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1 biology and advanced understanding of cancer pathophysiology.
2 spect to differences in underlying causes or pathophysiology.
3 isoform-specific AMPKalpha repression on AD pathophysiology.
4 ute and chronic GVHD, in the context of GVHD pathophysiology.
5 ing in splicing changes that promote disease pathophysiology.
6 echanisms connecting gut microbiota and host pathophysiology.
7 mune activation as central to stress-related pathophysiology.
8 cognitive function and psychiatric disorder pathophysiology.
9 del depicting numerous genes contributing to pathophysiology.
10 dressed by understanding the complex disease pathophysiology.
11 hly prevalent disease with poorly understood pathophysiology.
12 s (ICS) affect this important aspect of COPD pathophysiology.
13 lation (AF) share an underlying inflammatory pathophysiology.
14 ntification of patient subgroups with shared pathophysiology.
15 contribution of vascular dysfunction in CRS pathophysiology.
16 roviding insights into intracranial aneurysm pathophysiology.
17 lated adjunctive therapies to ameliorate HCC pathophysiology.
18 e essential for understanding kidney disease pathophysiology.
19 n could advance hormone-based physiology and pathophysiology.
20 tween in vitro experimental models and human pathophysiology.
21 endocrine development and associated disease pathophysiology.
22 derived microvesicles may influence arterial pathophysiology.
23 nd experimentally leveraged, to elucidate AD pathophysiology.
24 rs have deepened our appreciation of disease pathophysiology.
25 nsula, limbic structures key to the disorder pathophysiology.
26 result from both inflammation and non-immune pathophysiology.
27 I IFN mechanisms to address its role in TBI pathophysiology.
28 an important role in cellular physiology and pathophysiology.
29 +) myeloid cells, in RSV infection-triggered pathophysiology.
30 as new targets of potential relevance to ALS pathophysiology.
31 ast, AMPKalpha2 suppression did not alter AD pathophysiology.
32 for future work to elucidate the underlying pathophysiology.
33 ute and chronic phases of multiple sclerosis pathophysiology.
34 -processing network heavily implicated in AD pathophysiology.
35 erventricular differences in their molecular pathophysiology.
36 regulatory processes and implicated in some pathophysiology.
37 this toxin-receptor pair plays in S. aureus pathophysiology.
38 rare IBD variants on disease prediction and pathophysiology.
39 e contribution of cytokine storm to COVID-19 pathophysiology.
40 edge gap between in vitro models and in vivo pathophysiology.
41 tasis and the key pathways implicated in ALS pathophysiology.
42 limited treatment options and poorly defined pathophysiology.
43 tions in brain connectivity may underlie its pathophysiology.
44 disorders is important for understanding the pathophysiology.
45 e among the key markers for determining RA's pathophysiology.
46 native to animal testing for the study of BM pathophysiology.
47 lore pathways and mechanisms contributing to pathophysiology.
48 ny of which have plausible links to COVID-19 pathophysiology.
49 major determinant of cardiac physiology and pathophysiology.
50 as9 to study TNNT2 variant pathogenicity and pathophysiology.
51 cutive control of motor commands in dystonia pathophysiology.
52 a central role in both metabolic health and pathophysiology.
53 ation of nearby genes implicated in progeria pathophysiology.
54 ular mechanisms, which underlie preeclampsia pathophysiology.
55 lamus seem to be implicated in schizophrenia pathophysiology.
56 ns in the context of vascular physiology and pathophysiology.
57 nterneurons has been linked to schizophrenia pathophysiology.
58 rcuits and targeted to the root cause of the pathophysiology.
59 leles of a single locus and their associated pathophysiologies.
60 role of these Orai1 channels in the cardiac pathophysiology, a transgenic mouse was generated with c
62 here were no strong correlations between the pathophysiologies and no remarkable clusters among them.
63 d mortality requires knowing the responsible pathophysiologies and the therapeutic advances that are
65 na that may facilitate research into disease pathophysiology and biomarker development for diagnostic
66 y relevant insight into the underlying acute pathophysiology and biomarker release kinetics following
69 current knowledge on this disease, including pathophysiology and clinical presentation, moving on to
70 temporal and spatial development of ischemic pathophysiology and determining neuronal activity signat
71 ules with potentially deleterious outcome in pathophysiology and disease, "oxidative distress." Refle
72 paradigm shifts in our understanding of the pathophysiology and downstream end-organ complications o
73 er organoids (RCOs) closely recapitulate the pathophysiology and genetic changes of corresponding tum
74 the population, although key facets of their pathophysiology and host interaction remain unclear.
75 t further characterize PBDE-induced diabetic pathophysiology and identify critical developmental time
77 re short and underscore its relevance to the pathophysiology and interventions of human telomere-driv
78 osed framework unites many ideas of tinnitus pathophysiology and may catalyze cooperative efforts to
79 acological thresholds correspond to exercise pathophysiology and myocardial ischemia in patients with
81 al imaging has offered novel insights on its pathophysiology and prognosis, but its use in AF-related
82 mportantly, many promising findings focus on pathophysiology and reflect group-level comparisons, but
84 cussed as a potential factor influencing the pathophysiology and severity of inflammatory skin diseas
85 se that a better understanding of aetiology, pathophysiology and symptomatic treatments can arise fro
86 f these diseases could illuminate both their pathophysiology and the computational architecture of th
87 he complexity of immune dysregulation in MDS pathophysiology and the fine balance between smoldering
89 dditional work is needed to characterize the pathophysiology and to identify the definitive causes.
