ライフサイエンスコーパス: dim

1 The accumulation of Gr-1(dim)CD11b(+) cells is accompanied by the disappearance o

2 The Gr-1(dim)CD11b(+) cells suppress T cell proliferation and IFN

3 cells exhibit unsegmented nuclei, have Gr-1(dim)Ly-6G(dim)CD11b(+) phenotype, and express F4/80, CD4

4 ibit unsegmented nuclei, have Gr-1(dim)Ly-6G(dim)CD11b(+) phenotype, and express F4/80, CD49d, Ly-6C,

5 e-, fruit-, and soy-rich (VFS) pattern and a dim sum- and meat-rich (DSM) dietary pattern.

6 l and temporal frequencies was measured at a dim luminance level (2.6 .

7 te that brightness artifacts are caused by a dim nonpunctate membrane-bound fraction of Gag.

8 oupling, but the signal-to-noise ratio for a dim (multiphoton) light response is increased at night b

9 Maintaining diabetic animals in a dim-adapting light did not slow the progression of these

10 ize of evoked pupil dilation was larger on a dim versus bright background.

11 onstrated with transition from the dark to a dim light background.

12 Vertebrates acquired dim-light vision when an ancestral cone evolved into the

13 ve found that this knock-out does not affect dim-light vision mediated by rods acting as single-photo

14 8.87 [2.83] at baseline vs 7.33 [3.52] after dim-red LT) and the Parkinson's Disease Sleep Scale (97.

15 1 [19.86] at baseline vs 99.28 [16.94] after dim-red LT).

16 Mb output potentiation selectively amplifies dim retinal inputs at Mb --> ganglion cell synapses.

17 photoreceptors that function in daylight and dim light, respectively.

18 Both bright LT and dim-red LT were associated with improvements in sleep qu

19 AUGMIN subunit3 (AUG3), a homolog of animal dim gamma-tubulin 3, plays a critical role in gamma-tubu

20 t3 (AUG3), which encodes a homolog of animal dim gamma-tubulin 3/human augmin-like complex, subunit 3

21 dual cone central core reflectances appeared dim, suggesting loss of photoreceptor outer segments.

22 t image motion produces the same problems as dim light: photon noise and low signal-to-noise ratio.

23 d bipolar (RB) cell pathway that operates at dim backgrounds and a rod --> cone --> cone bipolar cell

24 ng the loss of visual information carried by dim scotopic signals.

25 s were derived, at least in part, from CD11c(dim)CD11b(int)Gr1(-) lung-resident monocytic cells trans

26 es over time in vivo even in initially CD123(dim) populations, and that human CD123-redirected T cell

27 the migration of purified CD4(+)CD25(+)CD127(dim) T regulatory cells.

28 CD14(dim)CD16(+) and CD14(+)CD16(+) monocytes showed a prefer

29 analyzed separately, the low-abundance CD14(dim) ("patrolling") subpopulation was more responsive to

30 ases on whole-mount histology, although CD14(dim) cells disappeared from blood.

31 tes, was observed in CD14(+)CD16(-) and CD14(dim)CD16(+) monocytes, but not in CD14(+)CD16(+) monocyt

32 TLR9-L mobilized the CD14(+)CD16(+) and CD14(dim)CD16(++) monocytes, and only TLR7/8-L and TLR9-L ind

33 + of T-cell subsets and %CD14+CD16+ and%CD14(dim)CD16+ monocyte subsets.

34 rtance of plasmacytoid dendritic cells, CD14(dim) monocytes, and C1q as key regulators of inflammator

35 dothelial migration was not observed in CD14(dim)CD16(+) monocytes during the 30-min observation peri

36 Long-range crawling behavior in CD14(dim)CD16(+) monocytes was abrogated by blockade of ICAM1

37 ate (CD14(+)CD16(+)), and nonclassical (CD14(dim)CD16(+)) monocytes.

38 ate (CD14(+)CD16(+)), and nonclassical (CD14(dim)CD16(+)) monocytes.

