ライフサイエンスコーパス: diseased

1 ng and removing brood that is parasitized or diseased.

2 almata that were grafted (inoculated) with a diseased A. cervicornis fragment.

3 iles of other tissues, including healthy and diseased adult cartilage, identified chondrocyte-specifi

4 failure is the loss of cardiomyocytes in the diseased adult heart.

5 ed with an increased proportion of spikelets diseased and amount of fungal biomass in spikelets, depi

6 etectable in GCF and saliva of periodontally diseased and healthy individuals, and the GCF levels of

7 ervation-based features, for SV call sets in diseased and healthy individuals.

8 probe incorporating S16 perfectly classified diseased and healthy prostates, supporting the relevance

9 Diseased and injured tendons develop fibrosis, driven by

10 and can be further adapted to SE analysis of diseased and non-diseased tissues from different organis

11 n challenging because of the small amount of diseased and nondiseased tissue available.

12 e train a diagnostic classifier (healthy vs. diseased) and extract instance-wise explanations for the

13 l of human tissue samples, including normal, diseased, and malignant liver.

14 sights into the myosin SRX state in healthy, diseased, and therapeutic conditions.

15 of beneficial effects in healthy as well as diseased animal models and cell systems.

16 ss of membrane potential in CA1 neurons from diseased animals and systemic LPS increased apoptosis in

17 ss of membrane potential in CA1 neurons from diseased animals and systemic LPS increased apoptosis in

18 ss of membrane potential in CA1 neurons from diseased animals and systemic LPS increased apoptosis in

19 y lower in Tregs obtained from periodontally diseased animals compared to controls (P < 0.05), as ide

20 e dysbiotic microbial community structure in diseased animals was further demonstrated by analysis of

21 stimuli to promote their accumulation in the diseased aorta.

22 tween blood and fibroblasts derived from the diseased areas detected a single novel variant predicted

23 terface of blood with the intimal surface of diseased arteries and propagate and amplify the regional

24 was shown to be significantly higher around diseased arteries and was confirmed to be a diacylglycer

25 fibro-fatty infiltration of subepicardium of diseased atria.

26 This approach offers a route for repairing diseased biocircuits and emulating their function with b

27 l and immunological disorders by replacing a diseased blood system with a healthy one, but this curre

28 The model captures ICP dynamics within the diseased brain and accounts for the ability/inability of

29 to advance the understanding of healthy and diseased brain circuit function through technological in

30 female mice, to examine vulnerability of the diseased brain to acute stressors, we showed that LPS (1

31 ntified major gene expression changes in the diseased brain, including sex-specific changes and marke

32 ibited increased process movement in the non-diseased brain, the Abeta rich environment in an AD-like

33 and impaired sleep is a common trait of the diseased brain.

34 cular microglial function in the healthy and diseased brain.

35 ons of DA neuron subtypes in the healthy and diseased brain.

36 rophage interactions in both the healthy and diseased brain.

37 ical seeds, particularly those isolated from diseased brains.

38 geal immunity and its effects on healthy and diseased brains.

39 cells with multiple functions in healthy or diseased brains.

40 ocycline reduced depressive-like behavior in diseased, but not healthy, animal models.

41 D. nodosus persisted in soil and on diseased, but not healthy, feet; similar strains were de

42 (AP) is vital for understanding healthy and diseased cardiac biology and drug safety testing.

43 However, the effects of normal and diseased cardiac MSCs on myocyte electrophysiology remai

44 8 genes analyzed differentially regulated in diseased cartilage.

45 similarities among periodontally healthy and diseased cats.

46 tally healthy cats were distinguishable from diseased cats.

47 (cGAMP) is an immunotransmitter exported by diseased cells and imported into host cells to activate

48 therapeutic transgenes site-specifically to diseased cells by responding to extracellular proteases

49 r differentiation to epigenetic responses of diseased cells upon drugging.

50 deliver destructive radiation discretely to diseased cells while simultaneously sparing the surround

51 Reprogramming diseased cells with mutated genes into induced pluripote

52 indicators of regional expression changes in diseased cells with only transcriptomic data.

