ライフサイエンスコーパス: disease state

1 uggested novel roles of EGR1 and SGK1 in the disease state.

2 biome can potentially impact host health and disease state.

3 atures of AMD and could represent an earlier disease state.

4 uences; change with age; and can change with disease state.

5 ment option in a therapeutically challenging disease state.

6 obustness of the developed model against the disease state.

7 manifesting in the condition that allows the disease state.

8 wn correlation between mutation identity and disease state.

9 mplications for characterizing an individual disease state.

10 gene expression and regulation varied in the disease state.

11 c phenomena and relationships that differ by disease state.

12 profiles differed significantly dependent on disease state.

13 rts that underwent hHTX/MU regardless of the disease state.

14 en by pay-offs or direct observations of the disease state.

15 rgets for cancers evolving into a metastatic disease state.

16 ses mice before symptomatic onset and tracks disease state.

17 on clinical NGS panels, despite a change in disease state.

18 rom perturbations such as drug treatment and disease state.

19 ly associated with any specific phenotype or disease state.

20 ons between changes in lesion morphology and disease state.

21 bute to the demise of normal behavior in the disease state.

22 cted in MDD, and may reveal biosignatures of disease-state.

23 genetic perturbations, drug treatments, and disease states.

24 tribute to the pathology of their associated disease states.

25 otential for distinguishing tissue types, or disease states.

26 out OSAS, as well as between ethnicities and disease states.

27 r cues and mediates pathogenic mechanisms in disease states.

28 ostasis, and defects can contribute to human disease states.

29 g rapid distinction between tissue types and disease states.

30 , with their misregulation leading to varied disease states.

31 S physiology and function both in normal and disease states.

32 ecules that are commonly altered in numerous disease states.

33 disorder lacking quantitative predictors of disease states.

34 es are significantly associated with certain disease states.

35 y counteract common inflammatory and myeloid disease states.

36 ation of this therapeutic strategy for other disease states.

37 ate and function and are implicated in brain disease states.

38 degree of adaptive plasticity in healthy and disease states.

39 endocrine system cause organ dysfunction and disease states.

40 O-glycan structure in a number of intestinal disease states.

41 oth GLUT and SGLT transporters in health and disease states.

42 l regulators of cell fate in both normal and disease states.

43 cuit motifs that might be generalized across disease states.

44 dysregulation can play a key role in various disease states.

45 eta- and BMP-regulated signaling pathways to disease states.

46 eir aberrant levels have been linked to many disease states.

47 iral signaling, and complex autoinflammatory disease states.

48 ow levels fluctuate in the course of certain disease states.

49 f cell-type definition, gene regulation, and disease states.

50 le in stimulating angiogenesis in normal and disease states.

51 anisms of BAF complex function in normal and disease states.

52 e been implicated in tumorigenesis and other disease states.

53 d the development of valvular-cardiovascular disease states.

54 bution of CD8alphabeta(+) T cells in various disease states.

55 otential markers and/or targets for cellular disease states.

56 e-cell sequencing in development, adult, and disease states.

57 he phenotype transitions between healthy and disease states.

58 ing newly-discovered cell types and cells in disease states.

59 ing exRNAs may reflect human physiologic and disease states.

60 ion of these interactions can easily lead to disease states.

61 promising TSPO PET tracers across different disease states.

62 cellular pathways associated with health and disease states.

63 nzymes have been implicated in several human disease states.

64 newly-discovered cell types and for cells in disease states.

65 model by which hnRNPs can impact health and disease states.

66 d assessment of responsiveness to changes in disease states.

67 outside of their textbook-defined regions in disease states.

68 H(2) O(2) , which is upregulated in several disease states.

69 ies-specific models for protein function and disease states.

70 enhance synaptic transmission in normal and disease states.

71 e in a multitude of biological processes and disease states.

72 equence data from donors with many different disease states.

73 in the context of physiologically normal and disease states.

74 te activity of reticular thalamic neurons in disease states.

75 erapeutic in patients with acute MI or other disease states.

76 edictors of prognosis in many cardiovascular disease states.

77 ndrial DNA, which if compromised can lead to disease states.

78 ng of the molecular basis of puberty and its disease states.

79 hen studying GNG in the context of metabolic disease states.

80 s related to lung function, development, and disease states.

81 re can perturb gene expression and result in disease states.

82 vide a framework to phenotype macrophages in disease states.

83 normal PFC function and in neuropsychiatric disease states.

84 as good diagnostic potential to predict many disease states.

85 elopment that may offer clues to its role in disease states.

86 bioelectric signaling within development and disease states.

87 ciation with progressive glomeruli damage in disease states.

88 uring the onset and progression of mammalian disease states.

