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 of VM DA progressively increased through 10 DIV.

8 iatal DA increased substantially, 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 4 d in vitro (DIV) compared with those at 14 DIV.

21 l glutamatergic responses are detected 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 After an additional 2 DIV in serum-free medium, the number of TH neurons had d

39 8 hours) exposure to bifenthrin commencing 2 DIV-enhanced neurite outgrowth and persistently increase

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

60 e elongation is significantly decreased at 4 DIV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 LtrA recognizes two intronic domains, DI and DIV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 ity and reaction time that was selective for DIV.

113 50 microM forskolin in the media on the four DIV induced surface galC expression in Schwann cells fro

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

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

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

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

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

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

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

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

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

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

124 the transcription factor MYBI, a homolog of DIV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 at DIV 6 and progressively increased through DIV 21.

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

158 nce of functional brain activity specific to DIV.

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

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

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

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

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

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

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

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

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

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

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

170 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

186 2 and were cultured for up to 60 d in vitro (DIV).

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

188 xcitotoxicity with increasing days in vitro (DIV).

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

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

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

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

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

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