ライフサイエンスコーパス: cone

1 for rods and v = 0.206 SD 0.069 min(-1) for cones).

2 m the flash response of a rod into that of a cone.

3 fferent dark excitons exist within the light cone.

4 raction of the stigma within the antheridial cone.

5 tes, such as the motor neuron and the growth cone.

6 which form the extremals of a linear convex cone.

7 ocalization of actin in the advancing growth cone.

8 ic filopodial domain that defines the growth cone.

9 work which we expect to exhibit a Dirac-like cone.

10 ive of an aberrant composition of the growth cone.

11 ucture, but not functional rescue in rods or cones.

12 vel was decreased twofold in cone-Bmal1(-/-) cones.

13 chondria and increased metabolic activity in cones.

14 m dynamics during the development of retinal cones.

15 cones (cone-Bmal1(-/-) ) and wild-type (WT) cones.

16 naptic terminals and scattered axonal growth cones.

17 o exert gain-of-function defects in rods and cones.

18 lipodia in migrating cells and axonal growth cones.

19 ent lipofuscin translocating inwardly within cones.

20 L cones, ~3% in M cones, and negligible in S cones.

21 ina, including the photon-sensitive rods and cones.

22 y local circuit neurons receiving input from cones.

23 its was dependent on activation of mTORC1 in cones.

24 in the axon shaft, at synapses or in growth cones.

25 may improve suboptimally functioning macular cones.

26 posite: signal flow through even the longest cones (0.4-mm axons) is essentially lossless.

27 h anesthesia distributed evenly to each nose cone (2.9 +/- 0.1 L/min).

28 long (L) and medium (M) wavelength-sensitive cones [3,4].

29 sin percentages in darkness, being ~30% in L cones, ~3% in M cones, and negligible in S cones.

30 Ultra-short Echo Time (UTE) MRI, using a 3D cones acquisition trajectory.

31 biases the stochastic fluctuations of growth cone actin to direct axon growth and guidance.

32 at mesopic light levels, where both rods and cones actively respond to light.

33 mpared morphologic and functional changes of cones after vitrectomy for macula-off retinal detachment

34 This S-cone amacrine cell makes highly selective inhibitory syn

35 ough inhibitory input from an undiscovered S-cone amacrine cell.

36 d the data within a model that describes how cone and melanopsin signals are weighted and combined at

37 Manipulation of the dynamic of the Taylor cone and phase separation of its ejected droplets enable

38 ERG cone and rod luminance response functions were recorded

39 ic vision tests, with their reliance on both cone and rod vision, may be a more comprehensive assessm

40 cones were transfated into ultraviolet (UV) cones and horizontal cells.

41 dentify a synaptic connectivity mechanism of cones and illustrate how interplay between adhesion mole

42 n nearly eliminates branched actin in growth cones and prevents growth cone recovery after repellent-

43 al acuity [VA], contrast sensitivity), mixed cones and rods (low-luminance VA, low-luminance deficit,

44 l cycle, as well as survival and function of cones and rods in patients with RPE65 mutations.

45 nsitions between the tilted anisotropic Weyl cones and the massive bulk bands.

46 It is selectively expressed in cones and transsynaptically recruits the key neurotransm

47 in darkness, being ~30% in L cones, ~3% in M cones, and negligible in S cones.

48 ters for the Bpin group: the A-value, ligand cone angle, and percent buried volume.

49 he core morphological features of the growth cone are strongly correlated with one another and define

50 Indeed, the majority of cones are contacted by single BC4 throughout development

51 Degeneration rates of S- and M-cones are negatively correlated with expression levels o

52 most important differences between rods and cones are: (1) decreased transduction gain, reflecting s

53 ae s.s. Kisumu strain to sprayed surfaces in cone assays and measuring mortality at 24 hours.

54 ield, which may use the signal from a single cone at a time.

55 The number of detectable cones at height of the inner-outer segment junction (IS/

56 ectric (PZT) patches, resulting in two Dirac cones at the K points.

57 TM4 was not detected at dendritic tips of ON-cone BCs.

58 hic findings from periapical radiographs and Cone Beam Computed Tomographies (CBCT) were analyzed to

59 It is unknown whether cone beam computed tomography (CBCT) image reconstructio

60 e implants on the change of BBT according to cone beam computed tomography (CBCT) scan analysis.

