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1 BIN1, to ameliorate synaptic dysfunction and disease progression.
2 erstand the molecular interactions governing disease progression.
3 zheimer's disease and can be used to monitor disease progression.
4 future for monitoring cellular functions and disease progression.
5 ceive open-label veliparib monotherapy after disease progression.
6 eins, ameliorate signs of disease, and delay disease progression.
7 itive cell interactions and how this affects disease progression.
8 ubule-interstitial damage, further worsening disease progression.
9 nt therapeutic approaches that delay or stop disease progression.
10 o either enhance or repress inflammation and disease progression.
11 icity and the propagation, which accompanies disease progression.
12 n spontaneously resolved without evidence of disease progression.
13  direct pathogenicity as well as the rate of disease progression.
14 er tissues, which positively correlated with disease progression.
15 ases, where neuroinflammation contributes to disease progression.
16 rder in which increased sphingosine mediates disease progression.
17 l of these changes in order to stop or delay disease progression.
18  burden and contribute to amyloid-associated disease progression.
19 gical processes that trigger ALS and promote disease progression.
20 ti-inflammatory response may slow or prevent disease progression.
21 ALS4, and hence they should be monitored for disease progression.
22 ibution of dysfunctional immune responses to disease progression.
23  rooted in their ability to evolve and drive disease progression.
24 es, ranging from neurological development to disease progression.
25  to promote long-term protection and prevent disease progression.
26  mg every 3 weeks for up to 2 years or until disease progression.
27 cellular and molecular mechanisms leading to disease progression.
28 sensitive measure than plasma NfL to monitor disease progression.
29  acute inflammation plays a critical role in disease progression.
30 EVD; however, little is known about temporal disease progression.
31 one scintigraphy was used to assess for bone disease progression.
32 ced upon C5 activation) were detected during disease progression.
33  is provided that details distinct stages of disease progression.
34 hich pericyte dysfunction contributes to the disease progression.
35 mplications is important in order to prevent disease progression.
36 nd their levels correlated with MRI signs of disease progression.
37 t may reflect immortalization and, possibly, disease progression.
38 es in prostate cancer cell proliferation and disease progression.
39 kers with potential utility as predictors of disease progression.
40 o the treatment of CHB and the assessment of disease progression.
41  the only proven treatment strategy to delay disease progression.
42 perexcitable and hypoexcitable states during disease progression.
43 ides new insights into the mechanisms behind disease progression.
44 h for 8 doses, and then once per month until disease progression.
45 ge so that treatment can be initiated before disease progression.
46 stric premalignancy, serving as a barrier to disease progression.
47 xial strains could be an important factor in disease progression.
48 ntal disease at baseline, were examined with disease progression.
49 level, are promising biomarkers to track the disease progression.
50 that drive fibrosis over the course of local disease progression.
51 erentiation into the squamous lineage during disease progression.
52 ng survival benefits, are not enough to halt disease progression.
53 d organelles within type1 NI plays a role in disease progression.
54 iptional regulators and essential drivers of disease progression.
55 inal vascular architecture as biomarkers for disease progression.
56 alternative drugs are clearly needed to slow disease progression.
57 f, from day 2 each cycle), or placebo, until disease progression.
58 ses on lowering intraocular pressure to slow disease progression.
59 onsidered to be the main risk factor for the disease progression.
60 via intravenous infusion every 4 weeks until disease progression.
61 hly follow-up scans throughout treatment and disease progression.
62  Wnt deregulated activity in LSCs attenuates disease progression.
63 carcinoma osimertinib-treated patients after disease progression.
64 ous, and their phenotype differed by rate of disease progression.
65 ein remains stably elevated with Parkinson's disease progression.
66 c CHCpatients and might have a role in liver disease progression.
67 s in the transcriptome as a whole to predict disease progression.
68 s abundance to understand driving factors of disease progression.
69 ncrease the rate of SIV oral transmission or disease progression.
70 effective pharmacologic treatment to prevent disease progression.
71 sease stages and increased in abundance with disease progression.
72 ction of autoreactive CD8+ T cells influence disease progression.
73 e competitive advantage of MDS HSPCs and for disease progression.
74 en deposition and serum C3M, a marker of IPF disease progression.
75 esponses to SARS-CoV-2 and the predictors of disease progression.
76     The most common cause of death is due to disease progression.
77 tions that can reinitiate growth and promote disease progression.
78 hus should be explored further as markers of disease progression.
