ライフサイエンスコーパス: DIV

1 cle velocity was about 30% less than after 1 DIV.

2 In cells of 7-10 DIV, glutamate caused only a modest and reversible drop

3 e to KCl or to glutamate in cultures at 7-10 DIV.

4 tion had decreased from those assessed at 10 DIV, thus providing an approximate limit to the effectiv

5 magfura-2 ratio reached maximum values by 10 DIV.

6 te, 100 microM kainate or 50 mM K(+) from 10 DIV onward.

7 iatal DA increased substantially, through 10 DIV.

8 of VM DA progressively increased through 10 DIV.

9 After 11 DIV, the peak GABA-activated current was largely pH inse

10 For granule cells before 11 DIV, the peak GABA-activated current was inhibited at lo

11 rams at both early (< 11 DIV) and late (> 11 DIV) development times at each H+ concentration.

12 ime frequency histograms at both early (< 11 DIV) and late (> 11 DIV) development times at each H+ co

13 ) were localized to GABAergic synapses at 14 DIV but were not expressed at 7 DIV.

14 t an increased number of granule cells at 14 DIV express delta subunit mRNAs as compared with 4 DIV g

15 after strong NMDA stimulation, whereas at 14 DIV phospho-CREB rose only transiently and fell back to

16 n none of the neurons at 7 DIV, in 20% at 14 DIV, and in 80% at 21 DIV.

17 Moreover, at 14 DIV, but not at 7 DIV, NMDA receptor stimulation induced

18 ssion at 7 DIV to clustered expression at 14 DIV.

19 ails the distribution of BDNF and TrkB at 14 DIV.

20 l glutamatergic responses are detected at 14 DIV.

21 4 d in vitro (DIV) compared with those at 14 DIV.

22 became vulnerable to the same stimulus by 14 DIV.

23 h-clubs at an early stage in development (14 DIV).

24 n increase in the number of precursors in 14 DIV cultures.

25 Overexpression of SALM1 in 14 DIV neurons recruits NMDA receptors (NR) and PSD-95 to d

26 ter 48 h, whereas transfection of neurons 14 DIV has no significant effect on neurite outgrowth.

27 of GABAergic synapses increased from 7 to 14 DIV, with a corresponding increase in frequency of mIPSC

28 The mIPSC decay quickened from 7 to 14 DIV, with a parallel change in the distribution of the a

29 approximately 10-fold between 8-9 and 14-15 DIV, changing little thereafter.

30 hen increased over 5 DIV values by 12 and 15 DIV.

31 In the majority of neurones at 11-17 DIV (71 %), exposure to glutamate for 10 min induced a p

32 tochondrial depolarisation in cells at 11-17 DIV and increased the proportion of neurones exhibiting

33 a small proportion of cells (29 %) at 11-17 DIV the [Ca2+]i increase induced by exposure to 100 micr

34 amine fibers from nigral neurons during 8-17 DIV.

35 By 17 DIV, many measures of DA function had decreased from tho

36 reased, in both the VM and striatum, over 17 DIV.

37 , followed by a decline in levels through 17 DIV; levels of striatal TH, in contrast, increased throu

38 At 18 DIV, the overall density of mitochondria within terminal

39 After an additional 2 DIV in serum-free medium, the number of TH neurons had d

40 8 hours) exposure to bifenthrin commencing 2 DIV-enhanced neurite outgrowth and persistently increase

41 CGNs), TRPC5 was detected at 2 d in vitro (2 DIV), a stage corresponding to CtxB-stimulated Ca2+ infl

42 een Dab1 ko and wt cultures were found at 20 DIV.

43 y 4 (four days in vitro or DIV 4) to day 20 (DIV 20), we observed that 1) GABA(A)Ralpha and GlyRalpha

44 at 7 DIV, in 20% at 14 DIV, and in 80% at 21 DIV.

