ライフサイエンスコーパス: diseased

1 thelial cells and tissues, whether normal or diseased.

2 re intended to treat bones which have become diseased.

3 cobacilli were isolated from 15 systemically diseased African bullfrogs (Pyxicephalus edulis), and we

4 y predictor of mortality in both healthy and diseased ageing populations.

5 otherapy and their ability to penetrate many diseased anatomic sites that characterize disseminated t

6 performed extensive cellular analysis of pre-diseased and diseased Sharpin(cpdm) mice and demonstrate

7 echanisms by which shock waves interact with diseased and healthy cellular components remain largely

8 d subgingival plaque was collected from LAgP diseased and healthy sites for each participant.

9 s of LAgP and subgingival presence of JP2 in diseased and healthy sites.

10 ng the difference in splicing events between diseased and healthy tissue is crucial in biomedical res

11 ent an essential part of the biology of both diseased and healthy tissues, it is of paramount importa

12 l tool for mapping cellular heterogeneity in diseased and healthy tissues, yet high-throughput method

13 iched genes of immune cell subsets from both diseased and healthy tissues.

14 Naturally diseased and laboratory infected coral systematically ex

15 ) transgenic mice, each including samples of diseased and non-diseased phenotypes.

16 g that qAF is elevated at the border between diseased and nondiseased retina in patients with AZOOR c

17 Infection was detected in overtly diseased and seemingly healthy animals.

18 A in human gingiva, with Wnt5a dominating in diseased and sFRP5 in healthy tissue.

19 Bone marrow was obtained from diseased animals and age-matched controls.

20 lish drug tolerances and withdrawal times in diseased animals results in frequent residue violations

21 In diseased animals, we showed an increased PET signal in t

22 n of the pulmonary microbiota was altered in diseased animals.

23 mined elimination routes in both healthy and diseased animals.

24 cilitate differentiation between healthy and diseased antibody repertoires, by serving as a point of

25 ssel wall albumin and microvessel density in diseased aortas and especially in ruptured plaque.

26 c disease, and that TGF-beta overactivity in diseased aortas is a secondary, unproductive response to

27 twork of bacteria and fungi differ between a diseased area of the sigmoid colon chronically affected

28 ried out either systemically or locally into diseased areas, both of which involve needles.

29 edical interventions that repair and replace diseased arteries a high priority for the cardiovascular

30 bility and improved adjunct drug delivery to diseased arteries.

31 cretory system in the context of healthy and diseased astrocytes.

32 der, and they suggest that circumventing the diseased BBB to deliver active TH to the brain could be

33 anomedicine targeted for collagen exposed on diseased blood vessel wall.

34 appears to be significantly impaired in the diseased blood vessel.

35 to target and deliver therapeutic agents to diseased bone sites could potentially provide an effecti

36 er microglia are efficient phagocytes in the diseased brain as well, we confronted them with a series

37 minate epigenetic determinants of normal and diseased brain development in longitudinal context.

38 rt of understanding their role in normal and diseased brain function poses experimental challenges.

39 and autoimmune diseases, but its role in the diseased brain is poorly explored.

40 method, no trace of BMAA was detected in the diseased brain or in the control specimens.

41 rified fH and prion rods enriched from prion-diseased brain.

42 degree of continued plasticity in the adult diseased brain.

43 eliorate neurogenic defects in the aging and diseased brain.SIGNIFICANCE STATEMENT We report an essen

44 glia in histological sections in healthy and diseased brains, as well as isolation of pure nonactivat

45 across widespread projections in normal and diseased brains.

46 te neuronal lipid homeostasis in healthy and diseased brains.

47 Conversely, healthy myocytes developed a diseased cAMP response if diseased neurons were introduc

48 y neurons onto diseased myocytes rescued the diseased cAMP response of the myocyte.

49 f congenital heart defects and the repair of diseased cardiac tissue.

50 el of single T-tubules, recently observed in diseased cardiomyocytes.

51 ers to stratify patients into disease or non-diseased categories.

