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1 eric ligand-gated ion channels that regulate synaptic activity in the central and peripheral nervous
2 ty and optimally supports the electrical and synaptic activity of neurons in culture.
3 eveal that detection inside the RF increases synaptic activity that depolarizes membrane potential re
4 mammalian brain circuits, activity-dependent synaptic adaptations, such as synaptic scaling, stabiliz
5 ng ribbon synapses colocalized with the post-synaptic afferent terminals is likely to increase, indic
6 APK-targets like gephyrin, and modulates the synaptic AMPAR/GluR composition both in the PFC and the
7  to longitudinally monitor the expression of synaptic AMPARs across multiple cortical layers in awake
8 modified MeCP2 in Mecp2-null neurons rescues synaptic and behavioral deficits in Mecp2 conditional kn
9 he release of gliotransmitters that regulate synaptic and neuronal functions.
10                 Immunogold staining revealed synaptic and perisynaptic GluD1 labeling at putative axo
11    These experiments are the first to record synaptic and spiking activity during sharp wave ripple (
12 cing miRNAs and analyzing their functions in synaptic and total tissue fractions obtained from dorsol
13                      Here, using focal trans-synaptic anterograde tracing, we show that the motor-act
14 on of C1ql3 in the dorsolateral AON impaired synaptic AON->OB connections and abolished acquisition,
15       These results illustrate a circuit and synaptic basis of aggression modulation by experience, w
16 ty in the awake, intact brain, we imaged the synaptic boutons of retinal axons in the superior collic
17                                          The synaptic calcium dysregulation is due to a loss of dendr
18                                        Local synaptic calcium transients decreased, leaving a GluR2 l
19 echanistic link between reduced transport of synaptic cargos and impaired maintenance of synaptic tra
20 ATEMENT Existing studies focus on excitatory synaptic changes after social stress, although little is
21 content imaging method for the assessment of synaptic changes and apply the method to brain homogenat
22 uals, but little is known about the relevant synaptic changes associated with social transmission and
23 ion tremor, our results thus characterized a synaptic circuit mechanism that may underlie the prevale
24 circular canal epithelia, the [K(+) ] in the synaptic cleft ([K(+) ](c) ) contributes to setting the
25 system, ions accumulate in diffusion-limited synaptic clefts during ongoing activity.
26 strocytes are active and integral players in synaptic communication, and that neuron-astrocyte intera
27 on-productively bound complexes and inactive synaptic complexes formed by Int.
28 mation of the AMPA-receptor-mediated maximal synaptic conductance based on numbers of GluR1s and GluR
29               Dendrogram analyses of all the synaptic connections between DAN-i1 and its two main tar
30                          Precise patterns of synaptic connections between neurons are encoded in thei
31 machinery immunostaining can define putative synaptic connections between neurons, as well as map put
32 ermis functions could be mediated by modular synaptic connections of distinct fastigial cell types wi
33                   A comprehensive mapping of synaptic connections reveals three recurrent circuit mod
34  homeostasis through continued refinement of synaptic connections.
35 versing the delayed enhancing effects on BLA synaptic connectivity and anxiety-like behavior.
36 duced increase of neuronal activity restores synaptic connectivity and function in the sensory-motor
37 sted circuit mapping revealed functional, di-synaptic connectivity between SCN(VIP) neurons and dorso
38 ngly, deletion of LAR-RPTPs had no effect on synaptic connectivity in cultured neurons or in vivo, bu
39                                 Sex-specific synaptic connectivity is beginning to emerge as a remark
40 ng, but display highly labile dynamics, when synaptic connectivity is continuously modified due to no
41                           This disruption of synaptic connectivity is linked to working memory impair
42                    These findings identify a synaptic connectivity mechanism of cones and illustrate
43 has facilitated the generation of a complete synaptic connectome.
44 ns in the VTA and were largely biased toward synaptic contact with local GABA neurons.
45 the symmetry and stability of the T cell-APC synaptic contact.
46 Nlgns) are adhesion proteins mediating trans-synaptic contacts in neurons.
47  T-stellate cells, and made local inhibitory synaptic contacts on principal cells of the VCN.
48  parallel to the dendrites and make multiple synaptic contacts support such coordination since incomi
49 e spillover and NMDA-receptor-mediated inter-synaptic cross-talk.
