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1 wo disparate cell fates, to a new epithelial disease state.
2 s known to be predictive of survival in this disease state.
3 e pathway or if it is altered in response to disease state.
4 tributions in virtually every CNS region and disease state.
5 the environment due to the high-cholesterol disease state.
6 insights into this devastating neurological disease state.
7 new molecular mechanism underpinning the FXS disease state.
8 the nasopharyngeal cavity, as opposed to the disease state.
9 was reproducible and reliably reflected the disease state.
10 are thought to contribute to this life-long disease state.
11 ression levels could be a novel measurer for disease state.
12 he hypothesis that cytokines could mark OPMD disease state.
13 first step in both the carrier state and the disease state.
14 hogenic effects, depending on the tissue and disease state.
15 ning peptides in human serum irrespective of disease state.
16 which genes are overexpressed in a specific disease state.
17 obiome-derived molecules may contribute to a disease state.
18 s, independent of stimulus, cell passage, or disease state.
19 erturb the gut microbiome to contribute to a disease state.
20 ulates inhibition of axonal transport in the disease state.
21 r elucidate the progression of the psychosis disease state.
22 and B cell signature were decreased at flare disease state.
23 l molecule compounds capable of inhibiting a disease state.
24 ) play crucial roles in the development of a disease state.
25 s that influence sensitivity to toxicity and disease states.
26 ible targets for new therapies for digestive disease states.
27 ulate their proliferation in both normal and disease states.
28 r model, and microsimulation of unobservable disease states.
29 ms under different environmental exposure or disease states.
30 gement of both metabolic and athrothrombotic disease states.
31 fer insights applicable to a wide variety of disease states.
32 an dyserythropoietic anemia and likely other disease states.
33 s predictive of clinical outcomes in several disease states.
34 act therapeutic strategies for as many as 50 disease states.
35 pheral immune responses and enhance relevant disease states.
36 activity in response to treatments and/or in disease states.
37 onses for host defence against infection and disease states.
38 e one cause of cognitive impairment in these disease states.
39 rther understanding of their role in certain disease states.
40 nd whose activity is linked to several human disease states.
41 or therapeutic targeting in neuropsychiatric disease states.
42 al studies exploring alterations observed in disease states.
43 ding lymphatic system function in normal and disease states.
44 and disease, including early transitions to disease states.
45 an systems in a variety of developmental and disease states.
46 novel therapeutic target for RAGE-dependent disease states.
47 on and reward processing, as well as several disease states.
48 ential information about human cognition and disease states.
49 s mechanism may be altered or exaggerated by disease states.
50 ases and identify key lessons learned across disease states.
51 lular responses and are involved in multiple disease states.
52 rial homeostasis associated with proteotoxic disease states.
53 dysregulation can contribute to a variety of disease states.
54 may be feasible in complex settings such as disease states.
55 tions and contributing to pathophysiology in disease states.
56 mately lead to complex phenotypes, including disease states.
57 e metabolic dysregulation of immune cells in disease states.
58 ionship to binding partners, and its role in disease states.
59 e elucidation of PPI biology under different disease states.
60 results in several well-characterized human disease states.
61 sitivity in the context of physiological and disease states.
62 avorable responses associated with different disease states.
63 n, and potentially other, protein misfolding disease states.
64 the detection of inflammatory foci in other disease states.
65 signaling pathways associated with multiple disease states.
66 tical for the transition between healthy and disease states.
67 man brain is vulnerable to neurodegenerative disease states.
68 t function that results in mutation-specific disease states.
69 ra are associated with a variety of distinct disease states.
70 repression during neural development and in disease states.
71 ety of tissues in both normal physiology and disease states.
72 nd worse in those with pre-admission chronic disease states.
73 Inflammation is linked to numerous chronic disease states.
74 l mutations have been shown to contribute to disease states.
75 ing in preclinical models of both normal and disease states.
76 ly model complex physiological conditions or disease states.
77 e transport and its regulation in normal and disease states.
78 uation of the macula in healthy patients and disease states.
