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1 which were missing in the singular MIA or HI insult.
2 stasis or induce cell death depending on the insult.
3 ns and is thought to arise from a congenital insult.
4 asting response to a prenatal immune-related insult.
5 terial infection and chemical and mechanical insult.
6 that is crucial for cell fate upon genotoxic insult.
7 e by 26% at 24 hours and 43% at 5 days after insult.
8 aimed at eliminating the original pathogenic insult.
9 xide lasting for over 48 h after the initial insult.
10 wn regulated when insects face a pro-oxidant insult.
11 pable of neutralizing a septic polymicrobial insult.
12 ing mediators or pathways that influence I/R insult.
13 l disorder, often develops following a brain insult.
14 ammation in response to persistent bacterial insult.
15 hematopoiesis or recovery from hematopoietic insult.
16 f organ architecture produced by the initial insult.
17 and high short-term mortality after an acute insult.
18 and memory behavior in response to repeated insult.
19 immune responses that adequately targets the insult.
20 or, even when combined with an environmental insult.
21 minished remyelination after a demyelinating insult.
22 n (i.e., scalp hair follicles) against redox insult.
23 ation, timing and severity of the hypoxaemic insult.
24 ation of E2F1 and are resistant to oxidative insult.
25 romise tolerance to a simulated haemorrhagic insult.
26 d implicated in secondary injury after a CNS insult.
27 agy, and protect cells from a subsequent OGD insult.
28 ficial in defending against the haemorrhagic insult.
29 omplement-mediated damage following ischemic insult.
30 gradation, essential for surviving genotoxic insult.
31 of the USP22-mediated response to genotoxic insult.
32 rotected bone integrity against osteoporotic insult.
33 rai1 inhibition strategy during hypertrophic insult.
34 eguarding of germline DNA from environmental insults.
35 shortage and to cope with diverse cytotoxic insults.
36 transient microbial, chemical, and physical insults.
37 maturity classically associated with hypoxic insults.
38 ubtle for disease-predisposing environmental insults.
39 cally in their resilience to injury or other insults.
40 and responsiveness to both acute and chronic insults.
41 ecting the organism's DNA from environmental insults.
42 increase resistance to common environmental insults.
43 ion is protective across a broad spectrum of insults.
44 chemical defenses against biotic and abiotic insults.
45 may be particularly susceptible to secondary insults.
46 erable to numerous genetic and environmental insults.
47 sing from physiological and/or environmental insults.
48 anging physiological demands or pathological insults.
49 stasis and responding to infections or other insults.
50 response in neuroprotection against various insults.
51 from degeneration after mechanical and toxic insults.
52 nfections and mediating control over sterile insults.
53 me capacity in response to other proteotoxic insults.
54 e span, including gestational and early life insults.
55 advantage during the response to excitotoxic insults.
56 patients exposed to potential epileptogenic insults.
57 powerful suppressor of PD-linked pathogenic insults.
58 jury is essential to prevent secondary brain insults.
59 ic environments and collateral pharmacologic insults.
60 orming a protective blanket against external insults.
61 long surveillance and protection from future insults.
62 sm, and an increased sensitivity to ischemic insults.
63 tive immunodominant epitopes from pathogenic insults.
64 sion were reversible upon clearance of brain insults.
65 orrecting cellular homeostasis after various insults.
66 rotection to liver cells exposed to chemical insults.
67 damage and neutralizing potentially harmful insults.
68 oded vMISTRAV exhibit resistance to the same insults.
69 sporadic delamination errors and teratogenic insults.
70 creased vulnerability to early environmental insults.
71 response to different initial cardiac muscle insults.
72 ritical to the health impact of inhalational insults.
73 ent for a range of neurological diseases and insults.
74 ate immune response to infection and sterile insults.
75 ort a MEWDS-like reaction to previous ocular insults.
76 is lost due to genetic and/or environmental insults.
77 lations vary in response to diverse paternal insults.
78 nsactivation in response to diverse cellular insults.
79 of genetic vulnerabilities and environmental insults.
80 a superior endurance to physiological redox insults.
81 n mount an inflammatory response to external insults.
82 immunological defense against environmental insults.
84 cells against reactive oxygen species (ROS) insults, (2) ER stress-generated ROS further promote ER
86 selective injury but more likely by systemic insults, a humanized xenograft model of FSGS resulted in
87 m physicochemical, biological and mechanical insults, a mono-layered or stratified epithelium that fo
93 e a framework for understanding how external insults alter immune cell phenotype during a period of r
94 t to adult-onset injury, developmental brain insults alter the ontogenetic pattern of brain organizat
95 TBI, appears to differ depending upon age-at-insult, although this response has not been well-charact
97 d be limited to the acute phases of ischemic insult and avoided for long-term treatment after MI.