52 example, identifying strategies to revert a diseased cell to a healthy state, or a mature cell to a

53 e necessary interventions to rejuvenate aged/diseased cells and improve their regenerative capacities

54 s have the potential to mechanically destroy diseased cells and/or increase cell membrane permeabilit

55 The chemobiomechanical signatures of diseased cells are often distinctively different from th

56 by the genome in the context of healthy and diseased cells will offer unique opportunities to uncove

57 Replacement of the diseased cells with a healthy donor endothelium is the o

58 identities of altered metabolite features in diseased cells, and infer experimentally undetected, dis

59 putative "droplet organelles" in healthy and diseased cells, connecting protein biochemistry with cel

60 , controlled drug delivery, and pathology of diseased cells, little is known about the molecular mech

61 essed on NK cell surfaces bind to ligands on diseased cells, they initiate a signal that is propagate

62 When these mediators were incubated with diseased cells, we only found a modest down regulation i

63 ds of gene delivery treat only a fraction of diseased cells, yielding retinas that are a mosaic of tr

64 fferential levels of ECM modification by the diseased cells.

65 o-inflammatory cytokines upon recognition of diseased cells.

66 favor of the former, allowing elimination of diseased cells.

67 al cellular events leading to destruction of diseased cells.

68 ic transcriptional regulation in healthy and diseased cells.

69 er chemotherapeutics often fail to reach all diseased cells.

70 urse of inflammatory cell recruitment at the diseased central nervous system (CNS).

71 with red light effectively terminates VT in diseased, ChR2-expressing human hearts.

72 tribution of 'Ca. Liberibacter asiaticus' in diseased citrus tissues.

73 ecurrent somatic mutations identified in the diseased clone in response to lenalidomide and the drug'

74 ation of mature microglia in the healthy and diseased CNS.

75 me to our knowledge, the presence of TiLV in diseased Colombian tilapia, indicating a wider distribut

76 rkedly induced prostaglandin biosynthesis in diseased compared to healthy tendon cells, and up regula

77 m K-edge on human bone tissue in healthy and diseased conditions and for different tissue maturation

78 spects of Ca signaling under both normal and diseased conditions.

79 lopmental processes and their disruptions in diseased conditions.

80 cases of various grades of severity and non-diseased controls.

81 ents with dilated cardiomyopathy and 108 non-diseased controls.

82 e area of fragmented fluorescent pigments in diseased coral extended 3.03 mm +/- 1.80 mm adjacent to

83 nadaceae abundances decrease dramatically in diseased corals.

84 The LED based unit displayed the diseased, critical, and fit conditions of the lungs by f

85 ed indentation provided clear delineation of diseased diaphragm, and together with organ bath assessm

86 tens of thousands of lines from healthy and diseased donors.

87 In a proinflammatory or diseased environment, CAR is lost from immature neurons

88 e main outcome measures were AC depth in the diseased eye and the fellow eye of the same patient and

89 hese four patients, the mean AC depth in the diseased eyes was 1.91 +/- 0.21 mm, which was much shall

90 The mean AC depth in the diseased eyes was significantly shallower than in the un

91 SR Ca(2+) release in the diseased fibers is also slower than in normal fibers, or

92 -rich microdomains in developing, ageing and diseased fibrocartilaginous tissues, and the impact of t

93 Mice diseased from experimental RA exhibited a 3-fold enhance

94 rix protein mindin (encoded by Spon2) in the diseased FVB/N Cd151 (-/-) GBM that did not occur in the

95 ction of mindin, its early expression in the diseased GBM could represent a trigger of both further p

96 hibit stiffness spanning that of healthy and diseased glomeruli, we demonstrate that kidney podocytes

97 st analytic function to separate healthy and diseased groups, achieving 94% sensitivity and 90% speci

98 Damaged or diseased HCEnCs may cause blindness.

99 Augmenting P2Y14 R expression levels in aged/diseased hCPCs antagonizes senescence and improves funct

100 ; (2) to understand what may go wrong in the diseased heart and why; (3) to identify possible novel t

101 It seems that stem cell delivery to the diseased heart as an adjunct to surgical palliation may

102 RNA (miRNA)-34a (miR-34a) is elevated in the diseased heart in mice and humans.

103 force production and pumping function in the diseased heart or stem cell-derived tissues.

