

16 anisms underlying the fragility of other DM1-affected tissues.

17 on, through modified blood vessels, and into affected tissues.

18 tiple point mutations of mtDNA in clinically affected tissues.

19 d maintenance of a reactive background in HL-affected tissues.

20 to be recruited to mitochondria, but only in affected tissues.

21 of glycogen ( approximately 5-fold) from the affected tissues.

22 Ca(V)1.2 is expressed in all affected tissues.

23 Tim23 in the mitochondrial inner membrane in affected tissues.

24 free DNA released from breakdown in disease-affected tissues.

25 r inability to selectively transduce disease-affected tissues.

26 nstrated the presence of mycobacteria within affected tissues.

27 rates glycosaminoglycan accumulation in some affected tissues.

28 restricted blood flow led to ischemia in the affected tissues.

29 sible for the increased contractility of the affected tissues.

30 KD mutations on the pattern of expression in affected tissues.

31 hages and lymphocytes in the lungs and other affected tissues.

32 thus correlating CPAMD8 expression with the affected tissues.

33 ondria and endoplasmic reticulum (ER) of ALS-affected tissues.

34 abnormally folded cellular prion protein in affected tissues.

35 capsid proteins were abundantly expressed in affected tissues.

36 which induces granulomatous inflammation of affected tissues.

37 canonical Hh signaling in some, but not all, affected tissues.

38 tissues leads to a black pigmentation of the affected tissues.

39 gen and its accumulation as Lafora bodies in affected tissues.

40 sma cells and numerous B cells were found in affected tissues.

41 osinophils, mast cells, and basophils in the affected tissues.

42 The cartilage is one of the principal affected tissues.

43 an elevation in the number of neutrophils in affected tissues.

44 response to growth factor signalling in the affected tissues.

45 sorders in which adipose is one of the first affected tissues.

46 nts, resulting in the rapid lignification of affected tissues.

47 e three-dimensional (3D) architecture of the affected tissues.

48 ese disorders, amyloid fibers are present in affected tissues.

49 ent of neutrophils through vessel walls into affected tissues.

50 mic vascular tissues; 2) can be found in the affected tissues; 3) live within the affected site; 4) i

51 pocampal slices (1) how glucose availability affected tissue acidosis during and after anoxia, (2) wh

52 nd may be present in bone marrow and disease-affected tissues although absent in the peripheral blood

53 ed by an increase in apoptotic cell death in affected tissues, although cell cycling rates are unalte

54 e the predominant inflammatory infiltrate in affected tissue and are thought to produce cytokines tha

55 degeneration and nucleocapsid inclusions in affected tissue and axons, providing further evidence fo

56 ween oxidation (8-OH guanosine) levels in AD-affected tissue and histological amyloid burden and foun

57 nic cells are thought to be recruited to the affected tissue and induce mineralization.

58 that AAV9-hGAA is able to replace GAA to the affected tissue and modify AChR mRNA expression, muscle

59 to shed light on the interaction between the affected tissue and the inflammatory cells and suggest t

60 he status of an IFN-induced signature within affected tissue and to gauge the integrity of IFN signal

61 by severe reduction in mtDNA copy number in affected tissues and are associated with progressive myo

62 ssociated death domain (TRADD) protein in AD-affected tissues and cell cultures.

63 ial to directly correct genetic mutations in affected tissues and cells to treat diseases that are re

64 nd showed remarkable selectivity for disease-affected tissues and cells.

65 of endogenous cytokine-producing cells into affected tissues and could potentially influence HIV dis

66 cross-linking would reduce elastic recoil in affected tissues and explain the cutis laxa phenotype.

67 eletion of UGT2B17, a gene expressed in GVHD-affected tissues and giving rise to multiple histocompat

68 release by overexpressed enzyme activity in affected tissues and offers the unique possibility of ac

69 to obesity and cancer, where they infiltrate affected tissues and orchestrate immune responses in tan

70 ctor-1 expression both in systemic sclerosis affected tissues and peripheral blood mononuclear cells.

71 egulation evidenced by inflammatory cells in affected tissues and production of autoantibodies.

72 res of NF1 are the wide range of potentially affected tissues and the great variation in expressivity

73 of SSc owing to its increased expression in affected tissues and to the specific stimulation of AIF-

74 associated with reduced bacterial burden in affected tissues and with recruitment and activation of

75 Cartilage appears to be the primary affected tissue, and in one patient, a biopsy of the ili

76 been shown to be uniformly expressed in the affected tissue, and it is associated and colocalizes wi

77 regeneration, aggressive debridement of the affected tissue, and treatment with amphotericin B.

78 n, IgG4-positive plasma cell infiltration in affected tissues, and elevated serum concentrations of I

79 sed in both animals and patients with TLE in affected tissues, and in plasma in response to epileptic

80 vered that inflammatory infiltrates from the affected tissue are dominated by a distinct phenotype of

81 is task, neighboring epithelial cells in the affected tissue are postulated to contribute to this pro

82 ling of these processes can be hidden unless affected tissues are challenged by physical constraints.

