ライフサイエンスコーパス: pathogenesis

1 ytokines associated with periodontal disease pathogenesis.

2 d autophagy as targetable components of ADOA pathogenesis.

3 onmental factors and lifestyle choices in AD pathogenesis.

4 e overexpressed in PMBL and involved in PMBL pathogenesis.

5 uroinflammation and Alzheimer's disease (AD) pathogenesis.

6 aureus and establish their importance during pathogenesis.

7 ins, in two widely used mouse models of ZIKV pathogenesis.

8 uggesting a role for this protein in disease pathogenesis.

9 , thereby facilitating viral replication and pathogenesis.

10 antibodies might impact HIV transmission and pathogenesis.

11 modynamic factors or lipid metabolism in MCI pathogenesis.

12 the molecular mechanisms that regulate ZIKV pathogenesis.

13 cer development and Alzheimer's disease (AD) pathogenesis.

14 ily of receptors functions in protection and pathogenesis.

15 of these findings in the wider context of RA pathogenesis.

16 cell maturation, a feature of BE, during EAC pathogenesis.

17 us a potential therapeutic approach for SCA5 pathogenesis.

18 on in understanding the HSV-1 life cycle and pathogenesis.

19 masomes during Leishmania spp. infection and pathogenesis.

20 of kinases in amyotrophic lateral sclerosis pathogenesis.

21 determine the underlying cellular arrhythmic pathogenesis.

22 function of this effector during Legionella pathogenesis.

23 ich SMC phenotypic transitions affect lesion pathogenesis.

24 overing hyperglycinemia as a driver of HLD10 pathogenesis.

25 g inflammatory pathways underlying psoriasis pathogenesis.

26 cal transfer of ZIKV that recapitulate human pathogenesis.

27 ons are required for cell-to-cell spread and pathogenesis.

28 dels suggest that CD8+ T cells drive disease pathogenesis.

29 nd JDP2 in BCC pathogenesis and FOXP1 in SCC pathogenesis.

30 pregulated during GvHD, and mediates disease pathogenesis.

31 pportunities to study the role of PRs in AMD pathogenesis.

32 ations potentially play a causal role in IBD pathogenesis.

33 a central issue regarding viral biology and pathogenesis.

34 potential of passive immunity in this fungal pathogenesis.

35 ion, have been suggested to contribute to UC pathogenesis.

36 mutations contribute significantly to GPP's pathogenesis.

37 believed to be a critical first step in ETEC pathogenesis.

38 1/5/8, mTOR, and VEGFR2 pathways opposes HHT pathogenesis.

39 st response, which may contribute to anthrax pathogenesis.

40 ior to metabolism and has been linked to GAS pathogenesis.

41 ed genes is necessary for unraveling disease pathogenesis.

42 e importance of LRP2BP in systemic sclerosis pathogenesis.

43 points to a role for CD8+ T cells in disease pathogenesis.

44 at specific cell types play during norovirus pathogenesis.

45 d innate receptors that may underlie disease pathogenesis.

46 rting the role of NETs in a late stage of TB pathogenesis.

47 me activation have a limited role on malaria pathogenesis.

48 nd discuss the role of vTRs in human disease pathogenesis.

49 in health and are implicated in Alzheimer's pathogenesis.

50 ucial hijacking point for a successful viral pathogenesis.

51 ifferentiation of Th2 cells important for AD pathogenesis.

52 nal microbes in human physiology and disease pathogenesis.

53 tive transcriptional pathways underlying DMD pathogenesis.

54 lar metals is essential for cell fitness and pathogenesis.

55 , rosetting has been associated with malaria pathogenesis.

56 ble new, systems-level insights into disease pathogenesis.

57 ion suggesting potential role of GQs in FSHD pathogenesis.

58 cluding fibrosis, plays a central role in DM pathogenesis.

59 erstand SARS-CoV-2 tropism, transmission and pathogenesis.

60 ntigens as important contributors to disease pathogenesis.

61 euroinflammatory responses implicated in AIS pathogenesis [9].

