ライフサイエンスコーパス: collateral

1 ation receives synaptic innervation from MOC collaterals.

2 from that of STN neurons without local axon collaterals.

3 , terminal segment stenosis and absent basal collaterals.

4 a contribution of climbing fibers and their collaterals.

5 outcomes due to a shutdown of leptomeningeal collaterals.

6 lum: the mossy fibers and the climbing fiber collaterals.

7 rs a proof of concept to target PI3K and the collateral-activated pathway to improve GBM therapy.

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

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

10 f blood to hypoperfused brain tissue through collateral anastomoses.

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

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

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

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

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

16 The alignment of local collaterals and T-stellate cell dendrites within the iso

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

18 gradient, aortic isthmus ratio, presence of collaterals, and exercise-induced hypertension.

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

20 traplaque hemorrhage (IPH), circle of Willis collaterals, and the presence and severity of arterial t

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

22 Central axon collaterals are found in subsets of primaries based on s

23 Collaterals are labeled by synaptophysin-tagged fluoresc

24 Collaterals are largely restricted to the neuropil, howe

25 including the influence of variations of the collateral arterial network and the effect on hand dysfu

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

27 tery in C57BL/6 J mice enlarged pre-existing collateral arteries and increased numbers of arterioles

28 Collateral arteries are an uncommon vessel subtype that

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

30 newborn mice and provides insights into how collateral arteries form.

31 mouse hearts use a novel mechanism to build collateral arteries in response to injury.

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

33 ng existing capillaries and reassembled into collateral arteries, which we termed "artery reassembly"

34 tetralogy of Fallot and major aortopulmonary collateral arteries.

35 f Tie2 receptor signaling, which limits pial collateral arteriogenesis following cerebrovascular occl

36 , which supply growth factors to preexisting collateral arterioles enabling them to grow.

37 CXCL12 or CXCR4 deletion impaired collateral artery formation and neonatal heart regenerat

38 e and Woo labs (Das et al., 2019) shows that collateral artery formation is a key mechanism contribut

39 e1 interfered with leukocyte recruitment and collateral artery growth.

40 low-up in separate LTR and family caregiver (collateral) assessments.

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

42 and 5.1% after MDA (P = .019), demonstrating collateral benefits of ivermectin MDA in this setting.

43 the Circle of Willis are a central source of collateral blood flow and play an important role in path

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

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

46 tine ganglion stimulation increased cerebral collateral blood flow, stabilised the blood-brain barrie

47 with no evidence of preinfarction angina or collateral blood flow.

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

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

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

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

52 phenotype that is consistent with increased collateral branch formation.

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

54 duces axonal filopodia dynamics and disturbs collateral branch formation.

55 lion cells (RGCs), and this pathway is not a collateral branch of the geniculate and collicular proje

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

57 Collateral branches from axons are key components of fun

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

59 quired for nerve growth factor (NGF)-induced collateral branching in vitro and expression of dominant

60 are validated solely on these advances, the collateral broader scientific progress resulting from th

61 influence became greater in the presence of collateral bypassing vessels, which sufficiently reduced

62 CC2D1A in the maintenance of LTP at Schaffer collateral-CA1 synapses and the formation of hippocampus

63 unction of SNAP-25a and SNAP-25b at Schaffer collateral-CA1 synapses in hippocampus using 4-week-old

64 he isolated NMDAR potentials at the Schaffer collateral-CA1 synapses, but without affecting basal neu

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

66 ses, but not in commonly studied in Schaffer collateral-CA1 synapses.

67 long-term potentiation (LTP) at the Schaffer collaterals-CA1 synapse.

68 gulating synaptic NMDAR function at Schaffer collateral (CA3)-CA1 synapses.

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

70 paraumbilical vein, number of portosystemic collateral channels and diameter of portal vein and posi

71 nalysed the number and type of portosystemic collateral channels in respect of age, sex, presence of

72 nce in diameter of portal vein and number of collateral channels was found in groups with and without

73 cal veins and higher number of portosystemic collateral channels.

74 tion of the palmar arch and forearm arterial collateral circulation during transradial access.

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

76 l hypertension and the dynamic physiology of collateral circulation, gastric variceal classification

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

78 to unravel the pathways leading to improved collateral circulation.

79 n of brain perfusion because, theoretically, collateral circulations may restore it.