79 strates the potential of using AI to predict disease progression.
80 1 and CHI3L1 levels correlate to the rate of disease progression.
81 -induced changes in metabolic homeostasis on disease progression.
82 ltered glycosylation patterns that relate to disease progression.
83 argeted immunotherapy could potentially slow disease progression.
84 ession models identified other predictors of disease progression.
85 d pharmaceuticals, as well as biomarkers for disease progression.
86 ation and how clonal complexity evolves with disease progression.
87 at symptoms rather than halting or reversing disease progression.
88 ires novel therapeutic approaches to prevent disease progression.
89 ith the option of on-study retreatment after disease progression (1-year fixed duration).
90 asyn in various models with implications for disease progression; 4) assess uniquely toxic properties
91          Perfusion increased from cycle 4 to disease progression (51% +/- 11; P < .001).
92 during the study, most frequently because of disease progression (61 [42%]); no deaths were deemed to
93                                     To track disease progression across the age spectrum, we defined
94 the modulation of key signaling pathways and disease progression, adding new perspectives to the func
95 scale index of 60% or higher, and documented disease progression after at least one previous line of
96 d endometrial carcinoma who have experienced disease progression after prior systemic therapy, regard
97 )-positive metastatic breast cancer who have disease progression after therapy with multiple HER2-tar
98                             Patients without disease progression after two cycles proceeded to receiv
99    Complex diseases with highly heterogenous disease progression among patient populations, cardiovas
100 ent (to reduce adverse clinical outcomes and disease progression among patients with stage C HF) and
101                 During follow-up, 8 cases of disease progression and 5 deaths occurred.
102     Neuroinflammation is known to accelerate disease progression and accentuate disease severity, but
103 aphs has been associated with higher risk of disease progression and adverse outcomes from coronaviru
104 aneurysm (AAA) pathogenesis, with effects on disease progression and anatomic stability.
105 ay serve as a useful diagnostic indicator of disease progression and as a therapeutic outcome measure
106 monella typhoid toxin contributes to typhoid disease progression and chronic infection, but little is
107 (12 weeks), after cycle 4 (24 weeks), and at disease progression and compared with the ORR by using t
108 cient (VAD) mice fared worst with more rapid disease progression and decreased survival.
109 portantly, accumulation is detected early in disease progression and decreases with successful therap
110 ld elucidate collective dissemination during disease progression and enable preclinical testing of ta
111      Inhibiting this interaction may inhibit disease progression and enhance patients' overall surviv
112 ty of splicing dysregulation correlates with disease progression and establish intron retention as a
113 strengthening their suitability for tracking disease progression and evaluating antifibrotic drug can
114 onstrates the feasibility of both monitoring disease progression and evaluating therapeutic efficacy.
115      The extent of expansion correlates with disease progression and formation of amyloid-like protei
116 e is a hallmark of HF and is associated with disease progression and higher mortality risk.
117 ension to slow and stabilize coronary artery disease progression and improve clinical outcome.
118                The 4-year cumulative risk of disease progression and intervention after uncomplicated
119                The 5-year cumulative risk of disease progression and intervention was 7%, 48%, and 89
120 n lung cancer and correlates with aggressive disease progression and poor patient prognosis.
121             Gut microbiome may contribute to disease progression and poor prognosis.
122 eting alpha cells are critically involved in disease progression and proper glucose control.
123 t neurological conditions and for monitoring disease progression and remission with distinct therapeu
124 if validated, may provide useful measures of disease progression and response to therapy.
125 metastatic cell recruitment and can identify disease progression and response to therapy.
126  diagnostic tool for quantitatively tracking disease progression and response to treatment.
127 tching to ocrelizumab therapy on measures of disease progression and safety in the open-label extensi
128             We analyzed rs111200466 in HIV-1 disease progression and showed a correlation with a fast
129 portance of neutralizing humoral immunity on disease progression and the need to develop broadly prot
130 onset disease is important for understanding disease progression and therapeutic development.
131 m outcomes using an established model of HCV disease progression and treatment (hepatitis C cost-effe
132 biomolecules which play significant roles in disease progression and tumor metastasis toward secondar
133 ance of albuminuria as a predictor of kidney disease progression and vascular disease has driven rese
134 athology is essential to better characterize disease progression and widen the spectrum of therapeuti
135  methods for the detection and monitoring of disease progression and, hopefully, to the development a
136 signature allows more accurate prediction of disease progression and, if prospectively validated, may
137            During follow-up, 112 experienced disease progression, and 69 died.
138 s, magnetic resonance imaging (MRI) markers, disease progression, and CoQ10 response data.