39 iate [CD14(+)CD16(+)] and nonclassical [CD14(dim)CD16(+)]) monocytes was increased in the peripheral

40 (CD14(++)/CD16(-), CD14(++)/CD16(+) or CD14(dim)CD16(++)), as determined by multi-colour flow cytome

41 bsets, CD14(+)CD16(-) (classical) and CD14(+/dim)CD16(+) (nonclassical/intermediate), have been descr

42 In particular, CD56(bright)CD16(-/dim) NK cells are the focus of interest.

43 weight, including 5 of 5 patients with CD19(dim) or CD19(-) B-ALL.

44 MS patients, increased levels of CD3(+)CD20(dim) T cells are effectively depleted by RTX.

45 ally demonstrate the existence of CD3(+)CD20(dim) T cells.

46 m MDH patients were found in the CD4(+) CD25(dim) T cell fraction and showed enhanced CD38 and PD-1 e

47 enic reporter mice to identify a Tie1(+)CD31(dim)vascular endothelial (VE)-cadherin(-)CD45(-) precurs

48 activated CD8(+) effector T cells with a CD4(dim) CD8(+) phenotype, both exhibiting exquisite specifi

49 ingle positive, CD8 single positive, and CD4(dim)CD8(bright)) were found in NSG-huPBMC mouse brain wi

50 This population is known as CD4(dim)CD8(bright) T cells.

51 Brain CD4(dim)CD8(bright) T cells from HIV-infected mice exhibited

52 ositive T cells into mouse brain induced CD4(dim)CD8(bright) T cells by 10-fold, which were prolifera

53 Wnts secreted from astrocytes induced CD4(dim)CD8(bright) T cells by 2-fold in vitro.

54 We evaluated the role of CD4(dim)CD8(bright) and CD8 single positive T cells in HIV-i

55 Further, higher frequency of CD4(dim)CD8(bright) T cells (R = -0.62; p </= 0.001), but no

56 Thus, CD4(dim)CD8(bright) T cells are capable of HIV control in th

57 NS during HIV infection can give rise to CD4(dim)CD8(bright) T cells, likely through a Wnt signaling-

58 for the first time that MHC class II(+)CD40(dim)CD86(dim)IL-10(+) microglia are potent inducers of A

59 se results indicate that MHC class II(+)CD40(dim)CD86(dim)IL-10(+) microglia have regulatory properti

60 EPCs (CD45(dim)/CD34(+)/kinase domain receptor(+)) from 36 HIV-unin

61 odstream for a longer time (CXCR4(bright)CD5(dim) cells).

62 responsive to BCR ligation than isolated CD5(dim)CXCR4(bright) cells of the same patient.

63 ng immunophenotypes: CD1a(-), CD8(-), CD5(-)(dim), and positivity for 1 or more stem cell or myeloid

64 CD56(dim) cells are generally considered more cytotoxic, wher

65 CD56(dim)CD16(+) NK cells made up the vast majority of NK cel

66 CD56(dim)CD57(+) NK cells are less responsive to IL-2 and pro

67 was most prominent within the adaptive CD56(dim) NK-cell population lacking PLZF expression.

68 ptor CD16 is present on essentially all CD56(dim) peripheral blood natural killer (NK) cells.

69 Also, CD56(dim) NK cells cocultured with M2 displayed lower degranu

70 a and degranulation by CD56(bright) and CD56(dim) NK cells following NKG2D stimulation were dependent

71 marily on conventional CD56(bright) and CD56(dim) NK cells from blood.