80 r and an augmented rate of LbCas12a-mediated collateral cleavage activity as high as 3.5-fold compare

81 etection by isothermal amplification and the collateral cleavage of reporter molecules by CRISPR-asso

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

83 Some patients with heart disease develop collateral coronary arteries, and this correlates with i

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

85 e to accumulating insights, and it may incur collateral damage (e.g., impairing cognitive processes a

86 ated immunosuppression protects tissues from collateral damage by antipathogen immune cells.

87 ning to insert foreign DNA and HDR to repair collateral damage caused by the microprojectiles.

88 n dogs with sDM and sDMPanc, suggesting that collateral damage from inflammation in the exocrine panc

89 deling following I/R injury secondary to the collateral damage from sustained myocardial inflammation

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

91 ither destroy foreign DNA directly or elicit collateral damage inducing death of infected cells.

92 How the immune response to this collateral damage influences brain maturation and functi

93 The collateral damage of early-life antibiotic treatment and

94 rget cancer cells have the ability to reduce collateral damage on normal tissue due to pan-toxic effe

95 x with aspect ratio of 12:1, and without the collateral damage that is observed in unmodulated CW dri

96 bundance target bacteria without significant collateral damage to complex microbial communities.

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

98 sponses counteract infections but also cause collateral damage to hosts.

99 ion of post-operative quality of life due to collateral damage to neighboring structures.

100 an promote genome evolution while minimizing collateral damage to overall chromosome architecture and

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

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

103 therapies in some cases, but issues such as collateral damage to the commensal microbiota and consis

104 as a general treatment, potentially causing collateral damage to the gut microbiome of the patient.

105 viral persistence and survival with minimal collateral damage to the healthy host.

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

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

108 ding histology sections exhibit only minimal collateral damage to the surrounding tissue and the dept

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

110 s, optimizing host protection and minimizing collateral damage(1,2).

111 chinery to protect against and tolerate this collateral damage.

112 endent apoptosis of individual cells without collateral damage.

113 he efficacy of cancer therapy while limiting collateral damage.

114 y impact on trafficker behavior and the many collateral damages associated with the militarized war o

115 ediate giant fiber activation coupled to MGF collateral dendrites.

116 We termed such genes "collateral dependencies" (CDs) and identified two classe

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

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

119 However, it is not known how these collaterals develop or how to stimulate them.

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

121 This study unveils a novel collateral drug sensitivity elicited by combining copper

122 Gepants worsened ischemic stroke in mice via collateral dysfunction.

123 We combine the collateral effect of Cas13a with isothermal amplificatio

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

125 We find that collateral effects are pervasive but difficult to predic

126 n extensive quantitative characterization of collateral effects in Enterococcus faecalis, a gram-posi

127 in different populations or species, or (ii) collateral evolution in which shared ancestry results fr

128 . elevatus is caused by a complex history of collateral evolution via introgression in the Amazon, co

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

130 Here, we report a collateral excitation mechanism in which high-frequency,

131 sized that the outcomes of dynamic Willisian collateral failure (DWF), induced during mechanical thro

132 Patients with initial Willisian collateral failure (IWF) were identified first, with rem

133 thrombus embolization resulting in Willisian collateral failure may lead to critical stroke outcomes

134 nd vascular imaging showing moderate-to-good collateral filling, as determined by multiphase CT angio

135 leterious, indicating that for some proteins collateral fitness effects occur as frequently as effect

136 Deleterious collateral fitness effects occurred more frequently in T

137 We comprehensively measured the collateral fitness effects of missense mutations in the

138 The surprising prevalence of deleterious collateral fitness effects suggests they may play a role

139 re, we reveal the importance of a mutation's collateral fitness effects, which we define as effects t

140 n of ASCs with downregulated miR-145 induced collateral flow and capillary formation evidenced by mag

141 ate occlusion of the descending aorta or any collateral flow and diverts flow away from the brain.

142 Both gepants consistently diminished collateral flow and reduced reperfusion success.

143 Collateral flow index (CFI), the ratio of mean occlusive

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

145 Collateral flow index in the untreated RCA and left coro

146 Collateral flow index is the ratio between simultaneousl

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

148 the aortic arch vessels to atmosphere allows collateral flow to be diverted away from the brain, main

149 We compared infarct risk and volumes, collateral flow, and neurological deficits after pretrea

150 , such as an increase in PC recurrent axonal collateral formation and hypertrophy of GABAergic basket

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

152 , and a reduction in the density of bridging collaterals from D1R-expressing neurons to pallidal area

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

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

155 Palmar arch and forearm collateral function was determined using radial artery p

156 nts an attractive new strategy for improving collateral function, neural tissue health, and functiona

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

158 is, induced neither pericyte recruitment nor collateral growth.

