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1 nd there is no clear relation to location of brain lesion.
2 ogical changes that occur distant to a focal brain lesion.
3 ulnerability of the behavior to a particular brain lesion.
4 ction in blood pressure and failed to reduce brain lesion.
5 iosis in the absence of any disease-specific brain lesion.
6 enotes brain dysfunction remote from a focal brain lesion.
7 ght intraorbital optic nerve tumor without a brain lesion.
8  may be indicated in HIV patients with focal brain lesion.
9  approach to the LV developed at least 1 new brain lesion.
10  denial of motor deficits contralateral to a brain lesion.
11 ry of the upper extremity after a unilateral brain lesion.
12 hich revealed a non-specific enhancing focal brain lesion.
13 ould be monitored for cognitive problems and brain lesions.
14 nal outcome, and survival in adult rats with brain lesions.
15  heavily on the study of patients with focal brain lesions.
16 ry), demyelinating disorders, and infectious brain lesions.
17  mainly been tested by modelization of focal brain lesions.
18 0.81 versus 2.23 mm, P=0.05) of new ischemic brain lesions.
19 8 patients, who presented with new/enlarging brain lesions.
20 nance imaging of the brain revealed multiple brain lesions.
21 oms, reduces neuroinflammation, and prevents brain lesions.
22  mammalian target of rapamycin and disabling brain lesions.
23  led to a marked increase in necrosis of the brain lesions.
24 2009 to identify progression of MRI-measured brain lesions.
25 ne of ten patients had reductions in size of brain lesions.
26 tibility to heat-induced seizures and cystic brain lesions.
27 ics of early active demyelinating NMO and MS brain lesions.
28 ssociation of retinal microvascular signs to brain lesions.
29  roles in the repair process after traumatic brain lesions.
30 trasbourg and Liverpool) for the presence of brain lesions.
31  the study of vascular and other acute focal brain lesions.
32  perceive than ungrouped ones after parietal brain lesions.
33 ic changes during recovery of function after brain lesions.
34 s distinguish CNS lymphoma from benign focal brain lesions.
35 f the second allele in the majority of human brain lesions.
36 y surgery in the absence of associated focal brain lesions.
37 fic to tuberous sclerosis complex-associated brain lesions.
38 nd H2R) are present on inflammatory cells in brain lesions.
39 bout 14% of infected mice but did not induce brain lesions.
40 d cerebrospinal fluid CD14+ cells, and in MS brain lesions.
41 ulation, which was before the development of brain lesions.
42 us indexes of cerebral blood flow with these brain lesions.
43  25 patients suffered from pre- or perinatal brain lesions.
44 zing neurological symptoms in the setting of brain lesions.
45 ls, thus contributing to tissue damage in MS brain lesions.
46 ially vulnerable to ischemic and hemorrhagic brain lesions.
47 mic disease have diminished efficacy against brain lesions.
48 lations and for understanding recovery after brain lesions.
49 12, respectively) than those without frontal brain lesions (1/11, P's < 0.05).
50     Clinical brain scans of 83 patients with brain lesions (67 in the training and 16 in the validati
51 evealed that 7 (12.5%) of the 56 total acute brain lesions after ablation formed a persistent glial s
52  incidence, number, and size of new ischemic brain lesions after CAS.
53         We describe the development of fetal brain lesions after Zika virus (ZIKV) inoculation in a p
54  of epileptogenesis in areas adjacent to the brain lesion and may trigger the formation of seizure-ge
55               In rats and monkeys, localized brain lesion and pharmacological approaches have been us
56 iteria, while 27 had not (13 had MRI-visible brain lesions and 14 did not).
57 ection in 50 stroke patients with unilateral brain lesions and 85 control subjects.
58 ative disorder characterized by pathological brain lesions and a decline in cognitive function.
59 neurons from the postnatal SVZ contribute to brain lesions and abnormal circuit remodeling in forebra
60 mental brain ischemia as a paradigm of acute brain lesions and additionally investigated a large coho
61                                     Vascular brain lesions and atherosclerosis are two similar condit
62 ment is, in turn, associated with structural brain lesions and autonomic dysfunction, which may predi
63 gle course of rituximab reduced inflammatory brain lesions and clinical relapses for 48 weeks.