50 and influences the electrical integration of synaptic currents.
51 r understanding of the mechanisms regulating synaptic d-serine availability remains limited.
52 he mechanisms regulating the availability of synaptic d-serine remains limited.
53       An overall trend was found for greater synaptic DA availability (DeltaBP(ND)) in CHR than contr
54 ether the penetrating property attributes to synaptic damage in vivo, we have generated adeno-associa
55  tau mislocalization to dendritic spines and synaptic deficits in cultured rat hippocampal neurons.
56 e respectively, in contrast to the increased synaptic density and decreased firing rate observed in g
57 ifidobacterium-treated mice exhibited normal synaptic density and neuronal activity as measured by de
58 dded autistic-like behaviors with diminished synaptic density and reduction of autism-related PSD-95
59 ion of alpha2delta3 increases the excitatory synaptic density as well but also facilitates spontaneou
60 suggests that PV(+) cell-mediated short-term synaptic depression influences the experimentally report
61                   GluA3 slows and attenuates synaptic depression, and makes it less dependent on the
62 vation by NAP suggests that ADNP may mediate synaptic development partly by activating EphB2.
63               EphB2 plays a critical role in synaptic development; its potent activation by NAP sugge
64 er, conflicting results around their role in synaptic differentiation arise from the various techniqu
65 ynapses in the lumbar spinal cord, detailing synaptic diversity that is dependent on developmental st
66 opamine transporter (DAT) availabilities, or synaptic dopamine levels in 983 patients and 968 control
67 veal that a selective decrease in excitatory synaptic drive to PV basket cells (PVBCs) likely underli
68 set point, caused a compensatory decrease in synaptic drive to the muscle affording robust and stable
69                                        These synaptic dynamics are timed by Rac1, with decreased and
70 ese synapses.SIGNIFICANCE STATEMENT Although synaptic dynamics have been extensively studied and mode
71 nsmission, together with BIN1, to ameliorate synaptic dysfunction and disease progression.
72 lyzed tau cleavage at aspartate 314 mediates synaptic dysfunction and memory impairment in mouse and
73 ell as tau hyperphosphorylation, and improve synaptic dysfunction in 3xTg mouse brain.
74 tion is pathogenic for NLGN4 and can lead to synaptic dysfunction in autism.
75                                              Synaptic dysfunction plays a central role in Alzheimer's
76  Abeta and tau pathology, neurodegeneration, synaptic dysfunction, and inflammation, highlight the ne
77 tsynaptic currents and potentials, inferring synaptic effects from extracellular spiking is challengi
78                 Given their robust impact on synaptic efficacy and neuronal signalling, neuronal rest
79 for in vivo neuronal sensing requires a post-synaptic electrode and its reference electrode and the t
80  that is involved in promoting the transient synaptic enlargement in D1-MSNs induced during reinstate
81  relapse, which is correlated with transient synaptic enlargement in the accumbens core.
82 with stress exposure, our findings suggest a synaptic entry point of the BDNF/TrkB system for adaptat
83 d pre-active" state that contributes to fast synaptic events and a "constrained pre-active" state tha
84 gate the astrocytic activity-driven neuronal synaptic events and behavioral consequences, we chemogen
85                            A balance between synaptic excitation and inhibition (E/I balance) maintai
86 e well-documented sleep-dependent changes in synaptic excitation.
87 lso cooperate to decrease and potentiate the synaptic excitatory and inhibitory tone onto mutant SF1
88        Other work has argued that short-term synaptic facilitation can serve as a substrate of memory
89 ctive role for K(v)1 channel inactivation in synaptic facilitation of excitatory hippocampal neurons.
90 ng high-frequency stimulation and eliminated synaptic facilitation without altering the initial proba
91 uronal structures subject to spatio-temporal synaptic fluctuations.
92                  The dentate gyrus expressed synaptic function and neurogenesis genes correlated with
93 se model of depression, at both the level of synaptic function and protein expression.
94 ates that the effects of ELS exposure on BLA synaptic function are sexually dimorphic and possibly re
95                    Alterations of excitatory synaptic function are the strongest correlate to the pat
96 trix directs synapse formation and regulates synaptic function in a model of human cortical brain dev
97  (D(2)R-GSK-3beta(-/-)) in the brain affects synaptic function in the medial PFC (mPFC).
