ライフサイエンスコーパス: collateral

1 Is and lateral inhibition from recurrent MSN collaterals.

2 on neighboring striatal neurons through axon collaterals.

3 irectly inhibit granule cells via their axon collaterals.

4 circulation, angiogenesis, and portosystemic collaterals.

5 stead promote the extension of specific axon collaterals.

6 r also sending extensive extra-striatal axon collaterals.

7 from that of STN neurons without local axon collaterals.

8 a contribution of climbing fibers and their collaterals.

9 s required unifocalization of aortopulmonary collaterals (17%).

10 This study investigates the collateral activity of glycosidases in commercial pectin

11 ptic inputs from entorhinal but not Schaffer-collateral afferents.

12 nds on the coincident activation of Schaffer collateral and temporoammonic inputs at the distal apica

13 es requires integration of both the Schaffer collateral and temporoammonic pathways.

14 rong association between the presence of ASL collaterals and a 1-point decrease in the mRS score at d

15 ly impairs synaptic potentiation of Schaffer collaterals and commissural inputs to the CA1 area of th

16 This novel association between ASL collaterals and improved neurologic outcome may help gui

17 ar to that of STN neurons without local axon collaterals and more generally to that of classically de

18 ons with consequent activation of inhibitory collaterals and reduction in background striatal firing

19 urprisingly little is known about their axon collaterals and their target neurons within the cerebell

20 lting from action potential bursts in single collaterals and variable times to spike threshold in con

21 ed by high-frequency stimulation of Schaffer collaterals, and that CN2097 attenuates this LTP impairm

22 e most commonly used methods for identifying collaterals are contrast-based angiographic imaging tech

23 Collaterals are restricted to the parasagittal plane, an

24 Distal CA3 (near CA2), where the recurrent collaterals are the strongest, maintained coherent repre

25 associated with an increase in the number of collateral arteries (1.5+/-0.7; 95% CI, 0.1-2.9; P=0.047

26 ytes into the perivascular space surrounding collateral arteries and their differentiation into macro

27 tetralogy of Fallot and major aortopulmonary collateral arteries at Lucile Packard Children's Hospita

28 etralogy of Fallot with major aortopulmonary collateral arteries is a complex and heterogeneous condi

29 hway is required for the formation of native collateral arteries that can restore circulation followi

30 increasing fluid shear stress in preexisting collateral arteries.

31 was specifically up-regulated in remodeling collateral arteries.

32 tetralogy of Fallot and major aortopulmonary collateral arteries.

33 ertain subgroups vascular imaging, including collateral assessment, can play a crucial role in determ

34 These expanded collateral axon branches resemble the extensive collater

35 ptors, acting specifically on intra-striatal collateral axons of striatopallidal neurons.

36 isual processing because elimination of axon collateral-bearing ipRGCs impairs light adaptation by li

37 r conditions were detected at a high rate, a collateral benefit of DR screening programs that may be

38 f an effective FDA-approved therapy, and the collateral benefits have included elucidation of the piv

39 ic stroke transferred for thrombectomy, poor collateral blood flow and stroke clinical severity are t

40 The adequacy of leptomeningeal collateral blood flow was rated as no or poor, decreased

41 tus were associated with ASPECTS decay, with collateral blood vessel status demonstrating the highest

42 ore, lower baseline ASPECTSs, and no or poor collateral blood vessel status were associated with ASPE

43 Robust collateral blood vessels have been associated with bette

44 crotubule-associated protein 7 (MAP7) during collateral branch development of dorsal root ganglion (D

45 In search of intrinsic factors that control collateral branch development, we identified a role for

46 phenotype that is consistent with increased collateral branch formation.

47 show that MAP7 is expressed at the onset of collateral branch formation.

48 duces axonal filopodia dynamics and disturbs collateral branch formation.

49 Like axon growth and guidance, formation of collateral branches depends on the regulation of microtu

50 Collateral branches from axons are key components of fun

51 esent either a novel retinotectal pathway or collateral branches from centrifugal neurons projecting

52 Finally, the collateral branches of the LOT were increased in LOTUS-K

53 ch regulation and the potential influence of collateral branches on pain sensitivity.