45 However, by 21 DIV, the number of synapses per neuron had jumped 30- to

46 ghts of high-density neuronal networks by 21 DIV, which were up to 18 mum thick, demonstrating the co

47 ampal neurons, and at synapses in mature (21 DIV) neurons.

48 y continued to increase, at least through 21 DIV.

49 f colocalization did not change from 7 to 21 DIV, this study details the distribution of BDNF and Trk

50 CNTF of lesioned SC neurons in mature (21-28 DIV) cultures may reflect a loss of sensitivity to CNTF

51 In long-term triple cultures (44 +/- 3 DIV), the striatal dopamine fiber density was high and w

52 sed relative to anterograde vesicles after 3 DIV, but this fact alone could not explain the decrease

53 After 3 DIV, the levels of striatal DA increased substantially,

54 In observations at 1, 2 and 3 DIV, larger vesicles moved more slowly than small vesicl

55 Neurite outgrowth in CGNs, determined at 3 DIV, was accelerated by CtxB and suppressed by TRPC5 siR

56 vealed large increases in VM TH after only 3 DIV, followed by a decline in levels through 17 DIV; lev

57 erved upon Munc18-1 or SNAP-25 loss within 3 DIV.

58 n neuronal activity in older neurones (20-33 DIV).

59 ell death, before synaptogenesis, within 1-4 DIV upon loss of t-SNAREs (syntaxin-1, SNAP-25) or Munc1

60 c length between mutant and wt cultures at 4 DIV, but detected no differences in complexity.

61 e elongation is significantly decreased at 4 DIV.

62 Furthermore, analyses of 4 DIV cultures derived from Dab1 heterozygotes or mice tha

63 taining 1% fetal bovine serum (FBS) on the 4 DIV, surface galC could be reexpressed in all +/+ and P1

64 press delta subunit mRNAs as compared with 4 DIV granule cells.

65 tein, OMP) numbers decreased between 1 and 5 DIV, then increased over 5 DIV values by 12 and 15 DIV.

66 ed to DM ([Formula: see text]) as early as 5 DIV, reducing SCO amplitude and depressing ESA and burst

67 d between 1 and 5 DIV, then increased over 5 DIV values by 12 and 15 DIV.

68 alpha5 subunit from diffuse expression at 7 DIV to clustered expression at 14 DIV.

69 ssed as clusters in none of the neurons at 7 DIV, in 20% at 14 DIV, and in 80% at 21 DIV.

70 Moreover, at 14 DIV, but not at 7 DIV, NMDA receptor stimulation induced a dephosphorylati

71 At 7 DIV, the mean number of synapses per neuron was less tha

72 napses at 14 DIV but were not expressed at 7 DIV.

73 In addition, by 7 DIV, all measures were statistically the same between cu

74 ined P/Q + R component), increased through 7 DIV.

75 At 7 d in vitro (7 DIV) phospho-CREB remained elevated 2 hr after strong NM

76 mbers of OMP-positive (OMP+) neurons after 9 DIV than ANM-alone cultures.

77 -old animals, we demonstrate that adjuvanted DIV vaccine provides protection against lethal disease i

78 II voltage sensor dynamics without affecting DIV.

79 In the absence of alum, DIV vaccine performed poorly in young animals challenged

80 ny interval between day in vitro (DIV) 0 and DIV 12, and knockdown of NOS1AP-L results in increased d

81 ssion in cultures treated between DIV 16 and DIV 21 but not in cultures treated between DIV 8 and DIV

82 density in the neurons in-between DIV 4 and DIV 20, but did not induce a major change in immature (D

83 ut not in cultures treated between DIV 8 and DIV 13.

84 LtrA recognizes two intronic domains, DI and DIV.

85 The DII and DIV S3-S4 loops of NaV channel voltage sensors are impor

86 ted that Asn residues in the S6s of DIII and DIV are important for coupling their pore domains to the

87 onserved Asn residues in the S6s of DIII and DIV in NaV1.5 and NaV1.4.