61 were: 1) to compare two phases of dual-phase cone beam computed tomography (DP-CBCT) achieved before

62 ntation on clinically diverse dataset of 637 cone beam CT volumes, with mandibular canals being coars

63 metal artifact reduction (MAR) algorithm of cone-beam computed tomography (CBCT) on the diagnostic a

64 owth, and density changes as quantified on a cone-beam computed tomography (CBCT) scan.

65 Corresponding cone-beam computed tomography images were used to measur

66 hanges were also evaluated radiographically (cone-beam computed tomography).

67 and the augmented tissues were evaluated by cone-beam computed tomography, microcomputed tomography,

68 ORS, parallel computing with GPU enables the cone-beam CT dose estimation nearly in real-time.

69 In this study, cone-beam single projection and axial CT scans are model

70 ilar to and mixes with POPC, also an inverse cone because of mobility of its unsaturated tail.

71 We propose that nestin changes growth cone behavior by regulating intracellular kinase signali

72 Vision tests probed cones (best-corrected visual acuity [VA], contrast sensi

73 -treated bednets was low (< 30% mortality in cone bioassays).

74 crine cell (AII AC) provides inhibition onto cone bipolar cell (BC) axons and retinal ganglion cell (

75 dent rod pathway(s) (e.g., direct rod to OFF cone bipolar cell synapses and/or glycinergic synapses f

76 between cone-specific Bmal1 knockout cones (cone-Bmal1(-/-) ) and wild-type (WT) cones.

77 X3 expression level was decreased twofold in cone-Bmal1(-/-) cones.

78 es but remained constitutively low in mutant cones both day and night.

79 regulated at night compared to the day in WT cones but remained constitutively low in mutant cones bo

80 CA1 blindness, both of which affect rods and cones, but they cannot explain the selective loss of rod

81 loped a quantitative, probabilistic model of cone cell decisions in the retinal tissue based on thyro

82 Identifying this S-cone circuit is particularly important because ipRGCs me

83 egulated at the transcriptional level by the cone clock.

84 Mice lacking functional cone CNG channel show endoplasmic reticulum (ER) stress-

85 Mutations in cone CNG channel subunits CNGA3 and CNGB3 are associated

86 for dendrite elaboration but not axon growth cone collapse.

87 nalysis between cone-specific Bmal1 knockout cones (cone-Bmal1(-/-) ) and wild-type (WT) cones.

88 onstructed the neurons and synapses of the S-cone connectome, revealing a novel inhibitory interneuro

89 equency signals (1) does not require the rod-cone Cx36 gap junctions as has been proposed in the past

90 ansduction pathway that regulates the growth cone cytoskeleton.

91 Cone death generally follows rod loss regardless of the

92 ly restore input synapse numbers when 50% of cones degenerate but one does not.

93 Progressive rod-cone degeneration (PRCD) is a small protein localized to

94 ed proteasome stress plays a major role in M cone degeneration in Lrat(-/-) model.

95 proteasome stress and completely prevents M cone degeneration in Lrat(-/-)Opn1sw(-/-) mice (a pure M

96 retina in the cpfl1 mouse model for primary cone degeneration, and in the rd1 and rd10 models for pr

97 to cGMP/PKG signaling-induced ER stress and cone degeneration.

98 ess, ranging from rod dysfunction to rod and cone degeneration.

99 endoplasmic reticulum (ER) stress-associated cone degeneration.

100 Rod-cone degenerations, for example, retinitis pigmentosa ar

101 bset of children to quantify FAZ metrics and cone densities at 0.2, 0.3, and 0.5 mm eccentricities.

102 icate that myopic children have lower linear cone densities close to the foveal center compared to no

103 ren as young as 5.8 years old by quantifying cone density and spacing, foveal avascular zone size, an

104 Despite improvement at FUP (P < .001), mean cone density at IS/OS and COST was still lower compared

105 ren, while myopic eyes have decreased linear cone density near the foveal center.