89 ora of cellular processes that contribute to disease states.

90 act therapeutic strategies for as many as 50 disease states.

91 nd whose activity is linked to several human disease states.

92 and disease, including early transitions to disease states.

93 PARP activity in these processes can promote disease states.

94 tic understanding of chromatin remodeling in disease states.

95 cells as they respond to signals, drugs, or disease states.

96 fort to understand common mechanisms of both disease states.

97 own of the epithelial barrier to model early disease states.

98 in remodeling the bone-matrix in healthy and disease states.

99 al convergence point of these three comorbid disease states.

100 n linked to diverse biological processes and disease states.

101 egulators to improve the therapy for several disease states.

102 ion of their biological roles in healthy and disease states.

103 ated modulation of angiogenesis in different disease states.

104 f these PTMs in metabolism, development, and disease states.

105 t levels of IgG glycosylation differ between disease states.

106 r morphologies are hallmarks of a variety of disease states.

107 h implications for a broad range of vascular disease states.

108 inflammation, and other platelet-associated disease states.

109 ous physiological, cognitive, behavioral and disease states.

110 on providing reliable markers of healthy and disease states.

111 e gene-expression signatures associated with disease states.

112 variety of cellular processes that influence disease states.

113 e of nucleic acids in aggregate formation in disease states.

114 ional damage to glycocalyx occurs in various disease states.

115 consequences in the etiology of a number of disease states.

116 chronic inflammation associated with several disease states.

117 e in cellular physiology, in both normal and disease states.

118 understanding of myocilin in its normal and diseased state.

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

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

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

122 erstanding of their functions in healthy and diseased states.

123 c and postsynaptic structures in healthy and diseased states.

124 aberrant genome reduplication, including in diseased states.

125 reatment of various types of maligancies and diseased states.

126 idney tissue to recapitulate both normal and diseased states.

127 logical processes and are often corrupted in diseased states.

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

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

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

131 s to the dysregulation of these processes in diseases states.

132 i.e., bioelectronic medicines, for treating disease states, accelerating wound healing processes and

133 Failure in proteostasis can trigger multiple disease states, affecting both human health and lifespan

134 lular and system-level phenotypes of the pre-disease state and allows users to construct predictive a

135 es in predicting tissue-of-origin, normal or disease state and cancer type of each sample.

136 een participants who were separated based on disease state and genetic status.

137 s mRNA coexpression patterns associated with disease state and induces neuronal cell death, establish

138 Low blood count is a fundamental disease state and is often an early sign of illnesses in

139 A levels may serve as markers of Parkinson's disease state and progression, respectively.

140 e complex biology of living organisms and of disease state and progression.

141 outcome measures were the data obtained per disease state and the interrelationships the data displa

142 Additionally, specific retinal disease states and anatomic variables such as extent of

143 tenuate extrapulmonary organ injury in other disease states and are neuroprotective in preclinical mo

144 e with critical and supporting roles in many disease states and conditions.

145 method will be useful in assessing metabolic disease states and developing therapies to improve PDH f

146 stand the heterogeneity of cell populations, disease states and developmental lineages.

147 ents, such as different genetic backgrounds, disease states and drug perturbations.

148 tworks subjected to perturbations, including disease states and drug-induced stress, relies on tracin

149 sequence analysis and the identification of disease states and effects of therapy are prerequisites

150 nding of epigenetic regulators in normal and disease states and enable development of new medicine po

151 an tissues, both for the scientific study of disease states and for diagnosis.

152 Neuroimmunoendocrine modulation in disease states and glucocorticoid-based therapeutics are

153 he damaging inflammation of non-communicable disease states and is considered an attractive therapeut

154 was originally described as associated with disease states and neuronal survival.

155 approach helps accuracy in identification of disease states and provides a route to a plausible mecha

156 ribed as sensitive biomarkers that represent disease states and response to therapies.

157 data can facilitate the characterization of disease states and subtypes, permitting pan-cancer analy

158 f cerebellar development to human behaviour, disease states and the design of better therapeutic stra

159 to provide deeper insights into the complex disease states and their causes than individual disconne

160 ntogeny, distribution across different HIV-1 disease states and their role in viral control remain un

161 ellular biomarkers of a variety of different disease states and therapeutic/vaccine responses.

162 671 are at a greater risk for numerous other disease states and thereby provide new targets for thera

163 herapies to protect these neurons in various disease states and to retain critical brain functions.

164 interactions have been implicated in various disease states and, consequently, disruption of BET-KAc

165 a functionally validated exon in normal and disease states - and reveal a potential target for the t

166 (BBA) has been implicated in motor tasks, in disease states, and as a potential signal for brain-mach

167 roles of bromodomain proteins in normal and disease states, and as a toolset for bromodomain target

168 sed by different environments, tissue types, disease states, and development stages.