62 r activation of MAPK signaling in iMCD-TAFRO pathogenesis and a rationale for exploring inhibition of

63 The underlying pathogenesis and appropriate management remain understud

64 on terminology that more accurately reflects pathogenesis and can help in patient stratification for

65 , thus, provide novel insights into COVID-19 pathogenesis and can serve as a model for understanding

66 mechanisms of environmental factors in FECD pathogenesis and demonstrates a strong link between UVA-

67 Specific topics include Pathogenesis and Epidemiology, Initial Evaluation, Imagi

68 bility of zebrafish for studying M. kansasii pathogenesis and for the first time identify extracellul

69 factors that implicated SMAD and JDP2 in BCC pathogenesis and FOXP1 in SCC pathogenesis.

70 Although CD4+ T cells are implicated in MS pathogenesis and have been the main focus of MS research

71 emphasizing an important role of 5hmC in AD pathogenesis and highlighting both ethnicity-specific an

72 is a valuable technique for studies of viral pathogenesis and host responses to infection in vivo.

73 alterations may improve understanding of AD pathogenesis and lead to new biomarkers and treatment ta

74 The pathogenesis and molecular features are unknown.

75 es new insight into how flaviviruses control pathogenesis and mosquito transmission through the nonst

76 ed for awareness of HS, understanding of its pathogenesis and novel treatments.

77 t phenotypic presentation as a reflection of pathogenesis and outline a practical approach to the eva

78 nes and proteases that contribute to disease pathogenesis and perpetuation.

79 icant for future investigations of filovirus pathogenesis and persistence as well as arthralgias in a

80 d peptide, Abeta, play a central role in the pathogenesis and progression of Alzheimer's disease.

81 nding of how inflammation contributes to the pathogenesis and progression of HF.

82 ntion because of their essential role in the pathogenesis and progression of kidney diseases.

83 tracellular S1P signaling contributes to the pathogenesis and progression of kidney diseases.

84 s a key defining factor to understand cancer pathogenesis and progression, which requires the develop

85 ation and ubiquitination are involved in SCD pathogenesis and provide further insight into the multif

86 nderstanding how GBA1 mutations influence PD pathogenesis and provides a platform for testing novel t

87 emonstrated that the spike has a role in MHV pathogenesis and retrograde axonal transport.

88 nnose as a marker of influenza virus-induced pathogenesis and severity of disease outcome.

89 nt HTT protein aggregates, a biomarker of HD pathogenesis and severity.

90 tial association between chronic ocular GVHD pathogenesis and stress-induced cellular senescence thro

91 -2 MA model demonstrates age-related disease pathogenesis and supports the clinical use of pegylated

92 ort the utility of AGM for studying COVID-19 pathogenesis and testing medical countermeasures.

93 histidine in the lung promotes Acinetobacter pathogenesis and that histidine serves as a crucial nitr

94 utoreactive CD4 T cell-mediated skin disease pathogenesis and that the NLRP3-dependent inflammasome i

95 ce regarding the common pathways for genetic pathogenesis and the anatomical distribution of meningio

96 itate future studies of DNA demethylation in pathogenesis and the development of 5hmC as biomarkers.

97 finitions, the uncertainties surrounding the pathogenesis and the highly variable clinical presentati

98 nd immediate utility to investigate COVID-19 pathogenesis and to evaluate new therapies and vaccines.

99 ogy and for the investigation of ACE2 in the pathogenesis and treatment of COVID-19.

100 rminants that could contribute to H5N1 virus pathogenesis and tropism.

101 ing a more profound understanding of disease pathogenesis and ultimately targeted therapies.

102 esistance to antibiotics and antimicrobials, pathogenesis, and adhesion to the mucosal surfaces to co

103 essive, site-specific nature of CLN1 disease pathogenesis, and highlight the importance of the neuroi

104 shed new light on the mechanisms of disease pathogenesis, and may help to guide the development of e

105 model provides a new tool to investigate HIV pathogenesis, and our results shed new light on the mole

106 ies in mediating protection, contributing to pathogenesis, and seeding the human placenta.

107 response; however, the mechanisms leading to pathogenesis are not well understood.

108 s in autistic brains, but their roles in ASD pathogenesis are still unclear.

109 st interactions inducing ocular and neuronal pathogenesis are unclear.

110 ing the exacerbated inflammation during DENV pathogenesis are unclear.

111 anism of feedback inhibition and its role in pathogenesis are unclear.