54 After axonal bundle formation, collateral branches sprout from primary axons of the LOT

55 mata in the interposed nucleus, and putative collateral branches terminating as mossy fibers in the c

56 Next, we found that the axonal collateral branches were increased in cultured OB neuron

57 ion resulted in increased corticospinal axon collateral branches with presynaptic puncta in the spina

58 ured OB neurons reduced the number of axonal collateral branches, suggesting that endogenous Nogo-A i

59 he cerebellar granule layer, consistent with collateral branching.

60 minals in the nucleus accumbens or local VTA collaterals; but reveal both excitatory and monosynaptic

61 , ASL images were graded for the presence of collaterals by 2 neuroradiologists.

62 long-term potentiation (LTP) at the Schaffer collateral CA1 synapse require stimulation of both betaA

63 lectrophysiological analysis of the Schaffer collateral-CA1 synapse in dorsal hippocampus, we find th

64 TP) of synaptic transmission at the Schaffer collateral-CA1 synapse in the hippocampus is substantial

65 receptors to synaptic plasticity at Schaffer collateral-CA1 synapses in acute slices of adult mice.

66 ces LTD of synaptic transmission at Schaffer collateral-CA1 synapses.

67 ng-term potentiation at hippocampal Schaffer collateral-CA1 synapses.

68 ular network, including the later-developing collateral cardinal, spinal, superficial lateral and sup

69 vein grafts (19% of post-CABG cases) versus collateral channels (36%) versus with an antegrade-only

70 No association between patent collateral circulation and favorable outcome was found.

71 underlines the importance of being aware of collateral circulation in patients with chronic aortoili

72 ng cardiomyocytes, suggesting that increased collateral circulation may provide an important source o

73 ts with BAO and to evaluate the influence of collateral circulation on outcome.

74 A well-developed coronary collateral circulation provides a potential source of bl

75 enous imaging-based biomarkers with grade of collateral circulation, the ischaemic penumbra and clini

76 to unravel the pathways leading to improved collateral circulation.

77 Long-term potentiation (LTP) at the Schaffer collateral-commissural synapses in the CA1 area of appro

78 ced long-term potentiation (LTP) of Schaffer collateral/commisural-CA1 pathway, phospho-alphaCaMKII (

79 c total coronary occlusion (CTO) and a large collateral contribution might alter the fractional flow

80 on of long-term potentiation at the Schaffer collateral/cornu ammonis 1 synapse in the dorsal hippoca

81 fidence interval [CI] -0.6 to 2.5; P=0.238), collateral count (0.9+/-0.6 arteries; 95% CI, -0.2 to 2.

82 line to 6 months in peak walking time (PWT), collateral count, peak hyperemic popliteal flow, and cap

83 of off-target cleavage events and potential collateral damage are still lacking.

84 mpaction, aggregates blood cells, and causes collateral damage due to leukocyte activation.

85 hus the host can benefit from suppression of collateral damage during parasite infection and from red

86 rance of pathogenic organisms while limiting collateral damage from the host inflammatory response, k

87 lation resulted in decreased cellularity and collateral damage in the tissue during viral infection.

88 in the protection of cells and tissues from collateral damage induced by inflammatory responses.

89 The collateral damage induced on healthy tissues during radi

90 exerts on an individual's own health via the collateral damage of the drug on bacteria that normally

91 fects harmful to hermaphrodites appear to be collateral damage rather than the goal.

92 t unfolding activity is prevented from doing collateral damage to cellular proteins are not well unde

93 . cancer cells or parasites) without causing collateral damage to healthy or to host cells is complic

94 e efficiency of targeted killing and prevent collateral damage to neighboring healthy cells.

95 nciple, yet it is accompanied by significant collateral damage to normal tissue and unwanted side eff

96 ced peripheral neuropathy (CIPN) arises from collateral damage to peripheral afferent sensory neurons

97 ness of the A1 pulley release and detect any collateral damage to the A2 pulley, interdigital nerves,

98 Causing collateral damage to the B-cell genome during CSR and SH

99 o tune the immune response, thereby limiting collateral damage to the host and the risk for sepsis.

100 , to prevent excessive inflammation to limit collateral damage to the host.

101 d downregulates Th1 responses that may cause collateral damage to the host.