98 ment, glutamatergic/cholinergic/dopaminergic synaptic function, calcium and PI3K-AKT signaling.
99 ttle is known about how AD risk genes impact synaptic function.
100 l pathways related to neural development and synaptic function.
101  groups to proteins important for axonal and synaptic function.
102 association study identified the interneuron synaptic gene ELFN1 as conferring significant genetic li
103 adenosine, which plays a role in fine-tuning synaptic glutamate transmission.
104 tle handling) suggest that sleep can promote synaptic growth and strengthening.
105 e terminally arrested, we have characterized synaptic growth, structure and function at the neuromusc
106 nit, enhancing ATP production efficiency and synaptic growth.
107 s critical for both cortical development and synaptic homeostasis.
108  channel inhibition, triggered intrinsic and synaptic homeostatic plasticity at different timescales
109 her this recovery simply reflects changes in synaptic immunostaining, or whether there is actual retr
110 ntial rescue of amyloid-beta (Abeta) induced synaptic impairment.
111 ition, we described the differences in their synaptic influence.
112 arval zebrafish that directly illustrate how synaptic inhibition and excitation are integrated by cer
113 otivated by these ideas, we examined whether synaptic inhibition changes over the 24-h day to compens
114                                        While synaptic inhibition is important for synchronization acr
115  chloride dynamics on dendritically targeted synaptic inhibition.
116 synapses, thereby regulating the strength of synaptic inhibition.
117 ygenase isoforms in modulating recovery from synaptic injury in SIV infection and suggest their thera
118                              Thus, acute SIV synaptic injury occurs throughout the brain, with sponta
119 sary to examine in detail the morphology and synaptic innervation pattern of the GIN cells, in order
120 s of abstinence, and then recorded GABAergic synaptic input evoked either electrically or optogenetic
121                                 In CA1, both synaptic input to single neurons and population activity
122           Both reduction of GABA release and synaptic inputs onto pyramidal cells erode the emergence
123 receive inhibitory GABAergic and glycinergic synaptic inputs.
124 opographically ordered retinal ganglion cell synaptic inputs.
125                              Corticostriatal synaptic integration is partitioned among striosome (pat
126 psilon4 show greater apoptosis and decreased synaptic integrity.
127 c shape, and intrastriatal and extrastriatal synaptic interactions of these neurons are quite well de
128 ynaptic active zones is controlled via trans-synaptic interactions remains unknown.
129 g trace metals together with proteins at the synaptic level.
130                         Our study proposes a synaptic-level mechanism of how memory consolidation is
131 e (g = 0.66, p = .03) capacities, as well as synaptic levels (g = 0.78, p = .0006), were greater in p
132 tween PKA and Ube3a in the regulation of SK2 synaptic levels might provide new platforms for developi
133 The discovery of keratinocyte-sensory neuron synaptic-like contacts may call for a reassessment of ba
134 features and molecular hallmarks of chemical synaptic-like contacts: narrow intercellular cleft, kera
135                             We conclude that synaptic loss is significant in chronic MS, likely contr
136  neurodegenerative disease, characterized by synaptic loss, motor neuron death, and reduced neuronal
137 how that correlative Brainbow and endogenous synaptic machinery immunostaining can define putative sy
138 es and spatial distribution of pre- and post-synaptic markers on cochlear inner hair cells, in guinea
139 s in protein synthesis that trigger impaired synaptic maturation and autistic behaviors.
140  NMDA-receptor-mediated responses by a trans-synaptic mechanism.
141 ects in a complex tissue environment and the synaptic mitochondrial changes that accompany its loss.
142 s of single stimuli are unable to induce any synaptic modification in 1.3 and 1.5 mM calcium and lead
143 ulation induces changes in the expression of synaptic molecules throughout the visual pathway and in
144 henotype that paralleled with alterations of synaptic morphology, transmission, and plasticity.
145                        Furthermore, the post-synaptic muscle fibers displayed increased distinct clus
146 allenging to illuminate the features of this synaptic network due to the small size and dense packing
147  pup vocalizations and discover a functional synaptic network embedded through acoustically selective
148 nize into localized and spontaneously active synaptic networks.