53 specific self-receptors to identify and lyse diseased cells without harming self-MHC I-bearing host c

54 chemical cross-linking of RBCs, a model for diseased cells, leads to striking changes in shape respo

55 In the diseased cells, the ERK1/2 inhibitor (PD98059) completel

56 f the Na(+) ,K(+) -ATPase as measured in the diseased cells.

57 f the Na(+) ,K(+) -ATPase as measured in the diseased cells.

58 es, leading to enzymatic cross-correction of diseased cells.

59 role in gene regulation for both normal and diseased cells.

60 ety of pharmacological knockdown of HDAC8 in diseased cells.

61 asculature may act as a surrogate marker for diseased cerebral vessels.

62 produced at high titers in the periphery of diseased cervids.

63 f1 expression was increased both in aged and diseased cholangiocytes, and in human cholangiopathies.

64 enously and allow local drug delivery to the diseased choroid via light-triggered targeting.

65 s and employed with the AFM/MEA platform for diseased CMs' drug response testing and DMD characteriza

66 ualization of spatial NE activity throughout diseased colon as well as changes in disease severity fr

67 g the lesion boundary) to diseased tissue on diseased colonies (DD; i.e. lesion front) was observed,

68 ealthy colonies (HH) to healthy tissue on WS-diseased colonies (HD; i.e. preceding the lesion boundar

69 mmunities of healthy and white syndrome (WS) diseased colonies of Acropora hyacinthus sampled from re

70 ignalling, TGFB1 and BMP2 mRNA expression in diseased compared to healthy tendon-derived cells.

71 ERK1/2 expression was reduced in torn (diseased) compared to healthy patient tendon tissues.

72 rivatives are favorable for the prognosis of diseased conditions associated with bacterial dysbiosis.

73 ncreas in neonates and adults in healthy and diseased conditions using single-cell sequencing approac

74 d neuronal excitability in physiological and diseased conditions.

75 with conspecifics and avoid stone crabs and diseased conspecifics.

76 ) blood-brain barrier (BBB) disruption and a diseased control group with cluster headache (n = 35).

77 body mass index: 32 +/- 2 kg m(-2) ) and non-diseased controls (age: 50 +/- 2 years: body mass index:

78 biased lipidomic analysis of plasma from non-diseased controls (n = 8) and patients with primary prog

79 gomonadaceae was significantly found in both diseased coral species.

80 eatability and reproducibility in normal and diseased cornea eyes through all map zones.

81 rature focus on assessing the center of this diseased cornea, there is growing evidence of peripheral

82 manual hyperemic pullback in 100 normal and diseased coronary arteries with single stenosis, using 4

83 ntervention for non-left anterior descending diseased coronary arteries.

84 hich recapitulates the in vivo phenomenon of diseased cystinotic cells stimulating thicker TNT format

85 Patients with damaged or diseased endothelium from Fuchs endothelial dystrophy or

86 Patients with damaged or diseased endothelium from Fuchs endothelial dystrophy or

87 Diseased endothelium had increased expression of chemoki

88 scans was similar across normal (10.7%) and diseased eyes (12.1%).

89 ng methods and representing both healthy and diseased eyes was circulated to the expert panel for ind

90 l mechanisms of HVS regression in normal and diseased eyes, which is not only important for advanced

91 f one parameter is more useful when studying diseased eyes.

92 begins to probe the function of healthy and diseased eyes.

93 ar strains were detected on both healthy and diseased feet of diseased sheep.

94 aradigm, F. necrophorum persisted on footrot diseased feet, and in mouths and faeces; different strai

95 tochondrial intercellular trafficking to the diseased fibroblasts.

96 criptional mechanisms are also active in the diseased fibrotic human heart.

97 their binary combinations) were planted in a diseased field plot in the Great Basin Desert of Utah.

98 nomic abundance occurred between healthy and diseased fish.

99 This score separated diseased from healthy samples, enabled discrimination of

100 eveals material heterogeneity and delineates diseased from healthy tissue.