106 Cone density of RDE was significantly reduced and ranged

107 However, linear cone density was lower in myopic versus non-myopic child

108 MainOutcomeMeasures: Cone density, cone pattern regularity and signal attenua

109 ssential for BDNF-stimulated neuronal growth cone development and dendritic protrusion formation, and

110 ytoskeletal reorganization within the growth cone direct axon navigation.

111 Using an unbiased proteomic strategy in cone-dominant species, we identified the cell-adhesion m

112 but not to slow temporal variations, whereas cone-driven responses supplement the loss in rod-driven

113 in abnormal dendritic protrusions and growth cone dynamics.

114 CNGB3 are associated with achromatopsia and cone dystrophies.

115 pigmentosa (RP), the most common form of rod-cone dystrophy, is caused by greater than 3100 mutations

116 nism by which SlitC constantly limits growth cone exploration, imposing ordered and forward-directed

117 sin Myo16 in cortical neurons altered growth cone filopodia density and axonal branching patterns in

118 of goldfish red (L), green (M), and blue (S) cones, finding with microspectrophotometry widely differ

119 onses and recent voltage-clamp recordings of cone flash responses, using a model incorporating the pr

120 e, mmachc mutants bred to express rod and/or cone fluorescent reporters, manifested a retinopathy and

121 rate eyes have rods for dim-light vision and cones for brighter light and higher temporal sensitivity

122 The long-held view is that Slits push growth cones forward and prevent them from turning back once th

123 h2R172W/Rom1+/- animals had worsened rod and cone function and exacerbated retinal degeneration compa

124 Prph2K/+/Rom1+/- mice had improved rod and cone function compared with Prph2K/+ as well as ameliora

125 ll Prph2 levels as well as decreased rod and cone function.

126 (NAC) reduces oxidative damage and increases cone function/survival in RP models.

127 ity (0.81 for rod-function anxiety, 0.83 for cone-function anxiety) and exhibits minimal test-retest

128 ction anxiety and rho = 0.83 [0.68-0.92] for cone-function anxiety).

129 re we provide the x-ray crystal structure of cone GAFab regulatory domain solved at 3.3 angstrom reso

130 Molecular dynamics simulations of cone GAFab revealed differences in conformational dynami

131 r-infrared stimulation increased activity in cones, ganglion cell layer neurons, and cortical neurons

132 The growth cone (GC) itself can generate very low intracellular for

133 1/2 as regulators of the temporal window for cone genesis and, given their widespread expression in t

134 utput by a remarkable non-divergent circuit: cone -> midget bipolar interneuron -> midget ganglion ce

135 activatable Rac1 to co-opt endogenous growth cone guidance machinery to precisely and non-invasively

136 oles: H1-H3 feed back onto different sets of cones, H4 feed back onto rods, and only H1 store and rel

137 that mitochondrial turnover is important for cone health.

138 e for apoptosis in secondary degeneration of cones, highlighting the importance of the spatial and te

139 ke TRP channels in light-insensitive retinal cones in a mouse model of retinal degeneration.

140 drives contact patterns downstream of single cones in Bax null mice and may serve to maintain constan

141 sole consisted of single, double, and triple cones in formations that differed from the traditional s

142 ion, here we characterize the arrangement of cones in individual Y-Junction cores as well as the spat

143 nub/pdm2, regulate the timely production of cones in mice.

144 By exciting Dirac-like cones in photonic honeycomb (pseudospin-1/2) and Lieb (p

145 ith variations between peripheral and foveal cones in primates and hint at a common mechanistic origi

146 The number of S-cones in the inferior retinas of 4- or 6-mo-old KI;Fatp4

147 Here, we show that UV cones in the larval zebrafish area temporalis are specif

148 In addition, true S-cones in the ventral retina form clusters, which may aug

149 nal role of GRK1 phosphorylation in rods and cones in vivo, we generated mutant mice in which Ser21 i

150 bly of charged droplets by control of Taylor cone instability and micro-electric field, enables the c

151 a mutants, neurons continue to sprout growth cones into adulthood, leading to a highly ramified nervo

152 t an electronic band connecting the two Weyl cones is flattened by electronic correlations and emerge

153 Moreover, the visual function of S- and M-cones is markedly preserved in the KI;Fatp4 (-/-) mice,

154 In mild cones (Kmax < 55 diopter [D]), mean keratometry remained

155 ation in Lrat(-/-)Opn1sw(-/-) mice (a pure M cone LCA model, Opn1sw encoding S-opsin) for at least 12