64 ynamic mechanisms contributing to structural brain lesions and cognitive impairment in the presence o
65 ses in which a temporal relationship between brain lesions and criminal behavior was implied but not
66 utant mice, brain stimulation and recording, brain lesions and direct pharmacological manipulations o
67 the brain at study entry for the presence of brain lesions and enhancing characteristics.
68 t with natalizumab led to fewer inflammatory brain lesions and fewer relapses over a six-month period
69 al mapping of visual cortex in patients with brain lesions and for studying patients with amblyopia,
70 ined from 15 consecutive patients with focal brain lesions and from 14 healthy control subjects.
71            Evidence from patients with focal brain lesions and from healthy volunteers using function
72 rred for neurosurgical assessment of unclear brain lesions and had undergone (18)F-FET PET.
73 del replicates several features of human TSC brain lesions and implicates an important function of Ts
74  (CNTF) has been shown to be expressed after brain lesions and in particular after demyelination.
75 rx1(-/-) mice exhibited significantly larger brain lesions and increased motor deficits following CCI
76           Importantly, the pathognomonic MRI brain lesions and neurohistopathologic findings are reve
77      Of these 94 patients, 11 had measurable brain lesions and no previous radiotherapy to the brain,
78 and two control groups: SCD patients without brain lesions and non-sickle cell sibling controls (n =
79 ils the microstructural abnormalities of the brain lesions and of the morphologically normal appearin
80   Hoarding has been shown to be sensitive to brain lesions and pharmacological agents, and is a suita
81  Neuropsychological studies on patients with brain lesions and rapid developments in brain imaging te
82  from the neonatal and juvenile SVZ generate brain lesions and structural abnormalities, which would
83 rmed to analyze the rate of ablation-related brain lesions and their effect on cognitive function.
84 psilateral hippocampal sclerosis as the only brain lesion, and underwent amygdalohippocampectomy.
85 nd overt cognitive impairment and structural brain lesions, and explored the role of autonomic dysfun
86 sodes of encephalopathy, bilateral symmetric brain lesions, and high excretion of organic acids that
87 ility of MSCs as OV carriers to disseminated brain lesions, and provides a clinically applicable ther
88 tients with multiple sclerosis, inflammatory brain lesions appear to arise from autoimmune responses
89                                        These brain lesions are associated with the symptom severity o
90                                    Ischaemic brain lesions are associated with white matter changes a
91                                        Focal brain lesions are assumed to produce language deficits b
92                                 MRI-detected brain lesions are common after left atrial catheter abla
93                            These parenchymal brain lesions are considered key contributors to cogniti
94 at the base of spontaneous regression of the brain lesions are discussed.
95                 Acute, subclinical ischaemic brain lesions are frequent but previously underestimated
96 ntibody-positive patients have revealed that brain lesions are not uncommon in NMO, and some patterns
97 reas and the disturbance introduced by focal brain lesions are poorly understood.
98                           Whereas multifocal brain lesions are present on MRI in many patients with a
99 ne in post-traumatic coma or when structural brain lesions are probable or possible causes.
100                                     Although brain lesions are readily detected, magnetic resonance i
101                       When clinically silent brain lesions are seen on MRI, the likelihood of develop
102 erous sclerosis complex (TSC) and associated brain lesions are thought to arise from abnormal embryon
103 n tremors, such as those induced by drugs or brain lesions, are also important to recognize because t
104 al and functional studies implicate multiple brain lesions as a basis for a functional dysconnectivit
105  functional differentiation in breast cancer brain lesions as a novel therapeutic strategy.
106 apamycin (mTOR) activation in TSC-associated brain lesions as well as in various cancers.
107 e initiating event in the development of TSC brain lesions as well as underscore the importance of Ts
108 lanning resective surgeries in patients with brain lesions, as well as investigations into structural
109 d how and when dysfunctional MCT8 can induce brain lesions associated with the Allan-Herndon-Dudley s
110 , aberrantly activated Erk was also found in brain lesions associated with tuberous sclerosis (TSC).