79 to the molecular basis of ER-driven neuronal disease states.
80 ascular growth is characteristic of multiple disease states.
81 ntification of glycosylation enzymes driving disease states.
82 ctive target to potentially treat a range of disease states.
83 s associated with both normal physiology and disease states.
84 tly linked with both congenital and acquired disease states.
85 o understanding mitochondrial dysfunction in disease states.
86 under normal physiological condition and in disease states.
87 PMCA conditional on simultaneously estimated disease states.
88 uction distinguishes health from an array of disease states.
89 toxic and associated with cataract and other disease states.
90 esses are increasingly identified in cardiac disease states.
91 of several disorders including pain-related disease states.
92 urinary tract and how dysfunction arises in disease states.
93 el regulator of cardiovascular and metabolic disease states.
94 y cis- and trans-acting mutations leading to disease states.
95 r elucidating their roles in development and disease states.
96 mines system can become dysfunctional during disease states.
97 otional processing underlie many psychiatric disease states.
98 ched at the transcriptional level in various disease states.
99 w these relationships change during aging or disease states.
100 e is large and addresses a broad spectrum of disease states.
101 Ca(2+) being indicators of several possible disease states.
102 dy-mediated pathology and protection in many disease states.
103 ciation with progressive glomeruli damage in disease states.
104 cidated how P. mirabilis causes all of these disease states.
105 ar oxidants, and accumulate across different disease states.
106 NA replication, observed in cancer and other disease states.
107 the function of TRIM14 protein in normal or disease states.
108 o multiple noxious environmental stimuli and disease states.
109 elopment or how this may, in turn, relate to disease states.
110 uring the onset and progression of mammalian disease states.
111 new targets for modulating Wnt signaling in disease states.
112 ora of cellular processes that contribute to disease states.
113 ridge between multiple different species and disease states.
114 in vivo, affecting its function in normal or disease states.
115 active means to therapeutically intervene in disease states.
116 ntributed to exacerbated MNC activity during disease states.
117 uitry and brain function in both healthy and disease states.
118 n bacterial metabolites and human health and disease states.
119 covery of peptides characteristic of various disease states.
120 exercise capacity with aging and in diverse disease states.
121 and will enhance our ability to intervene in disease states.
122 y contributes to mechanisms underlying these disease states.
123 at promise for the improved diagnosis of the diseased state.
124 ms disrupting lipid-protein complexes in the diseased state.
125 eractions that separate the healthy from the diseased state.
126 onse to external signals or as a result of a diseased state.
127 ynthesis, which ultimately gives rise to the diseased state.
128 as a patient transitions from a healthy to a diseased state.
129 as markers for future studies in healthy and diseased states.
130 rganisms' homeostasis and the development of diseased states.
131 the clonal evolution of progenitor cells in diseased states.
132 iven to mechanisms of platelet activation in diseased states.
133 s to the dysregulation of these processes in diseases states.
