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1 lopmental trajectories of tissue iron in the basal ganglia.
2 made by the corresponding systems within the basal ganglia.
3 ward-related and motivational signals in the basal ganglia.
4  (STN) neurons form a key network within the basal ganglia.
5 turation of tissue iron concentration in the basal ganglia.
6 affects learning and action selection in the basal ganglia.
7 nent in the striatum, the central hub of the basal ganglia.
8  a key, yet an understudied component of the basal ganglia.
9 key, centrally positioned network within the basal ganglia.
10  striatum is the main input structure of the basal ganglia.
11 lates with deposition of amyloid-beta in the basal ganglia.
12 ough dopamine-mediated interactions with the basal ganglia.
13 aints for future computational models of the basal ganglia.
14 aints for future computational models of the basal ganglia.
15  choice between GO and NO-GO pathways in the basal ganglia.
16 ex, frontal gyrus, amygdala, hippocampus and basal ganglia.
17 induced at specific coordinates in the right basal ganglia.
18 ed throughout the cerebellum, brainstem, and basal ganglia.
19 prediction errors that drive learning in the basal ganglia.
20 reduced vision /cataract or calcification of basal ganglia.
21 n subtype that preferentially innervates the basal ganglia.
22 the cerebral cortex, the cerebellum, and the basal ganglia.
23 d attention-related visual processing in the basal ganglia.
24 ease conditions associated with the mPFC and basal ganglia.
25 making systems residing in the brain, in our basal ganglia.
26 including white matter-enhancing lesions and basal ganglia abnormalities that could be related to sev
27                                              Basal ganglia abnormalities were seen in four other pati
28                  Second, we examine cortical-basal ganglia activation during inhibitory control in ch
29 l output will pave the way toward dissecting basal ganglia activity in both physiological and patholo
30 d to be permitted or triggered by changes in basal ganglia activity through gating- or rebound-like m
31 ng the normal and pathological patterning of basal ganglia activity.
32 eurodevelopmental syndromes characterized by basal ganglia agenesis are not known to date.
33  phenotype and molecular basis associated to basal ganglia agenesis in humans.
34 demonstrated abundant nitrergic cells in the basal ganglia, amygdaloid complex, preoptic area, basal
35  carrier status, mutation site within PSEN1, basal ganglia amyloid-beta as measured by Pittsburgh com
36 84% versus 63.3%; P = 0.006) and showed more basal ganglia amyloid-beta deposition (Pittsburgh compou
37 was significantly positively correlated with basal ganglia amyloid-beta deposition, Clinical Dementia
38 ers with motor findings more frequently were basal ganglia amyloid-beta positive (84% versus 63.3%; P
39 nd dorsal premotor cortex, as well as in the basal ganglia and anterior cerebellum.
40 memory (learning and memory that rely on the basal ganglia and associated circuitry) can explain nume
41 ional direct pathways running from cortex to basal ganglia and between basal ganglia and cerebellum i
42 ivated astroglia in the cortex, hippocampus, basal ganglia and brainstem; therefore, by measuring imi
43          Hypomyelination with atrophy of the basal ganglia and cerebellum (H-ABC) is a neurodegenerat
44 hy including Hypomyelination with Atrophy of Basal Ganglia and Cerebellum (H-ABC), a rare hypomyelina
45 ing from cortex to basal ganglia and between basal ganglia and cerebellum in the pathophysiology of m
46 ibuted to major neuropathology of mainly the basal ganglia and cerebral cortex.
47  inputs from upstream centers, including the basal ganglia and cortex, to regulate and modulate behav
48  relationship between neuronal firing in the basal ganglia and cortical gamma activity during movemen
49 port for models that link beta activity with basal ganglia and dopamine for the allocation of neural
50 he anatomy, physiology, and circuitry of the basal ganglia and highlight the mechanisms that underlie
51     Subtype 2 showed increased volume in the basal ganglia and internal capsule, and otherwise normal
52 normal and stable anatomy, except for larger basal ganglia and internal capsule, not explained by ant
53 he striatum is the main input nucleus of the basal ganglia and is a key site of sensorimotor integrat
54  gene expression patterns and found that the basal ganglia and medium spiny neurons were most enriche
55 ccupied restricted regions in the neocortex, basal ganglia and midbrain.
