ライフサイエンスコーパス: pathophysiology

1 ta for a comprehensive assessment of plaques pathophysiology.

2 n and signaling, to eosinophilic esophagitis pathophysiology.

3 nt of fundamental therapies that target ADHD pathophysiology.

4 mental disorders without any defined uniting pathophysiology.

5 s) play crucial roles in cell physiology and pathophysiology.

6 d provide insights into early cardiovascular pathophysiology.

7 ting to basophils as important players in CU pathophysiology.

8 tor (SR), is a key mediator in cholangiocyte pathophysiology.

9 ssing and in developmental models of anxiety pathophysiology.

10 tide (CGRP) pathway is important in migraine pathophysiology.

11 egrity, ARDS-associated GWAS genes, and lung pathophysiology.

12 c interneurons (SCIN), are involved in their pathophysiology.

13 ity of biological mechanisms influencing T2D pathophysiology.

14 role of the stress-signalling pathway in its pathophysiology.

15 are critical contributors to cardiovascular pathophysiology.

16 sufficient to broadly address the underlying pathophysiology.

17 her these reactions have the same underlying pathophysiology.

18 ep and breathing patterns on mouse models of pathophysiology.

19 ity/mortality and an incompletely understood pathophysiology.

20 y which inflammation might contribute to the pathophysiology.

21 stand gene regulation and ultimately disease pathophysiology.

22 H may reflect an underrated component of TBI pathophysiology.

23 nd thus advance knowledge of retinal hypoxia pathophysiology.

24 etao) in triggering Alzheimer's disease (AD) pathophysiology.

25 ng, which is central to NMDAR physiology and pathophysiology.

26 actions following DEC and IVM share a common pathophysiology.

27 y and bone metabolism may be involved in ALS pathophysiology.

28 rculosis, yet very little is known about the pathophysiology.

29 pain affects the sickle microenvironment and pathophysiology.

30 plicate 132 nearby genes in allergic disease pathophysiology.

31 cathepsin K plays a critical role in cardiac pathophysiology.

32 on inflammatory processes underlying disease pathophysiology.

33 can act as a unified mediator of downstream pathophysiology.

34 estation) in ways relevant to ASD-associated pathophysiology.

35 ipotent stem cells (iPSCs) to study cellular pathophysiology.

36 cular oxidative stress and diabetic vascular pathophysiology.

37 ber of currently competing hypotheses of SCZ pathophysiology.

38 cardiac excitation-contraction coupling and pathophysiology.

39 to understand its basic biology and clinical pathophysiology.

40 y, are currently suggested to underlie their pathophysiology.

41 e for neutrophils in pediatric severe asthma pathophysiology.

42 ide insight into mechanisms underlying sleep pathophysiology.

43 rosis are introduced in the context of their pathophysiology.

44 nvironmental determinant of bone marrow (BM) pathophysiology.

45 stigated for variants that may underlie SUDY pathophysiology.

46 e a valuable experimental model for human AF pathophysiology.

47 nd decreased repolarization reserve, lead to pathophysiology.

48 networks that may be perturbed in congenital pathophysiologies.

49 ic and causal links between SCRD and disease pathophysiology (3-5).

50 80 years) or with suspected non-Alzheimer's pathophysiology (A-T+N-, A-T-N+, and A-T+N+; 92% at age

51 regulation in GRB14 gene expression in human pathophysiology, a collection of 85 human HCCs was inves

52 gene expression that are highly relevant to pathophysiology affecting ASD.

53 amygdala function have been suggested in CU pathophysiology among antisocial populations, system-lev

54 tory skin disease characterized by a complex pathophysiology and a wide spectrum of the clinical phen

55 rove screening strategies, given the complex pathophysiology and clinical unpredictability of preecla

56 major limitation to better understanding the pathophysiology and diagnosis of this enteropathy is the

57 This syndrome has a discrete pathophysiology and differs genetically and clinically f

58 The model may be useful for studying disease pathophysiology and for developing experimental therapeu

59 nding deficient ABIN1[D485N] mice, and renal pathophysiology and glomerular inflammatory phenotypes w

60 has been an increase in the understanding of pathophysiology and important risk factors both for the

61 Understanding MGD pathophysiology and its relationship to dry eye is impor

62 hlight recent advances in understanding ZIKV pathophysiology and its underlying pathogenesis mechanis

63 , incomplete understanding of the underlying pathophysiology and lack of prognostic biomarkers.