139 ity, ocular surface health, quality of life, disease progression, and cost-effectiveness.
140 pairment could lead to improved detection of disease progression, and development and monitoring of n
141 e location and number of nicks affect cells, disease progression, and health outcomes.
142 ts, investigating biomarkers associated with disease progression, and identifying new drugs and route
143 y, pathophysiology, clinical manifestations, disease progression, and response to treatment.
144 s, create predictive computational models of disease progression, and reveal new drug targets and the
145        Low sKlotho in CKD is associated with disease progression, and sKlotho supplementation has eme
146 s within a tumor, the evolution of TPCs with disease progression, and their implications for therapy.
147 iologies, comorbidities, and factors driving disease progression, and therefore have limited value fo
148  connectivity in a way that matched proposed disease progression, and this loss of stability in conne
149 cantly associated with baseline DR severity, disease progression, and treatment requirement over 1 ye
150  these immunosuppressive cells decrease with disease progression, and whether they contribute to athe
151 ellular responses to environmental stresses, disease progression, and/or drug treatment; however, mos
152 herapies, effects on pulmonary pathology and disease progression are monitored by using histopatholog
153 tter understand the part which PRCD plays in disease progression as well as its contribution to photo
154                                              Disease progression, as defined in this study, correlate
155   Tamoxifen was administered at 4 months and disease progression assessed at 12 months.
156                                          The disease progression associated with the proinflammatory
157                                              Disease progression associates with increased genetic he
158  it was associated with an increased rate of disease progression at 12 months after treatment (RR, 4.
159 de that NPTX2 is a promising synapse-derived disease progression biomarker in genetic FTD.
160 linical assessment to curtail cardiovascular disease progression but are limited to the current clini
161         Current antiretroviral therapy slows disease progression but does not eliminate latently infe
162 iltration by glioma cells causes detrimental disease progression, but its multicellular coordination
163 to be associated with protection against HIV disease progression, but studies have been limited by th
164 f age-related macular degeneration (AMD) and disease progression, but the precise biological function
165 ates that type 2 immunity is associated with disease progression by promoting fungal growth and disse
166 t multiple sessions are usually required and disease progression can occur.
167 enders identifying different trajectories of disease progression challenging.Objectives: To identify
168                                     Although disease progression correlated with cardiovascular risk,
169 AD progression in this mouse model, and that disease progression could be ameliorated by inhibition o
170 f brain tissue, raising the possibility that disease progression could potentially be slowed by disru
171                                  The risk of disease progression decreased by 13% per 1,000-MBq incre
172 IC, when administered in the early stages of disease progression, decreases intestinal injury and pro
173 erozygous, indicating that the mutant drives disease progression despite the presence of wild-type (W
174 innate immunity exerts a mechanistic role in disease progression, determining the clinical outcomes.
175  or placebo and trastuzumab were given until disease progression; docetaxel was given for six cycles,
176 duals with varying clinical characteristics, disease progression, drug response, and risk of complica
177 rity of selected patients show no or limited disease progression during a trial period.
178 articularly if it changes over the course of disease progression (e.g., an evolving tumor).
179  could be used as a prognostic biomarker for disease progression, especially for the metastatic proce
180                                  Identifying disease progression, especially within clinical trials,
181 T-202), patients aged 18 years or older with disease progression following at least one previous trea
182  who maintain the EC characteristics without disease progression for more than 25 years.
183 patitis C virus transmission, treatment, and disease progression for Pakistan, calibrating using avai
184  to olaparib was allowed after imaging-based disease progression for patients who met certain criteri
185 ordering patients along a trajectory of LOAD disease progression from brain transcriptomic data.
186 is (TB) are not able to predict reactivation disease progression from latent TB infection (LTBI).
187 ablished prognostic ordinality: grade 1 = no disease progression; grade 2 = development of varices; g
188 plasma betaDG in correlation with markers of disease progression, gut damage, bacterial translocation
189 on admission, a model to predict in-hospital disease progression had an area under the curve of 0.85,
190 r plasmin (ogen) as a "second hit" in kidney disease progression has yet to have been demonstrated in
191 wo pathologies and the mechanisms underlying disease progression have remained unclear.