159 tural biology in order to lessen the risk of collateral harm and avoid the crisis of resistance now f

160 No pretectal structures in receipt of TGC collaterals have been described in this group.

161 onate response to the virus and mitigate the collateral impact.

162 nchial arteries (3%), and systemic bronchial collaterals in 1% of our patients.

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

164 Therefore, collateral inhibition of oncogenic signaling and mitocho

165 tion (PFA) would reduce PV stenosis risk and collateral injury compared with irrigated radiofrequency

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

167 CWs under mild cavitation conditions without collateral injury.

168 ar which of these neurons receive direct MOC collateral input due to conflicting results between in v

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

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

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

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

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

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

175 er, this DeltaNp63-low EMT state triggered a collateral loss of fitness.

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

177 Microscopic analysis revealed that MOC collaterals made some putative synaptic contacts with th

178 tations, but the possibility exists that the collaterals may also make contacts with neurons not proj

179 seek to highlight the potential problem of 'collateral mortality' from delayed or deferred treatment

180 ed features of the CRISPR-Cas mechanism: (i) collateral, nonspecific, cleavage of host nucleic acids;

181 fter ECA ligation because of the presence of collateral occipital-vertebral anastomosis.

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

183 The latter result demonstrates that axon collaterals of lumbar-projecting RVLM neurons project to

184 ns receive synaptic innervation from the MOC collaterals on their somata and proximal dendrites.

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

186 es onto GC proximal dendrites via their axon collaterals or terminals in the internal plexiform layer

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

188 + CA1) neurons of the hippocampal Schaeffer-collateral pathway in both female and male mice.

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

190 iated late-LTP in SOM-INs regulated Schaffer collateral pathway LTP in pyramidal neurons.

191 long-term potentiation (LTP) in the Schaffer collateral pathway of CA1 pyramidal neurons and in vitro

192 evealed that LTP stimulation of the Schaffer collateral pathway promoted MAP2 labeling in spine heads

193 of misfolded alpha-synuclein in the lateral collateral pathway, a region of the sacral spinal cord h

194 tic transmission in the hippocampal Schaffer collateral pathway.

195 non-invasive tool for direct measurement of collateral perfusion and delayed blood arrival in acute

196 Collateral perfusion at presentation was associated with

197 ging (MRI)-based method to directly quantify collateral perfusion in acute stroke patients.

198 Collateral perfusion is important for sustaining tissue

199 ime but was not consistently associated with collateral perfusion.

200 stand harsh tumor metabolic environments and collateral pharmacologic insults.

201 This variability typically emerged through collateral phylogenetic branching, leading to spatial va

202 iameter of paraumbilical vein, and number of collateral portosystemic channels.

203 ition of the anterior insula, which receives collateral projections from NAcC-projecting BLA neurons,

204 guided behavior, which is mediated by their collateral projections to both the motor-related layers

205 and motor-control circuits through extensive collateral projections.

206 n is strongly inhibited by the insurgence of collateral radical reactions.

207 identifying Mtb's glutamine synthetase as a collateral, rather than directly antimycobacterial, meta

208 sessment instruments obtain self-ratings and collateral ratings of behavioral, emotional, social, and

209 Unlike other collateral rearrangements, these fusion-oncogene-associa

210 Pial collateral remodeling is limited by the crosstalk betwee

211 yrosine kinase as a major suppressor of pial collateral remodeling, CBF, and functional recovery foll

212 EJ, underscoring the importance of MMEJ as a collateral repair pathway in the context of homologous r

213 previously sensitive lymphoma cells confers collateral resistance to the topoisomerase II poison dox

214 F domain activates the Csm6 HEPN domains for collateral RNA degradation, and how CARF domain-mediated

215 g is an RNA-guided ribonuclease (RNase) with collateral RNase and single-strand DNase activities.

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

217 ished long-term potentiation in the Schaffer collateral (SC) pathway through complex signaling involv

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

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

220 tentiates long-term potentiation of Schaffer collateral (SC) synapses.

221 tent potentiation of AMPAR-mediated Schaffer collateral (SC)-CA1 fEPSPs in slices derived from male a

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

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

224 might present unique, temporally restricted collateral sensitivities, absent in therapy naive or ful

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

226 One such strategy is the identification of collateral sensitivities, wherein evolution under a firs

227 Among numerous combative strategies, collateral sensitivity (CS) drugs have opened a new aven

228 ta-lactamase susceptibility is an example of collateral sensitivity (resistance to one antibiotic inc

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

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

231 tion of the tumour in our favour, leading to collateral sensitivity and proliferative costs.