64 hile, we have learned a great deal about the pathophysiology and mechanisms of acute coronary syndrom

65 rget for limiting the impact of PANR in PDAC pathophysiology and metastatic progression.Significance:

66 cell migration has been implicated in tumor pathophysiology and patient outcomes.

67 f sickle cell anemia that contributes to its pathophysiology and phenotypic variability.

68 actors that provide insights about molecular pathophysiology and potential drug targets.

69 ic genetic variables may be involved in both pathophysiology and response to treatment.

70 iate therapeutic approaches based on disease pathophysiology and stage and defined remaining research

71 d supports further studies to understand the pathophysiology and target treatments to pulmonary vascu

72 and the TJ have essential roles in podocyte pathophysiology and that claudin interactions with SD co

73 TLs may help identify cell types relevant to pathophysiology and the regulatory networks underlying d

74 Sex is an influential factor regarding pathophysiology and therapeutic response in human diseas

75 dies linking the glutamatergic system to the pathophysiology and therapeutics of mood disorders.

76 rophic factor (BDNF) plays a key role in the pathophysiology and treatment of depression.

77 nt signaling hub for stress response and for pathophysiology and treatment of depression.

78 creatic insulin production is pivotal in the pathophysiology and treatment of diabetes.

79 oncept study may offer new insights into the pathophysiology and treatment of MS.

80 Asthma pathophysiology and treatment responsiveness are predict

81 dy and its relation to the underlying cancer pathophysiology and tumor border on a per patient basis.

82 ecular bases of human gastric physiology and pathophysiology, and also represent a new platform for d

83 etwork disorder, understanding its causative pathophysiology, and identifying disorder-specific marke

84 There are limited data on the prevalence, pathophysiology, and management implications of pulmonar

85 nate immune responses are critical in stroke pathophysiology, and microglia are key cellular effector

86 se to cutaneous S. aureus contributes to DFU pathophysiology are unknown.

87 continue to be directed toward understanding pathophysiology as well as how best to approach surgical

88 expression may represent a lithium-sensitive pathophysiology, because both C57BL/6J and Pde11a KO mic

89 ta suggest that IL-17A contributes to asthma pathophysiology by increasing the capacity of IL-13 to a

90 nvestigated the role of Fut2 in murine liver pathophysiology by studying Fut2(-/-) mice.

91 As new research methods are developed, NEC pathophysiology can be more completely understood.

92 tibody-mediated pathogenicity as part of the pathophysiology cascade in humans.

93 rdiogenic shock summarizes the epidemiology, pathophysiology, causes, and outcomes of cardiogenic sho

94 eview will describe the underlying genetics, pathophysiology, classification and treatment of angioed

95 In this article, a brief explanation of the pathophysiology, classification, and treatment options f

96 overview of asthma, including epidemiology, pathophysiology, clinical diagnosis, asthma phenotypes,

97 inar describes the epidemiology, lifecycles, pathophysiology, clinical diagnosis, management, and pub

98 ex-specific differences in the epidemiology, pathophysiology, clinical presentation, clinical treatme

99 The review discusses the following topics: pathophysiology, clinical presentation, rationale for st

100 h-quality studies providing insight into the pathophysiology, diagnosis, and management are lacking;

101 We review the pathophysiology, diagnosis, and treatment of chronic dia

102 Our goal in this review is to discuss the pathophysiology, diagnosis, and treatment of stroke caus

103 this Seminar, we summarise the presentation, pathophysiology, diagnosis, and treatment options availa

104 In malaria pathophysiology, divergent hypotheses on the inhibition

105 earch and care communities of evidence about pathophysiology, drug class effects, and the value of su

106 mune cells, specifically mast cells in their pathophysiology, eluding to a potential role for these c

107 eminar discusses the important topics of the pathophysiology, epidemiological trends, and modern mana

108 differentiated cells to study physiology or pathophysiology, examine drug interactions or toxicities

109 e suggesting each subtype may have different pathophysiology, few neuroimaging studies have examined

110 n contribute to our understanding of disease pathophysiology for epigenetic disorders, paving the way

111 These are arguments to consider a step-wise pathophysiology for these diseases, with therapy adjuste

112 echanisms by which MSI2 alters breast cancer pathophysiology have not been clearly identified.

