ライフサイエンスコーパス: affected tissue

1 mulation of lymphocytes and monocytes in the affected tissue.

2 tal diseases were managed mainly by excising affected tissue.

3 mited T cell populations are concentrated in affected tissue.

4 pothesized that they carry more mutations in affected tissue.

5 affected by diverticulitis and adjacent non-affected tissue.

6 ture and severely impede the function of the affected tissue.

7 ce site- and time-specific activation in the affected tissue.

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

9 ammation requires their recruitment into the affected tissue.

10 at facilitated leukocyte infiltration to the affected tissue.

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

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

13 system (CNS) appears to be the most commonly affected tissue.

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

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

16 ces inflammation and oxidative stress in the affected tissue.

17 response to growth factor signalling in the affected tissues.

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

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

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

21 s involved, and the role of G(s)alpha in the affected tissues.

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

23 ent of neutrophils through vessel walls into affected tissues.

24 d activities of respiratory chain enzymes in affected tissues.

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

26 accumulation of multiple mtDNA deletions in affected tissues.

27 rofiling and immunohistochemical analysis of affected tissues.

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

29 tiple point mutations of mtDNA in clinically affected tissues.

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

31 tions and display autoantibodies against the affected tissues.

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

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

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

35 rage), (2) a broad gene set, and (3) testing affected tissues.

36 Tim23 in the mitochondrial inner membrane in affected tissues.

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

38 r inability to selectively transduce disease-affected tissues.

39 nstrated the presence of mycobacteria within affected tissues.

40 rates glycosaminoglycan accumulation in some affected tissues.

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

42 sible for the increased contractility of the affected tissues.

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

44 s, with few focusing on samples derived from affected tissues.

45 infections rely on structural changes in the affected tissues.

46 es in blood and in all examined autoimmunity-affected tissues.

47 rders by increasing or restoring function to affected tissues.

48 nt of alloreactive effectors from blood into affected tissues.

49 ver and skeletal muscle are usually the most affected tissues.

50 is was evident upon direct inspection of the affected tissues.

51 by expanding antigen-specific Treg cells in affected tissues.

52 athogenesis, both in the kidney and in other affected tissues.

53 rculating peripheral blood cells rather than affected tissues.

54 which induces granulomatous inflammation of affected tissues.

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

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

57 cyte detection and response in periodontitis-affected tissues.

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

59 thus correlating CPAMD8 expression with the affected tissues.

60 odels to individualized therapy that targets affected tissues.

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

62 abnormally folded cellular prion protein in affected tissues.

63 d T lymphocytes, suggesting extravasation to affected tissues.

64 capsid proteins were abundantly expressed in affected tissues.

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

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

67 protein aggregates from cell-to-cell within affected tissues.

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

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

70 The cartilage is one of the principal affected tissues.

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

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

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

74 early and localized suppression of cilia in affected tissues after injury as a therapeutic strategy

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

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

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

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

79 9 infection exhibit a low level of oxygen in affected tissue and blood.

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

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

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

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

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

85 oth proliferative and apoptotic cells in the affected tissue and were largely suppressed by rapamycin

86 tion is a common, reversible change in lupus-affected tissues and appears to reflect damage downstrea

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

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

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

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

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

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

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

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

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

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

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

98 ese results suggest that therapies targeting affected tissues and progenitor T cells within them woul

99 In diseases, RAGE levels increase in the affected tissues and sustain chronic inflammation.

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

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

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

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

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

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

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

107 s a unique communication between healthy and affected tissues, and highlights the potential benefits

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

109 and found that mutant CHCHD10 aggregated in affected tissues, applying a toxic protein stress to the

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

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

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

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

114 gs point to somatic CAG repeat expansions in affected tissues as a key pathological mechanism.

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

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

117 olving inflammation is thought to return the affected tissue back to homoeostasis but recent evidence

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

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

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

121 se requires demonstration of the organism in affected tissue by microscopy and, preferably, PCR.