135 e vascular wall progenitor cells in vascular disease states, adding weight to the notion that the adv
136 ultiple mechanisms regulating the normal and diseased state (age related macular degeneration, AMD) i
139 Given the strong association of GM-NDI with disease state and neurocognitive performance, its potent
140 bility of several of these measures, and how disease state and number of beats impact their reproduci
142 relationships between these pathways across disease state and relative to modifiable risk factors su
143 tokine expression with quantified pathologic disease state and then used neuron cultures to test whet
144 otherwise appear incongruous with a clinical disease state and/or contribute to the development of sy
145 gregated admissions to 91 hospitals into 119 disease states and 22 disease subcategories of the WHO G
146 tenuate extrapulmonary organ injury in other disease states and are neuroprotective in preclinical mo
147 erential expression of microRNAs (miRNAs) in disease states and between different treatments, tissues
148 dge gap regarding associations between known disease states and breath metabolite profiles in cetacea
149 with health or disease state, (ii) health or disease states and community structure associated with a
150 exhibit differences in abundance in several disease states and have, therefore, been proposed for us
151 ltered tissue structure is a feature of many disease states and is usually measured by microscopic me
153 y sensitivity and specificity to distinguish disease states and provide diagnostic potential for this
154 II-based cell mechanics across phylogeny and disease states and provides proof of concept that cell m
155 ESRD, with effects increasing with worsening disease states and the contribution of genetic African a
156 ause of its significance to the detection of disease states and the manufacturing of biopharmaceutica
157 lmination of a multiplicity of heterogeneous disease states and their varied health trajectories lead
159 ons with many different cell types, to model disease states and to determine the functions of poorly
160 gut mucosal immune development in health and disease states and to help discover ways of repairing or
161 entify functional phenotypes associated with disease states and to identify compounds that improve ce
163 ypertension in a number of cardiorespiratory diseases states and has therefore been identified as a p
164 iota can be altered to ameliorate or prevent disease states, and engineering the gut microbiota to th
165 endogenous adenosine levels, particularly in disease states, and have potential for treatment of seiz
166 oplantar epidermis in both physiological and disease states, and how this 'stress' keratin is regulat
167 a, the fungal microbiota is often altered in disease states, and increasingly studies are being desig
168 sbiosis) have been implicated in a number of disease states, and the prototypical example is Clostrid
169 tivity Map (CMap), whereby genes, drugs, and disease states are connected by virtue of common gene-ex
171 sion, despite their importance in normal and disease states, are poorly understood, largely because o
174 ding the cellular mechanisms associated with disease states as well as assessing cell-based targeting
175 entially be generalized to a wide variety of disease states, as well as other immunological phenotype
176 ible link between hyperglycemia and vascular disease states associated with smooth muscle contractili
177 s (immune response, angiogenesis) as well as diseased states (atherosclerosis, cancer, thrombosis).
181 al processes in normal physiology as well as disease states, but requires noninvasive methods for ide
182 release in heart cells is altered in several disease states, but the physiological mechanisms that re
183 cellular-level function in both healthy and diseased states, but these variations remain difficult t
184 increased contractility in the short term in disease states characterized by enhanced renin-angiotens
186 er adherence did not differ significantly by disease state (diabetes, 3.0% [CI, 1.5% to 4.6%]; hypert
187 cated bacterial effectors that propagate the disease state, drawing common parallels and showing the
190 ot achieve minimal residual disease negative disease state following chemoimmunotherapy approaches.
192 ) microbial groups associated with health or disease state, (ii) health or disease states and communi
195 ave significant capability in discriminating disease states in bodily fluids, cells and tissues.
198 d family of co-chaperones that are linked to disease states in mammals and responses to environmental
204 ysregulation of talin activators can lead to disease states in which aberrant integrin activation and
205 association of vitamin D status with various disease states in which vitamin D status was measured on
206 aditional imaging in the high-risk localized-disease state, in patients with biochemical recurrence a
208 pathway is implicated in a variety of human disease states including angiogenesis, autoimmune diseas
209 tors have been utilized for studying various disease states including cancer, sexual function disorde
212 d perception are associated with a number of disease states, including autism spectrum disorders, sch
213 ling and DAN inhibition can lead to numerous disease states, including cancer, kidney nephropathy, an
215 ular and vascular structures in a variety of disease states, including malignancies and ataxia telang
216 ate Fe/S cluster scaffold proteins can cause disease states, including multiple mitochondrial dysfunc
217 ndings may translate to healthy humans or to disease states involving the brain or the gut/brain axis
218 expected that mechanisms underlying several disease states involving the interactions between microb
222 tion of biomarkers that represent health and disease states is vital for disease diagnosis and treatm
223 se phenomena and how they are modulated in a diseased state is very important for aiding our understa
228 on would help physicians detect diseases and disease states more rapidly, efficiently, and accurately
229 species exhibit a synergism that produces a disease state not seen with any of the individual specie
230 c cargo to treat a range of cancer types and disease states obeys the 'one material fits all' rule.