113 rst, categorizing PH according to underlying pathophysiologies, hemodynamic characteristics, and trea

114 Further understanding of asthma pathophysiology in aged patients is needed to improve ma

115 ple lines of evidence support a muscle-based pathophysiology in HD mouse models.

116 mation, a condition proposed to underlie CNS pathophysiology in heritable brain disorders and age-rel

117 neurotransmission are two novel pathways to pathophysiology in mood disorders.

118 pment and suggest a possible contribution to pathophysiology in neurodevelopmental disorders.

119 ble of accurate detection of critical plaque pathophysiology in the coronary arteries.

120 nset before 2 years of age and has a complex pathophysiology in which genetic factors are important.

121 ery disease or those with a specific driving pathophysiology in whom a therapeutic or preventive appr

122 ways disease and showed a marked decrease in pathophysiology, including lung function and airway eosi

123 Both link to discrete pathophysiology: irritability with disruptions in prefro

124 ors are scarce, and our understanding of EVD pathophysiology is limited.

125 t strategies for TBI are supportive, and the pathophysiology is not fully understood.

126 Although the underlying pathophysiology is not well understood, inhibition of bl

127 al sclerosis (ALS) is rapid and, because its pathophysiology is unclear, few effective treatments are

128 dometriosis, its contribution to the disease pathophysiology is unknown.

129 he disorder, providing information about its pathophysiology, is needed.

130 ing or plays an active role in these various pathophysiologies, it is suggested here that treating or

131 We sought to study the molecular pathophysiology leading to susceptibility to infection i

132 The goal of this paper is to review the pathophysiology, mechanism, and management of VT in the

133 Here, the authors discuss the pathophysiology, mechanism, and management of VT that oc

134 Our results suggest that asthma pathophysiology might be differentially associated with

135 mposium, "The Differentiation of Diabetes by Pathophysiology, Natural History and Prognosis" on 10-12

136 ll be for understanding human physiology and pathophysiology, nor how the model will be modified to i

137 EAE transfer experiments suggested that the pathophysiology observed in active EAE was linked to the

138 elucidation and understanding of the unique pathophysiology of AA.

139 Despite recent insights into the pathophysiology of acute and chronic itch, chronic itch

140 Insight into the pathophysiology of acute kidney injury is gleaned from t

141 mation and aberrant immune regulation in the pathophysiology of AD.

142 origin of ORT provides new insights into the pathophysiology of advanced retinal disease highlighting

143 enetic processes have been implicated in the pathophysiology of alcohol dependence, but the specific

144 reticulum (ER) stresses are hallmarks of the pathophysiology of ALS and other neurodegenerative disea

145 ctive for examinations and understanding the pathophysiology of ALS.

146 rought tremendous progress in unraveling the pathophysiology of Alzheimer's disease (AD).

147 gulated proteins, 122 were found linked with pathophysiology of Alzheimer's disease (AD).

148 s biology may have relevance not only to the pathophysiology of Alzheimer's disease but also diet-ass

149 loid beta production are associated with the pathophysiology of Alzheimer's disease, it is clear that

150 The pathophysiology of AMN is not well understood, and the r

151 ortant knowledge gap remains in terms of the pathophysiology of AMR and how detection of immune activ

152 A (Nogo-A) is thought to have a role in the pathophysiology of amyotrophic lateral sclerosis (ALS).

153 ent of the cerebrocerebellar circuits in the pathophysiology of an increasing number of neuropsychiat

154 ural code and also be used to understand the pathophysiology of and design novel therapies for neurol

155 This review describes the epidemiology and pathophysiology of aortic stenosis with heart failure an

156 y allow cross-sectional investigation of the pathophysiology of AR and may also be useful as a potent

157 considerable debate regarding the underlying pathophysiology of ASD.