56 imultaneous intracranial recordings from the basal ganglia and motor cortex, we found that response-c
57 the hyperdirect and indirect pathways of the basal ganglia and movement control.
58  of the ventral telencephalon from which the basal ganglia and olfactory tubercles originate, where i
59 mal and patients demonstrate the role of the basal ganglia and other interconnected structures, such
60 ciated with blunted reward activation in the basal ganglia and other regions such as the medial prefr
61 from the frontal and occipital white matter, basal ganglia and pons was used to obtain a global cereb
62 the nervous system, such as the spinal cord, basal ganglia and pontine nuclei in the brainstem, can b
63 ic nucleus (STN) is a pivotal element of the basal ganglia and serves as target for deep brain stimul
64 ificity and multi-network integration in the basal ganglia and thalamus of individual human subjects.
65 knockouts had higher manganese levels in the basal ganglia and thalamus than controls.
66 hology, myelin and iron concentration of the basal ganglia and thalamus were estimated from 182 MRI d
67 racterize the functional interaction between basal ganglia and thalamus, we demonstrated that patient
68        We review the connections between the basal ganglia and the thalamus and cortex, address the b
69 havior both via ascending projections to the basal ganglia and through descending projections to brai
70 d target engagement (lowering of iron in the basal ganglia), and seemed to somewhat slow disease prog
71 sential tremor within higher-level cortical, basal ganglia, and cerebellar regions.
72  define axonal trajectories of the cortical, basal ganglia, and cerebellar systems.
73 ral lobe, the diencephalon, cerebral cortex, basal ganglia, and cerebellum.
74 ing and correlating the variable cerebellar, basal ganglia, and neocortical neuropathology with the v
75 ing posterior cingulate and parietal cortex, basal ganglia, and temporal cortex.
76 nderstand the functional organization of the basal ganglia, and with the discovery of the neurotoxin
77                                          The basal ganglia are a collection of nuclei in vertebrates
78                                          The basal ganglia are a group of subcortical nuclei that con
79 ursts of beta frequency band activity in the basal ganglia are associated with slowing of voluntary m
80                                          The basal ganglia are implicated in a range of perceptual fu
81                                          The basal ganglia are important for movement and reinforceme
82 o how decision processes and learning in the basal ganglia are modulated by the motivation.
83                    In particular, dysplastic basal ganglia are part of the malformative spectrum of t
84 hat D2 MSNs and specific circuits within the basal ganglia are preferentially vulnerable to HIV-1.
85                                              Basal ganglia are subcortical grey nuclei that play esse
86 h brain slices we show that within each bird basal ganglia Area X-projecting (HVC(X)) neurons share s
87 f the arcopallium) and from HVC to the avian basal ganglia (Area X).
88 gly connected with the prefrontal cortex and basal ganglia, areas which have been implicated in inter
89 and marked deposition of amyloid-beta in the basal ganglia, autosomal dominant Alzheimer's disease co
90                                         Both basal ganglia (BG) and orbitofrontal cortex (OFC) have b
91  in brain regions linked to ASD, such as the basal ganglia (BG) and the dorsomedial prefrontal cortex
92      Reinforcement learning models treat the basal ganglia (BG) as an actor-critic network.
93 nds to treatments that decrease pathological basal ganglia (BG) beta oscillations (10-17 Hz in primat
94 antia nigra pars reticulata (SNr), where the basal ganglia (BG) direct and indirect pathways converge
95 es in PD are generally attributed to altered Basal Ganglia (BG) function.
96 ad hoc behavioral protocol to understand how basal ganglia (BG) is affected by cannabinoids.
97 ter sensory-motor cortical loop and an inner basal ganglia (BG) loop, controlling their respective ha
98                                  As a rodent basal ganglia (BG) output nucleus, the substantia nigra
99 egulates sensory thalamic activity through a basal ganglia (BG) pathway.
100                                       In the basal ganglia (BG), anatomically segregated and topograp
101 culated in the neocortex and cortical lobes, basal ganglia (BG), hippocampi, and thalami.
102 d connect the prefrontal cortex (PFC) to the basal ganglia (BG).
103 ars reticulata (SNr), the main output of the basal ganglia, blocks signaled active avoidance, while i
104 ere located in the following areas: level of basal ganglia (caudate nucleus, putamen, corpus callosum
105                            In contrast, some basal ganglia, cerebellar, and limited cortical areas sh
106 tely treated HIV, except a MRS alteration in basal ganglia choline.