112 ment of EoE, but other cytokines involved in pathogenesis are unknown.

113 s expression might provide insights into its pathogenesis as well as improving risk stratification st

114 ow this manipulation can influence microbial pathogenesis as well as the host cell metabolism and imm

115 conceptual shift in the understanding of MS pathogenesis, away from the classical model in which T c

116 and evaluation.IMPORTANCE Differences in HIV pathogenesis between males and females, including immuni

117 ates the critical role of SFTSV NSs in viral pathogenesis but also suggests potential future therapeu

118 ells has implications not only for H. pylori pathogenesis but for host tumorigenesis.

119 plays a primary role in Alzheimer's disease pathogenesis, but longitudinal Abeta, tau, and neurodege

120 le for T-cell-mediated immunopathology in LF pathogenesis, but the mechanisms by which T cells influe

121 eciated role in sHLH/cytokine storm syndrome pathogenesis by preventing macrophages from becoming bot

122 tion while potentially contributing to HIV-1 pathogenesis by triggering T cell activation and cell de

123 The pathogenesis, classification and assessment of SSc-assoc

124 3 immunity is modulated and immune-mediated pathogenesis controlled.

125 er beneficial or detrimental roles in lesion pathogenesis, depending on the nature of their phenotypi

126 tation of circadian influences contribute to pathogenesis during distinct disease states (ie, the ugl

127 ritical for P. mirabilis urease activity and pathogenesis during infection.

128 trophilic inflammation is central to disease pathogenesis, for example, in chronic obstructive pulmon

129 addressing plaque psoriasis have been in its pathogenesis, genetics, comorbidities, and biologic trea

130 Pathogenesis hallmarks for tuberculosis (TB) are the Myc

131 For many years, the prevailing view of AD pathogenesis has been that changes in Abeta precipitate

132 cible models for the study of M. haemolytica pathogenesis has hampered efforts to better understand t

133 e contribution of genetic risk factors to UC pathogenesis has not been systematically defined.

134 the muscle-specific role of TRIM32 in LGMD2H pathogenesis has proven difficult, as neurogenic phenoty

135 To better understand neuroblastoma pathogenesis, here we analyze whole-genome, whole-exome

136 is may suggest a role for epigenetics in T1D pathogenesis; however, functional validation is warrante

137 clinical isolates affects transmissibility, pathogenesis, immune modulation, and drug resistance.

138 n order to study herpesvirus replication and pathogenesis in animals.

139 or the HIV envelope, to mitigate HIV-induced pathogenesis in bone marrow, liver, thymus (BLT) humaniz

140 ute to early stages of neurodegeneration and pathogenesis in HAND.

141 for postnatal HIV transmission or increased pathogenesis in infants.

142 y novel modifiers of different aspects of HD pathogenesis in medium-spiny neurons and highlight a com

143 r results identify a novel pathway of asthma pathogenesis in patients with obesity/metabolic syndrome

144 tiochelin is required for full S. marcescens pathogenesis in the bloodstream.

145 a druggable epigenetic mechanism of disease pathogenesis in this heritable HF syndrome.

146 ent key islet miRNA families involved in T2D pathogenesis including miR-200, miR-7, miR-184, miR-212/

147 genome evolution and are a notable source of pathogenesis, including cancer.

148 ogical processes that contribute to delirium pathogenesis, including neuroinflammation, brain vascula

149 lly ill patients that mediate the associated pathogenesis, including vascular dysfunction, thrombosis

150 y help decipher the mechanisms underlying KS pathogenesis induced by HIV and KSHV coinfection.

151 selves in susceptibility to infection, early pathogenesis, innate viral control, adaptive immune resp

152 ese studies unveil a unique mechanism for Ft pathogenesis involving a virulence-specialized RNAP that

153 rheumatoid arthritis and osteoporosis, whose pathogenesis is associated with a Th17/Treg imbalance.

154 In this study, we test whether AD pathogenesis is associated with dysregulation in brain t

155 These findings suggested SCAD pathogenesis is noninflammatory and screening for autoim

156 arries a poor prognosis, in part because its pathogenesis is not well understood.