88 ements of the S4 helices within the DIII and DIV voltage sensors in response to membrane potential ch

89 cantly altered the dynamics of both DIII and DIV.

90 hway through a fenestration between DIII and DIV.

91 age sensor domains (VSDs; DI, DII, DIII, and DIV) in which their S4 segments contain a variable numbe

92 CYC-like gene and downstream targets RAD and DIV.

93 To investigate the role of CYC, RAD, and DIV in the development of ray and disc florets within a

94 d excitotoxic necrosis, which was minimal at DIV 6 and progressively increased through DIV 21.

95 rast, the dynamic in vitro model of the BBB (DIV-BBB) mimics both functionally and anatomically the b

96 GlyRalpha1 density in the neurons in-between DIV 4 and DIV 20, but did not induce a major change in i

97 osporine or cyclosporine was maximal between DIV 4-10 and declined from DIV 10 through 18.

98 PDE4A expression in cultures treated between DIV 16 and DIV 21 but not in cultures treated between DI

99 d DIV 21 but not in cultures treated between DIV 8 and DIV 13.

100 played greater activation or deactivation by DIV than the sum of signal change by the two selective a

101 We suggest that AmMYBML1 is regulated by DIV in association with the B-function proteins DEFICIEN

102 In contrast, DIV vaccines (both adjuvanted and unadjuvanted) performe

103 an unadjuvanted double-inactivated SARS-CoV (DIV) vaccine, we demonstrate an eosinophilic immunopatho

104 d with 64 MHz, and 1 hour daily for 14 days (DIV 21) had significantly reduced levels of secreted AB4

105 with conformational changes within the 4 (DI-DIV) VSDs to define molecular mechanisms of NaV1.5 modul

106 sors from the four alpha-subunit domains (DI-DIV) to monitor the activity of individual voltage-senso

107 nery composed of four homologous domains (DI-DIV), with a pore domain formed by the S5 and S6 segment

108 itively charged residues in the hNav1.4 DIII-DIV linker differentially regulate the kinetics of fast

109 tal muscle channels, using mutations of DIII-DIV linker charges.

110 Because the DIII-DIV linker is an essential structure in Na(V)1.5 inactiv

111 mutations at D1309 and EE1314,15 in the DIII-DIV linker of the human skeletal muscle sodium channel h

112 M with the C-terminal IQ domain and the DIII-DIV linker, combined with the similarity in phenotypes w

113 was slowed to a greater extent for the DIII/DIV double mutation than that calculated from additive e

114 transmembrane segments S3-S5+S6 and the DIII/DIV linker region were associated with high probability

115 toma (DICH), Radialis (RAD), and Divaricata (DIV) specify the development of floral bilateral symmetr

116 DIALIS (RAD), and a ventral gene DIVARICATA (DIV).

117 The DIVARICATA (DIV) gene is required for ventral petal identity.

118 ndrite number only when overexpressed during DIV 5-7.

119 ity and reaction time that was selective for DIV.

120 50 microM forskolin in the media on the four DIV induced surface galC expression in Schwann cells fro

121 s maximal between DIV 4-10 and declined from DIV 10 through 18.

122 wavelet coherence of calcium transients from DIV 12-15 hippocampal neurons from GCaMP6s mice after ap

123 tudies of the molecular mechanisms governing DIV-induced eosinophilia and vaccine failure, especially

124 t did not induce a major change in immature (DIV 4) and mature (DIV 20) neurons; 3) during normoxia G

125 Even though substitutions for the Asn in DIV-S6 in NaV1.5, N1764A and N1764C, produce little ioni

126 In contrast, cell death in DIV 7-8 neurons was prevented by the protein-synthesis i

127 The single R1H, R2H, and R3H mutations in DIV did not produce appreciable proton currents, indicat

128 reast cancer sera promoted neuritogenesis in DIV 12 embryonic day 18 rat hippocampal neurons and neur

129 Local flexibility of domain IV (DIV) governed by molecular hinges at its interdomain jun

130 major change in immature (DIV 4) and mature (DIV 20) neurons; 3) during normoxia GABA, glycine and ta

131 ow-based in vitro blood-brain barrier model (DIV-BBB) we have also investigated the BBB physiological

132 Here, using hippocampal neurons (DIV 15-20) cultured in microfluidic devices in order to

133 the transcription factor MYBI, a homolog of DIV.