107 ays a distinct role in the prefrontal cortex-basal ganglia circuit for reinforcement learning and is
108                            Therefore, the M2-basal ganglia circuit is critical for the assembly of th
109  plausible biophysical models of the cortico-basal ganglia circuit that could explain the functional
110                                   Within the basal ganglia circuit, the external globus pallidus (GPe
111 pallidus (GPe) is a critical node within the basal ganglia circuit.
112 milar manner as the hyperdirect and indirect basal ganglia circuitry.
113 eflecting derangements in the cerebellar and basal ganglia circuitry.
114 ctivity in HVC and occurred independently of basal ganglia circuitry.
115  Our findings provide insights into cortical-basal ganglia circuits and global brain organization und
116 ulates glutamatergic transmission in cortico-basal ganglia circuits and represents a major target of
117                                      Cortico-basal ganglia circuits are thought to mediate goal-direc
118 ical and fundamental studies have identified basal ganglia circuits as critical for this process.
119 y oscillations (15 to 35 Hz) in cortical and basal ganglia circuits become abnormally synchronized in
120  scenarios emerge that shed new light on how basal ganglia circuits modulate self-paced movement init
121 ing and to establish that downstream cortico-basal ganglia circuits serve a learning role that is onl
122 l spatial attention, then the involvement of basal ganglia circuits should incorporate the subject's
123 or symptoms are attributed to dysfunction of basal ganglia circuits under conditions of low dopamine.
124 bition critically relies on frontal cortex - basal ganglia circuits.
125 y among cognitive, motor, and limbic cortico-basal ganglia circuits.
126 apturing prefrontal, anterior cingulate, and basal ganglia connections linked to the limbic system.
127 on has both behaviour-independent effects on basal ganglia connectivity, as well as behaviour-depende
128 demonstrated elevated tau PET binding in the basal ganglia, consistent with prior work with amyloid-b
129 lanation for these diverse roles is that the basal ganglia control the level of commitment to particu
130 (47.4%) developed T1 hyperintensities of the basal ganglia, corresponding to accumulated lipid phagoc
131  also discuss where beta might be generated: basal ganglia, cortex, or both.
132 unique but complementary spatial patterns of basal ganglia degeneration that are strikingly reminisce
133 cifications, necrotic and calcified areas in basal ganglia, dentato-olivary dysplasia and severe hypo
134 telencephalic signaling center important for basal ganglia development known in other vertebrates (i.
135 ic diseases are associated with dysregulated basal ganglia direct-pathway activity.
136 ons (SPNs) are thought to contribute to many basal ganglia disorders, including early-onset neurodeve
137 d to PD and Dystonia are likely amplified by basal ganglia downstream structures.
138 tory of tissue iron concentration across the basal ganglia during adolescence and provide evidence th
139 ly, the increase in beta oscillations in the basal ganglia during sleep paralleled decreased NREM sle
140                                        While basal ganglia dysfunction is observed in many neurodegen
141 established physiological criteria to define basal ganglia dysfunction, correlations between individu
142 ous research has linked SHANK3 deficiency to basal ganglia dysfunction, motor stereotypies, and socia
143 related directed medial prefrontal cortex to basal ganglia effective connectivity is abnormally incre
144                                              Basal ganglia encephalitis (BGE), representing a subset
145 d by abrupt phase slips between cortical and basal ganglia ensemble signals.
146                                          The basal ganglia, especially the caudate nucleus 'head' (CD
147 tes, and executive function, mediated by the basal ganglia, extended amygdala, and frontal cortex, re
148 mplex modes of information processing in the basal ganglia for different motor and nonmotor functions
149 ood-brain barrier (BBB) openings in the left basal ganglia for three consecutive weeks.
150 red in the basal ganglia in PD and models of basal ganglia function and dysfunction were proposed.
151 striatal output is crucial for understanding basal ganglia function and related behaviors.
152 ing.SIGNIFICANCE STATEMENT Current models of basal ganglia function are often based on a distinction
153 pathways provides striking predictions about basal ganglia function that have been used to develop de
154 sting parallel functional pathway concept of basal ganglia function to include the study of limbic-mo
155 nals in the striatum play a critical role in basal ganglia function, such as reinforcement and motor
156 nd dopamine, both of which are essential for basal ganglia function.