157 Its pathogenesis is poorly understood, and there are no effe

158 Molecular pathogenesis is preserved between V-EoE and L-EoE.

159 y epithelial proliferation and breast cancer pathogenesis likely via the modulation of Wnt/beta-caten

160 Parkinson's disease (PD) pathogenesis may involve the epigenetic control of enhan

161 6 and AIM2 contribute to periodontal disease pathogenesis may lead to treatment options that address

162 43 and CHCHD10 mutations drive mitochondrial pathogenesis, mechanisms underlying such phenotypes are

163 To address the role of NK cells in PD pathogenesis, NK cell function was investigated in a pre

164 dosteronism syndrome and implicate it in the pathogenesis of "essential" hypertension.

165 well as players in an important role in the pathogenesis of a variety of human diseases.

166 Dysregulated autophagy contributes to the pathogenesis of acute kidney injury, to incomplete kidne

167 Inflammation plays a central role in the pathogenesis of acute lung injury (ALI) during both the

168 how this might impact the neuropathology and pathogenesis of AD.

169 tion of the identified ADAM17 variant in the pathogenesis of AD.

170 of these 2 emerging key pathways driving the pathogenesis of AF.

171 iated by zinc deficiency and involved in the pathogenesis of AH.

172 T1E1 appears to have a novel function in the pathogenesis of AKI.

173 ictive biomarkers, but also in capturing the pathogenesis of Alzheimer dementia.

174 ls of amyloid-beta, which is critical in the pathogenesis of Alzheimer's disease.

175 sting a retinal vascular contribution to the pathogenesis of AMD.

176 e the role of neuronal NF-kappaB activity in pathogenesis of amyotrophic lateral sclerosis (ALS), we

177 of this probability may be critical for the pathogenesis of anxiety or reckless and impulsive behavi

178 The pathogenesis of ASD is not known, but it involves activa

179 egarding the role and function of EVs in the pathogenesis of asthma via the PRISMA statement method.

180 has been recognized as a major player in the pathogenesis of atherosclerosis.

181 L-17 production, play important roles in the pathogenesis of autoimmune diseases (such as arthritis,

182 ondrial calcium transport contributes to the pathogenesis of Barth syndrome, and more generally, show

183 -grade inflammation are major players in the pathogenesis of cardiovascular disease (CVD) and Alzheim

184 termine whether these bacteria contribute to pathogenesis of CD.

185 nhancement (ADE) is a mechanism by which the pathogenesis of certain viral infections is enhanced in

186 ir involvement in palate development and the pathogenesis of cleft palate.

187 oles for inherited noncoding variants in the pathogenesis of CLL.

188 es, leading to significant insights into the pathogenesis of complex human diseases, little is known

189 thrombocytopathy and endotheliopathy to the pathogenesis of COVID-19 and discuss potential therapeut

190 wever, the participation of platelets in the pathogenesis of COVID-19 remains elusive.

191 Inflammation has a pivotal role in the pathogenesis of CVD.

192 ered regulatory phenotype and ultimately the pathogenesis of DCM.

193 rker of neurotoxicity, may contribute to the pathogenesis of delirium independent of inflammation.

194 To further understand the molecular pathogenesis of desmoplastic small round cell tumor (DSR

195 esponse is thought to both contribute to the pathogenesis of disease and provide protection during it

196 s a role for HOPS complex dysfunction in the pathogenesis of dystonia, although variants in different

197 Finally, further insights into the pathogenesis of EoE have revealed several novel disease

198 ) play an important role in the etiology and pathogenesis of esophageal squamous cell carcinoma (ESCC

199 venue for advancing our understanding of the pathogenesis of ET; however, until recently, the number

200 results provide a paradigm for the molecular pathogenesis of ETEC in which the bacteria use toxin to

201 Our results suggest that pathogenesis of FXII-, ANGPT1-, and U-HAE moves through

202 isorders and has also been implicated in the pathogenesis of gastrointestinal (GI)-related cancers, i

203 activation, which has been implicated in the pathogenesis of heart failure (HF) with preserved ejecti

204 r dysfunction plays an important role in the pathogenesis of heart failure with preserved ejection fr

205 he innate and adaptive immune systems in the pathogenesis of heart failure, and highlights the result

206 renal system, and has a putative role in the pathogenesis of Hirschsprung disease.