102 ective antimicrobial protection with minimal collateral damage to the host.

103 lance of initiating immunity without causing collateral damage to the lungs because of an exaggerated

104 s and can treat microvessels without causing collateral damage to the surrounding tissue.

105 Collateral damage to the vagal nerve and the upper gastr

106 this beneficial activity comes at a cost of collateral damage when the immune system overreacts to i

107 am to prevent excessive inflammation, repair collateral damage, and restore tissue homeostasis, and f

108 endent apoptosis of individual cells without collateral damage.

109 f lymphocytes, while minimizing the risk for collateral damage.

110 a thermally confined manner without causing collateral damage.

111 that downregulate hyperinflammation to avoid collateral damage.

112 he efficacy of cancer therapy while limiting collateral damage.

113 y of cognitive tests and provided a range of collateral data.

114 7 approximately 92 results in an increase in collateral density limbs and hearts and in ischemic limb

115 ojection to the TeO, cells in FRLx send, via collaterals, descending projections through tectopontine

116 these cells can be regulated to mitigate the collateral destruction associated with macrophage activa

117 a the climbing fibre projection, which sends collaterals directly to large premotor neurons of the mo

118 e first population-based survey data to show collateral disruptions to facility-based delivery caused

119 ese results suggest that newly sprouted axon collaterals do not preferentially innervate functionally

120 odest increase in the FFR of the predominant collateral donor vessel associated with a reduction in c

121 We combine the collateral effect of Cas13a with isothermal amplificatio

122 gets on homologous chromosomes, an undesired collateral effect that has not been described previously

123 as13a (previously known as C2c2) exhibits a "collateral effect" of promiscuous ribonuclease activity

124 ongly suggest that NETs mediate the negative collateral effects of tumors on distal organs, acting to

125 ogram focused on 1 dietary change results in collateral effects on other untargeted healthy diet comp

126 ate streams, but few studies have considered collateral effects on species composition or ecosystem f

127 MSX1 induction in collateral endothelial cells (ECs) was shear stress driv

128 UV protection, using chemicals that lead to collateral environmental consequences.

129 Activating climbing fibre collaterals evoked well-timed increases in firing probab

130 nd in vitro data suggest that climbing fibre collateral excitation is weak in adult mice, raising the

131 ary end point was the change of the coronary collateral flow index (CFI) after 4 weeks.

132 The primary study end point was coronary collateral flow index as obtained during a 1-minute prox

133 Collateral flow index in the untreated RCA and left coro

134 Collateral flow index is the ratio between simultaneousl

135 iferation of collateral vessels and promoted collateral flow restoration in a model of rat hind limb

136 ratios (RR) were pooled for good versus poor collaterals for outcomes based on a random-effects model

137 e OB developmentally increased during axonal collateral formation.

138 onal growth and in ipsilateral intracortical-collateral formation.

139 ments enable the spatial specificity of axon collateral formation.

140 at thalamocortical input to layer 1 includes collaterals from axons innervating layers 3b/4 and is la

141 of synaptic transmission was larger at axon collaterals from iMSNs than their projections to the ven

142 hich each CbN neuron receives input from 4-7 collaterals from inferior olivary neurons as well as fro

143 ellar nuclear afferent comprised of feedback collaterals from premotor rubrospinal neurons can direct

144 degenerative lesions induce sprouting of new collaterals from surviving axons, but the extent to whic

145 al mammary artery device closure on coronary collateral function and myocardial ischemia.

146 Several layers of regulation prevent collateral genomic DNA damage by restricting RAG activit

147 different arterial occlusions and different collateral grading methods.

148 adiology/Society of Interventional Radiology collateral grading system) were assessed by a blinded co

149 he association between exercise training and collateral growth still unclear.

150 ss efficiently than in wt hearts, similar to collateral growth.

151 is, induced neither pericyte recruitment nor collateral growth.

152 activity as modelled in NE(-/-) mice prevent collateral host tissue damage.