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

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

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

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

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

127 s disease (HD), ongoing repeat expansions in affected tissues contribute to disease onset, progressio

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

129 In affected tissue, cytotoxic CD8(+) T cells express privat

130 erformed bulk RNA-seq molecular profiling of affected tissues derived from a cohort of client-owned c

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

132 In the affected tissues, differentiation is initiated and many

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

134 nce of distinct phenotypes of B cells in HSV-affected tissue; dissecting their role in reactivation m

135 e-relevant cells and the microenvironment of affected tissue domains.

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

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

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

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

140 Moreover, within affected tissues, expression of specific selenoproteins

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

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

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

144 548G-->A, p.Arg183Gln) in GNAQ in samples of affected tissue from 88% of the participants (23 of 26)

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

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

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

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

149 Previous studies of affected tissue from pediatric cohorts have identified p

150 tailed examination of the protein in disease-affected tissues from amyotrophic lateral sclerosis pati

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

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

153 0% reduction in phosphorylated AKT (pAKT) in affected tissues from five of six individuals.

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

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

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

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

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

159 Accordingly, affected tissues had defects in mitochondrial respiratio

160 Affected tissues harboured a marked biochemical defect i

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

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

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

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

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

166 27b levels declined significantly in colitis-affected tissue in mice in the presence of increased A(2

167 12 family cytokines by cells of the CNS, the affected tissue in MS.

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

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

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

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

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

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

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

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

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

177 se (NTE), yet the role of NTE dysfunction on affected tissues in the large spectrum of associated dis

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

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

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

181 Affected tissues include the bone marrow, spleen, thymus

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

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

184 resemble fibroblast states in other disease-affected tissues including skin and colon.

185 Neuroinflammation is apparent in affected tissues, including increased T cell infiltratio

186 ccumulation of globotriasylceramide (Gb3) in affected tissues, including the heart.

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

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

189 ssion changes precede disease; and (iii) The affected tissue is a homogeneous single cell monolayer,

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

191 udying how RNA triggers disease because: (i) Affected tissue is routinely removed during surgery; (ii

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

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

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

195 The ability of immune cells to penetrate affected tissues is highly dependent on energy provided

196 iles and the inflammatory environment within affected tissues is pivotal for uncovering mechanisms dr

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

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

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

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

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

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

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

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

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

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

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

208 OMA1 was found to be activated similarly in affected tissues of mutant C10 knock-in (KI) mice, demon

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

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

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

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

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

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

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

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

217 cs at concentrations that can be achieved in affected tissues or organs and models conditions of inte

218 y for pilonidal disease involves excision of affected tissue paired with a variety of closure types i

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

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

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

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

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

224 t the nociceptive fibers densely innervating affected tissues regulate disease progression; therefore

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

226 stribution and persistence of CAR T cells in affected tissues remains a major challenge.

227 Analyses of the affected tissues revealed that these compartments failed

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

229 Subsequently affected tissue samples were investigated histologically

230 is often impeded by lack of accessibility to affected tissue samples, mosaicism or insufficient seque

231 e B receptors are expressed by astrocytes in affected tissue, selegiline was administered to one pati

232 The affected tissues show remarkable disrupted gap junction

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

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

235 Among affected tissues, skeletal muscle is particularly vulner

236 Affected tissues slowly accumulate mutations, some of wh

237 tive cells were found ex vivo in biopsies of affected tissues, such as kidney and skeletal muscle.

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

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

240 tion between directly injured tissue and non-affected tissues that are distant from injury, which war

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

242 In periodontitis-affected tissues, the imbalance between T-helper type-17

243 both T and NK cells expand and accumulate in affected tissues, the role of NK cell expansion in tumor

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

245 operatively to promote the adaptation of the affected tissue to any subsequent stress.

246 ion of systemic signals that travel from the affected tissue to the entire plant.

247 ignaling pathways that transmit signals from affected tissues to all parts of the plant.

248 mitochondrial integrated stress response in affected tissues, tying mutant C10 pathogenesis to C2/C1

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

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

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

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

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

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

255 Using single-cell spatial transcriptomics in affected tissue, we found ectopic suprabasal activation

256 and high-depth next-generation sequencing of affected tissues, we discover here clonal mosaic variant

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

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

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

260 ed by mitochondrial DNA (mtDNA) depletion in affected tissues with variable organ involvement.

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

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

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