156 n of rods triggers secondary degeneration of cones, leading to significant loss of daylight, color, a

157 Rods evolved from cone-like precursors through expression of different tra

158 We know that rods evolved from cone-like precursors through the expression of different

159 Al(3)O(4)(+) exhibits a cone-like structure with a central trivalent O atom (C(3

160 es encode only two opsins for use in retinal cones, limiting their adaptive flexibility and color vis

161 als from both sexes revealed that disrupting cone LINC complexes resulted in mislocalization of cone

162 By histologic analysis, cone lipofuscin was found in outer retinal layers of 25%

163 Visual deficits are dominated by cone loss, which progresses slowly, leaving a window dur

164 We examined associations between rod- and cone-mediated vision and HRF plus smaller hyperreflectiv

165 systems is fundamental to understanding how cone-mediated vision is sustained in vivo.

166 We also report dense material shared between cone mitochondria that is extruded from the cell at nigh

167 directly examine Ca(2+) uptake in zebrafish cone mitochondria, we found that loss of MCU reduces but

168 reveal an elaborate set of daily changes to cone mitochondrial structure and function.

169 ared to HFE and ranged between 7790 and 9555 cones/mm(2) (P < .001).

170 (2), P < 0.001) and 0.3 mm (43,944 +/- 5,547 cones/mm(2) vs 48,622 +/- 3,538 cones/mm(2), P < 0.001).

171 es of 0.2 mm (mean +/- SD = 50,022 +/- 5,878 cones/mm(2) vs 58,989 +/- 4,822 cones/mm(2), P < 0.001)

172 22 +/- 5,878 cones/mm(2) vs 58,989 +/- 4,822 cones/mm(2), P < 0.001) and 0.3 mm (43,944 +/- 5,547 con

173 44 +/- 5,547 cones/mm(2) vs 48,622 +/- 3,538 cones/mm(2), P < 0.001).

174 organization and its consequences for growth cone morphogenesis and motility.

175 developing neurons where it regulates growth cone morphology and responsiveness to the guidance cue S

176 lar mechanism by which nestin affects growth cone morphology and Sema3a sensitivity.

177 Changes in growth cone morphology require rearrangements of cytoskeletal n

178 Changes in growth cone morphology require rearrangements of cytoskeletal n

179 cal cultures, nestin regulates axonal growth cone morphology.

180 we demonstrate that grain boundaries in the cone mosaic instead appear during initial mosaic formati

181 llary is that lattice-like patterning of the cone mosaic may improve visual acuity.

182 species with lattice-like periodicity in its cone mosaic.

183 environments and do not possess lattice-like cone mosaics are congruent with this claim.

184 The cone mosaics of the common sole and the Senegalese sole

185 the cytoskeleton to produce directed growth cone motility.

186 the cytoskeleton to produce directed growth cone motility.

187 s) are essential for the apical migration of cone nuclei during development.

188 demonstrate that the apical localization of cone nuclei in the ONL is required for the timely dark a

189 his evolutionarily conserved localization of cone nuclei is unknown.

190 INC complexes resulted in mislocalization of cone nuclei to the basal side of ONL in mouse retina.

191 drothermal systems on the volcanic resurgent cones of Brothers volcano harbor communities of thermoac

192 ubule tips toward the leading edge in growth cones of hippocampal neurons.

193 light-sensitive chromophore of both rod and cone opsin visual pigments.

194 e lambdamax of phylogenetically distant Sws2 cone opsins.

195 expression of the visual receptors, rod and cone opsins; inhibit the inflammatory reactions; and ind

196 the inner-outer segment junction (IS/OS) and cone outer segment tips (COST) was counted manually in A

197 s; rather, it localizes to a small region of cone outer segments: the cell membranes surrounding the

198 n and retina-based alterations mostly in the cone pathway.

199 isual information processing in both rod and cone pathways.

200 MainOutcomeMeasures: Cone density, cone pattern regularity and signal attenuation, retinal

201 mparison to HFE, RDE showed highly irregular cone patterns in AO-OCT and irregular outer retinal band

202 hich BMAL1 alters signal transmission at the cone pedicle, we performed an RNA-seq differential expre

203 evidence that this protein is present at the cone pedicles, as well as in other synapses of the chick

204 nkeys' and approached the upper bound set by cone photocurrents.