101 ic curves were calculated for discriminating diseased from nondiseased prostate segments, and optimal

102 biologic activities occurring in healthy and diseased gingival tissues in this human-like periodontit

103 s CC chemokine ligand 2 and interleukin 6 in diseased gingival tissues.

104 identify a pro-fibrotic gene network in the diseased heart and show that this network is regulated b

105 ight into the fetal shifts that occur in the diseased heart and unveil strategies for driving maturat

106 both of these mechanisms eventually lead to diseased heart tissue and symptoms of a failing heart.

107 YAP as a key player in ECM remodeling in the diseased heart via transcriptional activation of focal a

108 applied to interrogating regeneration of the diseased heart, exemplifying the importance of understan

109 crophage populations in the steady-state and diseased heart, focusing on the human heart and mouse mo

110 via Mcp1 silencing reduced leukocytes in the diseased heart, improved healing after infarction and at

111 ies have revealed PDE10A upregulation in the diseased heart.

112 ucing the mechanical behavior of healthy and diseased hearts, but it also provides important insights

113 e translation of target transcripts in human diseased hearts.

114 ne the strain differences between normal and diseased hearts.

115 structure and function appeared preserved in diseased human and murine specimens in the presence of m

116 althy animals or to extrapolate such data to diseased human arteries.

117 ell interactions and novel drug screening in diseased human brain.

118 associated with SMC phenotypic modulation in diseased human coronary arteries, and higher levels of T

119 Staining of healthy and diseased human gastric tissue samples paralleled these r

120 ges in cardiac metabolism in the healthy and diseased human heart.

121 ardiac fibroblasts obtained from healthy and diseased human hearts, we identify an endogenous target

122 ns with high-level engraftment of normal and diseased human immune/hematopoietic cells has made in vi

123 In diseased human olfactory tissue, activated HBCs in a P63

124 by generating new results across normal and diseased human samples.

125 and potentially differentiating healthy and diseased human skin tissues based on changes in detected

126 ding of how inflammation induces fibrosis in diseased human tendons.

127 d the landscape of chimeric RNAs in 9495 non-diseased human tissue samples of 53 different tissues fr

128 However, limited access to non-diseased human tissues has hindered efforts to profile a

129 ity, and functional potential of ILCs in non-diseased human tissues.

130 ibited increased vasculature, while isolated diseased human TMJ cells exhibited marked increased in v

131 Aged, diseased, human saphenous vein (HSV) remnants obtained f

132 and mammalian species, including healthy and diseased humans across the lifespan.

133 Our data demonstrate that B cells infiltrate diseased iBA and BASM biliary remnant tissue.

134 sbiotic oral microbiome from a periodontally diseased individual into a healthy individual will lead

135 lso affected by endurance (the propensity of diseased individual to survive the infection) and infect

136 itable shelter and cues from stone crabs and diseased individuals are used to determine shelters to b

137 Here, we show that photoreceptors (PRs) of diseased individuals display increased expression of two

138 t anti-AM IgG from asymptomatic but not from diseased individuals was protective and provided data su

139 d in fetal and adult brains from healthy and diseased individuals.

140 Furthermore, comparison of diseased KCs and infiltrating macrophages revealed that

141 1) in Fusarium-damaged rachis rate, Fusarium-diseased kernel rate and DON content in harvested kernel

142 ) TCR Valpha7.2(+) CD161(hi)) in healthy and diseased kidney tissues, detecting expression of tissue-

143 s activate endogenous EPO gene expression in diseased kidneys and are being developed, or are already

144 ompared with either nonfibrotic samples from diseased kidneys or tissue samples from healthy kidneys.

145 r INF2 function and for robust evaluation of diseased-linked variants of formin.

146 origin of the instability and found that the diseased lipid membrane has a 25% lower bending rigidity

147 well-defined multilayer structures, whereas diseased lipid membranes form folded assemblies with hig

148 into its bilayer leaflet side in case of the diseased lipid mixture, whereas there is no insertion fo

149 decrease of the sphingomyelin content of the diseased lipid mixture.