153 lateral axon branches resemble the extensive collaterals in CA3 of the mammalian hippocampus but prob

154 Here, we find that all PCs have collaterals in young, juvenile, and adult mice.

155 .38 to 0.63; p<0.001), as compared with poor collaterals, in patients with acute ischaemic stroke und

156 ferentially expressed miRNAs in FSS-stressed collaterals including miRNA-352 which was down-regulated

157 Overall, good pretreatment collaterals increased the rate of favourable functional

158 n of inflammation revealed enhanced Schaffer collateral-induced excitatory field potentials in CA1 st

159 Therefore, collateral inhibition of oncogenic signaling and mitocho

160 ds on creation of transmural lesions without collateral injury to contiguous structures.

161 CWs under mild cavitation conditions without collateral injury.

162 Here we show that newly sprouted CF collaterals innervate multiple Purkinje cells (PCs) over

163 Nonetheless, the spatial gradient of collateral innervation might help to loosely maintain fu

164 s modulate synaptic function at the Schaffer collateral input to CA1 pyramidal cells, thereby lowerin

165 We therefore examined climbing fibre collateral input to large premotor CbN cells over develo

166 more, a single SCN-projecting ipRGC can send collateral inputs to many other brain regions.

167 ortance and functional relevance of coronary collaterals is controversial with the association betwee

168 ervation of cerebellum by rubrospinal neuron collaterals is remarkably selective for the IN compared

169 Following AIS, the presence of ASL collaterals is strongly associated with better neurologi

170 Synthetic lethality and collateral lethality are two well-validated conceptual s

171 perspective, we review the novel concept of "collateral lethality", which has served to identify canc

172 impaired NADPH production, provides a prime 'collateral lethality' therapeutic strategy for the treat

173 f neighbouring housekeeping genes can confer collateral lethality, we sought to determine whether los

174 For the evaluation of ulnar collateral ligament (UCL) tears with stress US, the inte

175 eover, TRPV1 knockouts have reduced Schaffer collateral LTP, which is rescued by activating OLM neuro

176 ee lines of evidence showing that these axon collaterals make connections with upstream dopaminergic

177 orescence microscopy reveals that ipRGC axon collaterals make putative presynaptic contact with DACs.

178 ic treatments are associated with widespread collateral microbiome impact by enrichment of AR genes t

179 ivariable analysis, the presence of suitable collaterals, no smoking, no previous coronary artery byp

180 opagation of action potentials into the fine collaterals of axons and dendrites in two of the largest

181 ei to the cerebellar cortex in mice includes collaterals of cerebellar premotor output neurons, mappe

182 Moreover, optogenetic stimulation of axon collaterals of double-projecting vCA1 neurons induced mo

183 tomical and physiological evidence that axon collaterals of ipRGCs constitute a centrifugal pathway t

184 be modulated by suggested intraocular axonal collaterals of ipRGCs traveling to the eye's ciliary bod

185 ofiles of granule cells, indicating that the collaterals of nuclear output neurons contact both Golgi

186 ated in the somata and axons, including axon collaterals, of somatostatin-expressing interneurons are

187 The convergence of climbing fibre collaterals onto CbN cells decreases from approximately

188 and cognitive disorders, a broad spectrum of collateral oral disease may be encountered.

189 but have more synaptic area on PCs near the collateral origin than on distant PCs.

190 isease score (P < 0.001), more portosystemic collaterals (P = 0.01) and splenomegaly (P = 0.01) on ul

191 bellar cortex, implicates the climbing fibre collateral pathway in early postnatal development.

192 rmined in acute brain sections; the Schaffer collateral pathway was stimulated and the field excitato

193 ebellar premotor output neurons, mapped this collateral pathway, and identified its postsynaptic targ

194 ecific and were not observed in the Schaffer collateral pathway-associated inhibitory synapses.

195 Collateral pathways in vascular disease are important na

196 epletion of Tregs resulted in restoration of collateral priming in the skin.

197 new antigens in the lungs, which we called "collateral priming".

198 y 50% of PAG-projecting VMHdm/c neurons send collateral projection to the AHN and vice versa.

199 ey are the only central neurons that receive collateral projections from motor outputs, yet the effic

200 roximately 30 parvocellular OT neurons, with collateral projections onto magnocellular OT neurons and

201 Collaterals provide fast, slow, and tonic inhibition to

202 expanded the system of intrahippocampal axon collaterals, relative to turtles and lizards.