149 e bioenergetics, leading to abnormalities in synaptic neurotransmission and cognitive function in a r
150 ritical for the localization and activity of synaptic neurotransmitter receptors and ion channels.
151 roviding a feedforward mechanism to increase synaptic NMDAR activation.
152 at neuronal NAMPT is important for pre-/post-synaptic NMJ function, and maintaining skeletal muscular
153 rs (ASD) can be classified broadly as either synaptic or developmental.
154 yriad tissues including neurite guidance and synaptic organisation within the nervous system.
155  of subcortical and cortical inputs, but its synaptic organization in humans is still unknown due to
156 B/SEM) can be applied to study in detail the synaptic organization of the human brain obtained from a
157  profoundly alter the timing and strength of synaptic output.
158 oup of molecules, are potent determinants of synaptic partner choice and therefore ultimately control
159  of neurons constrains the pool of available synaptic partners and influences the electrical integrat
160 system, RGC interactions extend beyond their synaptic partners such that they guide development befor
161                                         Such synaptic patterns usually involve some partners receivin
162           This daily variation in microglial synaptic phagocytosis was abrogated by global REV-ERBalp
163 deletion, which caused persistently elevated synaptic phagocytosis.
164  the first evidence that Dscam2 can regulate synaptic physiology and highlights how diverse roles of
165  (2) cellular adaptations and (3) excitatory synaptic physiology in the basolateral amygdala (BLA) in
166 tal determinant of their coactivation and of synaptic physiology.
167 s that incorporated the signature short-term synaptic plasticity (STP) profiles of the inhibitory par
168  can be 'silently' maintained via short-term synaptic plasticity (STSP) without the need for persiste
169 ers are characterized by impaired functional synaptic plasticity and abnormal dendritic spine morphol
170 mental role of the endocannabinoid system in synaptic plasticity and emotional memory processing.
171 aired with tactile rehabilitation to enhance synaptic plasticity and facilitate recovery of sensory f
172 lar pathway is triggered by the induction of synaptic plasticity and in response to object location l
173 tle is known about stress-induced inhibitory synaptic plasticity and its relevance for neuropsychiatr
174 m channel, SK2, contributes to impairment of synaptic plasticity and learning in AS mice.
175 tion of activity-dependent genes, as well as synaptic plasticity and memory formation.
176 pression of proteins essential for long-term synaptic plasticity and memory.
177 pheric asymmetry, we investigated changes in synaptic plasticity and neuronal excitability of BLA neu
178 ncreased synaptic transmission and long-term synaptic plasticity at the Cornu Ammonis (CA) 3-CA1 syna
179 tation/inhibition (E/I) balance and aberrant synaptic plasticity at the cortical level.
180                    Motor learning depends on synaptic plasticity between corticostriatal projections
181 mice exhibited normal cognitive function and synaptic plasticity but had increased dendritic spine de
182 are involved in neuronal differentiation and synaptic plasticity but the molecular mechanisms behind
183  increased receptor membrane trafficking and synaptic plasticity during memory reconsolidation.
184 persistent activity, excitatory feedback, or synaptic plasticity for storage.
185 nce of isoform-specific functions of GSK3 in synaptic plasticity has not been fully explored.
186 functional signaling protein that suppresses synaptic plasticity in dendritic spines of hippocampal n
187 amate receptors (NMDARs) plays a key role in synaptic plasticity in the central nervous system (CNS).
188        The discovery of impaired hippocampal synaptic plasticity in the heterozygous mouse model shed
189 H) mice) display motor deficits and impaired synaptic plasticity in the striatum.
190 evealed that 3 mo of OLT1177 diet can rescue synaptic plasticity in this mouse model of AD (P = 0.007
191 nucleus accumbens, opioid-induced excitatory synaptic plasticity involves presynaptic and postsynapti
192  We hypothesized that the cell type-specific synaptic plasticity is associated with parallel cell-spe
193 dent plasticity, it is still unclear whether synaptic plasticity rules inferred from in vitro experim
194 ts of Abetaos on glutamatergic transmission, synaptic plasticity, and dendritic spine structure.