150 For both native and diseased lipid mixtures we find that MBP forms dense liq

151 xcess extracellular matrix deposition in the diseased liver and as such are important in the progress

152 Exome sequencing of diseased liver samples from 82 patients revealed a compl

153 Increased CHOP levels were detected in diseased livers of children homozygous for the Z allele.

154 CEPT1 was found to be elevated in diseased lower-extremity arterial intima of individuals

155 pes at implants was analogous to that in the diseased lung and had distinct dynamics compared with bl

156 a major site of Il13 gene expression in the diseased lung; and second, at an upstream level, this sa

157 cleus transcriptomes of 46,500 nuclei in non-diseased lungs from donors of ~30 weeks gestation,~3 yea

158 These breath signals can identify diseased mice with high sensitivity as early as 10 min a

159 Terminally diseased mice with severe neurological symptoms showed e

160 -) Bcl-6(-) T cells specifically expanded in diseased mice.

161 fects of antibiotic therapy on periodontally diseased mice.

162 healthy mice, and improved liver function in diseased mice.

163 xpression is very low or absent in normal or diseased middle ear in mouse and human, and salivary exp

164 gest a link between primary MMUT deficiency, diseased mitochondria, mitophagy dysfunction and epithel

165 l's propensity to avoid becoming infected or diseased), mortality rates of populations undergoing an

166 Ki67 immunohistochemistry demonstrating that diseased muscle-invading T cells are minimally or non-pr

167 would provide selective, timely delivery to diseased muscle.

168 and to calcified fibrotic tissues, including diseased muscle.

169 brosis obstructs the regenerative efforts of diseased muscles.

170 into the structure-function relationship of diseased myocardium that will help pave the way toward m

171 ples were collected from healthy (n = 5) and diseased (n = 5) sites of each patient.

172 rong impact on understanding the healthy and diseased nervous system.

173 ch these neurochemicals regulate healthy and diseased neural circuitry, one needs to measure their sp

174 t impact on the understanding of healthy and diseased neural processes.

175 t uses embolic agents to intentionally block diseased or injured blood vessels for therapeutic purpos

176 ch for facilitating axon regeneration in the diseased or injured human CNS, thus helping to reduce an

177 lusion of blood vessels for the treatment of diseased or injured vasculature.

178 tic strategy and number of coronary arteries diseased or severity of ischemia.

179 ponse factors is a key survival strategy for diseased or stressed cells.

180 ic rodents to monitor signalling pathways in diseased organs using whole-body bioluminescence imaging

181 Diseased PAECs had increased proximate glycolysis pathwa

182 iciency of the method were explored in n = 7 diseased patient bifurcations of varying anatomical comp

183 Although microarray data from diseased patient kidneys and fibrotic mouse model kidney

184 ts and platelet antagonists and studies with diseased patient plasma demonstrate the ability of the s

185 The addition of 3059 diseased patients uncovered pan-disease and disease-spec

186 We collected brain autopsies on diseased patients with NDs, and found a dynamic increase

187 vealed increased binding of (18)F-PM-PBB3 in diseased patients, reflecting cortical-dominant AD and s

188 lis and can be detected in lipid extracts of diseased periodontal tissues and teeth of humans.

189 issection, (iii) distinguishing healthy from diseased PGs, and (iv) minimizing postoperative hypocalc

190 sion of healthy PGs or inability to localize diseased PGs, resulting in postsurgical complications.

191 ncreased vascular permeability, leading to a diseased phenotype both in vitro and in vivo.

192 itions, and keep experts' attention on these diseased pixels.

193 Specifically we compare the removal of diseased plants by roguing, preferential selection of pl

194 cognition and motor learning in healthy and diseased populations of all ages.

195 n-behavior relationships in both healthy and diseased populations.

196 te analysis, the number of coronary arteries diseased predicted long-term mortality, but severity of

197 The number of coronary arteries diseased predicted survival (HR, 1.25; 95% CI, 1.09-1.43

198 rces glucose pathways from the normal to the diseased range, thereby exposing novel metabolic links.