203 Collateral remodeling is critical for blood flow restora

204 Flow recovery and collateral remodeling were significantly blunted in EC-s

205 rmore, PLX-4032-resistant cells demonstrated collateral resistance to conventional chemotherapy, yet

206 e administered drug, and may also select for collateral resistances to other drugs.

207 ors Csx27 and Csx28, as well as non-specific collateral RNA damage.

208 ct repeats, cleaves target RNA, and exhibits collateral RNase activity.

209 ion of entorhinal cortical (EC) and Schaffer collateral (SC) inputs to hippocampal CA1 pyramidal neur

210 short- and long-term plasticity at Schaffer collateral (SC) synapses in the dorsal and ventral hippo

211 nd plasticity at dorsal and ventral Schaffer collateral (SC) synapses in the mouse hippocampus.

212 long-term potentiation (LTP) at CA1 Schaffer collateral (SC) synapses.

213 is expressed presynaptically at the Schaffer collateral (SC)-CA1 synapse in the hippocampus in adult

214 erm depression (LTD) at hippocampal Schaffer collateral (SC)-CA1 synapses.

215 farct core, pretreatment alteplase), and the collateral score.

216 tivities in the resistant population, termed collateral sensitivities, and then using these as second

217 e we tested 6 further anti-cancer agents for collateral sensitivity among resistant cells, uncovering

218 2) to a panel of 4 ALK TKIs, and performed a collateral sensitivity analysis.

219 one in which patterns of drug resistance and collateral sensitivity change substantially, and therefo

220 apy, another ALK TKI is administered, though collateral sensitivity is not considered.

221 indeed find that temporal and/or persistent collateral sensitivity to non-classical BCR-ABL1 drugs a

222 nerabilities-a notion that we term "temporal collateral sensitivity." Using a combined pharmacologica

223 large-vessel occlusion/stenosis with sparse collaterals showed hypoperfusion by both of the two appr

224 oth of the two approaches, one with abundant collaterals showed neither TTP nor TSA time delay.

225 ruption of sebaceous glands without damaging collateral skin.

226 ecule coordinating NGF signaling to regulate collateral sprouting and structural plasticity of intact

227 tein levels were increased in neurons during collateral sprouting but decreased following injury, sug

228 om the rat in vivo spared dermatome model of collateral sprouting identified the adaptor protein CD2-

229 To understand how collateral sprouting proceeds in the adult brain, we ima

230 olecule associated with adult sensory axonal collateral sprouting, and this association may offer new

231 ct axons of noninjured neurons, often termed collateral sprouting, contributes to both adaptive and p

232 n Cerebral Infarction [TICI] score 2b-3) and collateral status (using the American Society of Interve

233 ary 2000, investigating correlations between collateral status and any efficacy or safety outcome in

234 ent predictors of recanalization were better collateral status and the use of a stent retriever.

235 imed to investigate the role of pretreatment collateral status in predicting the efficacy and safety

236 Good pretreatment collateral status is associated with higher rates of fav

237 Beside initial stroke severity, the collateral status predicts clinical outcome and recanali

238 al Institutes of Health Stroke Scale scores, collateral status, and the use of magnetic resonance ima

239 ould alter the estimate of overall effect of collateral status, but there were moderate to significan

240 CA1 pyramidal cells in response to Schaffer collateral stimulation in slices from young adult mice.

241 s, evoked in CA1 principal cells by Schaffer collateral stimulation, were detected in hippocampal sli

242 se data suggest that oncogenic MYC confers a collateral stress on splicing, and that components of th

243 selectivity that tracked the fusiform gyrus/collateral sulcus.

244 ctional dynamics of the hippocampal Schaffer collateral synapse by using data-driven nonparametric mo

245 rast, AMPAR-mediated input at local Schaffer-collateral synapses on neurogliaform cells remains norma

246 s the release of NPY that modulates Schaffer collateral synapses requires integration of both the Sch

247 we show that at mature hippocampal Schaffer collateral synapses the magnitudes of Ca2+ transients du

248 eficits in synaptic transmission at Schaffer collateral synapses, and blunted plasticity and imbalanc

249 AMPAR and NMDAR currents evoked at Schaffer collateral synapses.

250 provides strong evidence that the recurrent collateral system underlies the associative network func

251 ls, which are possibly expressed in the axon collateral terminals of ipRGCs; and (3) fluorescence mic

252 receptors at neighboring excitatory Schaffer collateral terminals, which could counteract effects of

253 Some neurons have long collaterals that form autapses.

254 pulation of M1 ipRGCs have intraretinal axon collaterals that project toward the outer retina.