111 fference in new positive postprocedure DWMRI brain lesions at 2 days after TAVI in potentially protec
112 had central veins visible in the majority of brain lesions at baseline.
113           CSF from MS patients with enhanced brain lesions at magnetic resonance imaging was able to
114 ledge of different types of hypoxic-ischemic brain lesions based on our personal experience and MR im
115                  Additionally, patients with brain lesions but not controls exhibited significant dif
116    Neglect signs do not only depend on focal brain lesions, but also on dysfunction of large-scale br
117                                   Mechanical brain lesion by controlled cortical impact.
118                                   Mechanical brain lesion by controlled cortical impact.
119 nce nitrogen) treatment following mechanical brain lesion by controlled cortical impact.
120 se from the Cardiovascular Abnormalities and Brain Lesions (CABL) study.
121 phy as part of the Cardiac Abnormalities and Brain Lesions (CABL) study.
122 ing given powerful demonstrations that focal brain lesions can affect specific aspects of cognition.
123 curacy and the loss of such functions due to brain lesions can be catastrophic.
124 her differences between benign and malignant brain lesions can be depicted with fluorine 18 ((18)F) f
125  evidence that propofol sedation after acute brain lesions can have a deleterious impact and implicat
126                                        Focal brain lesions can have important remote effects on the f
127  and we conclude that static models of adult brain lesions cannot be used to account for the dynamics
128                                In metastatic brain lesions carrying activated alpha(v)beta(3), VEGF e
129                              Here we analyze brain lesions causing acute onset freezing of gait to id
130 c resonance imaging measures of infarct-like brain lesions, cerebral microbleeds, total brain volume,
131  immune target is not the main substrate for brain lesion characteristics.
132                These results based on causal brain lesions complement prior neuroimaging studies in P
133 tic resonance imaging of angiomyolipomas and brain lesions, computed tomography of lung cysts, and pu
134 aine with clinical and sub-clinical vascular brain lesions, congenital heart defects, coronary heart
135 g outcome of having T2-weighted hyperintense brain lesions consistent with the 2010 McDonald MRI crit
136                                              Brain lesions containing filamentous and aggregated alph
137                                 How a single brain lesion could cause such a complex disorder is uncl
138 ; P=0.03), and significant reductions in the brain lesion count on magnetic resonance imaging (MRI) (
139                                              Brain lesion count was recorded from brain magnetic reso
140  were performed to determine whether age and brain lesion count were associated with adrenal findings
141                               Similar to the brain lesions described for human EEE, the NA EEEV-infec
142  (with 1 exception) were not associated with brain lesion development.
143 three main mechanisms of coma are structural brain lesions, diffuse neuronal dysfunction, and, rarely
144                                     Ischemic brain lesions discovered on DWI after CAS seem to be a m
145                                          MRI brain lesion distribution criteria were able to distingu
146 ncluding psychiatric and neurologic disease, brain lesions, drug effect, and hearing impairment.
147 tive than flow reversal in reducing ischemic brain lesions during CAS through femoral approach.
148 umulative number of new gadolinium-enhancing brain lesions during the treatment phase and was analyse
149 y untreated patients, 25% had more than four brain lesions, eight (7%) achieved an objective response
150        The model also describes how specific brain lesions enhance the strength of the startle respon
151  A number of CD4(+) and CD8(+) T cells in MS brain lesions expressed GM-CSF.
152  fulminant encephalopathy and characteristic brain lesions following viral infection.
153 ciated with the clinical compensation of new brain lesion formation in RR-MS.
154 l giant cell astrocytomas (SEGAs) are common brain lesions found in patients with tuberous sclerosis
155 thways may facilitate delivery to the global brain lesions found in these disorders.
156 rst, we assessed ASIC1 expression in chronic brain lesions from post-mortem of patients with progress
157 eta(3) activation state that is critical for brain lesion growth.