195 for the APP family in neuronal excitability, synaptic plasticity, and memory in adulthood, despite th
196                 MARCKS supports development, synaptic plasticity, and regeneration after injury.
197                         However, hippocampal synaptic plasticity, learning, and memory are impaired i
198                Because of its involvement in synaptic plasticity, SynGAP has emerged as a critical pr
199 lactate supply alone rescued stress-impaired synaptic plasticity, which was blocked by inhibiting neu
200 t the outcome of activity-dependent forms of synaptic plasticity, yet activity-independent processes
201 nges in synaptic transmission that influence synaptic plasticity.
202 tions for various MAPs in activity-dependent synaptic plasticity.
203 receptor trafficking, which is essential for synaptic plasticity.
204 akening and dendritic spine shrinkage during synaptic plasticity.
205 can have profoundly negative consequences on synaptic plasticity.
206 naptically located receptors that can impair synaptic plasticity.
207 e, innate immunity, synapse development, and synaptic plasticity.
208 th previously been implicated in hippocampal synaptic plasticity.
209 stigation of more powerful directed types of synaptic plasticity.
210 elty suppressed feeding tests, and increased synaptic plasticity.
211 fects in mice of either sex on cognition and synaptic plasticity.
212 as required for contextual fear learning and synaptic potentiation in the vCA1-BA pathway.
213                                              Synaptic potentiation of the MeApv-VmH and MeApv-BNST pa
214 ve emotional behavior, and a deficit in BNST synaptic potentiation.
215  translation initiation factors that dampens synaptic protein translation.
216 eviated excessive fragmentation of important synaptic proteins.
217 n [dpi]) and quantified viral (SIV gag RNA), synaptic (PSD-95; synaptophysin), axonal (neurofilament/
218 eas, in guinea pigs, counts of immunostained synaptic puncta can recover with increasing post-exposur
219                                          The synaptic Ras homologous (Rho) guanine nucleotide exchang
220 ter a synaptopathic exposure, shows dramatic synaptic re-organization during the recovery period in w
221  social memory formation, through regulating synaptic receptor trafficking in pyramidal neurons by So
222 nvestigated due to postmortem degradation of synaptic receptors.
223 eficiency on microglia and on climbing fiber synaptic refinement during cerebellar postnatal developm
224 hfully transfer action potentials to distant synaptic regions but also to maintain their timing.
225 ediate the dopamine- and amphetamine-induced synaptic regulation, revealing a novel cellular pathway
226 e olfactory bulb (OB) glomeruli, where their synaptic release is subject to local and cortical influe
227 nsequence of inefficient clearance following synaptic release.
228                                Developmental synaptic remodeling is important for the formation of pr
229 by reducing the peak amplitude of subsequent synaptic response.
230 havioral stimulation likewise elicited focal synaptic responses within grafts.
231 roduce short-term plasticity and variance of synaptic responses.
232 vity-dependent synaptic adaptations, such as synaptic scaling, stabilize neuronal activity in the fac
233                                      NK cell synaptic secretion, triggered by ligation of NKp30 or NK
234                            This blueprint of synaptic sharing provides an efficient way of controllin
235 nce electrode and the tissue becomes the pre-synaptic signal.
236 This module contained many genes involved in synaptic signaling and neuroplasticity.
237 r signaling in addition to conventional fast synaptic signaling, and that spillover transmission medi
238 differentiation, protein phosphorylation and synaptic signaling.
239 t might be involved in the time averaging of synaptic signals, which can then lead to the high precis
240 rons with no history of activity whatsoever, synaptic sizes are no less diverse.
241                            The efferent post-synaptic SK2 channels appear prior to the establishment
242 ransmitter receptors orchestrates functional synaptic specification in a neural circuit.
243 and spatial topologies, thereby rivaling the synaptic specificity of chemical synapses.
244 genous activation of CB1Rs modifies afferent synaptic strength and coordinated downstream network sig
245            Overall, LRRK2 mutations reshaped synaptic structure and function, an effect exaggerated i
246 iatric disorders, including those related to synaptic structure and function.
247                In turn, photoreceptor ribbon synaptic structure depends on the cytoskeleton arrangeme
248 rotein shown to regulate the trafficking and synaptic targeting of AMPARs, is required for LTP and le
249 These findings indicate that there are lower synaptic terminal protein levels in schizophrenia in viv
250  reflected in VIP(+)/ChAT(+) interneuron pre-synaptic terminals, as quantitative molecular analysis s
251 ets in a preferential manner and with larger synaptic terminals, providing a putative explanation for
252 nding for the rapidly growing field of local synaptic translation.