199 teristics in one healthy and three different diseased rat models.

200 e the effects of all-trans-RA in healthy and diseased reconstructed human epidermis.

201 MFS patients, many of which were specific to diseased samples.

202 In 26 individuals, median most diseased segment TBR(max) (interquartile range) was high

203 F-NaF tissue-to-background ratio of the most diseased segment: 2.16 vs. 1.97; p = 0.043).

204 otic and deformed bowel loops separated by 2 diseased segments with sequential strictures.

205 otic and deformed bowel loops separated by 2 diseased segments with sequential strictures.

206 After the resection of the 3 severely diseased segments, the remaining 2 discontinuous segment

207 how PRC2 activity is regulated in normal and diseased settings.

208 etected on both healthy and diseased feet of diseased sheep.

209 ht interdigital swabs from eight, preferably diseased, sheep.

210 ngival biopsy was obtained from one selected diseased site from each patient and prepared for immunoh

211 eduction of 0.73 +/- 0.11 mm and decrease of diseased sites (PD >3 mm) were measured at 6 months illu

212 Diseased sites had significantly (P <0.05) higher levels

213 vels of LL-37 and HNP 1-3 when compared with diseased sites of non-smokers.

214 Diseased sites of smokers presented significantly lower

215 ttern from HNP 1-3: LL-37 was upregulated in diseased sites, and HNP 1-3 was increased in periodontal

216 improvement in topical delivery of drugs at diseased sites, when compared to prevalent spray techniq

217 icrobial heterogeneity between skin sites in diseased skin, such as atopic dermatitis (AD) lesions.

218 d have long been associated with healthy and diseased skin.

219 stems that only partially recapitulate human diseased skin.

220 tivity and 94.6% specificity for identifying diseased spectra.

221 This diseased state can be rescued by administering a glucose

222 Our results suggest that the diseased state is a manifestation of a phase change of t

223 However, in a diseased state, host-microbial networks lead to dysbiosi

224 can shift from homeostasis to dysbiosis or a diseased state, it is crucial to understand how the inna

225 understanding of myocilin in its normal and diseased state.

226 the wide capacity of neurons to respond in a diseased state.

227 ta (SNr) transitions from the healthy to the diseased state.

228 the body depending on its solubility, and in diseased states such as RA, deposited ApoE may induce lo

229 ay are introduced, covering both healthy and diseased states, and we discuss the potential promise of

230 sferases (PRMT) are generally not mutated in diseased states, but they are overexpressed in a number

231 In normal and diseased states, dozens of chromatin effectors alter the

232 st in right ventricular form and function in diseased states, there is a paucity of data regarding ch

233 r to unveil the mechanistic details of these diseased states, we analyzed protein families relevant t

234 erstanding of their functions in healthy and diseased states.

235 ata on living human microglia, especially in diseased states.

236 c and postsynaptic structures in healthy and diseased states.

237 aberrant genome reduplication, including in diseased states.

238 reatment of various types of maligancies and diseased states.

239 idney tissue to recapitulate both normal and diseased states.

240 logical processes and are often corrupted in diseased states.

241 l modeling of the human brain in healthy and diseased states.

242 icrobiome axis and suggest that the feces of diseased subjects might be enriched with miRNAs with the

243 istinct grouping of samples from healthy and diseased subjects, with excellent reproducibility of res

244 a-induced CTGF mRNA expression in healthy or diseased tendon cells.

245 n of TGF-beta1 and BMP-2 between healthy and diseased tendon tissues and cells, advancing understandi

246 The study uses two HMECs derived from a diseased tissue (e.g. MCF10A) and reduction mammoplasty

247 We verified expression of AFP in normal and diseased tissue and generated an affinity-optimized T-ce

248 amined the immunoglobulin (Ig) repertoire of diseased tissue from each BA group.

249 n to understanding their role in healthy and diseased tissue microenvironments.