158  extensive literature involving experimental brain lesions has implicated the hippocampus in context
159                   The study of patients with brain lesions has made major historical contributions to
160  new study mapping the functional effects of brain lesions has revealed a surprising map of human int
161                             Although various brain lesions have been found to affect performance on t
162  pure-tone thresholds and central MS-related brain lesions have not been assessed.
163 ic brain areas and direct induction of focal brain lesions, human research has so far utilized predom
164 be assessed in patients suffering from focal brain lesions (i.e. connectomal diaschisis).
165 resently, no evidence exists for a localized brain lesion in IED subjects.
166  inattention to the side of space opposite a brain lesion in patients with unilateral neglect, primin
167  activity in anatomical reorganization after brain lesion in the adult.
168                  These techniques detect new brain lesions in 25% to 50% of patients after both coron
169     Our observation of ZIKV-associated fetal brain lesions in a nonhuman primate provides a model for
170 al QT, no sexual dimorphism was detected for brain lesions in either intact or gonadectomized mice.
171 n antagonist that reduced the development of brain lesions in experimental models and in a preliminar
172  used to precisely map and selectively model brain lesions in human and animals studies.
173 cm2 in adult mice recapitulates the CCM-like brain lesions in humans; the lesions display disrupted v
174 variants of these cells derived from bone or brain lesions in immunodeficient mice.
175 igraine with progression of any MRI-measured brain lesions in men.
176  spontaneously disseminate into the CSF from brain lesions in mice in a COX-2-dependent manner and ca
177 ) is the primary imaging technique to detect brain lesions in MS.
178                             Investigation of brain lesions in multiple sclerosis (MS) reveals a coord
179  of the nature, prognosis, and ways to treat brain lesions in neonatal infants has increased remarkab
180          Establishing the diagnosis of focal brain lesions in patients with unexplained neurologic sy
181  MRI sequences is important to differentiate brain lesions in pediatric patients.
182 ction of CSF spermine reflects correction of brain lesions in these animals.
183 g has led to further characterization of the brain lesions in TSC.
184 iagnostic algorithms for the workup of focal brain lesions in which lymphoma is a consideration.
185      Eight patients with anterior prefrontal brain lesions including the FPC performed a four-armed b
186                                        Focal brain lesions increased EV release, and, following isola
187                                        Acute brain lesions induce profound alterations of the periphe
188                        We also observed that brain lesioning induced several metabolites with neuropr
189                                        Acute brain lesions induced dysbiosis of the microbiome and, i
190 ansplantation of fecal microbiota normalizes brain lesion-induced dysbiosis and improves stroke outco
191              Humans with pharmacological and brain lesion-induced suppression of REM sleep do not sho
192 predictable, and consistently sized necrotic brain lesions, inflammatory responses, and behavioral de
193 findings in stroke patients, with unilateral brain lesions involving at least one of these areas, who
194 halopathy, which is characterized in part by brain lesions, lactic acidemia, excretion of ethylmaloni
195 hat affordances can be effective even when a brain lesion limits the use of other properties in searc
196 , age of onset, disease severity, as well as brain lesion load and normalized brain volume from magne
197 ne hundred three patients with focal, stable brain lesions mapped onto a reference brain were tested
198 hat language system organization after focal brain lesions may be marked by complex signatures of alt
199                       While it is known that brain lesions may selectively affect orthographic long-t
200 kely to be toxoplasmosis (n=8, 42.1%), focal brain lesion (n=5, 26.3%) or both (n=3, 15.8%).
201 ) with single or multiple contrast-enhancing brain lesions (n = 40) on MRI after radiation therapy of
202 g superior parietal cortex (n = 146), and no brain lesions (n = 55).
203  we assembled the largest known set of focal brain lesions (n = 581), derived from unselected patient
204                           Neither persistent brain lesions nor the ablation procedure itself had a si
205 leiotropic, clock-independent functions; and brain lesions not only disrupt cellular circadian rhythm
206 n peripheral blood, cerebrospinal fluid, and brain lesions of MS patients.
207 cs, we observed that RAAS is up-regulated in brain lesions of MS.