207 mmatory caspases may also play a role in the pathogenesis of human disease.

208 a role for the adaptive immune system in the pathogenesis of IADRs.

209 however, and their potential contribution to pathogenesis of ICL remain unclear.METHODSWe hybridized

210 e of sputum cells and its implication in the pathogenesis of immune function and the development of C

211 irus and the host immune response and of the pathogenesis of infection is crucial to identify valid t

212 Diet plays a significant role in the pathogenesis of inflammatory bowel disease (IBD).

213 unocytes could provide key insights into the pathogenesis of inflammatory skin diseases that have thu

214 for deciphering the location, regulation and pathogenesis of internal mRNA m7G.

215 cific modulations, pharmacology, and disease pathogenesis of K(V)7.1, and likely applies to numerous

216 late KSHV ORF21 and, thus, contribute to the pathogenesis of KSHV-MCD and the activity of zidovudine

217 nown to play a crucial role in virulence and pathogenesis of M. tuberculosis In our earlier study, we

218 hey provide a platform for understanding the pathogenesis of macular degeneration and other related d

219 of caspase-8 and caspases-1/11/GSDM-D in the pathogenesis of malaria.

220 l dysfunction is a common contributor to the pathogenesis of most types of diabetes.

221 y autoreactive CD4 T cells contribute to the pathogenesis of MS.

222 tigate their respective contributions in the pathogenesis of mucoinflammatory airway disease.

223 Our findings provide insights into the pathogenesis of myeloid transformation and how clonal co

224 have implicated glycosyltransferases in the pathogenesis of neurodegenerative diseases but different

225 5, in attenuating mechanisms involved in the pathogenesis of neurodegenerative diseases, using both i

226 , as such, may be critically involved in the pathogenesis of neurodevelopmental abnormalities and cog

227 eral nervous system (PNS) contributes to the pathogenesis of neuropathy remains poorly understood.

228 the intestinal crypts may be involved in the pathogenesis of normalization of hyperglycemia caused by

229 P53 has been implicated in the pathogenesis of obesity and diabetes; however, the mecha

230 ess in adipocyte plays a central role in the pathogenesis of obesity as well as in the associated car

231 rticularly the brainstem, contributes to the pathogenesis of obesity-associated cerebrovascular dysfu

232 importance of dietary acid load (DAL) in the pathogenesis of osteoporosis is still debated.

233 ein (AHSG), all of which are involved in the pathogenesis of other types of crystal-induced nephropat

234 The dual hit hypothesis about the pathogenesis of Parkinson disease (PD) suggests that the

235 ings support a critical role of Tregs in the pathogenesis of persistence induced by intracellular bac

236 monocyte lineage, play a direct role in the pathogenesis of PH.

237 the trajectories and targets underlying the pathogenesis of prenatally triggered asthma are largely

238 Future research must investigate the pathogenesis of recurrent pregnancy loss and evaluate no

239 the expression and mechanisms of HE4 in the pathogenesis of renal fibrosis.

240 stent with mCH playing a central role in the pathogenesis of Rett Syndrome.

241 cell dysregulation as a central event in the pathogenesis of rheumatoid arthritis.

242 r expand on what is known about ClpXP in the pathogenesis of S. aureus to include the respiratory tra

243 The pathogenesis of salmonellosis has been extensively studi

244 erging at a steady pace, some aspects of the pathogenesis of SARS-CoV-2 can be studied in detail only

245 OVID-19 disease, an effect that might be for pathogenesis of SARS-CoV-2 infection and indicate that i

246 els that are important for understanding the pathogenesis of SARS-CoV-2, vaccine development, and the

247 These results offer insight into the pathogenesis of scarlet fever-causing GAS mediated by pr

248 ests that gut microbiota plays a role in the pathogenesis of schizophrenia via the microbiota-gut-bra

249 signaling is a prevailing hypothesis for the pathogenesis of schizophrenia.

250 ic regulation may play a central role in the pathogenesis of sepsis.