231 hese viral factors may help to determine the disease state of patients more accurately, and identify
232 ined positions enable assessment of relevant disease state of tissue within the tumor mass and examin
235 both understand the nexus between health and disease states of the respiratory virome, and drive a pa
237 oped to recapitulate many of the healthy and diseased states of native tissues and can be used as a c
238 small molecule compounds that may enhance a disease state or increase the risk of developing that di
243 n of statistical learning methods to predict disease states or the immune response to perturbations.
245 ategy to modify inflammation in a variety of disease states, particularly those that depend on Ag-ind
246 ties, but the enhanced local disorder in the disease state perpetuates high-affinity platelet aggluti
247 valuable molecular insight into healthy and diseased states persevered in their native ultrastructur
248 ant, elevated levels of FA are implicated in disease states ranging from asthma to neurodegenerative
252 on mechanism is also a major obstacle during disease state since it dramatically hinders the drug del
254 ool that could yield accurate assessments of disease state such as the risk or presence of SSc-ILD, t
255 the literature yet may provide insights into disease states such as age-related macular degeneration
256 rent challenges, including the monitoring of disease states such as autism and chronic diseases invol
257 lyltransferases, particularly ST6Gal-1, with disease states such as cancer and a variety of inflammat
258 ation equilibrium is associated with several disease states such as cancer and infections, however th
259 if they go awry, they are poised to promote disease states such as cancer cell metastasis and loss o
260 ntial to provide information on a variety of disease states such as cancer, cardiovascular complicati
261 pecies associated with many life-threatening disease states such as cancers and neurodegenerative dis
263 in individual enzymes leading to dissimilar disease states such as CHARGE syndrome or autism spectru
264 pathologic, psychological, and physiological disease states such as depression, post-traumatic stress
268 emostasis, but may also cause acute ischemic disease states such as myocardial infarction or stroke.
269 er has to rely on leaky vessels arising from disease states such as pathological angiogenesis and inf
270 t of myocardial infarction, and more chronic disease states such as stable angina and ischemic cardio
271 aviour, and has been associated with several disease states, such as cancer and neuronal diseases.
272 tions of signaling proteins are perturbed in disease states, such as cancer, and are modulated by dru
273 cells were shown to play a role in different disease states, such as cancer, autoimmunity, neuroinfla
275 the impact of defects occurring in the MMDS1 disease state that result from a point mutation (Gly208C
276 cle pain and altered sympathetic reflexes in disease states that are based in problems with periphera
277 strating its relevance to a broad variety of disease states, the bioenergy production phenotype has b
278 surprisingly, given its exploration in many disease states, the gut microbiota has also been studied
281 gical roles and being implicated in numerous disease states, there has been a lack of clarity about t
282 R profile which could influence responses to disease states through autocrine or paracrine mechanisms
283 ht into normal cellular function and various disease states through molecular characterization of gen
284 lly be personalized according to a patient's disease state to achieve optimal diagnostic and therapeu
285 iduals with one, two, or three microvascular disease states versus none, the multivariable-adjusted H
286 ups according to the age at disease onset or disease state, we again obtained no significant associat
287 ortical oscillatory activity to movement and disease state, we recorded local field potentials from h
288 To advance studies of iron in healthy and disease states, we now report the synthesis and characte
289 hyl-lysine (Kme) binding proteins to various disease states, we recently developed and reported the d
290 biomarkers to predict a patient's health or disease state when one can pair his or her current test
291 the barrier achieves full integrity, and in disease states when barrier integrity is compromised.
292 ng pathway networks associated with specific disease states when compared to published pathway networ
293 vitro and in vivo correlates in healthy and diseased states when ROS-free or ROS-containing media ar
294 ntribution of the MPC activity to health and disease states where pyruvate metabolism is expected to
295 actions of metabolites, proteins, genes, and disease states, while advancing personalized medicine.
296 genous carriers for therapeutics in multiple disease states, while the second part discusses the use
298 ocess in complex tissues, including fibrotic disease states with high collagen, is now utilizing 'omi
300 erstand fundamental biological processes and disease states, yet most researchers do not perform a si
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