253 hat exogenous Amh protein addition increased synaptic transmission and long-term synaptic plasticity
254      At low (nanomolar) levels, it modulates synaptic transmission and neuronal activity, but at much
255 y but also connect homeostatic regulation of synaptic transmission and neuronal excitability.
256        However, these changes did not impair synaptic transmission and plasticity and synaptic vesicl
257  of PFC DA homeostasis, leading to defective synaptic transmission and plasticity as well as impaired
258 SD symptoms, and a novel locus implicated in synaptic transmission and plasticity may serve as a poss
259  synaptic cargos and impaired maintenance of synaptic transmission and plasticity, contributing to au
260 receptor trafficking, ultimately controlling synaptic transmission and plasticity.
261 d 11] results in long-lasting alterations in synaptic transmission and reduced PV expression in the a
262 mportant roles of GluA3 in the maturation of synaptic transmission and short-term plasticity in endbu
263                    Many proteins involved in synaptic transmission are well known, and their features
264  GPCR that binds C1ql3, similarly suppressed synaptic transmission at AON->OB projections and abolish
265 el cellular mechanism that supports reliable synaptic transmission at high frequency in the CNS.
266 n induced by traumatic stress, and weakening synaptic transmission at these synapses blocks the effec
267 ctively boosts excitatory synaptogenesis and synaptic transmission by a novel mechanism that is indep
268  in the developing eye causes roughening and synaptic transmission defect, common findings in neurode
269 eptors, negatively modulates corticostriatal synaptic transmission from the first postnatal week onwa
270 s and the endocannabinoid (eCB) system tunes synaptic transmission in brain regions regulating emotio
271 , and may provide a general means to enhance synaptic transmission in normal and disease states.
272 ed ion channels that mediate fast excitatory synaptic transmission in the nervous system.
273 uce a long-lasting suppression of inhibitory synaptic transmission onto OFC pyramidal neurons in a re
274 red mutations in SNAP25 give rise to related synaptic transmission phenotypes, specific alterations i
275 cularly enriched in synapses but its role in synaptic transmission remains poorly understood.
276                               Within the CNS synaptic transmission set, we identify individual signif
277 e machinery, causing long-lasting changes in synaptic transmission that influence synaptic plasticity
278  function, the regulatory effects of MORs on synaptic transmission were recapitulated in two sets of
279 age induces long-term deficits in inhibitory synaptic transmission within the spinal superficial dors
280             Therefore, during high-frequency synaptic transmission, when large amounts of glutamate a
281 uces a long-lasting suppression of GABAergic synaptic transmission, which depends on subregional diff
282 oid tone mimics GEE effects on cognition and synaptic transmission.
283 quantal release by exocytosis that underlies synaptic transmission.
284 ognized as regulatory elements of excitatory synaptic transmission.
285  the synaptic vesicle cycle to ensure normal synaptic transmission.
286 logical role of cholesterol in glutamatergic synaptic transmission.
287                                              Synaptic vesicle (SV) endocytosis is coupled to exocytos
288 roton and chloride concentrations during the synaptic vesicle cycle to ensure normal synaptic transmi
289 WT mice, while nCLCa-only mice had increased synaptic vesicle numbers, restoring normal neurotransmis
290           Mice with only nCLCb had a reduced synaptic vesicle pool and impaired neurotransmission com
291 esin-3 KIF1A known for its fast shuffling of synaptic vesicle protein transport vesicles in axons.
292     However, how neuronal activity regulates synaptic vesicle recycling is largely unknown.
293 air synaptic transmission and plasticity and synaptic vesicle release kinetics.
294                                              Synaptic vesicles accumulate neurotransmitters, enabling
295 ts: narrow intercellular cleft, keratinocyte synaptic vesicles expressing synaptophysin and synaptota
296  influences cerebral bioenergetics, enhances synaptic viability and dendritic spine formation, and in
297 w safer and more effective anterograde trans-synaptic viral vectors for neural circuit analysis in mu
298 e NMDAR, independent of ion flow, in driving synaptic weakening and dendritic spine shrinkage during
299                 Here, we show, however, that synaptic weight changes caused by spike timing dependent
300 l networks in hardware by implementing their synaptic weights using memristive devices.

 
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