158 s the role of Dyrk1a loss of function in the pathophysiology of autism.

159 long been known to be a crucial part of the pathophysiology of B-cell lymphomas; however, several ea

160 es, suggesting that our understanding of the pathophysiology of blood vessel disease in diabetes is l

161 The pathophysiology of both movement disorders is largely un

162 ediate-early gene may also contribute to the pathophysiology of brain disorders including schizophren

163 ironmental factors and/or epigenetics in the pathophysiology of CAKUT.

164 The pathophysiology of carcinoid heart disease is poorly und

165 al interest to better understand the complex pathophysiology of cardiovascular diseases.

166 B and T cells play a role in the pathophysiology of cGVHD.

167 care and confounds efforts to elucidate the pathophysiology of commonly occurring symptoms in youths

168 phy (SD-OCT) can provide an insight into the pathophysiology of congenital Zika syndrome (CZS).

169 The pathophysiology of CVD in T1D is poorly defined.

170 ta point to ACC MKP-1 as a key factor in the pathophysiology of depression and a potential target for

171 These findings provide new insight into the pathophysiology of depression, which can aid in future a

172 udies implicate dopamine hypofunction in the pathophysiology of depression.

173 sly unknown role of DNA damage repair in the pathophysiology of DFUs colonized with S. aureus.

174 om the islet of Langerhans is central to the pathophysiology of diabetes.

175 in hyperglycemic heart and contribute to the pathophysiology of diabetic cardiomyopathy.

176 A better understanding of the pathophysiology of DWMI is therefore of critical importa

177 nitive and psychomotor abnormalities, in the pathophysiology of early-stage MDD.

178 ity) as an integral and specific part of the pathophysiology of EoE and implicated protease- and IL-1

179 pite many advances made in understanding the pathophysiology of epileptic disorders, seizures remain

180 is known about the mechanisms underlying the pathophysiology of epithelial injury and intestinal barr

181 nge and were inconsistent with a role in the pathophysiology of FPIES.

182 opic glutamate receptors (mGlu1/5) is a core pathophysiology of fragile X syndrome (FX); however, the

183 erations in GABAergic inhibition play in the pathophysiology of FXS are ill defined.

184 gnificantly, this deficit contributes to the pathophysiology of FXS as the GABABR agonist (R)-baclofe

185 cortical development underlying the sensory pathophysiology of FXS.SIGNIFICANCE STATEMENT Fragile X

186 ointestinal tract, with implications for the pathophysiology of gastrointestinal comorbidities of ASD

187 ld (VF) defects may provide insight into the pathophysiology of glaucoma.

188 L-17A is recognized as being involved in the pathophysiology of Helicobacter pylori-associated diseas

189 tudies are warranted to better elucidate the pathophysiology of hepatic immune-mediated diseases and

190 moreflex pathway plays a pivotal role in the pathophysiology of HF with reduced ejection fraction.

191 of coronary microvascular compromise in the pathophysiology of HFpEF.

192 The pathophysiology of HSRs to IVIPs remains currently uncle

193 rtant and specific role for basophils in the pathophysiology of human anaphylaxis.

194 d suggest a potential role for GRASP1 in the pathophysiology of human cognitive disorders.

195 er, the T-lymphocyte subsets involved in the pathophysiology of hypertension remain unclear.

196 tions that relate to the cells, tissues, and pathophysiology of IBD.

197 rogenesis during infancy are critical to the pathophysiology of ID.

198 r RvD2-DRV2 and their downstream pathways in pathophysiology of infectious inflammation.

199 ort in normal physiologic conditions and the pathophysiology of intestinal diseases.