98 cultative regenerative organ when exposed to insult and contribute to repair in either the airway or
99 ic snoRNAs in safeguarding against oncogenic insult and demonstrate a functional link between H/ACA s
101 hemical processes beginning with the initial insult and lasting for days, months and even years post-
103 and the molecular links between the primary insult and the changes in the matrix environment are unk
106 both tumor cell-intrinsic and cell-extrinsic insults and develop acquired resistance to therapeutic i
107 s axonal degeneration in response to various insults and is therefore considered an attractive drug t
108 pression in the presence of oxidative stress insults and measured the metabolic response by the nanos
109 contributes to a lower exposure to secondary insults and nosocomial adverse events, increasing the op
111 otects the lung and kidney from pro-fibrotic insults and that this circulating factor is attenuated i
112 he Men1 protein is stabilized in response to insult, and loss of Men1 is associated with the overexpr
113 irment in human cases with early hippocampal insult, and on the clinical implication of the hippocamp
114 etion of USP22 sensitized cells to genotoxic insult, and the role of USP22 in response to genotoxic i
115 growth, mostly depending on the sequence of insults, and allow deciphering the immune mechanisms and
116 ormation of a protective dentin bridge after insult are necessary to seal the pulp chamber in an effo
121 t resist numerous internal and environmental insults associated with neoplasia that jeopardize proteo
122 tubular damage in mice exposed to cisplatin insult, associated with enhanced autophagy in renal tubu
123 ut mice despite ongoing carbon tetrachloride insult, associated with increased numbers of CD68 and F4
124 ct "danger" signals (pathogenic or traumatic insult), become activated, produce proinflammatory cytok
127 ates pathological responses to many types of insults by enhancing oxidative stress and inflammation.
128 giocyte response to genetic or environmental insults can lead to a heterogeneous response; that is, a
131 k, caused by various combinations of genetic insults, can facilitate the assessment of cancer severit
133 phic muscles follows or leads the mechanical insults caused by the muscle's disrupted contractile mac
134 signalling through genetic or environmental insults causes a constellation of neurodevelopmental dis
135 at hypoxia and endoplasmic reticulum stress, insults commonly present in inflammatory bowel diseases,
136 showed an increased vulnerability to stress insults, compared with neurons overexpressing wild-type
138 (UBE3A), but it is unclear how this genetic insult confers vulnerability to seizure development and
139 t independent muscular, neural, and vascular insults contribute to neuromyopathy and that there is me
140 ralateral and ipsilateral to an inflammatory insult demonstrate different functions as inflammation p
141 (DGCs) generated in response to an epileptic insult develop features that promote increased excitabil
142 (TLE) generally takes years after an initial insult during which maladaptation of hippocampal circuit
144 thology, repeated focal seizures, and global insults each contribute to atrophy in specific tracts.
147 IV infection, and demonstrate that these two insults exert significant neuroinflammatory activity.
148 the extent and location of maximum ischemic insult following RVO compared to FFA, hence represents a
149 eneration (e.g. developmental pruning, toxic insult from neurodegenerative disorder), Wallerian degen
151 serves as a barrier to physical and chemical insults from mastication, food, and microorganisms.
152 rly after the 1960s, biological and chemical insults from the surrounding environment-the exposome-ha
153 rigenesis, its combination with an oncogenic insult, illustrated by Pten heterozygosity, elicited let
154 anding of basic mechanisms by which prenatal insults impact offspring brain function, and suggest gut
155 to POAG, which might show a primary vascular insult in addition to secondary vascular damage due to g
159 s R-837 and R-848 were used to mimic a viral insult in the upper airways represented by primary human
160 combined with random potential environmental insults in an immunologically susceptible individual.
161 prevent organ damage from ischemic or toxic insults in animals, but clear evidence in humans is miss
162 and inflammatory reactions to environmental insults in humans with impaired skin barrier functions.
163 ese STFs, we show several pathophysiological insults in hypertrophic cardiomyopathy, including the R4
164 ithelium is critical for recovery from these insults in order to rebuild the epithelial barrier and r
165 will address the role of perinatal vascular insults in the development of late pulmonary vascular dy
166 optic nerve (ON) diseases caused by various insults including glaucoma, inflammation, ischemia, trau
167 oenvironment components respond to different insults including inflammation, malignant haematopoiesis
169 also be used to assess the effects of airway insults, including coinfections by recognized respirator
170 tested their potential for modelling neural insults, including hypoxic-ischaemic and Ca(2+)-dependen
171 as increased in beta-cells upon diabetogenic insults, including in human type 2 diabetic islets.
173 tection for the bacterium from environmental insults, including other bacteria and the host immune sy
176 ination of genetic factors and environmental insults, including viral infection during pregnancy.
178 pressed postnatal peripheral proinflammatory insult-induced systemic inflammation and normalized comp
179 reased in number after relevant pathological insults (infarcts), suggesting a similar expansion of ce
182 ment of neutrophils to sites of inflammatory insult is a hallmark of the innate immune response.
183 njury resulting from repeated mild traumatic insult is associated with cognitive dysfunction and othe
187 Effective adaptation to such environmental insults is essential for the preservation of pulmonary f
188 ence that risk associated with developmental insults is unmasked in female offspring following period
189 often remarkably robust to lesions and other insults, it may be fragile when these take place in spec
191 angiocytes react to exogenous and endogenous insults, leading to disease initiation and progression.