83 The presence of ACR3 hardly affected tissue arsenic levels, but increased arsenic tr

84 l inflammation and macrophage density in the affected tissues (as indicated by paw swelling and histo

85 at p57KIP2 is not imprinted in at least some affected tissues at a critical stage of development and

86 neutrophilic and histiocytic inflammation in affected tissues became progressively more fibrinous and

87 Arg183Gln) in GNAQ was identified in the PWS-affected tissue but not in the normal skin sample.

88 utations were detected at very low levels in affected tissues but were undetectable in the blood, ind

89 f fever and serositis and by infiltration of affected tissues by large numbers of neutrophils.

90 be due to relative lack of imprinting in the affected tissue, cardiac muscle, representing a novel me

91 we found elevated (3-fold) FAS levels in UL-affected tissue compared to matched myometrial tissue.

92 pression and existing immune infiltration of affected tissue compared with normal lung and melanoma a

93 IL-23p19 was detected in periodontal disease-affected tissues compared to healthy gingival tissues.

94 nique and genetic background of donor plants affected tissue culture-induced variation.

95 endent on the developmental potential of the affected tissue, different caspases trigger distinct for

96 In the affected tissues, differentiation is initiated and many

97 When dissected from affected tissue, digested into protein fragments of diff

98 During inflammation, T cell traffic into the affected tissue dramatically increases; however, the dyn

99 surface antigens expressed in multiple cGVHD affected tissues, due to their potential functional impa

100 O production and iNOS mRNA expression in the affected tissues (eg, native lung and grafted heart); an

101 cells, macrophages, and endothelial cells in affected tissues expressed AIF-1.

102 Moreover, within affected tissues, expression of specific selenoproteins

103 SPM) that limit the host response within the affected tissue; failure of effective resolution may lea

104 or (BCR) repertoires, in blood as well as in affected tissue, for IgG4+ clones.

105 ine stains, but not in any of the samples of affected tissue from 4 participants with an unrelated ce

106 548G-->A, p.Arg183Gln) in GNAQ in samples of affected tissue from 88% of the participants (23 of 26)

107 generation sequencing using a panel to assay affected tissue from a diverse cohort of subjects with v

108 formed massively parallel mRNA sequencing on affected tissue from eight participants.

109 his mutant allele in unaffected tissue or in affected tissue from individuals with other types of vas

110 allele frequencies ranged from 3% to 30% in affected tissue from multiple embryonic lineages.

111 docosahexaenoic acid levels are decreased in affected tissues from cystic fibrosis-knockout mice.

112 ation of a genus-specific 16S rRNA gene from affected tissues from each cat.

113 Using exome sequencing of DNA from multiple affected tissues from five unrelated individuals with EC

114 d SALS, but not present in normal or disease-affected tissues from other neurodegenerative diseases,

115 In contrast, it was not detectable by PCR of affected tissues from patients with several other autoim

116 study was to investigate AIF-1 expression in affected tissues from patients with SSc and to examine t

117 ibing the presence of microchimeric cells in affected tissues from patients with systemic sclerosis,

118 Accordingly, affected tissues had defects in mitochondrial respiratio

119 Affected tissues harboured a marked biochemical defect i

120 restriction of the biochemical defect to the affected tissue has important implications for the scree

121 disorder, in which the majority of mtDNAs in affected tissues have deletions (Delta-mtDNAs).

122 In addition, many affected tissues have neural crest-derived components an

123 s been implicated as a major factor, but the affected tissues have not been identified.

124 ng recurrence following surgical excision of affected tissue in advanced disease.

125 27b levels declined significantly in colitis-affected tissue in mice in the presence of increased A(2

126 12 family cytokines by cells of the CNS, the affected tissue in MS.

127 lity of C4F6 to differentiate pathologically affected tissue in mutant SOD1 ALS rodent models and hum

128 MPK to intercalated discs in human heart, an affected tissue in myotonic dystrophy.

129 ipitants, all of which stress the particular affected tissue in some way and aid in propelling its ac

130 mechanism that underlies the defects in the affected tissues in both human and mouse diseases.

131 ted hydrophobic SOD1 species in lysates from affected tissues in G85R and G93A mutant but not wildtyp

132 wn why there are aggregates or inclusions in affected tissues in mice with such mutations and in most

133 ation can be drawn from the genomic study of affected tissues in PAH, in particular, pulmonary vascul

134 could change the architecture of the ECM of affected tissues in patients harboring mutations in gene

135 of the immune system, rapidly migrating into affected tissues in response to injury or infection.