104 rdiac fibrosis; however, their origin in the diseased heart remains unclear, warranting further inves

105 ophages as the mediators of calcification in diseased heart valves and atherosclerotic plaques.

106 ulation of miRNAs was also identified in the diseased heart, and may explain the differential respons

107 Reductions of Ito,f are common in the diseased heart, which is also associated with enhanced s

108 esis and energy metabolism in the normal and diseased heart.

109 roles of cardiac K(+) channels in normal and diseased heart.

110 oninvasively assess metabolic changes in the diseased heart.

111 his new tool to aid in the assessment of the diseased heart.

112 of excitation-transcription coupling in the diseased heart.

113 ing use of biomaterials to mimic healthy and diseased hearts and how these matrices can contribute to

114 Altered Ca(2+) handling is often present in diseased hearts undergoing structural remodeling and fun

115 develops during volume loading in normal and diseased hearts with the chest intact.

116 r protocols to study LTP in both healthy and diseased human brains, a previously unattainable goal.

117 t need to identify inherent deficits in aged/diseased human CPCs (hCPCs) derived from HF patients in

118 ined retinal pigment epithelium (RPE) to the diseased human eye.

119 Previous Mossbauer spectra of unenriched diseased human hearts lacked mitochondrial and blood dou

120 In diseased human hearts, LOXL2 is upregulated in cardiac i

121 The lack of accessibility to normal and diseased human intestine and the inability to separate t

122 licles to allow future studies on normal and diseased human ovaries.

123 in studies of shape variation in healthy and diseased humans.

124 However, basal and diseased immune states in humans show vast inter-individ

125 dy we show that the amyloid fibrils within a diseased individual can vary considerably in their three

126 rk examining the organization of healthy and diseased individual human brains.

127 dependencies between microbes in healthy and diseased individuals remain far from understood.

128 Analysis of the diseased individuals' tumor tissue demonstrated high mic

129 t but declined with increasing prevalence of diseased individuals.

130 enerally have higher entropy values than non-diseased individuals.

131 ge product of C4 activation, is found in the diseased joint and can bind covalently to complement-act

132 s modulated the inflammatory response in the diseased kidney in favor of an anti-inflammatory milieu

133 Analysis of diseased kidneys and purified UMOD-producing cells revea

134 Targeting diseased kidneys for pharmacologic treatment has had lim

135 tyrosine residues and the chemokine CCL2 in diseased kidneys.

136 evascularization (CR) for all CTOs and other diseased lesions.

137 quirements between healthy hematopoietic and diseased leukemic stem cells for core circadian transcri

138 However, their roles in normal and diseased limbal epithelial stem cells (LESC) remain unkn

139 + NK were strikingly enriched in healthy and diseased liver compared to blood (p < 0.0001).

140 and biliary epithelial cells from healthy or diseased liver tissues.

141 t, we confirmed expression of RXFP1 in human diseased liver.

142 +, CD40 ligand-positive T cells was found in diseased livers explanted from patients with chronic hep

143 Treg from diseased livers expressed high levels of CD95, and their

144 This process is often impaired in fatty or diseased livers, leading to cirrhosis and other deleteri

145 binding to ECM proteins for homeostatic and diseased livers.

146 onary vascular cells and various types of PH-diseased lung tissue and determined that ECM stiffening

147 ovide a precedent for comparative studies in diseased lungs and potential targets for therapeutics.

148 r injury, fibrosis in chronically injured or diseased lungs can occur at the expense of regeneration.

149 cheal delivery of stem cells into injured or diseased lungs can provide a variety of therapeutic and

150 pertoires and repertoires from preimmune and diseased mice demonstrated that public TCR were preferen

151 with the pulmonary microbiota isolated from diseased mice enhanced IL-17A production in the lungs of

152 Th cell subsets in the spleen and kidney of diseased mice, and expression correlated with disease se

153 Thus, in prion-diseased mice, both trazodone and dibenzoylmethane treat

154 hyperactivated in the skin and the lungs of diseased mice.