72 +) NK cells, including CD56(bright) and CD56(dim) subsets, exhibit impaired cell activation and IFN-g

73 major NK cell subsets (CD56(bright) and CD56(dim)) exist in humans and have distinct anatomical local

74 ets, namely the CD56(bright)CD16(+) and CD56(dim)CD16(-) subsets, were increased in the peripheral bl

75 im)CD57(-)KIR(-)NKG2A(+) (NKG2A(+)) and CD56(dim)CD57(-)KIR(-)NKG2A(-) (lacking inhibitory receptors;

76 The relationship between CD56(dim) and CD56(bright) proliferating cells indicates that

77 Peripheral blood CD56(dim)CD16(+) and CD56(bright)CD16(-) NK cells expressed s

78 revealed that the ratio of CD56(bright):CD56(dim) NK cells differed in the GPI+ and GPI(neg) populati

79 PD-1 is expressed by CD56(dim) but not CD56(bright) NK cells and is confined to fu

80 CD57 was mostly expressed by CD56(dim)CD16(+) NK cells.

81 3(-) CD56(+) total NK cells and CD16(+) CD56(dim) NK cells were inversely correlated with HIV-1 DNA l

82 CD3(-) CD56(bright) CD16(-) and CD3(-) CD56(dim) CD16(+) subsets.

83 CD3(+)CD56(+) NKT-like cells and CD3(-)CD56(dim) and CD3(-)CD56(hi) NK cells at baseline, BCG revacc

84 granzyme B but less perforin than CD3(-)CD56(dim) NK cells.

85 6(bright), canonical, or adaptive CD3(-)CD56(dim) NK cells.

86 predominantly to differentiated CD57(+)CD56(dim) NK cells.

87 c CD56(bright) NK cell to the cytolytic CD56(dim) NK cells.

88 er frequency of predominantly cytotoxic CD56(dim) NK cells (p = 0.011), higher frequency of predomina

89 D16(-) NK cells and less differentiated CD56(dim)CD16(+) NK cells.

90 Our data suggest that some dying CD56(dim) cells become CD16(+)CD56(-) NK cells and that CD16(

91 pansion of a novel subset of FcRgamma(-)CD56(dim) NK cells with an altered activation receptor repert

92 Functionally, CD56(dim) NK cells responded poorly to target cells at the ti

93 nal, whereas CD107a(+) and IFN-gamma(+) CD56(dim) NK cells presented a different pattern of HLA class

94 of mouse NK cells are enriched in human CD56(dim) cells.

95 r the IgG Fc portion expressed on human CD56(dim) NK cells and involved in Ab-dependent cell cytotoxi

96 Human CD56(dim) NK cells were costimulated specifically by HVEM but

97 und that in addition to the known human CD56(dim)CD16(+), CD56(bright)CD16(-), and CD56(-)CD16(+) NK

98 ed for the generation of hyporesponsive CD56(dim) NK cells with limited degranulation and cytotoxic c

99 with STAT1 GOF mutations have immature CD56(dim) NK cells with decreased expression of CD16, perfori

100 P1), and RORA mRNA levels are higher in CD56(dim) cells.

101 in vivo restored perforin expression in CD56(dim) NK cells and partially restored NK cell cytotoxic f

102 In CD56(dim) NK cells, the memory-like IFN-gamma response was co

103 enotype characterized by an increase in CD56(dim) NK cells.

104 s higher in CD56(bright)CD16(-) than in CD56(dim)CD16(+) NK cells.

105 human peripheral blood, the more mature CD56(dim) NK cell efficiently kills malignant targets at rest

106 is expressed on essentially all mature CD56(dim)CD16(+) NK cells and is expressed heterogeneously in

107 nduced an increased frequency of mature CD56(dim)NKG2A(+)CD57(+) NK cells in the blood that persisted

108 n of NK CD56(bright) cells toward an NK CD56(dim) phenotype was tightly dependent on MCM4-dependent c

109 n addition, the specific loss of the NK CD56(dim) subset in patients was associated with a lower rate

110 with degranulation when a wide range of CD56(dim) NK cell activating receptors were stimulated, where

111 Activation of CD56(dim) NK cells by cross-linking CD16 with antibodies resu

112 s the percentage and absolute number of CD56(dim) NK cells decreased.

113 NKp30 and NKp46 to approximately 90% of CD56(dim) NK cells in some VS HIV(+) individuals may influenc

114 RBV pretreatment, both the frequency of CD56(dim) NK cells with cytotoxic effector functions and the

115 8(+) T cells plus a milder expansion of CD56(dim) NKG2A(+) KIR(-) natural killer (NK) cells.