192 in the metastatic liver, which leads to fast disease progression, high recurrence rate, and short sur
193 ically relevant prion-induced changes during disease progression in a cell-type-specific and genome-w
194 ly, PG protected against HSV-1 infection and disease progression in a murine model of ocular infectio
195 xpression profiling of the bone marrow along disease progression in a spontaneous model of mammary ca
196 and 1992, who never showed signs of clinical disease progression in absence of any antiretroviral tre
197 ature of muscle denervation that may reflect disease progression in ALS.
198 uggested as a potential approach for slowing disease progression in ALS.
199  have shown to ameliorate cyst formation and disease progression in animal models of ADPKD.
200 ocked IL-23 signaling in vitro and inhibited disease progression in animal models of SpA.
201 tial for regulatory T cells (Tregs) to limit disease progression in bacterially triggered fibrosis ex
202 ctive age-related macular degeneration (AMD) disease progression in both eyes.
203  were also associated with increased risk of disease progression in both the F3 and F4 groups (P < .0
204 ed as a predominant driver of disability and disease progression in central nervous system (CNS) dise
205 ons: We demonstrate two distinct patterns of disease progression in COPD using SuStaIn, likely repres
206 n Results: We identified two trajectories of disease progression in COPD: a "Tissue->Airway" subtype
207  identified as major risk factors for severe disease progression in COVID-19.
208 sity measurements to predict possible severe disease progression in COVID-19.
209 CPT1), it is possible to reverse or slowdown disease progression in experimental models of autoimmune
210  and management strategies for modulation of disease progression in hereditary spastic paraplegias an
211 >G is activated in the intermediate phase of disease progression in high-risk MM.
212 1 deletion variant is associated with kidney disease progression in human cohorts: the African Americ
213  and their predictive value as biomarkers of disease progression in idiopathic Parkinson's disease (i
214                                              Disease progression in many tumor types involves the int
215 anges are associated with tumor response and disease progression in metastatic RCC treated with vascu
216 hatic muscle cells (LMCs), is a biomarker of disease progression in mice with inflammatory arthritis.
217 ortant oral hygiene behavior to prevent oral disease progression in older adults.
218 tween subgingival microbiota and periodontal disease progression in older women, for which limited pu
219 nses in patient-derived cells and attenuates disease progression in PAH mice.
220 d CRAF can modulate therapeutic response and disease progression in patients treated with ATP-competi
221  fine-tunes the balance between dormancy and disease progression in PC dyscrasias.
222 disease onset also contribute to the rate of disease progression in SCA3/MJD.
223 tamine (polyQ) tract form of ataxin-1 drives disease progression in spinocerebellar ataxia type 1 (SC
224                             We also assessed disease progression in subgroups of patients according t
225                                     Although disease progression in the mouse does not perfectly mode
226 nt COPD exacerbation events, contributing to disease progression in these individuals.
227 ging as key players in tissue physiology and disease progression, including cancer, the mechanism ide
228 f the transcriptome rearrangements affecting disease progression independently of inflammation and re
229                                Virulence and disease progression involve life-history decisions that
230 receptor degeneration in the central retina, disease progression involves epigenetic changes in chrom
231                              Our analysis of disease progression is based on a stochastic model of a
232 plastic syndrome (MDS); however, its role in disease progression is unclear.
233 although IPSS-R is an excellent predictor of disease progression, it is an ineffective predictor of r
234 f knowledge about the factors that influence disease progression, making this a key challenge for the
235                    Patients discontinued for disease progression (n = 25), adverse events (AEs; n = 7
236 n BTKi and 12 had stopped therapy because of disease progression (n = 8) or toxicity (n = 4).
237                                              Disease progression occurred in 18 of 56 patients (32%)
238 n Hox-B13 (HOXB13) have been associated with disease progression of ER-positive breast cancer patient
239                     The role of FATP4 in the disease progression of retinal dystrophies associated wi
240 R mutation-positive, advanced NSCLC, who had disease progression on a previous EGFR TKI.
241                                Patients with disease progression on placebo could cross over to pembr
242 ts who completed the previous trials without disease progression on siltuximab.
243  of first subsequent therapy (TFST), time to disease progression on subsequent therapy or death (PFS2
244 actors were ECOG performance status, time to disease progression on the previous androgen signalling-
245  9.0 months], respectively; hazard ratio for disease progression or death, 0.51 [95% CI, 0.39 to 0.66
246  placebo-combination group (hazard ratio for disease progression or death, 0.54; 95% confidence inter
247 ) on day 2 and day 9 of a 21-day cycle until disease progression or intolerable toxicity.