157 l or physiological framework that highlights basal ganglia function.
158 g mice of either sex, we found that the main basal ganglia GABAergic output in the midbrain, the subs
159 nt, however, is increased motor cortical and basal ganglia gamma synchrony.
160  anatomy of the medial prefrontal cortex and basal ganglia has been extensively studied and the forme
161 The ventral pallidum, located in the ventral basal ganglia, has long been recognized as an obligatory
162                                          The basal ganglia have been implicated in action selection a
163                  While prefrontal cortex and basal ganglia have been implicated in interval timing in
164   Whereas subcortical structures such as the basal ganglia have been widely explored in relation to m
165 n CD36 protein with age in several cortices, basal ganglia, hippocampus, and midbrain, a decrease wit
166  in the white matter in children, and in the basal ganglia in adults.
167                           Pathophysiology of basal ganglia in focal seizures appears to be much more
168 ticipation or an even more prominent role of basal ganglia in focal seizures, the mode of interaction
169 ation of potential volumetric changes of the basal ganglia in patients with PD who underwent staged S
170 e physiological changes that occurred in the basal ganglia in PD and models of basal ganglia function
171  depends on the interconnected nuclei of the basal ganglia in the CNS.
172       Recent work has implicated the primate basal ganglia in visual perception and attention, in add
173 intracerebral electrode contact explored the basal ganglia, in either their putaminal or caudate part
174                                          The basal ganglia include two pathways, which have been asso
175        Increases were most pronounced in the basal ganglia, including the caudate-putamen, striatum a
176  Ndufs4 deletion in GABAergic neurons causes basal ganglia inflammation without motor or respiratory
177 t in the integration of limbic, sensory, and basal ganglia information to guide effective response st
178 ant as firing rate for understanding cortico-basal ganglia information transfer.
179 ings suggest that the broken balance between basal ganglia inhibition and thalamus synchronization ca
180                                      Cortico-basal ganglia interactions continuously shape the way we
181  of the motor system by including cerebellar-basal ganglia interactions, and compared the modulatory
182 e of Pontocerebellar Hypoplasia with typical basal ganglia involvement on neuroimaging.
183 r, the normative developmental trajectory of basal ganglia iron concentration during adolescence and
184 r, our results suggest a prolonged period of basal ganglia iron enrichment that extends into the mid-
185           Atypical iron concentration in the basal ganglia is associated with neurodegenerative disor
186          A set of sub-cortical nuclei called basal ganglia is critical for learning the values of act
187                     A pivotal element of the basal ganglia is the subthalamic nucleus (STN), which se
188 lar nucleus (PF), an excitatory input to the basal ganglia, is targeted with deep-brain stimulation t
189 m(2)/sec; right, 1.15 x10(3)mum(2)/sec), and basal ganglia (left, 1.26 x10(3)mum(2)/sec; right, 1.23
190 years +/- 0.32; right, 1.45 years +/- 0.33), basal ganglia (left, 1.79 years +/- 0.31; right, 1.70 ye
191 in connectivity between the habenula and the basal ganglia, limbic, and sensory systems was already p
192 on effective connectivity within the cortico-basal ganglia loops at rest, as well as further modulati
193 esults demonstrate that activity through the basal ganglia may play an important and distinct role am
194         These findings demonstrate a cortico-basal ganglia mechanism responsible for motivating actio
195 ectively) suppressed by an inhibitory fronto-basal ganglia mechanism.
196 he striatum is the main input nucleus of the basal ganglia, mediating motor and cognitive functions.
197  extremity hemiparesis, we propose a cortico-basal ganglia model capable of performing reaching tasks
198 n's disease, leading to abnormal function of basal ganglia motor circuits and the accompanying charac
199         PSD-95 was reduced in the brainstem, basal ganglia, neocortex, and cerebellum within 13 dpi,
200 utility of actions can be implemented in the basal ganglia network.
201 pected action or inhibition recruit a fronto-basal-ganglia network just like stopping.
202 pected nogo signal recruited the same fronto-basal-ganglia network which is usually assigned to stopp
203 s just like global stopping recruit a fronto-basal-ganglia network.