116 mediate CXCR3 levels on the majority of CD56(dim)CD16(+) pNK cells.

117 We show an expansion of CD56(dim)CD57(dim)CD69 + CCR7 +KIR+ NK cells in TILN.

118 tion, characterized by the expansion of CD56(dim)NKG2A(-)KIR(+) cells, even in the absence of NKG2C e

119 rs CD319 and CD229 on pDCs and CD319 on CD56(dim) NK cells was selectively increased.

120 xpression of CD319 on pDCs and CD229 on CD56(dim) NK cells, but RNA-IC stimulation increased CD319 an

121 cells and inhibitory receptor NKG2A on CD56(dim) NK cells, compared with nonresponders.

122 ated activation than do CD56(bright) or CD56(dim)CD57(-) NK cells.

123 n maintained independently from GPI(pos)CD56(dim).

124 ting cells indicates that proliferating CD56(dim) cells both self-renew and are derived from prolifer

125 ve compared the behavior of FACS-sorted CD56(dim)CD57(-)KIR(-)NKG2A(+) (NKG2A(+)) and CD56(dim)CD57(-

126 ls to be more metabolically active than CD56(dim) cells, which supports their production of large amo

127 action of GPI-negative cells within the CD56(dim) NK cells was markedly lower than that of neutrophil

128 ficiency characterized by a lack of the CD56(dim) NK subset.

129 ge preceding terminal maturation to the CD56(dim) stage, considered the most enabled for cytotoxicity

130 ficient patients are exclusively of the CD56(dim) subset, which is recapitulated on in vitro NK cell

131 K cells and downregulated CX3CR1 in the CD56(dim) subset.

132 degranulation, is maintained across the CD56(dim) subsets.

133 essed on highly mature cells within the CD56(dim)CD16(+) NK cell compartment.

134 infections, drives the expansion of the CD56(dim)CD57(+)NKG2C(+) NK cell population, skewing the NK c

135 forin(low) NK cells, with others by the CD56(dim)perforin(high) cytotoxic counterpart.

136 oduce IFN-gamma at levels comparable to CD56(dim) NK cells.

137 ma(-) NK cells as a proportion of total CD56(dim) NK cells increased in cART-naive viremic HIV-infect

138 r rates of glucose uptake compared with CD56(dim) cells.

139 more metabolically active compared with CD56(dim) cells.

140 me 10 (PTEN) protein when compared with CD56(dim) NK cells.

141 We show an expansion of CD56(dim)CD57(dim)CD69 + CCR7 +KIR+ NK cells in TILN.

142 profound nuclear hypersegmentation, a CD62L(dim), CD16(bright), CD11b(bright), CD66b(bright), CD63(b

143 The differences between CD62L(dim) and mature neutrophils are unlikely to have been a

144 red much earlier in blood than labeled CD62L(dim) and segmented neutrophils, which shared similar lab

145 remely low transcriptional capacity of CD62L(dim) neutrophils and the fact that neutrophils do not di

146 Therefore, we propose CD62L(dim) neutrophils are a truly separate neutrophil subset

147 banded nucleus, and T-cell-suppressing CD62L(dim) neutrophils with a high number of nuclear lobes.

148 omes by cluster analysis revealed that CD62L(dim) neutrophils were clearly separate from conventional

149 a very immature thymic, CD34(+)/CD1a(-)/CD7(+dim) stage, before Ddelta2(Ddelta3)-Jdelta1 rearrangemen

150 responses occur within the CD38(+)CD27(-)CD8(dim)T cell population, the minority populations of CD8(b

151 Furthermore, the frequency of CD8(dim)T cells directly correlates with viral load and clin

152 ytokines coincides with the emergence of CD8(dim)T cells, and the size of this population inversely c

153 the low expression of the CD8 receptor (CD8(dim)).