134 opleurin-A toxin, which inhibits movement of DIV-S4, still reduced Qmax by nearly 30%, a value simila

135 ces via a hydrophobic interaction with S6 of DIV and an aromatic/hydrophobic interaction with S6 of D

136 However, the septum of DIV is longer, which prevents water molecules from hydra

137 ne-fourth is due to partial stabilization of DIV-S4 (a reduction of 8-10%).

138 spartate at the analogous SF site in DIII or DIV, but not DI, indicating that Ca(V) SF asymmetry is k

139 al neurons from day 4 (four days in vitro or DIV 4) to day 20 (DIV 20), we observed that 1) GABA(A)Ra

140 I/F960V and DIII/F1449V, but not DI/Y405V or DIV/F1752V, regulate Na(v)1.7 activation, consistent wit

141 Inhibition of NKCC1 did not protect DIV 7-8 neurons against OGD-mediated cell death.

142 harge (Qmax), was mutated to a cysteine (R1C-DIV).

143 Gating charge could be fully restored in R1C-DIV by exposure to extracellular MTSEA, a positively cha

144 inactivation, and the gating currents of R1C-DIV-ICM(MTSET) were recorded before and after modificati

145 the individual S4s in R3C-DIII + ICM and R2C-DIV + ICM.

146 DIII + ICM, R2C-DIV + ICM and R3C-DIII + R2C-DIV + ICM, and compared to WT-ICM.

147 ls containing both mutations (R3C-DIII + R2C-DIV) the IC50 for rested-state lidocaine block decreased

148 block was determined for R3C-DIII + ICM, R2C-DIV + ICM and R3C-DIII + R2C-DIV + ICM, and compared to

149 he 2nd outermost Arg in S4 of domain IV (R2C-DIV) in Na(V)1.5.

150 se data raise significant concerns regarding DIV vaccine safety and highlight the need for additional

151 PC-1505 was active against T-20-resistant ("DIV") virus with a G36D substitution in gp41.

152 The RIC-DIV mutation was combined with ICMMTSET to remove fast i

153 gments in domains III and IV (S4-DIII and S4-DIV).

154 demonstrate that the slow movement of the S4-DIV during repolarization is not dependent upon the norm

155 a) in which the outermost arginine in the S4-DIV, which contributes approximately 20% to total gating

156 taflumizone shares the domain IV segment S6 (DIV-S6) binding determinants identified for other SCI in

157 low-inactivated Na(v)1.4 channels and shares DIV-S6 binding determinants with other SCI insecticides

158 erformed in parallel using Transwell systems DIV-BBB models and data were then cross compared.

159 eas modulated by the divided attention task (DIV).

160 The DIV mutation would cause a phenotype of sodium channel h

161 PI(4,5)P(2) reduces the mobility of both the DIV S4-S5 linker and the DIII-IV linker, responsible for

162 th Transwell, C6 and BAEC co-cultured in the DIV-BBB demonstrated predominantly aerobic metabolism ev

163 ng BBB tightness, thus making the use of the DIV-BBB well suited for pharmacological studies.

164 A serine residue on the DIV S2 helix was found to be sufficient to explain Pre1a

165 nced inward gating-pore currents through the DIV voltage-sensor.