204 ther, these findings demonstrate that fronto-basal ganglia networks buttress action-selection under r
205  previous findings on the essential role for basal ganglia networks in absence seizures, in particula
206 ry of beta bursting, both locally and across basal ganglia networks, impacts on motor performance in
207 ry of beta bursting, both locally and across basal ganglia networks, may impact on motor performance.
208 ht compromise information coding capacity in basal ganglia networks.
209                                         Many basal ganglia neurodevelopmental disorders are thought t
210 logical methods to detail the progression of basal ganglia neuron type-specific pathology and the def
211 s issue by defining the firing properties of basal ganglia neurons around the emergence of cortical b
212       The thalamus also receives inputs from basal ganglia nuclei (BG) involved in value-based decisi
213 ally control the flow of information through basal ganglia nuclei that eventually project back to the
214        Beta dynamics therefore differ across basal ganglia nuclei.
215  We found that beta dynamics differed across basal ganglia nuclei.
216 ursts of beta frequency band activity in the basal ganglia of patients with Parkinson's disease (PD)
217        The PFB-induced increase of TH in the basal ganglia of the NGR was documented by immuno-histoc
218 vus, meninges, substantia nigra, but not the basal ganglia or choroid plexus.
219 tical injury had an AUC of 0.67 (0.60-0.73), basal ganglia or thalamic injury had an AUC of 0.81 (0.7
220 or signs improved with lesions involving the basal ganglia or thalamus.
221 osphodiesterase 10A (PDE10A) activity in the basal ganglia orchestrates the control of coordinated mo
222  sampled single-unit activity from connected basal ganglia output and thalamic nuclei (globus pallidu
223 a convergence, illuminating how synchrony of basal ganglia output during motor learning or in patholo
224 y in the ventral thalamus, a major target of basal ganglia output, is often assumed to be permitted o
225 ssion and resulted in reduced direct pathway basal ganglia output.
226 ing the impact of the subthalamic nucleus on basal ganglia output; then, at ~160 ms, suppression was
227 ow direct and indirect pathways can modulate basal ganglia outputs to facilitate movement initiation,
228 actions and directly or indirectly modulates basal ganglia outputs.
229                             Further study of basal ganglia pathophysiology is required to better unde
230                       One limitation is that basal ganglia pathophysiology is studied only at end-sta
231 plementing this complex balancing act is the basal ganglia pathway, but its roles have not yet been e
232 ex and the sensory system with an overlooked basal ganglia pathway.
233 epended upon the direct but not the indirect basal ganglia pathway.
234                 Here we investigate cortical-basal ganglia pathways underlying inhibitory control in
235 ought to be nodes in circuits extending, via basal ganglia pathways, from mood-related neocortical re
236 lation has modulatory effects on a number of basal ganglia pathways.
237                                          The basal ganglia play an important role in decision making
238 ject to the subthalamic nucleus (STN) of the basal ganglia, play a key role in inhibiting impulsive r
239 ons of primate anterior cingulate cortex and basal ganglia predict the moment of gaining information
240 TEMENT The striatum is the main input of the basal ganglia processing information from different brai
241 kdown of Sgce in the cerebellum, but not the basal ganglia, produced motor symptoms, likely due to ab
242  dynamic functional connectivity between the basal ganglia (r = - 0.53, P = 0.003) and thalamic netwo
243 m represents the main input structure of the basal ganglia, receiving massive excitatory input from t
244  RPE signals in the ventral pallidum (VP), a basal ganglia region functionally linked to reward-seeki
245                                              Basal ganglia regions may be relatively preserved in TS
246 centration using R2* relaxometry within four basal ganglia regions, including the caudate, putamen, n
247 ntum across patients, but not in cortical or basal ganglia regions.
248 ity between the medial prefrontal cortex and basal ganglia related to depression.
249  left temporoparietal region, but not in the basal ganglia, relative to typically-developing matched
250 ting locomotion by releasing dopamine in the basal ganglia, spinal networks, and the mesencephalic lo
251 phase-locked action potential firing in each basal ganglia structure was shifted during burst initiat
252     Neuronal ensemble recordings in multiple basal ganglia structures of parkinsonian rats revealed t
253 ssibly related to the smaller volume of some basal ganglia structures.