154 of a functionally impaired HIV-specific CD8(dim)T cell population less efficient in controlling HIV

155 first time that MHC class II(+)CD40(dim)CD86(dim)IL-10(+) microglia are potent inducers of Ag-specifi

156 s indicate that MHC class II(+)CD40(dim)CD86(dim)IL-10(+) microglia have regulatory properties potent

157 ibility complex class II-restricted CD8alpha(dim) T cells that are generated through CD4 downregulati

158 ession-like phenotype observed under chronic dim LAN.

159 nstant routine of enforced posture, constant dim light, hourly isocaloric meals, and sleep deprivatio

160 pulation of CLL cells that migrate are CXCR4(dim)CD5(bright) with higher CD49d, CD80, CD86, and HLA-D

161 t and moved into the peripheral blood (CXCR4(dim)CD5(bright) subpopulation) have higher cell surface

162 Also, isolated CD5(bright)CXCR4(dim) cells, representing CLL that had been newly release

163 ed CLL cells manifest a proliferative, CXCR4(dim)CD5(bright) phenotype compared with those in the PB

164 metry as CD63(bright)CD203c(+)CD123(+)HLA-DR(dim/-)CD41a(-)lineage(-).

165 re alleviated by imipramine treatment during dim night-time light.

166 hesized that nocturnal light exposure (i.e., dim LAN) would induce depressive responses and alter neu

167 igh-energy intermediate, capable of emitting dim light by itself, formed from the reaction between gu

168 of co-expressed bfloGFPc1 showing extremely-dim brightness due to low (0.1%) quantum efficiency.

169 phids possess several visual adaptations for dim-light conditions, including enlarged eyes, an aphaki

170 le for GABA in sensitizing the circuitry for dim-light vision, thereby complementing GABA's tradition

171 g insects are hypothesized to compensate for dim conditions by integrating light over longer times.

172 tude is only slightly perturbed, optimal for dim light and for small shifts 2) another class of sched

173 nd high photosensitivity in rod pigments for dim-light vision.

174 orming the transduction channel required for dim light vision and the ON pathway.

175 the vertebrate retina and is responsible for dim light vision.

176 r cells with differing sensitivity: rods for dim light and cones for bright light and colour detectio

177 tes have a duplex retina containing rods for dim light vision and cones for bright lights and color d

178 sed upon three photoreceptor types: rods for dim light vision and two types of cones (M and S) for co

179 alia was dominated by positive selection for dim-light vision, supporting the predominate nocturnalit

180 ght vision and relatively weak selection for dim-light vision.

181 gle-QD properties, principally emitting from dim gray states but having high two-exciton (biexciton)

182 over a wide range of light intensities, from dim starlight to bright sunshine.

183 n can modulate the kinetics of recovery from dim light stimulation.

184 eme lighting, peripheral vision, and general dim lighting.

185 GR(dim)-LPS mice also exhibited sustained locomotor impairm

186 GR(dim)-LPS mice exhibited elevated and prolonged levels of

187 responses to a systemic immune challenge, GR(dim) mice, in which absent GR dimerization leads to impa

188 h a GR mutation that blocks dimerization (GR(dim) mice).

189 r (lethargy, piloerection, ptosis) in the GR(dim)-LPS mice was associated with increased early brain

190 We also provide directions on how to image dim signals such as those of radioluminescence (1-1.5 h)

191 In dim light conditions, AHA2 is found in intracellular com

192 In dim light, rod-photoreceptors are active, but colour vis

193 six types of photoreceptors: rods, active in dim light, double cones that are thought to mediate achr

194 can explain certain experiences of colour in dim lights, such as a 'blue shift' in twilight.

195 ion cell performs a different computation in dim light--averaging contrast within its receptive field

196 tant bright light and a control condition in dim light.

197 erin potentiates the sensitivity of cones in dim light conditions but does not contribute to their ca

198 hifts were calculated from the difference in dim light melatonin onset (DLMO) between CRs.

199 se development preserves retinal function in dim light.

200 ily apparent when the seedlings are grown in dim white light, were attenuated by treatment with eithe

201 ort, during a limited time of fast growth in dim white light beginning 2.5 days after germination.