250 (HD; i.e. preceding the lesion boundary) to diseased tissue on diseased colonies (DD; i.e. lesion fr

251 a crucial reference set for comparisons with diseased tissue samples to map the cellular foundations

252 expanding the availability and use of human diseased tissue stored in brain banks.

253 NA copy number and dynamics in any normal or diseased tissue that can be used for monitoring the effe

254 A major limitation comes from the amount of diseased tissue that can be used for research purposes.

255 e identified, with T7 and T8 enriched in the diseased tissue.

256 lux kinetics of medical agents in normal and diseased tissues could be a new strategy for tackling ch

257 Detection of protease activity in diseased tissues could therefore be useful for diagnosis

258 tool to study the cellular heterogeneity in diseased tissues for a variety of biological problems.

259 r adapted to SE analysis of diseased and non-diseased tissues from different organisms.

260 genome-wide studies of chimeric RNAs in non-diseased tissues have been scarce.

261 Biological constraints in diseased tissues have motivated the need for small nanoc

262 delivery of oligonucleotides selectively to diseased tissues in the body, and specifically to the ce

263 heart and used them to replicate healthy and diseased tissues in vitro.

264 identified candidate proteins for analyzing diseased tissues near or distal to salivary glands using

265 f drug delivery is insufficient targeting of diseased tissues or cells.

266 mportantly, our list of chimeric RNAs in non-diseased tissues overlaps with some entries in several c

267 ts, and by the low levels of free calcium in diseased tissues that restrict the use of annexins.

268 erentiate the healthy colon tissues from the diseased tissues were identified to be in the phosphodie

269 of the mutant form of HTT is a key aspect of diseased tissues, and the most promising therapeutic app

270 ple macrophage phenotypes are represented in diseased tissues, but we lack deep understanding of mech

271 to extracellular cGAMP levels in healthy and diseased tissues, such as cancer.

272 ments, which are based on PS-induced harm to diseased tissues, the photoinduced cycle of singlet oxyg

273 e repository of chimeric RNAs present in non-diseased tissues, which can be used as a control dataset

274 uently seed fibrillation and deposition into diseased tissues.

275 ize the composition of the ECM of normal and diseased tissues.

276 cules to accelerate the repair of injured or diseased tissues.

277 ersistence of proinflammatory macrophages in diseased tissues.

278 flows (IFs) are present in both healthy and diseased tissues.

279 to enhance maintenance and repair of aged or diseased tissues.

280 ility for prodrug delivery and activation in diseased tissues.

281 ng of mutational heterogeneity in normal and diseased tissues.

282 implicated in promoting apoptosis in various diseased tissues.

283 target the acidic environments of different diseased tissues.

284 g healthy tissues, which decreased by 75% in diseased tissues.

285 patial cholesterol metabolism in healthy and diseased tissues.

286 bone transdifferentiation using healthy and diseased TMJ tissues from miniature pigs and humans.

287 tes to the propagation of the pathology from diseased to healthy neurons.

288 ycle that propagates synaptic pathology from diseased to healthy neurons.SIGNIFICANCE STATEMENT Here

289 identification and comparison of normal and diseased transcriptional cell populations.

290 etabolite profiles of skeletal muscle across diseased, treated, and normal states.

291 iac valve development are also implicated in diseased valves.

292 rately placing the ablation fiber within the diseased vein.

293 these correlations increased by 2.5-fold in diseased versus healthy tissues of adult animals.

294 r insights into the PCSK6 role in normal and diseased vessel wall.

295 yzed qualitatively and semiquantitatively in diseased vessels by measuring maximum tissue-to-backgrou

296 n evaluating individual stenoses in serially diseased vessels.

297 n conclusion, upregulation of SK channels in diseased VMs is mediated by hyperadrenergic drive in car

298 Separate subgroup analyses were conducted on diseased vs healthy animal models, different rodent spec

299 sted models, the number of coronary arteries diseased was not associated with increased mortality.

300 ope was more virulent; the number of dead or diseased wild birds found and the severity of pathologic

301 e cells in live human eyes, both healthy and diseased, with the unique capabilities of our adaptive o