92 essential for the elucidation of the ME/CFS pathophysiology, and lead to accurate diagnoses, prevent
93 ronchiectasis, likely contributes to disease pathophysiology, and may be a target for pharmacotherapy
94 othelial cells that regulates cardiovascular pathophysiology, and provide a mechanism by which a sing
97 oups based on features reflecting underlying pathophysiology, are likely to have less clinical utilit
98 into normal human organ function and disease pathophysiology, as well as more accurately predict the
99 and neuroimaging can identify the underlying pathophysiology at the earliest stage of some neurodegen
100 ides an opportunity to dissect human disease pathophysiology at unprecedented resolutions(6), particu
102 romotes thrombotic events and drives obesity pathophysiology, but a lack of essential analytical tool
103 ial dysfunctions appear also involved in ASD pathophysiology, but the mechanisms by which such altera
104 des evidence that MPs play a key role in SCD pathophysiology by triggering a proinflammatory phenotyp
105 n our Review Article, we discuss the disease pathophysiology, clinical manifestation, evidence based
106 These disparities are noted in epidemiology, pathophysiology, clinical manifestations, disease progre
108 ients attending the HIV outpatient clinic of Pathophysiology Department at <<Laiko>> General Hospital
109 chronic GVHD preclinical models that have a pathophysiology distinct from acute GVHD, Itpkb-/- donor
111 logy (eg, heart rate and blood pressure) and pathophysiology (eg, onset of adverse cardiovascular eve
112 We review the rapidly changing epidemiology, pathophysiology, emerging therapy, and clinical outcomes
114 ss has been made in the understanding of CRS pathophysiology: from the epithelium and epithelial-mese
115 esult of our incomplete understanding of its pathophysiology, functional dyspepsia is difficult to tr
117 hese results elucidating somatotroph adenoma pathophysiology identify pathways for targeted treatment
118 our understanding of disease mechanisms and pathophysiology in a disorder with diverse clinical phen
119 sociations between neuroimmune responses and pathophysiology in brain disorders such as Alzheimer's d
121 will provide insights into the BDNF mediated pathophysiology in coronary artery disease (CAD) that ma
122 d treatment for hypertension, the underlying pathophysiology in each patient has to be taken into con
123 y kidney disease according to its underlying pathophysiology in order to develop more precise and eff
125 y has potential downstream effects on asthma pathophysiology, including on airway epithelial cells, m
128 demonstrates the diversity of sensory neuron pathophysiology is due in part to subtype-dependent sens
129 eater understanding of aetiopathogenesis and pathophysiology is emerging and includes intestinal comp
130 ding of atopic dermatitis (AD) and psoriasis pathophysiology is largely derived from skin biopsy stud
134 ynuclein, which is critically involved in PD pathophysiology, is upregulated in inflamed segments of
135 ailures, and CNS trauma were the most common pathophysiologies leading to morbidity and mortality in
136 y may be increased because of the underlying pathophysiology leading to Fontan palliation, remodellin
142 oxygen species are centrally involved in the pathophysiology of airway diseases such as asthma and ch
143 e epithelial barrier to the forefront of the pathophysiology of airway inflammation, different approa
144 heterozygous mouse model sheds light on the pathophysiology of altered memory and cognitive function
146 that vHipp-NAcSh activity is relevant to the pathophysiology of anhedonia and depression as well as t
147 r responses have been well documented in the pathophysiology of anxiety and may play an important rol
148 in AT(1) receptor pathway contributes to the pathophysiology of ARDS, whereas activation of the ACE-2
154 sly unappreciated clues in understanding the pathophysiology of behavioural, psychiatric and neurodeg
157 local B cell response may contribute to the pathophysiology of CAV through a mechanism that needs to
158 isease, which would provide insight into the pathophysiology of chronic cachexia and a tool to test t
159 nflammasome substantially contributes to the pathophysiology of chronic cerebral hypoperfusion-induce
162 cortex maturation has been implicated in the pathophysiology of cognitive deficits in psychiatric dis
163 s, provide insight into the potential immune pathophysiology of COPD exacerbations, and indicate that
165 st x-ray tomography as a tool to unravel the pathophysiology of Covid-19, extending conventional hist
168 In this review, the latest research on the pathophysiology of CRS with a focus on potential novel b
170 ting TRD provided a new understanding of the pathophysiology of depression, a paradigm shift from mon
173 on has emerged as a central component of the pathophysiology of diffuse parenchymal diseases includin
174 he context of both normal physiology and the pathophysiology of disease and then extended to discuss
176 f UPR signalling and its implications in the pathophysiology of disease might open new therapeutic av
177 itical to advancing our understanding of the pathophysiology of diseases involving the cerebellum.