202 mmalian retina encodes visual information in dim light using rod photoreceptors and a specialized cir

203 These cells swam normally in dim light but could not maintain typical swimming trajec

204 responses of SbC-RGCs, which are observed in dim and bright light conditions.

205 (AMD) have vision problems, particularly in dim light conditions.

206 ltiday, in-laboratory protocols performed in dim light, throughout which behavioral and environmental

207 tial circadian phase assessment procedure in dim light (<3 lux), and were then randomized for exposur

208 ompleted constant routine (CR) procedures in dim light (<3 lux) before and after the light exposure t

209 that typically maximize light production in dim strains of luminous bacteria.

210 the other session (control) they remained in dim room light, counterbalanced.

211 mpact of diabetes on contrast sensitivity in dim light is unknown.

212 at the moth's visual processing does slow in dim light.

213 in bright and self-selected lighting than in dim light for both chronotypes, whereas visual comfort w

214 asmin and experienced darkening of vision in dim illumination for 4 months, despite improvement in vi

215 e specialized neurons that mediate vision in dim light and are the predominant photoreceptor type in

216 tion of ocular specializations and vision in dim light are discussed.

217 Vision in dim light depends on synapses between rods and rod bipol

218 Vision in dim light, when photons are scarce, requires reliable si

219 -photon responses are critical for vision in dim light.

220 oise and limits the sensitivity of vision in dim light.

221 receptors, the cells that initiate vision in dim light.

222 communication is indispensible for vision in dim light.

223 e visual signal, thereby improving vision in dim light.

224 an ultradian light-dark cycle (2.5 h wake in dim light, 1.5 h sleep in the dark), forced desynchrony

225 n is for imaging signals that are inherently dim and undetectable using standard microscopy technique

226 ro measurements of rhodopsins to investigate dim-light adaptation.

227 of spatial details on bright days and large dim objects on moonless nights.

228 ittermates were housed in a 12:12 hour light-dim light photocycle (30 lux during the day and 3 lux at

229 d 6.7 h bright white light PRC and a <15 lux dim background light PRC constructed under similar condi

230 f either bright white light (n=18) or <3 lux dim background light (n=18) scheduled at 1 of 18 circadi

231 o discernible PRC was observed in the <3 lux dim background light PRC.

232 000 lux) and to compare this PRC to a <3 lux dim background light PRC.

233 ither 7,000-lux bright white light or 50-lux dim red placebo light (N=23 for each group).

234 ce photoreceptor degeneration or maintenance dim light (25 lux).

235 Rhodopsin, the mammalian dim-light receptor, is a unique test case for understand

236 on where rod and cone photoreceptors mediate dim- and bright-light vision, respectively.

237 mperature-sensitive visual pigment mediating dim-light vision, offers an opportunity to enhance our u

238 Finally, neither dim light alone nor a shortened night is sufficient for

239 Interestingly, we also observed dim ORF1p immunoreactivity in histologically NE of all p

240 reduced sucrose preference, in weeks 2-3 of dim light at night, whereas WT mice did not.

241 ming than WT mice during weeks 1, 2 and 4 of dim light at night exposure.

242 Continuation of dim light is unnecessary for T15/30 behavioral entrainme

243 two important factors in the development of dim-light vision.

244 Mutation of dim-5, which encodes an H3K9 methyltransferase responsib

245 vels (41 min) and delayed circadian phase of dim-light melatonin offset (1.37 h), partially mediated

246 re calculated as the difference in timing of dim light melatonin onset (DLMO) during pre- and post-st

247 rly defined cell subsets than those based on dim markers and for rare populations.

248 2 hr bright lightratiodark (1000lux, BLD) or dim lightratiodark (50lux, DLD) condition.

249 ffect dCRY phototransduction under bright or dim light in vivo as measured by light-induced proteolys

250 rences, such as optimization for computer or dim-light working, or night driving, could be useful too

251 n either a standard light-dark cycle (LD) or dim LAN (dLAN).