166 This indicates that trapping the DIV voltage-sensor in the resting configuration selectiv

167 activated Nav at a conserved site within the DIV S4-S5 linker, which couples the voltage-sensing doma

168 cillations from day in vitro (DIV) 6 through DIV 10.

169 at DIV 6 and progressively increased through DIV 21.

170 (E18) rat cortical neurons were cultured to DIV (days in vitro) 14.

171 nce of functional brain activity specific to DIV.

172 ated as a dual intraoperative visualization (DIV) approach.

173 As of 18 days in vitro (DIV 18), ESNs were synaptically coupled, exhibited spont

174 citotoxic death during development in vitro (DIV 4-21).

175 ressed at any interval between day in vitro (DIV) 0 and DIV 12, and knockdown of NOS1AP-L results in

176 eous calcium oscillations from day in vitro (DIV) 6 through DIV 10.

177 At days in vitro (DIV) 7-8 PSD-95gfp-transfected cells had NMDA-mEPSCs wit

178 In most cells (96 %) at 6-7 days in vitro (DIV) and in a small proportion of cells (29 %) at 11-17

179 reased in number between 1 and 5 d in vitro (DIV) and in mass thereafter.

180 ages during the initial three days in vitro (DIV) but the proportion of Schwann cells expressing surf

181 mRNA, was detected as early as 5 d in vitro (DIV) by RT-PCR.

182 ellar granule cell cultures at 4 d in vitro (DIV) compared with those at 14 DIV.

183 cy for GABA between 11 and 12 days in vitro (DIV) resulting in a shift of the EC50 from 10.7 to 2.4 u

184 trophysiological data over 95 days in vitro (DIV) showed an age-dependent increase of axonal conducti

185 tical neurons cultured for 14-15 d in vitro (DIV) with 100 microm glutamate for 24 hr resulted in 50%

186 ion of hippocampal neurons for 4 d in vitro (DIV) with SALM1 more than doubles the dendritic lengths

187 After 1 d in vitro (DIV), a small population of TH-immunostained neurons tha

188 tamate/10 microM glycine at 5 days in vitro (DIV), but became vulnerable to the same stimulus by 14 D

189 After 3-4 days in vitro (DIV), cells that are plated into the somal compartment h

190 At 11 days in vitro (DIV), DFO reduced average mitochondrial speed by increas

191 In cells of > 11 days in vitro (DIV), exposure to 50 mM potassium or 100 microM glutamat

192 In young cultures after 1-7 days in vitro (DIV), GABA induced depolarizing membrane potentials (+16

193 neurons were cultured 8 or 9 days in vitro (DIV), loaded with the Ca(2+) indicator Fluo-4, and image

194 After 3 days in vitro (DIV), the average vesicle velocity was about 30% less th

195 pses appeared between 3 and 8 days in vitro (DIV), with GABAA receptor subunit clusters appearing fir

196 lar granule cells (CGCs) 6-14 days in vitro (DIV).

197 tory markers at 7, 14, and 21 days in vitro (DIV).

198 ell bodies, was observed at 2 days in vitro (DIV).

199 C expression was lost after 3 days in vitro (DIV).

200 2 and were cultured for up to 60 d in vitro (DIV).

201 see text]) mice between 5 and 14 d in vitro (DIV).

202 a immunocytochemistry over 21 days in vitro (DIV).

203 xcitotoxicity with increasing days in vitro (DIV).

204 boxylase (GAD 65/67), over 17 days in vitro (DIV).

205 n immature cultures [< or = 6 days in vitro (DIV)] and cytoarchitectural analyses of mutant mice have

206 ps of growth cones in young [2-5 d in vitro (DIV)] cultured embryonic hippocampal neurons, and at syn

207 l neurons increases over age [days in vitro (DIV)] in long-term primary cultures, apparently contribu

208 with formation of a fully open pore, whereas DIV voltage sensor movement underlies formation of a dis

209 which through an antagonistic activity with DIV participates in establishing floral asymmetry.