255 tage of nearby MSNs in contrast to local MSN collaterals that provided only sparse and weak inhibitor

256 ents who had obvious MRA lesions with sparse collaterals, those with abundant collaterals would keep

257 ized Slit inhibit formation of specific axon collaterals through modulation of Dscam1 activity.

258 nosine is a key immune regulator that limits collateral tissue damage due to an intracellular pathoge

259 eutrophil antimicrobial armaments allows for collateral tissue damage.

260 ation, which are associated with NET-induced collateral tissue injury.

261 pamine in the NAc primarily by an excitatory collateral to the ventral tegmental area (VTA).

262 ieval of emotional memories, VH neurons with collaterals to both areas may be particularly important

263 dual-labeling revealed many cells extending collaterals to both target regions.

264 r muscle IMAs issued specialized polymorphic collaterals to myenteric ganglia, and a subset (41%) of

265 transgene suppression, resistant MNs sprout collaterals to reinnervate previously denervated neuromu

266 ionally, however, these climbing fibres send collaterals to the cerebellar nuclei (CbN).

267 scribed in previous studies to send feedback collaterals to the cerebellum.

268 ng-evoked defensive responses through axonal collaterals to the dorsal raphe nucleus (DRN) and SC.

269 e potent, sustained antitumor responses, but collateral toxicity often limits dosages.

270 It has been proposed that PC collaterals transiently control circuit assembly in earl

271 We show that synchronized stimulation of collateral transmission from multiple indirect-pathway M

272 al anomalies, older age, a greater number of collaterals unifocalized, and higher postrepair right ve

273 In this rare and extremely lucky case no collateral vascular or neurological damage was detected.

274 incomplete MOIVC above the level of a large collateral vein and it may lead to prostatic and urethra

275 part of intrahepatic IVC proximal to a large collateral vein as well as prostatic and urethral conges

276 ination revealed tense ascites and abdominal collateral veins.

277 ce up to the level of the obliterated IVC, a collateral venous branch was identified at the confluenc

278 CA) is an invasive procedure used to assess collateral ventilation and select candidates for valve-b

279 e yielded modest group benefits because when collateral ventilation is present it prevents lobar atel

280 atients with heterogeneous emphysema without collateral ventilation resulted in clinically meaningful

281 patients with homogeneous emphysema without collateral ventilation results in clinically meaningful

282 with heterogeneous emphysema and absence of collateral ventilation.

283 3-fold, suggesting that Il21r modulates both collateral vessel anatomy and innate neuroprotection.

284 Collateral vessel connections were moderately reduced in

285 Nineteen patients had ASITN/SIR collateral vessel grades of 0 or 1, 63 patients had a gr

286 N)/Society of Interventional Radiology (SIR) collateral vessel grading system, while reperfusion was

287 tify miRNAs involved in elevated FSS-induced collateral vessel growth in rat hind limbs.

288 We conclude that enhanced collateral vessel growth is controlled by miRNAs, among

289 Although collateral vessel growth is distinctly enhanced by eleva

290 At multivariable analysis, collateral vessel status independently predicted reperfu

291 In this patient population, collateral vessel status independently predicted the piv

292 onset-to-treatment time (OTT) of 0-3 hours, collateral vessel status predicted final infarct size an

293 e analyzed at a blinded core laboratory, and collateral vessel status was assessed by using the Ameri

294 of patient selection for EVT on the basis of collateral vessel status.

295 52 increased the number and proliferation of collateral vessels and promoted collateral flow restorat

296 sess the association between the presence of collateral vessels identified using arterial spin labeli

297 Better collateral vessels were associated with higher reperfusi

298 In 25 of 38 patients (65.8%), collaterals were detected using ASL, which were signific

299 nificantly increasing formation of lymphatic collaterals with minimal systemic absorption.

300 with sparse collaterals, those with abundant collaterals would keep intact local perfusion.