254 ntal cortex with reward prediction errors in basal ganglia support exploration of latent task represe
255 IM1 in neurotransmitter release at prominent basal ganglia synapses, and provide evidence that RIM1-d
256       The temporal evolution of cortical and basal ganglia synchronization is cell type-selective, wh
257 entify a novel intrinsic property of cortico-basal ganglia synchrony that suggests the phase of ongoi
258                     The current model of the basal ganglia system based on the 'direct', 'indirect' a
259  the beta band, restrict the capacity of the basal ganglia system to encode physiologically relevant
260 y, thus providing a novel perspective on the basal ganglia system.
261 medial temporal lobe, cerebellum, brainstem, basal ganglia, thalami, and orbitofrontal and sensorimot
262 CHD were demonstrated bilaterally within the basal ganglia, thalami, corpus callosum, occipital, temp
263 yelination and iron concentration within the basal ganglia-thalamic circuit over 2 years post-SCI.
264 tive and reorganizational changes across the basal ganglia-thalamic circuitry occur early after SCI a
265 Abnormally increased beta bursts in cortical-basal ganglia-thalamic circuits are associated with rigi
266 ly related within dopamine-modulated cortico-basal ganglia-thalamic circuits in schizophrenia.
267                  Thus, in the healthy state, basal ganglia-thalamic communication during learned move
268 and temporal aspects of large-scale cortical-basal ganglia-thalamic interactions using dynamic functi
269 hat dynamic interactions within the cortical-basal ganglia-thalamic loop might play a role in the mod
270 ple known targets of plasticity (the cortico-basal ganglia-thalamic network), suggesting that feedbac
271                                      Cortico-basal-ganglia-thalamic (CBGT) networks are critical for
272 cortico-thalamic connectivity within cortico-basal-ganglia-thalamic circuits.
273  (mPFC) is a critical component of a cortico-basal ganglia-thalamo-cortical loop regulating limbic an
274 ease (PD), gamma oscillatory activity in the basal ganglia-thalamo-cortical network is altered and th
275 d, and gamma oscillations are altered in the basal ganglia-thalamo-cortical network.
276                    We will then describe the basal ganglia-thalamocortical circuit, the major locus o
277 ich is a key component of the limbic cortico-basal ganglia-thalamocortical loop.
278 erspective of the interactive pathways among basal ganglia, thalamus and cortex, to explore the impri
279 etrical lesions found on neuroimaging in the basal ganglia, thalamus, and brainstem and by a loss of
280                                          The basal ganglia, thalamus, and cerebral cortex form an int
281  synchronization in the insular, cerebellum, basal ganglia, thalamus, operculum, frontoparietal corti
282 nificant hippocampal inhibition of amygdala, basal-ganglia, thalamus, orbital frontal cortex, inferio
283 these changes in interactive profiles of the basal ganglia-thalamus network in the current history gr
284  of both the thalamocortical network and the basal ganglia-thalamus network with resting state functi
285 cture to the classic indirect pathway of the basal ganglia that also targets the STN.
286 e, we show that a major input station of the basal ganglia, the caudate nucleus, plays a causal role
287                               In the primate basal ganglia, the caudate tail (CDt) encodes the histor
288            These include the striatum of the basal ganglia, the dorsolateral prefrontal cortex (DLPFC
289                                   Within the basal ganglia, the globus pallidus pars externa (GPe) ha
290                The main input nucleus of the basal ganglia, the striatum, receives inputs from fronta
291                                     Atypical basal ganglia tissue iron levels have been linked to imp
292 ally relevant variables, and possibly by the basal ganglia to coordinate movement.
293           Despite clear evidence linking the basal ganglia to the control of outcome insensitivity (i
294    Mild worsening was identified in post-ATI basal ganglia total choline MRS, suggesting an alteratio
295 n and gray matter as well as hippocampal and basal ganglia volumes in NMDARE children.
296 D n = 19,099, control sample n = 34,194), 2) basal ganglia volumes, and 3) fractional anisotropy in t
297  A key role in this process is played by the basal ganglia, where neural activity and plasticity are
298 (2+) currents in HVC neurons that target the basal ganglia, whereas tutor exposure increased the rest
299 s through their ascending projections to the basal ganglia, which in turn project to the mesencephali
300 ry brings together models of learning in the basal ganglia with the incentive salience theory in a si

 
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