155 uces neuropathology and prolongs survival of diseased mice.

156 re to BQCA markedly extended the lifespan of diseased mice.

157 s were common infiltrates of spinal cords in diseased mice.

158 ons with neighboring cells or factors in the diseased microenvironment can underlie white matter defe

159 h case, OCTA yields images of the normal and diseased microvasculature at all levels of the retina, w

160 ocal microenvironment in many ways to rescue diseased motor neurons.

161 f healthy photoreceptor precursor cells into diseased murine eyes leads to the presence of functional

162 llagen deposition, which is seen in aged and diseased muscle, interferes with muscle function and lim

163 cells and driving regeneration in normal and diseased muscle.

164 ng the failure of inflammation to resolve in diseased musculoskeletal soft tissues are unknown.

165 Similar curvatures are also found in vivo in diseased myelin sheaths.

166 on of multi-cellular physiology in normal or diseased myocardium.

167 nd release that are important in healthy and diseased myocardium.

168 reover, cross-culturing healthy neurons onto diseased myocytes rescued the diseased cAMP response of

169 ical and mechanical properties of normal and diseased myocytes, and to determine whether Orai channel

170 at is mostly expressed by fibroblasts in the diseased nerve and exists in three isoforms.

171 injury.SIGNIFICANCE STATEMENT In injured and diseased nerves, the transcription factor c-Jun in Schwa

172 antly larger whole-cell Ca(2+) currents from diseased neurons that were largely mediated by the N-typ

173 ocytes developed a diseased cAMP response if diseased neurons were introduced.

174 so decreased cAMP levels and PKA activity in diseased neurons.

175 inhibitor slightly decreased the current in diseased neurons.

176 astrointestinal motility disorders caused by diseased or absent enteric neurons.

177 S, which can be used to objectively assess a diseased or healing tendon.

178 d to be exclusively intracellular (except in diseased or injured tissues), our data show that schisto

179 ests that NKG2DL induced on T cells within a diseased organ can calibrate NKG2D-dependent activation

180 contexts across biology in both healthy and diseased organisms.

181 s to improve or even restore the function of diseased organs.

182 cognate receptor were present in normal and diseased parathyroid glands, and if so, whether they had

183 100 to 300 mg of adenomatous or hyperplastic diseased parathyroid tissue was prepared and processed a

184 ons and endogenous PaO2 oscillations in lung-diseased patients have different origins, it is likely t

185 Importantly, microbiota transplantation from diseased patients or mice (IBD, metabolic syndrome, etc.

186 ponse pathway were down-regulated in PMNs of diseased patients.

187 els that differ between healthy subjects and diseased patients.

188 healthy (probing depth [PD] </=3 mm) and two diseased (PD >/=6 mm), at baseline and at 3 and 6 months

189 esents a generalized challenge to regenerate diseased pediatric tissues that must grow to avoid organ

190 y to neural cells could instead underlie the diseased phenotype.

191 , each including samples of diseased and non-diseased phenotypes.

192 ons, with the organism being detected in the diseased placenta.

193 ate processes that result in both normal and diseased pregnancies.

194 tributes to cognitive defects in healthy and diseased-primed brains.

195 nuclear translocation, might be a sign of a diseased profibrotic epithelial phenotype.

196 rs the spectrin network and lipid bilayer of diseased RBCs may be significantly altered, leading to i

197 echanical characteristics of the healthy and diseased RBCs, including Plasmodium falciparum-infected

198 (-/-) GBM that did not occur in the C57BL/6 diseased-resistant strain.

199 ch to develop cell replacement strategies in diseased retinas with degenerating RGCs.