178 ium dynamics and their potential role in the pathophysiology of disorders characterized by dysfunctio
180 early 2000s, a greater understanding of the pathophysiology of diverticulosis and diverticular disea
183 ling may provide additional insight into the pathophysiology of emphysema and inflammatory lung disea
185 Findings may provide novel insights into the pathophysiology of epileptic seizures with respect to AN
189 g recognition of duodenal alterations in the pathophysiology of functional dyspepsia (FD), the effect
192 ent stem cells as a model to investigate the pathophysiology of FXS in human neurons, we reveal key n
199 tile output for energy conservation and that pathophysiology of HCM results from destabilization of t
200 Myocardial fibrosis may contribute to the pathophysiology of heart failure with preserved ejection
201 is recognized as playing a major role in the pathophysiology of heart failure; however, clinical tool
202 Thus, our model provides explanations of the pathophysiology of hemoglobinopathies and other disease
204 we examine our current understanding of the pathophysiology of HRS-1 and existing challenges in its
206 16 mice can be a useful model to examine the pathophysiology of increased upper airway collapsibility
212 Despite its public health importance, the pathophysiology of Lassa fever in humans is poorly under
213 rotrophic factor (BDNF), a key player in the pathophysiology of major depression and the action of an
214 ) microstructure have been implicated in the pathophysiology of major depressive disorder (MDD).
219 ggests that cytokines play a key role in the pathophysiology of MDD and alterations in peripheral cyt
220 rest has been consistently implicated in the pathophysiology of MDD, potentially driven in part by ex
224 cellular studies of the normal function and pathophysiology of mural cells in a variety of disease m
226 studies implicating selected variants in the pathophysiology of NAFLD and highlight opportunities for
227 s of this motor cortex microcircuit with the pathophysiology of neurodegenerative diseases affecting
228 e reveal potential neural substrates for the pathophysiology of neuropsychiatric disease-associated c
229 circadian misalignment, contributing to the pathophysiology of OSA and potentially other diseases th
230 our findings expand our understanding of the pathophysiology of OSB and support the need for an early
231 ensory perception and sheds new light on the pathophysiology of pain and itch as well as the physiolo
236 dysregulation may be transdiagnostic of the pathophysiology of psychotic disorders such as DD and SZ
238 analysis may facilitate comprehension of the pathophysiology of respiratory drive in critically ill p
239 nsequences of AHT are controversial, and the pathophysiology of retinal research findings is still no
240 ecognized to play a role in the etiology and pathophysiology of schizophrenia and other psychiatric d
247 ances understanding of the genetic basis and pathophysiology of Takayasu arteritis and provides clues
248 t that gamma oscillations have a role in the pathophysiology of the abnormal LTP-like plasticity in P
249 d antioxidants are a critical contributor of pathophysiology of the CSD, and that is first explored t
255 the need for further investigation about the pathophysiology of this disease to provide clues for dev
256 s may open new avenues for understanding the pathophysiology of this disease, especially via longitud
260 owledge on the role of beta-cell mass in the pathophysiology of type 1 and type 2 diabetes by enablin
265 ay to study human intestinal development and pathophysiology, perhaps for therapeutic discovery.
266 nderstand its clinical relevance, underlying pathophysiology, possible means of early diagnosis and p
267 ntestinal disease of incompletely understood pathophysiology predominantly affecting premature infant
269 utions of transporter dysfunction to disease pathophysiology remain ambiguous as the fundamental rela
273 rther studies are required to understand the pathophysiology, response to treatment, and outcomes of
275 on (AF) may improve the understanding of the pathophysiology, risk prediction, and development of new
276 a translational mouse model of the dopamine pathophysiology seen in schizophrenia and test approache
277 d age and cardiovascular risk factors, their pathophysiology, systemic implications, and management d
280 es will provide insights into physiology and pathophysiology that more closely resemble intact intest
281 eizure activity in the brain is a widespread pathophysiology that, in principle, should yield to inte
282 ing sphingolipid biology with cardiovascular pathophysiology, these results suggest the potential uti
284 diagnosis of MS induced cardiac and vascular pathophysiology, to assess prognosis, and understand the
285 widely used for research in the physiology, pathophysiology, toxicology, and pharmacology of the ren
286 iew discusses current evidence regarding the pathophysiology, transmission, diagnosis, and management
291 recognition surrounding the diversity of AD pathophysiology underscores the need for holistic system
292 (VBM) studies and resting-state voxel-based pathophysiology (VBP) studies of blood flow, glucose met
293 cognitive function and psychiatric disorder pathophysiology, via its hypothesised effects on adult h
294 onin gene-related peptide (CGRP) in migraine pathophysiology was identified over 30 years ago, but th
296 the group with both elevated amyloid and tau pathophysiology were declining approximately three times
297 is a neurological disorder of heterogeneous pathophysiology, which causes involuntary muscle contrac
299 ed pathways in nACD, providing insights into pathophysiology with the potential to unravel novel ther
300 Therefore, a blood-based marker for such pathophysiology would have greater utility in a primary