252 were randomized 1:1 to receive bright LT or dim-red LT (controlled condition) twice daily in 1-hour

253 rerequisite for rod cells, which mediate our dim-light vision.

254 The struggle to perceive dim downwelling light and bioluminescent sources and the

255 All candidate signatures appear radio-dim and do not have the X-ray to radio flux ratios requi

256 inct classes of puncta, including relatively dim puncta that were located at active zones and may ref

257 brate retinas are generally composed of rod (dim-light) and cone (bright-light) photoreceptors with d

258 more reliable flight reactions in the fish's dim and turbid habitat as compared with fish lacking thi

259 light exposure were assessed using salivary dim-light melatonin onset (DLMO) and wrist-worn photomet

260 nificant for all parameters (except scotopic dim-flash b-wave implicit time), ranging from 0.34 to 0.

261 ponses of rod photoreceptors, which subserve dim light vision, are carried through the retina by thre

262 The dim population showed similar trends, though velocities

263 he self-selected and the bright, but not the dim lighting condition, the onset of melatonin secretion

264 from the difference in the clock time of the dim light melatonin onset (DLMO) between the initial and

265 mechanism optimizing the performance of the dim-light channel of vision, which consists of sensitizi

266 ontinued activation of the photocycle of the dim-light receptor rhodopsin leads to the accumulation o

267 ey are nearer to ancestral pigments than the dim-light rod photoreceptor rhodopsin.

268 Scale score comparing the bright LT with the dim-red LT.

269 nt was also agravitropic but when adapted to dim red light it displayed a reversed gravitropic respon

270 cently demonstrated that chronic exposure to dim (5 lux) LAN provokes depressive-like behaviors and r

271 Exposure to dim light at night (dLAN) disrupts natural light/dark cy

272 Bdnf expression after 3 weeks of exposure to dim light at night, but only mice deficient for the PERI

273 Firstly, exposure to dim nocturnal illumination (<0.1 lux), rather than compl

274 asuring: (1) the variability in responses to dim flashes, (2) Neurobiotin tracer coupling, and (3) ju

275 action of both regions sustains responses to dim light, allows for the integration of light over time

276 Rod-driven responses to dim scotopic single-flash stimuli were normal in 7 patie

277 es reduces retinal and visual sensitivity to dim light flashes.

278 t light should not compromise sensitivity to dim light.

279 s, implying strong selective pressure toward dim-light vision in Cambrian ecosystems.

280 visited by the LMCs differed between the two dim-light species, their dendritic extents were very sim

281 Rods, active under dim illumination, are thought to saturate at higher (pho

282 ght sunlight to single-photon counting under dim starlight.

283 than with a spherical IOL, especially under dim light.

284 paired in rh7 mutant flies, especially under dim light.

285 ina but not in the retina of mice kept under dim lighting.

286 ng 3 balanced crossover segments, once under dim light (DL: 8 lx), and once under either white light

287 efficiency that allows them to operate under dim light conditions.

288 tina, which triggers a visual response under dim light conditions.

289 ntrols the threshold responses of RGCs under dim ambient light.

290 such responses to be mediated by rods under dim lighting conditions, rods/M-cones/melanopsin under i

291 ht light to enhancing the same signals under dim illumination.

292 n, the visual pigment mediating vision under dim light, is composed of the apoprotein opsin and the c

293 But very dim-light exposure quickly translocates them to the oute

294 For animals active in very dim light the visual system is challenged by several sou

295 Arch fluorescence, however, is very dim and is not optimal for applications in live-cell ima

296 through associated limitations with the very dim-fluorescent acceptor ShadowG for mTFP1 and the red-s

297 fects on heterochromatin compaction, whereas dim-3 caused more drastic changes, specifically decreasi

298 idual trajectories and can be used also with dim and dense molecules.

299 onstrate how altering light/dark cycles with dim LEN (dLEN) speed the development of breast tumors, i

300 hotoreceptor cells are light-responsive with dim-flash kinetics similar to adult wild-type photorecep