200 Innate immune signaling is important in the pathophysiology of ischemia/reperfusion (stroke)-induced

201 ivo lung perfusion (EVLP) to investigate the pathophysiology of isolated lungs, we aimed to identify

202 These findings demonstrate that the pathophysiology of KATPHI is complex, and they provide a

203 ecreased WNT/beta-catenin contributes to the pathophysiology of LMNA cardiomyopathy and that drugs ac

204 The pathophysiology of lymphatic disruption is unknown, and

205 de an overview of lymphatic development, the pathophysiology of lymphedema, and the role of leukotrie

206 Inflammatory processes play a key role in pathophysiology of many neurologic diseases/trauma, but

207 contributors to the pathogenesis and disease pathophysiology of many reproductive pathologies, includ

208 is in the eye is an important feature in the pathophysiology of many vision-threatening diseases, inc

209 is and causes DNA damage, accounting for the pathophysiology of megaloblastic anemia observed in vita

210 ter system has been widely implicated in the pathophysiology of mood-related disorders such as anxiet

211 identified allergens may play a role in the pathophysiology of mosquito allergy in the tropics, and

212 t brain phenotype not only implicated in the pathophysiology of multiple disorders, but also used as

213 ects of PDGF-BB on myoblasts involved in the pathophysiology of muscular dystrophies and confirmed ou

214 te select microglial activity to improve the pathophysiology of neurodegenerative conditions or the p

215 CSF flux is involved in the pathophysiology of neurodegenerative diseases and cognit

216 The pathophysiology of neurodegenerative diseases is poorly

217 function has been strongly implicated in the pathophysiology of neurodevelopmental disorders, raising

218 function with relevance to understanding the pathophysiology of neuropsychiatric illness.

219 MiR-146b may play a role in the pathophysiology of OA.

220 Glu may be involved in the pathophysiology of OCD and may moderate response to CBT.

221 Mitochondria play a primary role in the pathophysiology of Parkinson's disease (PD), and small m

222 uss their impact on our understanding of the pathophysiology of PD, and the implications that this mi

223 These findings may be tied to the underlying pathophysiology of periodontal disease progression in sm

224 njury to developing lungs contributes to the pathophysiology of persistent asthma remains poorly unde

225 The focus is on the heterogeneous etiology/pathophysiology of PH in the young, and particularly on

226 In this review, we first consider the pathophysiology of placental infection and transplacenta

227 as inflammation and oxidative stress, in the pathophysiology of polycystic ovary syndrome (PCOS), the

228 vered locus may enhance understanding of the pathophysiology of preeclampsia and its subtypes.

229 us to develop and propose a new view on the pathophysiology of primary biliary cholangitis and PSC i

230 , the three pathways were underscored in the pathophysiology of psychiatric disorders in bioinformati

231 ternal vaginal microbiota contributes to the pathophysiology of PTB, but conflicting results in recen

232 Our current understanding of the pathophysiology of pulmonary vascular disease is incompl

233 nate immune system, has defined roles in the pathophysiology of renal allograft rejection.

234 dating the role of exosomes in the molecular pathophysiology of retinal diseases and help identify po

235 act, but rather implicated in the underlying pathophysiology of schizophrenia and bipolar disorder.

236 l-d-aspartate receptors (NMDARs) in both the pathophysiology of schizophrenia and in neuronal plastic

237 g disrupted PFC-thalamic connectivity in the pathophysiology of schizophrenia and mechanisms of cogni

238 lap between genetic variation underlying the pathophysiology of schizophrenia and the molecular effec

239 t one-carbon metabolism is implicated in the pathophysiology of schizophrenia.

240 ative of a role for immune activation in the pathophysiology of schizophrenia.

241 genes that may provide new insight into the pathophysiology of schizophrenia.

242 Finally, we propose a new vision of the pathophysiology of sepsis that includes the invariable l

243 and, in particular, mTOR alterations in the pathophysiology of sepsis-induced T cell alterations.

244 ular division, repair, and metabolism in the pathophysiology of septic shock.

245 immune system, which has been linked to the pathophysiology of suicidal behavior.

246 vances in the molecular understanding of the pathophysiology of systemic mastocytosis have provided n

247 findings could offer novel insight into the pathophysiology of TBM.

248 me because of HO activity contributes to the pathophysiology of thalassemia.

249 les to investigate the role of miRNAs in the pathophysiology of the disease and to identify novel bio

250 nction associated with ATP production in the pathophysiology of the disease.