136 f interactions among genes, environment, and affected tissues in the setting of complex and heterogen

137 Histological analysis of affected tissues in these mice shows abundant iron store

138 ntal processes most commonly involved in the affected tissues include epithelial-mesenchymal interact

139 Affected tissues include the bone marrow, spleen, thymus

140 ly to the heart, and ultimately to all other affected tissues including brain.

141 ntify Wnt-active self-renewing stem cells in affected tissues including hair follicles, sebaceous gla

142 utant disrupted early inductive signaling in affected tissues, indicating that FGF signaling is requi

143 Transgene transcription was detected in affected tissues, indicating that the C3(1)-based vector

144 ient ischaemic attack it is assumed that the affected tissue is penumbral but rescued by early sponta

145 s procedure, in which a tiny fraction of the affected tissue is selected for pathological examination

146 her fibrocytes are stimulated to home to the affected tissue is unknown.

147 Targeted excitation and photokilling of affected tissues is achieved through focal light irradia

148 Pathogenic CD4(+) T cells within affected tissues may be identified by expression of mark

149 nal fluid (CSF) of patients, but also in the affected tissue, most often localized in cells of mononu

150 Blood flow to the affected tissue must be restored quickly if viability an

151 n mutations (E542K, H1047L or H1047R) in the affected tissue of five additional unrelated patients; m

152 ed TCRs therefore predominate in the disease-affected tissue of patients with HLA-DQ8-mediated CD.

153 ggest that the high level of TN found in the affected tissue of patients with SSc results from the hi

154 sidues within its kinase or RCC1 domains, in affected tissue of three out of three NC-affected subjec

155 ynein-dynactin complex in cultured cells and affected tissues of ALS mice.

156 ecrosis factor, IL-1beta, IL-6, and IL-17 in affected tissues of diseased mice.

157 rotein levels were reduced in skin and other affected tissues of heterozygous mice.

158 protein were significantly decreased in the affected tissues of K5.Smad7 mice.

159 distribution, which was abnormal only in the affected tissues of noggin-exposed inner ears.

160 FUS form abnormal cytoplasmic aggregates in affected tissues of patients with amyotrophic lateral sc

161 in dusp-5 and snrk-1 have been identified in affected tissues of patients with vascular anomalies, im

162 ecific antioxidant superoxide dismutase-2 in affected tissues of SBMA knock-in mice.

163 However, affected tissues of SCO1 and SCO2 patients exhibit a com

164 eases are characterized by prevalence in the affected tissues of type 1 T lymphocytes, which secrete

165 the extent or nature of the gene defect, the affected tissue or cell type and the context of other ca

166 sseminated delivery of cells or genes to the affected tissues or organ.

167 CLU expression is markedly elevated in FED-affected tissue, pointing to a yet undiscovered form of

168 ritis, there is evidence indicating that the affected tissues produce large amounts of oxygen-free ra

169 ulated in Fkbp52-deficient males but only in affected tissues, providing further evidence of tissue-s

170 The prevalence of the mutant allele in affected tissues ranged from 1.0 to 18.1%.

171 receptors that are locally expressed in the affected tissues rather than with receptors constitutive

172 eir cells, but the oncogenetic mechanisms in affected tissues remain unknown.

173 Analyses of the affected tissues revealed that these compartments failed

174 d whole-exome sequencing of paired blood and affected tissue samples isolated from a PEODDN lesion of

175 The affected tissues show remarkable disrupted gap junction

176 ent of leukocytes and plasma proteins to the affected tissue site.

177 nd was present in a high percentage (87%) of affected tissue (skeletal muscle) and a low percentage (

178 Affected tissues slowly accumulate mutations, some of wh

179 ficiencies, and the differential response of affected tissues, suggest that the cerebum gene may norm

180 In contrast, the mutation V252/911A affected tissue targeting in the human intestinal explan

181 progression and the inability to biopsy the affected tissue, the brain, making it difficult to desig

182 In two affected tissues, the two imprinted genes appear to act

183 e response to this exaggerated immune state, affected tissue typically develops tertiary lymphoid org

184 pairs, the target is expressed in a disease-affected tissue under healthy conditions.

185 hen assayed activation of the AKT protein in affected tissues, using phosphorylation-specific antibod

186 tical imaging, where gel localization to the affected tissue was observed with near complete clearanc

187 The volume of affected tissue was on the average 42% smaller in MT-TG

188 The intensity of images of affected tissues was greatly reduced in the presence of

189 d suppression of signatures of cell death in affected tissue, whereas mitochondrial morphology and ge

190 s was performed, including the biopsy of the affected tissue which revealed the presence of Mycobacte

191 endothelial cells of microvessels in stroke-affected tissue, whilst expression of other receptors fo

192 er, infections were rapidly cleared from all affected tissues, with no clinical signs of disease.

193 in Drosophila results in hyperplasia of the affected tissue without significant disruptions in diffe

194 d cornea are required to clear bacteria from affected tissue, yet their persistence may contribute to