251 nflammatory processes are known to drive the pathogenesis of several chronic diseases, including card

252 A better understanding of the pathogenesis of SFTS is crucial to improving medical cou

253 n of complement components contribute to the pathogenesis of some autoimmune neurological disorders a

254 These results shed light on the pathogenesis of Spn and identify therapeutic targets.

255 lococcal alpha-hemolysin is critical for the pathogenesis of Staphylococcus aureus skin and soft tiss

256 ould thus be considered a risk factor in the pathogenesis of synucleinopathies or a subset of mental

257 the contributions of GRA12 to the molecular pathogenesis of T. gondii infection were examined in vit

258 ion of the antiviral response underlying the pathogenesis of the disease, COVID-19.

259 rly event and plays a functional role in the pathogenesis of the diseases by impacting several mechan

260 oronavirus and evaluated the replication and pathogenesis of the DUB mutant virus (DUBmut) in culture

261 We compared the pathogenesis of the DUBmut virus to that of the wild-typ

262 Much of the pathogenesis of these diseases is related to dysregulate

263 fundamental understanding of the biology and pathogenesis of these viruses.

264 nd migration of ECs that are critical in the pathogenesis of transplant vasculopathy.

265 novo, uptake of cobalamin has been linked to pathogenesis of tuberculosis(2).

266 The pathogenesis of Type 1 diabetes (T1D) arises from the de

267 between signaling pathways that regulate the pathogenesis of UC and summarize the macrophage-based na

268 CRI) is very important for understanding the pathogenesis of various human diseases-notably autoimmun

269 role in organ homeostasis, immunity and the pathogenesis of various inflammation-driven diseases.

270 VD may improve our understanding on glaucoma pathogenesis, offering new treatment insights.

271 isms by which coronavirus infection dictates pathogenesis or counters the host immune response would

272 y associated with neuronal homeostasis or HD pathogenesis, or both.

273 current dilemmas was reviewed, and possible pathogenesis proposed, based on advances in immunology t

274 e assessment of host signaling in SARS-CoV-2 pathogenesis provides some complex yet important strateg

275 propagation of tau protein misfolding and AD pathogenesis, providing a new conceptual framework that

276 ew the role of ppGpp and pppGpp in bacterial pathogenesis, providing examples of how these nucleotide

277 cid induction deficient2 and nonexpressor of pathogenesis-related genes1 (npr1) mutant backgrounds.

278 omics was used to sequence and identify four pathogenesis-related proteins (PRPs) from the haze of a

279 eptides, camalexin, and 4-OH-ICN, as well as pathogenesis-related proteins.

280 tory influence of TEs and their links to AML pathogenesis remain unexplored.

281 elevance of CP-GAS interactions to bacterial pathogenesis remain unknown.

282 o role of the STING pathway during bacterial pathogenesis remains unclear.

283 oarthritis, yet its relative contribution to pathogenesis remains unknown.

284 In contrast, PML pathogenesis research has been greatly hindered because

285 NPR1 nuclear roles include pathogenesis response (PR) gene regulation.

286 g of disease-causing mutations suggests that pathogenesis results from folding defects and the disrup

287 epithelial cell apoptosis in gastric cancer pathogenesis, suggesting a mechanism for prolonged epith

288 and the repertoire of animal models of CCHFV pathogenesis that can be used for therapeutic developmen

289 ls a critical gap in our understanding of CM pathogenesis that is impeding development of therapeutic

290 tery disease-and its contribution to disease pathogenesis, there is increased interest in understandi

291 or an essential role of the PfELC in malaria pathogenesis, these structures provide a blueprint for t

292 findings suggest that UBQLN2 mutations drive pathogenesis through a dominant-negative loss-of-functio

293 une effector that controls CoV infection and pathogenesis via a mechanism distinct from other factors

294 HIKV replication in skeletal muscle cells to pathogenesis, we engineered a CHIKV strain exhibiting re

295 ne molecules with a novel function in cancer pathogenesis, we found the cluster of differentiation 17

296 ehensive understanding of APOE4's role in AD pathogenesis, we performed a transcriptomics analysis of

297 the contribution of the immune system to CDC pathogenesis, we undertook a prospective multicentric ex

298 eted and its roles in fungal development and pathogenesis were investigated using approaches includin

299 eralized stepwise model for MCD/C5 and PENLs pathogenesis, whereby acquisition of founder mutations i

300 , PRMT7 is a cytoplasmic protein implicit in pathogenesis with unknown substrates.