169 derepression is associated with a number of disease states, and has the potential to cause significa

170 oplantar epidermis in both physiological and disease states, and how this 'stress' keratin is regulat

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

172 as valuable biomarkers for health status and diseases states, and enable personalized medicine, sensi

173 host and microbial signatures of a number of disease states are currently being examined to identify

174 ative index cases of various prostate cancer disease states are presented, including suspected high-r

175 diating these learning systems in normal and disease states are unknown.

176 tudies on the effects of TRAILshort in other disease states are warranted.

177 e or several user-provided annotations (e.g. disease states) are possible.

178 es in normal lung development, as well as in disease states, are not well defined.

179 sion, despite their importance in normal and disease states, are poorly understood, largely because o

180 t, as measured by the CGI-I, and less severe disease states, as measured by the CGI-S.

181 ng and can be applied to compare healthy and disease state associated to mitochondria morphology.

182 In disease states associated with impaired angiogenesis, we

183 hophysiology of hemoglobinopathies and other disease states associated with unstable globins and red

184 Methods to distinguish disease states based on pattern recognition in the adapt

185 powerful tool in providing readouts of early disease states before clinical manifestation.

186 ion of proteins in blood that could serve as disease-state biomarkers in individuals with FXS.

187 They are not only tools for studying disease states but are also a crucial part of efforts to

188 R1 and CR2 have been implicated in modifying disease states but the mechanisms are not known.

189 behaviour which may have some relevance for disease states, but may also be useful as a screening te

190 biome is dysbiotic and heterogeneous in both disease states, but the metabolome reveals disease-speci

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

192 ing critical transitions from a healthy to a disease state by using early-warning signals is of prime

193 Cells respond to inflammatory disease states by releasing exosomes containing highly s

194 from individuals with a common experience or disease state can be clustered by their repertoire finge

195 such as age, gender, ethnicity, genotype and disease state can cause inter-individual variability in

196 on of excess oxygen, suggesting that certain disease states can potentially be treated by modulating

197 This diseased state can be rescued by administering a glucose

198 plified centrioles, known to be tolerated in disease states, can occur as part of a normal developmen

199 periority in assessment of renal function in disease states characterized by muscle wasting.

200 In disease states, closure of critical periods limits the a

201 n-invasive detection and characterization of disease states could benefit from optical-imaging biomar

202 her anti- or pro-inflammatory effects due to disease-state-dependent changes in AR profiles.

203 king molecular and chemical changes to human disease states depends on the availability of appropriat

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

205 vival and lead to the development of certain disease states, drug persistence, and resistance.

206 Updated disease state durations were incorporated into a simulat

207 These are often employed to characterize disease state early in the process of discovery and prio

208 xpression, causing overexpression during the disease state early-use critical period.

209 ffector cells can potentially influence many disease states, especially those with a chronic inflamma

210 l and continuing discovery of their roles in disease states, focusing particularly on cancer and neur

211 Subgroup analyses by disease state found statistically significantly better v

212 e needed mechanistic insight into normal and disease state functions, as well as afford evaluation fo

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

214 ite cell dysfunction occur in tandem in many disease states; however, no data exist examining the imp

215 erve enhancement is a sign seen in different disease states; however, perineural enhancement is less

216 s contribute to pathogenesis during distinct disease states (ie, the ugly).

217 e has suggested potential benefit in several disease states impacting critically ill patients includi

218 otential to serve as sensitive biomarkers of disease state in both idiopathic and gene-identified PD

219 a direct colorimetric urinary readout of the disease state in less than one hour.

220 ants a need for additional methods assessing disease state in the renal transplant.

221 these two biological processes in health and disease states in chickens, cellular and global expressi

222 To examine podocytes in early disease states in FSGS mouse models, we used podocyte fr

223 omarkers are unlikely to distinguish between disease states in HIV-1 co-infected individuals, and com

224 ret such patterns of immune response between disease states in the absence of functional data.

225 unction; however, excess iron contributes to disease states in the eye.

226 S acquisition closely recapitulate the human disease state, in which GBS colonizes the intestine and

227 stablished as a major risk factor for common disease states including hypertension, type 2 diabetes m

228 otransmission display altered glycans in the disease state, including AMPA and kainate receptor subun

229 is important in normal physiology as well as disease states, including cancer.

230 mmunity changes are associated with numerous disease states, including cardiovascular disease (CVD).