251 recognized to have a significant role in the pathophysiology of the disorder.

252 ing to characterize and treat the underlying pathophysiology of the disorder.

253 models that can faithfully recapitulate the pathophysiology of the original tumor.

254 s system has been directly implicated in the pathophysiology of these complex mental illnesses.

255 Research into the pathophysiology of these conditions has been limited by

256 is believed to play an important role in the pathophysiology of these conditions.

257 xcessive CRF is thought to contribute to the pathophysiology of these diseases.

258 The risk factors and pathophysiology of this condition are also not yet fully

259 in our understanding of the still enigmatic pathophysiology of this disease.

260 spective and broaden our view of the complex pathophysiology of this disease.

261 transporter homoeostasis might underlie the pathophysiology of this disorder.

262 res between AMR and TCMR, suggesting similar pathophysiology of tissue injury.

263 However, knowledge of the pathophysiology of TTP has inspired new ways to prevent

264 aim of the present review is to discuss the pathophysiology of TTS with particular emphasis on the r

265 tial improvement in our understanding of the pathophysiology of TTS, a number of knowledge gaps remai

266 idea that the BCAA genes are relevant in the pathophysiology of type 2 diabetes, and that mitochondri

267 udy can additionally yield insights into the pathophysiology of type 2 diabetes.

268 t and contribute to our understanding of the pathophysiology of urinary retention and incontinence wh

269 y disease models that can help elucidate the pathophysiology of vascular inflammation.

270 he role of haemolysis in sickle cell disease pathophysiology, optimal management of pregnancy, and st

271 kinematics or coordination units may reflect pathophysiology or compensatory mechanisms.

272 her exenatide affects the underlying disease pathophysiology or simply induces long-lasting symptomat

273 The authors review the pathophysiology, pathobiology, and emerging clinical per

274 Data on BIA-ALCL, such as pathophysiology, patient demographics, presentation, dia

275 tanding of the cardiovascular system and its pathophysiology refined all aspects of care for these pa

276 The pathophysiology reflects an imbalance between alpha- and

277 re critical next steps in the development of pathophysiology-relevant, evidence-based practice parame

278 he downstream mediators of insulin-resistant pathophysiology remain unclear.

279 Although HFpEF pathophysiology remains incompletely understood, endothe

280 ally toxic immunosuppressive strategies, the pathophysiology remains incompletely understood.

281 ance is a cardinal symptom of HFpEF, yet its pathophysiology remains uncertain.

282 ion antiretroviral therapy (cART), but their pathophysiology remains unclear.

283 Insights on pathophysiology reveal a complex interplay of the epithe

284 ure was performed to discern MGD in terms of pathophysiology, risk factors, and ocular surface impact

285 urgical outcomes, are heterogeneous in their pathophysiology, severity, and reporting accuracy.

286 T4 receptors are promising candidates in IBS pathophysiology since they regulate gut motor function a

287 el of syndemics that addresses transactional pathophysiology, socioeconomic conditions, health system

288 immune diseases, but its participation in BP pathophysiology still needs to be clarified.

289 demiology, the newer insights of anatomy and pathophysiology, the imaging characteristics with emphas

290 , despite hENT3's prominent role in lysosome pathophysiology, the molecular basis of hENT3-mediated t

291 actors is warranted to further elucidate the pathophysiology underlying this novel finding.

292 gesting gender-dependent regulation of their pathophysiology underpinnings.

293 Here, we explored the underlying pathophysiology using induced pluripotent stem cell-deri

294 ions could contribute to nonsyndromic autism pathophysiology using induced pluripotent stem cells mod

295 d inflammation was pursued and a link to PAH pathophysiology was investigated by next-generation sequ

296 pathways relevant to cardiovascular disease pathophysiology, we performed studies in a cell-model sy

297 lymphocyte alterations are central to sepsis pathophysiology, whereas related mechanisms remain poorl

298 A better understanding of the pathophysiology will aid in developing physical and phar

299 Improved understanding of CMML pathophysiology will hopefully lead to the exploration o

300 hallmarks of AD and its associated onset and pathophysiology with age.