232 surements, we measure phenotypic profiles of collateral sensitivity and resistance for a total of 900

233 exhibit qualitatively different profiles of collateral sensitivity as well as markedly different fit

234 e than on the parental cell line, exerting a collateral sensitivity effect.

235 ions in several genes previously linked with collateral sensitivity in other species.

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

237 Here we study collateral sensitivity patterns of the globally distribu

238 horizontally transferred genes by exploiting collateral sensitivity patterns.

239 ion that conferred resistance to AsnEDAs and collateral sensitivity to an inhibitor of the Pf20S beta

240 However, biofilm populations developed collateral sensitivity to cephalosporins, demonstrating

241 Collateral sensitivity to inhibitors among respective pr

242 ment of resistance against one drug leads to collateral sensitivity to the other drug.

243 ikely due to variation in the effect size of collateral sensitivity, epistasis among adaptive mutatio

244 is to exploit evolutionary trade-offs, like collateral sensitivity, where evolved resistance to one

245 ce to one antibiotic may be associated with "collateral" sensitivity to other drugs.

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

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

248 vein (PUV) and the presence of portosystemic collateral shunts and their relationship with age and po

249 the inhibition of these enzymes can trigger collateral side effects that could preclude the practica

250 tients classified into the DWF and Willisian collateral sparing (WCS) groups.

251 35-day-old rat, we previously demonstrated a collateral sprouting response that reinnervates the part

252 sment of the microcirculation, the impact of collateral steal as well as assessing the severity of a

253 in the frequency of sEPSC following Schaffer collateral stimulation.

254 monary vein (PV) isolation without damage to collateral structures.

255 to reachable views, located in the posterior collateral sulcus, the inferior parietal sulcus, and sup

256 r arch and forearm arterial function reveals collateral supply to the briefly occluded in comparison

257 d suppression of autoimmune diseases without collateral suppression of normal immunity remains an elu

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

259 omposition between commonly studied Schaffer collateral synapses and perforant path-dentate gyrus (DG

260 ptor-mediated synaptic responses at Schaffer-collateral synapses monitored in juvenile mice, but agai

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

262 neurons in the modulation of LTP at Schaffer collateral synapses onto pyramidal cells.

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

264 ect formation of perforant-path and Schaffer-collateral synapses, respectively, to hippocampal CA1-re

265 ellular engagement assays defined RIPK2 as a collateral target.

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

267 t bypasses the AMMC via the saddle and forms collaterals terminating in the posterior slope (PS) (T6I

268 Some neurons have long collaterals that form autapses.

269 ts of spinal motor neurons also exhibit axon collaterals that influence motor output centrally.

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

271 on assessing the function and regression of collaterals, the assessment of the microcirculation, the

272 mited precision and the risk of harm through collateral thermal damage to the adjacent healthy tissue

273 puts are not as strong as piriform recurrent collaterals, they are less constrained by disynaptic inh

274 itionally, neutrophils were thought to cause collateral tissue damage before dying at the site.

275 This was achieved without steam pops or collateral tissue damage.

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

277 ling that many afferent neurons project axon collaterals to both the lateral and medial NTS subdivisi

278 ial olivocochlear (MOC) neurons also project collaterals to cochlear nucleus and make synaptic contac

279 gnificant minority of RVLM neurons send axon collaterals to disparate spinal segments (T(2) and T(10)

280 vessel (the vessel supplying the majority of collaterals to the CTO).

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

282 urgical area of tumor resection, without any collateral toxicity.

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

284 liver cirrhosis occurred (thrombocytopenia, collateral venous circulation, first degree varices oeso

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

286 Flow bypass through the collateral vessel caused a decrease in TPA flux in the c

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

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

292 ompression by right common iliac artery with collateral vessels in the pelvis in a postpartum female.

293 Leptomeningeal anastomoses or pial collateral vessels play a critical role in cerebral bloo

294 ive, require contrast agents and demonstrate collateral vessels, rather than measuring perfusion dire

295 POLR2A in the TP53-neighbouring region as a collateral vulnerability target in TNBC tumours, suggest

296 nd a facet of mode-of-action biology we term collateral vulnerability, knowledge of which has the pot

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

298 Biocytin abundantly labeled MOC collaterals which entered cochlear nucleus.

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

300 ributor to be slow conduction through axonal collaterals within HVC, which typically adds between 1 a