205 tors on immediate, early, and late phases of cone photopic vision.

206 Chromophore regeneration of cone photopigments may require the retinal pigment epith

207 +) dysregulation is thought to cause rod and cone photoreceptor cell death.

208 applied ncRNA profiling to identify rod and cone photoreceptor CREs from wild-type and mutant mouse

209 The retinas of nonmammalian vertebrates have cone photoreceptor mosaics that are often organized as h

210 development with lack of a foveal pit and no cone photoreceptor outer segment lengthening.

211 otein essential for the formation of rod and cone photoreceptor outer segments (OS).

212 inal rod pathways that ultimately connect to cone photoreceptor pathways via Cx36 gap junctions or vi

213 precise chronological order, but how exactly cone photoreceptor production is restricted to early sta

214 identified synapse in the mouse retina, the cone photoreceptor type 4 bipolar cell (BC4) synapse, an

215 r middle- (M-) and long- (L-) wave sensitive cone photoreceptors [2].

216 We show that cone photoreceptors and P-type pathway bipolar cells are

217 maintain continuous rod function and support cone photoreceptors as well although its throughput has

218 Rod and cone photoreceptors convert light into electrochemical s

219 In mammalian retinas, rod and cone photoreceptors form selective synaptic connections

220 Cone photoreceptors in the retina enable vision over a w

221 the resolution afforded by a dense array of cone photoreceptors is preserved in the retinal output b

222 Retinal rod and cone photoreceptors mediate vision in dim and bright lig

223 Expression of opsin photopigments in the cone photoreceptors of the mouse retina provides an exce

224 Rod and cone photoreceptors of the retina are responsible for th

225 n photons of the light interact with rod and cone photoreceptors that are present in the neural retin

226 highly expressed protein secreted by rod and cone photoreceptors that has major roles in photorecepto

227 ope (AOSLO) images of foveal capillaries and cone photoreceptors were acquired in a subset of childre

228 Preventing the secondary loss of cone photoreceptors would preserve central visual acuity

229 e cell types, including Muller glia, rod and cone photoreceptors, and bipolar cells.

230 rrelated with epigenetic profiles of rod and cone photoreceptors, identified thousands of candidate r

231 long-wavelength-sensitive opsin (lws) in red cone photoreceptors, while in retinal pigment epithelium

232 egulating the dark adaptation of rod but not cone photoreceptors.

233 ation and efficient synaptic transmission in cone photoreceptors.

234 sociated with the visual pigments of rod and cone photoreceptors.

235 sociated with the visual pigments of rod and cone photoreceptors.

236 feration and selective failure to regenerate cone photoreceptors.

237 visual pigment remains stable in darkness, a cone pigment has some tendency to dissociate spontaneous

238 otted to summarise the topography of rod and cone pigment kinetics and descriptive statistics conduct

239 Cones produce energy using a large cluster of mitochondr

240 pression in late-stage RPCs triggers ectopic cone production at the expense of late-born fates.

241 u2f1 or Pou2f2 in RPCs expands the period of cone production, whereas misexpression in late-stage RPC

242 alysis reveals two separate groups of growth cone properties that together account for growth cone st

243 ment-binding protein, leading to early-onset cone protection.

244 ed actin in growth cones and prevents growth cone recovery after repellent-induced collapse.

245 microperimetry is a powerful tool to capture cone regeneration after vitreoretinal surgery.

246 s a newly developed Center-Surround model of cone resilience and rod vulnerability.

247 Finally, Crb1 plays a role in cones' responsiveness to light through an arrestin-trans

248 ed by retinitis pigmentosa in 14% (3/23) and cone-rod dystrophy (4%, 1/23).

249 one family with macular dystrophy, nine with cone-rod dystrophy (CORD), and three with retinitis pigm

250 n EYS-RD: retinitis pigmentosa (RP; 85.94%), cone-rod dystrophy (CORD; 10.94%), and Leber congenital

251 8, associated with human autosomal recessive cone-rod dystrophy, negatively regulates EV levels in th

252 's congenital amaurosis (LCA1), and dominant cone-rod dystrophy-6 (CORD6) affected RetGC1 activity an

253 2_P355del associated with autosomal dominant cone-rod dystrophy.