231 tune cell homeostasis and are deregulated in disease states, including hepatocellular carcinoma (HCC)

232 olved in the pathogenesis of several chronic disease states, including IBD, but they have been largel

233 Disease states, including neurodegeneration, are associa

234 For all disease states, individuals exhibited a statistically si

235 expected that mechanisms underlying several disease states involving the interactions between microb

236 ns has been previously implicated in various disease states, ion-exchange chromatography, microfluidi

237 ing these genes in an attempt to improve the disease state is challenging.

238 The disease state is usually preceded by disruption of the h

239 of altered organelle connectomics related to disease states is emerging.

240 An alternative approach to alleviate disease states is to utilize insulin-producing pancreati

241 contribute to neurohumoral activation during disease states is unknown.

242 blood lipids in a broad range of health and disease states is well recognised but less explored is t

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

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

245 a history of acute myocardial infarction, a disease state linked to peripheral inflammation.

246 Moreover, knowledge of disease state may bias assessment.

247 systemic homeostasis and mirrors the global disease state of individuals.

248 cates that FAAH may represent a biomarker of disease state of potential utility for clinical studies

249 used as a diagnostic tool in identifying the disease states of an individual.

250 m for systematic interrogation of normal and disease states of neurons.

251 d underlie both homeostasis and a variety of disease states of the brain.

252 ately, when treatments are discontinued, the disease state often returns as patients relapse.

253 d a number of lipids that were reflective of disease state or injury.

254 However, whether IgE glycans differ in disease states or affect biological activity is complete

255 ng the potential utility of this approach in disease states other than cancer.

256 abnormalities develop into more recognizable disease states over time is unknown but warrants further

257 endently across all five TMAs, regardless of disease state (p = 8.66e-15).

258 stasis and the molecular basis of associated disease states relies on the use of animal models.

259 ytes under beta-adrenergic stimulation or in disease states remains undefined.

260 but their role in cardiovascular health and disease states remains unknown.

261 rom Ang II, in both normal conditions and in disease states, remains only partially understood.

262 that could have therapeutic implications for disease states resulting from reduced TET2 levels or act

263 ofiles were observed during colonization and disease states, revealing specific genes/operons whereby

264 arate validation cohort (N = 540) and across disease states, showing that our findings are robust.

265 with understanding the causes of health and disease states so that we can improve the health of popu

266 protocol compared with Snellen in 4 of the 5 disease states studied.

267 N is dysregulated, the cell may enter into a disease state such as cancer.

268 nctional implications for tissue biology and disease states such as cancer.

269 in individual enzymes leading to dissimilar disease states such as CHARGE syndrome or autism spectru

270 network perturbations that may contribute to disease states such as diabetes, obesity and cancer are

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

272 echanical cues likely contributes to various disease states, such as fibrosis, muscle diseases, and c

273 accepted definitions of remission and other disease states, such as low disease activity or vessel d

274 maintenance lenalidomide in more aggressive disease states, such as patients with cytogenetic high-r

275 Sepsis is a heterogeneous disease state that is both common and consequential in c

276 acers may have potential utility in multiple disease states that are associated with upregulation of

277 Beyond the diseased state, there was an age-related robust decline

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

279 t defective ESCRT function may contribute to disease states through altered sEV signaling.

280 r the shift from an asymptomatic subclinical disease state to advanced clinical disease is not fully

281 levant neural circuit and how they change in disease states to allow rational choices of drugs target

282 NR1 may decrease ARDS development from other disease states to prevent ARDS globally.

283 Moreover, the breadth of disease states to which mechanisms induced by muscle-spe

284 d has the potential to be applied to diverse disease states using clinical or animal-model tissue sam

285 curately classified rats according to their `disease state' using frequency-domain data from steady-s

286 Furthermore, each disease state was associated with a loss of microbial di

287 Prevention of more advanced disease states was not demonstrated.

288 ions contribute to metabolic homeostasis and disease states, we analysed the steady state response of

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

290 ulators of the transition from the normal to disease state were inferred, a number of which are linke

291 robial content, biomarkers of each naive and disease states were identified.

292 ramatically improves recovery of the correct disease state when considering realistic allele effect s

293 ng pathway networks associated with specific disease states when compared to published pathway networ

294 based recommendations are concerning in this disease state where mortality is so integrally related t

295 metabolic comorbidities have in the COVID-19 disease state, which can be key in screening potential t

296 ike RP is used colloquially to describe this disease state, which can present at the time of RP diagn

297 patients due to the additive effects of both disease states, while A. muciniphila may play a non-redu

298 lating a clinical parameter, which manifests disease state, with a laboratory parameter.

299 ) are a growing target class across multiple disease states, with several inhibitors now reported.

300 nked genes in a variety of healthy human and disease state X diploid (XX) cells.