248  not clear how the epicardium contributes to disease progression or repair in the adult.
249 andomly assigned to continue nivolumab until disease progression or unacceptable toxicity or to stop
250 eeks thereafter as maintenance therapy until disease progression or unacceptable toxicity).
251 15 mg/kg every 3 weeks in both groups) until disease progression or unacceptable toxicity.
252 y, given continuously in 4-week cycles until disease progression or unacceptable toxicity.
253  mg orally once daily in 28-day cycles until disease progression or unacceptable toxicity.
254 elinexor orally on days 1 and 3 weekly until disease progression or unacceptable toxicity.
255  weekly dexamethasone in 28-day cycles until disease progression or up to 6 cycles after complete hem
256                             Because of rapid disease progression or worsening of clinical condition,
257 ity of MRI and (1)H MR spectroscopy to track disease progression over a wide range of ages in partici
258 t provided sustained benefits on measures of disease progression over the 6.5 study years of follow-u
259 nce of covariates or factors determining the disease progression over time.
260     Virus RNA clearance time lengthened with disease progression (P = 0.0001).
261 ety profile among patients with a history of disease progression (PD).
262                     We identified 4 distinct disease progression profiles based on limb-specific pare
263 uggested that earlier surgery could mitigate disease progression, providing better pain control and p
264 ly significant reductions in lesion size and disease progression rates during masked treatment.
265 ere precolectomy (shortest projected time to disease progression), rectal or ileal pouch polyposis af
266 :2 were detected in patients with more rapid disease progression, regardless of therapy and these fin
267 lignant brain cancer but the early stages of disease progression remain elusive.
268 ip between SARS-CoV-2 viral load and risk of disease progression remains largely undefined in coronav
269 nd point was progression-free survival, with disease progression requiring the development of end-org
270                    In sum, muscle BDNF slows disease progression, rescuing select cellular and molecu
271 ong the 78 patients (of 396) retreated after disease progression, response was seen in 5 of 34 retrea
272                                  Mechanistic disease progression studies using animal models require
273 FL thickness may be a more stable measure of disease progression that clinicians can use to monitor a
274 that BMP signaling regulates GI function and disease progression that involve stem/progenitor cells a
275 scle tissue provides reliable benchmarks for disease progression that may be valuable in testing the
276 ective in clearing the infection, leading to disease progression that may result in gastric adenocarc
277 n which drusen collapsed without evidence of disease progression, the CC parameters were similar once
278 hat loss of TBK1 kinase activity impacts ALS disease progression through distinct pathways in differe
279 r-associated macrophages (TAMs) that promote disease progression through induction of angiogenesis, t
280 tumorigenesis, from cellular transformation, disease progression to metastatic disease.
281 scovery of genomic alterations that underlie disease progression to MM could improve current risk mod
282 t background accelerated motoneuron loss and disease progression to twice the rate observed in litter
283  days off (starting on cycle 1 day 15) until disease progression, unacceptable toxicity, loss to foll
284 and 35-day cycles from the ninth cycle until disease progression, unacceptable toxicity, or patient w
285 ce per day in continuous 28-day cycles until disease progression, unacceptable toxicity, or withdrawa
286 2)) orally once daily in 28-day cycles until disease progression, unacceptable toxicity, the investig
287  up to 7 days after treatment start, patient disease progression using the WHO scale up to 28 days, a
288 fy cases in early stages to prevent or alter disease progression via appropriate interventions.
289 ly living, avoidance of visual symptoms, and disease progression via maintenance of IOP control.
290 e average follow-up time without evidence of disease progression was 10.1 months.
291 t the contribution of hyper-succinylation to disease progression, we develop a zebrafish model of the
292 dy of perinatal hepatitis B transmission and disease progression, we estimated the coverage impact an
293                                         With disease progression, we observed nominally significant i
294     Overexcitation of neurons can facilitate disease progression whereas the induction of cortical ga
295    During follow-up, 23 patients experienced disease progression, whereas 13 patients died from their
296 y in preclinical models and in patients with disease progression while on immunotherapies.
297  and prematurely degenerate in the course of disease progression, while the discovery of new therapeu
298 derstanding the causes of immune evasion and disease progression will identify potential immune-media
299 erm reductions in new infections and delayed disease progression, with Atlanta, Baltimore, and Miami
300 ppressive therapy may be helpful in limiting disease progression, with rituximab showing efficacy in

 
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