200 and Slc16a2 were significantly higher in the diseased retinas, suggesting locally elevated TH signali

201 For reasons that remain unclear, diseased RP photoreceptors begin to deteriorate, eventua

202 G) and 8-oxo-2'-deoxyadenosine (8-oxo-dA) in diseased RPE could provide important insights into the m

203 ntibody produced positive results with CaLas diseased samples when the primary scFv were not used.

204 The observed pathology of NMJs in diseased SBMA mice is likely the morphological correlate

205 g corneal power are encountered in eyes with diseased, scarred, and postsurgical corneas.

206 -background ratio [p = 0.010], and mean most diseased segment [p < 0.001]), but did not significantly

207 ivity at differing vascular sites and a most diseased segment approach.

208 nt, targeted thermal vapour ablation of more diseased segments and preservation of less diseased segm

209 e diseased segments and preservation of less diseased segments resulted in clinically meaningful and

210 The severity of luminal narrowing in the diseased segments was unchanged in the intervention grou

211 ensive cellular analysis of pre-diseased and diseased Sharpin(cpdm) mice and demonstrated that cellul

212 ITS sequencing were performed on chronically diseased sigmoid colon tissue (DT) and adjacent tissue (

213 ny advantages including direct access to the diseased site, potent knockdown of disease symptoms, and

214 nize targets expressed preferentially at the diseased site.

215 to 17.5%, 6.45%, and 3.23%, respectively, in diseased sites (P <0.001) and to 2.5%, 3.23%, and 0%, re

216 at baseline could differentiate healthy from diseased sites (sensitivity and specificity >/=77%).

217 e JP2 sequence was identified in 75% of LAgP diseased sites and in 56.67% of healthy sites.

218 l plaque bacteria from clinically healthy or diseased sites in the same individuals.

219 that predict extinction, populations in long-diseased sites persist.

220 Chondrocytes in injured and diseased situations frequently re-express phenotypic bio

221 nd cholesterol preferentially accumulated in diseased skin and these autoantigens directly activated

222 res extracted from OCT images of healthy and diseased skin are analyzed and, in conjunction with deci

223 ry systems at therapeutic doses in models of diseased skin.

224 white, genetically revertant macules in red, diseased skin.

225 epidermal adhesion structures in normal and diseased skin.

226 nhanced PDT response by AFXL pretreatment in diseased skin.

227 ght the potential role of OCT4 in normal and diseased somatic cells.

228 ultiple mechanisms regulating the normal and diseased state (age related macular degeneration, AMD) i

229 se phenomena and how they are modulated in a diseased state is very important for aiding our understa

230 as a patient transitions from a healthy to a diseased state.

231 at promise for the improved diagnosis of the diseased state.

232 ms disrupting lipid-protein complexes in the diseased state.

233 eractions that separate the healthy from the diseased state.

234 s (immune response, angiogenesis) as well as diseased states (atherosclerosis, cancer, thrombosis).

235 oped to recapitulate many of the healthy and diseased states of native tissues and can be used as a c

236 valuable molecular insight into healthy and diseased states persevered in their native ultrastructur

237 cellular-level function in both healthy and diseased states, but these variations remain difficult t

238 rganisms' homeostasis and the development of diseased states.

239 as markers for future studies in healthy and diseased states.

240 the clonal evolution of progenitor cells in diseased states.

241 as the alterations of fractal pattern during diseased statuses.

242 rogeneous responses that occur in healthy or diseased subjects, or during treatment.

243 ic human antibody repertoires in healthy and diseased subjects.

244 ions, e.g. multiple samples from healthy and diseased subjects.

245 ndreds of synapses supports the idea that AD-diseased synapses are intrinsically defective in LTP.

246 However, DPSCs isolated from diseased teeth with irreversible pulpitis (IP-DPSCs) are

247 In diseased tendon cells, we also found increased 15-Prosta

248 roscopic resection in patients with limited (diseased terminal ileum <40 cm), non-stricturing, ileoca

249 Patients with diseased terminal ileum longer than 40 cm or abdominal a

250 was similarly refractory to deer prions from diseased TgD infected with mink prions.