194 a contribution of genetic and environmental insults, many of which molecularly converge on transcrip
195 hypothesized that a prevalent form of renal insult may accelerate cystic progression and investigate
199 dogenesis, is upregulated by cerebrovascular insult; moreover, its activity is increased both in brai
201 endritic mitochondrial changes, oligomycin A-insulted neurons displayed spine loss and altered spine
202 y, we show that continuous targeting of post-insult new neurons in a therapeutically relevant time pe
212 nerated by diverse chemical and physical DNA insults; oxidative stress, chemotherapeutic drugs, envir
213 lness (P < 0.001) and severity of neurologic insult (P = 0.02) were higher in neonates with adverse o
214 in patients who had experienced major immune insults, particularly prior immunosuppressive drug expos
215 umulating evidence indicates that infectious insults perturb ACE2 activity, allowing for uncontrolled
216 Our study demonstrates that maternal immune insults perturb microglial phenotypes and influence neur
217 pes exposed to a high level of environmental insults possess cell type-specific prosurvival mechanism
222 es that anticipated mating-associated immune insult received measurable fitness benefits (survival an
223 in which initial demographic and ecological insults reduce the size and heterogeneity of the populat
224 duced new neurons at the time of the initial insult reduces the frequency of recurrent seizures.
227 n cellular adaptation following pathological insults remains blurred, which makes p75NTR's related si
228 eatment with these flavonoids prior to light insult remarkably protected retina from deterioration an
234 S 15 min prior or adenosine 3 h after E.coli insult significantly attenuated the E.coli-mediated incr
235 This implies that exposure to environmental insults such as hypoxia could explain variable expressiv
242 e reaction to various types of intracellular insults, such as nutrient deficiency or endoplasmic reti
245 s (hemodynamic, biological, renal, and liver insults) than donors without extracorporeal membrane oxy
246 accumulation has been considered the initial insult that drives both the accumulation of tau patholog
247 I/PNN, even if performed after an additional insult that exacerbated the long term PVI/PNN impairment
249 ble-strand breaks (DSBs) are serious genomic insults that can lead to chromosomal rearrangements if r
250 cells of both maternal and fetal origin, and insults that disrupt the maternal-fetal dialogue could r
251 but most studies have overlooked neurotoxic insults that impair development, such as lead exposure.
256 l mechanisms operate together to combat this insult: the ER luminal chaperone Grp170 prevents proinsu
257 an lead to abnormal responses to a secondary insult, these results suggest that chronic sleep loss, t
258 e barrier epithelium in response to external insults, these epithelial cell-derived cytokines were in
259 o the exceptional vulnerability of the DG to insults, these findings provide a further rationale for
260 ime points between the initial precipitating insult through to the establishment of chronic epilepsy.
261 exert the protective effects against lethal insults through conferring apoptosis resistance to hepat
262 ost's immune system to cope with the initial insult (tissue invasion by pathogens and malignant cell
263 ew neurons generated after the epileptogenic insult to alleviate the development of chronic seizures.
266 eckmann et al. showed that an acute ischemic insult to the heart, which induces sterile inflammation,
267 nd and persistent memory loss resulting from insult to the hippocampus in infancy was absent in early
270 phalopathy of prematurity employ significant insults to generate gross central nervous system abnorma
272 ppocampal neurons were exposed to two common insults to preterm brain: transient hypoxia-ischemia (HI
273 ause hypoxia, cytotoxicity, and inflammatory insults to renal tubular epithelial cells (RTECs), resul
275 Neuroinflammation can be caused by various insults to the brain and represents an important patholo
278 Microglia are also profoundly sensitive to insults to the brain to which they respond with process
281 isruption of hormones involved in sleep, and insults to the hypothalamus, brain stem, and reticular a
283 ion coupled with unique acute and persistent insults to their immune function after CAR-T-cell infusi
285 ied, how neutrophils advance an inflammatory insult towards epithelial neoplasia is less understood.
287 tations, environmental toxins and biological insults typically act during developmental windows of su
289 d the role of USP22 in response to genotoxic insult was further confirmed using mouse adult fibroblas
290 the muscle stem cell in response to ischemic insults, we explored cellular interactions between the v
291 pression unless they encounter environmental insults, whereas developing lungs are highly susceptible
292 ar responses following cytotoxic therapeutic insult which promotes their survival and subsequent outg
293 flammatory response are influenced by age-at-insult, which may be an important consideration for trea
294 Importantly, connectivity is impaired by insults, which mimic the diabetic milieu, including high
296 pocampal neuronal cells from the excitotoxic insult, while efavirenz (EFV) did not contrast the neuro
297 ceptors involved in the response to pathogen insults will facilitate the study of changes that occur
298 ndering these genes susceptible to mutagenic insults, with carcinogenesis accelerated by germline DNA
299 least-squares-path modeling we found that WM insult within the optic radiations, V1, and cuneus is a