208                                   In chronic brain lesions of patients with progressive multiple scle
209 al studies provide correlative evidence, and brain lesions often comprise both white and gray matter
210                                              Brain lesions on diffusion-weighted imaging (DWI) are fr
211 ent ischemic attack, and definitive ischemic brain lesions on fluid-attenuated inversion recovery mag
212 rated differential effects of left and right brain lesions on immune function, but human studies are
213  The primary end point was the number of new brain lesions on monthly gadolinium-enhanced magnetic re
214 initial demyelinating event, had two or more brain lesions on MR images, and had two or more oligoclo
215       The UCCA and the number of hypointense brain lesions on T1-weighted images were the strongest M
216  parameters, including number of hypointense brain lesions on T1-weighted MR images, presence of diff
217                  UCCA, number of hypointense brain lesions on T1-weighted MR images, presence of diff
218 % with placebo (P=0.04); the total volume of brain lesions on T2-weighted magnetic resonance imaging
219               In previous follow-up studies, brain lesions on T2-weighted MRI are associated with inc
220 ere employed to test the mediating effect of brain lesions on the association of diabetes with cognit
221         This study showed that microvascular brain lesions on ultra-high field MRI are not significan
222 sly treated patients, 21% had more than four brain lesions, one had a partial response, and six (18%)
223 ansferring the three-dimensional volume of a brain lesion onto a reference brain; (ii) assessing the
224 ry obliterations associated with tumefactive brain lesions or nephropathy.
225 of fumarate-treated patients presenting with brain lesions or seizures even in the absence of severe
226 s can go unnoticed for years, and incomplete brain lesions or silencing of neurons often fail to prod
227 sue to resect, such as the location of focal brain lesions or the presence of epileptiform rhythms, d
228 s than male mice [odds ratio (OR) = 2.28 for brain lesions; OR = 2.37 for spinal cord (SC) lesions].
229 orrelation with age (P < .001) and number of brain lesions (P < .001).
230                       Here, we studied human brain lesion patients to determine whether the superior
231 the detection of awareness in anesthesia and brain-lesioned patients.
232 ssessment of patients with a newly diagnosed brain lesion; patients who had no radiotherapy, surgery,
233              Ablation-related acute ischemic brain lesions persist to some extent but do not cause co
234    Nesting has been shown to be sensitive to brain lesions, pharmacological agents and genetic mutati
235                                    While the brain lesions predominantly originate prenatally, it rem
236                                        These brain lesions present a mixed glioneuronal phenotype and
237                                     Vascular brain lesions, present in advanced atherosclerosis, shar
238                                    Following brain lesions, previously normal patients sometimes exhi
239                                              Brain lesions produced by the tetravalent ChimeriVax-DEN
240              Much uncertainty has surrounded brain lesions producing deficits in these tests, with st
241      Eleven subjects with PBC had structural brain lesions quantified via magnetic resonance imaging.
242 hin 48 hours after ablation, showed that new brain lesions (range, 1-17) were present in 16 (43.2%) p
243 besity were not associated with infarct-like brain lesions (relative risk (RR) = 0.82, 95% confidence
244                  The treatment of metastatic brain lesions remains a central challenge in oncology.
245 onditions, of which neurological disease and brain lesions represent a substantial proportion, and th
246  rodents induces cortical neuronal migration brain lesions resembling those of autism.
247              Phosphoproteomic analysis of MS brain lesions revealed S1P1 phosphorylation on S351, a r
248 ical findings for patients with EEE included brain lesions, seizures that evolved to status epileptic
249                               Looking at the brain lesion should always be done from the whole patien
250          After adjusting for age, NIHSS, and brain lesion size (computed tomography), PENK-A predicte
251 r function after brain trauma, and decreases brain lesion size induced by trauma.
252 ody (0.8 mg/kg) caused a twofold decrease in brain lesion size, whereas that of tPA (10 mg/kg) had a
253 observations of visual-field scotomas across brain-lesioned soldiers to produce a schematic map of th
254 m the CABL (Cardiovascular Abnormalities and Brain Lesions) study by traditional and tissue Doppler i
255 t in understanding functional recovery after brain lesions such as stroke.