254 obilities of both unsaturated tails confer a cone shape to DOPC, and PGPC separates form DOPC.

255 on the solvent nature-aromatic or aliphatic-cone-shaped C(3)-symmetric subphthalocyanine 1 can under

256 s and their physiological counterparts where cone-shaped lipids, like cardiolipin, are involved.

257 ngstrom resolution, revealing an asymmetric, cone-shaped structure.

258 ntrols in the manner in which melanopsin and cone signals are combined.

259 ecifies selective wiring and transmission of cone signals.

260 ncrease the difference of anomalous M- and L-cone signals.

261 diversity primarily aligns with that of the cone sites and magmatically influenced hydrothermal syst

262 e neurotoxic peptides in the venom of marine cone snails and have broad therapeutic potential for man

263 Caprella spp.; sea anemones, Actinia equina; cone snails, Conidae; male platypus, Ornithorhynchus ana

264 seq differential expression analysis between cone-specific Bmal1 knockout cones (cone-Bmal1(-/-) ) an

265 , identified thousands of candidate rod- and cone-specific CREs, and identified motifs for rod- and c

266 mpanied by marked decreases of both rod- and cone-specific gene expression.

267 are fundamental for the constitution of the cone-specific glycocalyx stained by the PNA (peanut aggl

268 ncRNA expression, whereas CRX alone favored cone-specific ncRNA expression, providing quantitative e

269 fic CREs, and identified motifs for rod- and cone-specific TFs.

270 properties that together account for growth cone structure and dynamics.

271 magnetic Dirac fermions with simplest double cone structure near the Fermi level emerge in the antife

272 radiation on the Si substrate, and a twisted cone structure with a height of 3.5 um was created at th

273 , the precise dark apo-opsin contents across cone subtypes are mostly unknown, as are their dark acti

274 a mechanism by which the clock controls the cone synaptic transfer function to second-order cells an

275 oidal neovascularization (RCN) in enhanced S-cone syndrome (ESCS).

276 Enhanced S-cone syndrome has a highly variable phenotype with relat

277 0/26) showed evidence of generalized rod and cone system dysfunction.

278 Remarkably, ELFN2 in cone terminals functions in synergy with a related adhes

279 ive widening of the rhabdoms and crystalline cone tips.

280 ochastic fluctuations of actin in the growth cone to produce axon growth and guidance.

281 for comparing short (S) wavelength-sensitive cones to long (L) and medium (M) wavelength-sensitive co

282 cues act during development to guide growth cones to their proper targets in both the central and pe

283 f impenetrable barriers, forcing axon growth cones to traverse one half of each somite as they extend

284 Birds have four color cone types (compared to three in humans) and might perce

285 Here, we analyzed the distribution of all cone types across the entire retina for two commonly use

286 ese materials as wires, coils, films, tubes, cones, unimorphs, bimorphs, and printed elements enables

287 Rods and cones use intracellular Ca(2+) to regulate many function

288 Here we show that Vangl2 controls growth cone velocity by regulating the internal retrograde acti

289 However, the processes enabling cone vision in bright light (i.e. photopic vision) are n

290 Rod and cone visual pigment synthesis rates in those with AMD (v

291 icipants, AO-IRAF structure corresponding to cones was observed, as we have demonstrated previously.

292 In contrast, dark adaptation of cones was unaffected by the S21A mutation.

293 ean regularity indices for single and double cones were conspicuously lower than those of other fishe

294 ods and red/green cones, whereas blue and UV cones were relatively unaffected.

295 , retinal progenitors destined to become red cones were transfated into ultraviolet (UV) cones and ho

296 ding decreased numbers of rods and red/green cones, whereas blue and UV cones were relatively unaffec

297 This performance originates in the foveal cones, which are extremely narrow and long to form a hig

298 evelopmental or phototransduction defects in cones with mislocalized nuclei, their dark adaptation wa

299 2 to be pivotal for the functional wiring of cones with the ON type of BC.

300 olar cell types that rewire, two contact new cones within stable dendritic territories, whereas one e