251 s within a lobe are often substantially more diseased than others, thereby warranting a more targeted

252 ilage where we observed a 2-fold increase in diseased tissue (P < 0.0001).

253 ling of the fibronectin matrix in injured or diseased tissue elicits an EDA-dependent fibro-inflammat

254 icrobial ecosystem distinguishes chronically diseased tissue from adjacent tissue.

255 ve ions inside a cell in vitro, and inside a diseased tissue in vivo, may indicate growth or recurren

256 dogenous stem cells to regenerate injured or diseased tissue may circumvent these challenges.

257 population of patients, DCs recruited at the diseased tissue produce high levels of CCL-2 and IL-8 an

258 w top-down strategy for directly employing a diseased tissue to produce biofunctional nanovesicle-bas

259 umber of functional progenitors delivered to diseased tissue, and prevents correction of underlying p

260 enabling discrimination between healthy and diseased tissue, with the cell-killing ability of cytoto

261 ly relevant protein processing in normal and diseased tissue-from 40 to 70% of proteins also occur in

262 lymer chains to favour their accumulation in diseased tissue.

263 mechanotransductive processes in normal and diseased tissue.

264 we aim to study the molecular signature of a diseased tissue.

265 stered nanomaterials and prevent delivery to diseased tissue.

266 racellular matrix or to deliver a payload to diseased tissue.

267 Harsh environments within damaged and diseased tissues and limited retention and survival of i

268 g-term repair and regeneration of injured or diseased tissues and organs.

269 achieved to harness nature's ability to cure diseased tissues and organs.

270 e complex mechanisms of crystal formation in diseased tissues and their interplay with the nutrients,

271 It has been observed that many diseased tissues are acidic and that tumors are especial

272 ies when the differences between healthy and diseased tissues are small; clinically, CT image noise i

273 o an imaging agent, to select patients whose diseased tissues display sufficient targeted receptors f

274 datasets as input: an expression dataset of diseased tissues from patients with a disease of interes

275 though genome-wide transcriptome analysis on diseased tissues has greatly advanced our understanding

276 fferentially transcribed between healthy and diseased tissues in colorectal cancer and chronic lympho

277 , protein, and activity levels in normal and diseased tissues indicate targeting applicability in a v

278 nment is an integral component of normal and diseased tissues that is poorly understood owing to its

279 ly occurring differences between healthy and diseased tissues, and active targeting, which utilizes v

280 identify the sequences of microorganisms in diseased tissues, i.e., to identify organisms that appea

281 d to image wound healing in other injured or diseased tissues, or to monitor tissue changes over time

282 ve pharmacodelivery of cytotoxic payloads to diseased tissues, providing an innovative platform in ch

283 e examination of a variety of developing and diseased tissues, with specific focus on the dynamics of

284 NA-seq data from diverse types of normal and diseased tissues.

285 proteomes and their dynamics in healthy and diseased tissues.

286 pression of specific nucleic acid sensors in diseased tissues.

287 ted by unfavorable environments in aging and diseased tissues.

288 f fundamental questions about the genomes of diseased tissues.

289 tanding the function of cells in healthy and diseased tissues.

290 the enrichment of cell subset signatures in diseased tissues.

291 t selective sequential treatment of the more diseased upper lobe segments with bronchoscopic vapour a

292 and Mycoplasma were significantly higher in diseased versus healthy animals, and the total bacterial

293 tive disease is comparing gene expression in diseased versus healthy tissues.

294 ontrast-filled lumen rather than imaging the diseased vessel itself.

295 graft thrombosis or in situ thrombosis of a diseased vessel, and often results in limb loss.

296 tudy was to evaluate the impact of number of diseased vessel, lesion location, and severity of the no

297 n vascular biomechanics and can be extend to diseased vessels for better understanding of initiation,

298 t-MI HF among patients with 0 or 1, 2, and 3 diseased vessels were 10.7%, 14.6%, and 23.0% at 30 days

299 outcomes with respect to LVEF and number of diseased vessels, including proximal left anterior desce

300 oth luminal and microvascular endothelium in diseased vessels.