256                               However, acute brain lesions, such as traumatic brain injury, reactivat
257 racterized by significant neurodevelopmental brain lesions, such as tubers and subependymal nodules.
258 ed to test the association between miRNA and brain lesions (T2 hyperintense lesion volume [T2LV]), th
259 ot significantly affected by the presence of brain lesions [T2 lesions (P = 0.918), periventricular T
260 emained obscure, which we addressed by using brain lesion techniques combined with modern immunohisto
261     However, on the basis of the location of brain lesions that produce acquired impulsive aggression
262 were previously at high risk for destructive brain lesions that resulted in cystic white matter injur
263 6 men; age range, 26-79 years) with solitary brain lesions that were enhanced at magnetic resonance (
264                       Multiple, disseminated brain lesions, that are characterised by restricted diff
265 lthough chronic exposure is known to produce brain lesions, the influence of DA toxicosis on behavior
266 clinical relapses and new focal inflammatory brain lesions throughout the 2 years of immune monitorin
267 ing biomaterials for injection into cavitary brain lesions to recruit endogenous NPCs and enhance neu
268 distortions, contrasting patients with focal brain lesions to the ventromedial prefrontal cortex (vmP
269 ermined, although it is impaired by discrete brain lesions to ventromedial prefrontal cortex, anterio
270 tactic cues and structural support, cavitary brain lesions typically fail to recruit endogenous neura
271 rmance on the different tasks; patients with brain lesions under-produced but over-estimated time int
272 cal studies are important in determining the brain lesions underlying dementia.
273 ropathological information on the structural brain lesions underlying seizures is valuable for unders
274 asymptomatic NTZ-associated PML (NTZ PML, 18 brain lesions) underwent 3-T MR imaging.
275  isolated from rats after focal inflammatory brain lesions using IL-1beta, to activate a systemic APR
276 m of Deinagkistrodon acutus, on MRI-detected brain lesion volume and tissue perfusion deficit in a hy
277 roved motor function recovery, and decreased brain lesion volume compared with wild-type controls.
278 limited cerebral ischemic injury and reduced brain lesion volume significantly more effectively than
279  reflected by better motor function, reduced brain lesion volume, and diminished neurodegeneration.
280                             We also measured brain lesion volume, cervical spinal cord lesion number
281 tical gray matter and cerebral white matter, brain lesion volume, spinal cord gray and white matter a
282 ic mice, BI-1 transgenic mice showed reduced brain lesion volumes and better performance in motoric t
283                                      The new brain lesion was treated with stereotactic radiosurgery,
284           GM-CSF production by T cells in MS brain lesions was analyzed by immunofluorescence.
285                          Using patients with brain lesions we show that, relative to nonfrontal lesio
286 velopmental perturbations that lead to these brain lesions, we created a mouse model that selectively
287  Studying a group of 192 patients with focal brain lesions, we show a significant association between
288 lated brainstem syndromes in whom multifocal brain lesions were absent, showed trajectories more clos
289                                     Ischemic brain lesions were assessed by a 3T magnetic resonance i
290                                   N = 302 MS brain lesions were detected, and generalized linear mixe
291                               No parenchymal brain lesions were evident on imaging, but transient cer
292               Neurological disease and focal brain lesions were found in 25% and 9% of the total subj
293                                   Structural brain lesions were found in PBC, the density of which co
294 12 s stimuli demonstrated that patients with brain lesions were more variable than controls on the es
295 erm equivalent age without focal parenchymal brain lesions were studied with 20 full-term control inf
296  for stimuli in the field contralateral to a brain lesion when stimuli are simultaneously presented o
297  The authors discussed a few T1-hyperintense brain lesions which did not include metastases (except f
298 rn before 33 weeks' gestation are at risk of brain lesions, which have the potential to disrupt subse
299 th a post-neonatally acquired or progressive brain lesion who could grasp before the operation, and a
300 logical cost, we predicted that pathological brain lesions would be concentrated in hub regions.

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