ライフサイエンスコーパス: VD

1 VD class GABAergic neurons are generated in the late L1

2 VD could therefore be a strong candidate for liver cance

3 VD motor neurons develop after the L1 moult; they take o

4 VD(T) measured in muscle in 15 monkeys was reasonably co

5 VD(T) values were high in the thalamus, intermediate in

6 VD, as well as the nonhypercalcemic analogue RO-25-6760,

7 We report that (1) VD:VI inhibition is critically dependent on the Gbetagam

8 (2+) and by mutagenesis of a conserved D(149)VD(151) sequence motif that is considered to act in cati

9 Instead, 1,25(OH)(2) VD(3) decreases the stability of the hTERT mRNA.

10 that 1,25-dihydroxyvitamin D(3) (1,25(OH)(2) VD)(3)induces OCa cell apoptosis by down-regulating telo

11 resistant to apoptosis induced by 1,25(OH)(2)VD(3) .In contrast to parental cells, which lose prolife

12 ulation of telomerase activity by 1,25(OH)(2)VD(3) and the resulting cell death are important compone

13 1,25(OH)(2)VD(3) binds the nuclear VD receptor (VDR) that binds tar

14 These findings suggest that 1,25(OH)(2)VD(3) can affect human immune responses by regulating FO

15 Although 1,25(OH)(2)VD(3) can promote FOXP3 expression in CD4(+) T cells wit

16 scription-PCR analysis shows that 1,25(OH)(2)VD(3) decreases the level of human telomerase reverse tr

17 is unknown whether this effect of 1,25(OH)(2)VD(3) is mediated through direct binding of VDR to the F

18 expressing hTERT is inhibited by 1,25(OH)(2)VD(3) to a similar degree as that of the parental cells,

19 proliferation potential after the 1,25(OH)(2)VD(3) treatment, hTERT-expressing clones resume rapid gr

20 cells decreases their response to 1,25(OH)(2)VD(3)-induced growth suppression.

21 s of the response of OCa cells to 1,25(OH)(2)VD(3)-induced growth suppression.

22 clear whether FOXP3 expression in 1,25(OH)(2)VD(3)-induced Treg (VD-iTreg) cells is critical for the

23 vity by such VDREs in response to 1,25(OH)(2)VD(3).

24 rapid growth after withdrawal of 1,25(OH)(2)VD(3).

25 1,25-Dihyroxyvitamin D(3) [1,25(OH)(2)VD(3)] affects the functions of immune cells including T

26 ity was the main mechanism for ajoenes and 2-VD.

27 ,3-dithiin (3-VD), 2-vinyl-4H-1,2-dithiin (2-VD) and (E)- and (Z)-ajoene, which are the most importan

28 )- and (Z)-ajoene, 2-vinyl-4H-1,2-dithiin (2-VD), diallyl sulphide (DAS) and diallyl disulphide (DADS

29 d from apoptosis by the cell permeant KE(217)VD tetrapeptide or C/EBPbeta-Glu(217).

30 at is mimicked by C/EBPbeta-Glu(217) (KE(217)VD).

31 ase substrate/inhibitor box (K-Phospho-T(217)VD) that is mimicked by C/EBPbeta-Glu(217) (KE(217)VD).

32 ole in the antiproliferative effects of 1,25-VD and restoration of androgen responsiveness by 1,25-VD

33 ockdown of miR-98 led to a reduction of 1,25-VD anti-growth effect and overexpression of miR-98 suppr

34 te cancer and a potential biomarker for 1,25-VD anti-tumor action.

35 Furthermore, we demonstrated that 1,25-VD can increase E-cadherin expression in PCa cells and p

36 ive to the growth inhibitory effects of 1,25-VD compared to the AR-negative prostate cancer cell line

37 s that the antiproliferative actions of 1,25-VD in AR-positive prostate cancer might be mediated thro

38 storation of androgen responsiveness by 1,25-VD might be beneficial for the treatment of hormone-refr

39 The inhibitory effects of 1,25-VD on PCa cell heterotypic adhesion were further confirm

40 mical carcinogenesis to investigate how 1,25-VD prevents malignant transformation.

41 ing of the molecular mechanism by which 1,25-VD prevents tumorigenesis remains incomplete.

42 In this model, 1,25-VD promoted expression of the DNA repair genes RAD50 and

43 Taken together, our data revealed that 1,25-VD promoted PCa cell aggregation by increasing E-cadheri

44 Correspondingly, 1,25-VD protected cells from genotoxic stress and growth inhi

45 growth inhibitive miR-98 is induced by 1,25-VD provides a potential therapeutic target for prostate

46 arker potential of miR-98 in predicting 1,25-VD response.

47 R-98 levels in blood are increased upon 1,25-VD treatment in mice suggesting the biomarker potential

48 Interestingly, we also found that 1,25-VD treatment induced the expression of AR, and that the

49 1,25-VD treatment inhibited cyclin-dependent kinase 2 (cdk2)

50 vity of 1alpha, 25-dihydroxyvitamin D3 (1,25-VD) and its analogues has been demonstrated in many pros

51 ced by 1alpha,25-dihydroxyvitamin D(3) (1,25-VD) in LNCaP.

52 cts of 1alpha,25-dihydroxyvitamin D(3) (1,25-VD) in tumorigenesis.

53 d that 1alpha,25-dihydroxyvitamin D(3) (1,25-VD), the bioactive form of vitamin D, reduced PCa cell r

54 ormation that could not be prevented by 1,25-VD, defining an essential role for VDR in mediating the

55 Mechanistic dissection revealed that 1,25-VD-induced miR-98 is mediated through both a direct mech

56 Furthermore, a reduction in 1,25-VD-mediated growth inhibition was observed when AR signa

57 R transactivation activity, diminishing 1,25-VD-mediated induction of ATM and RAD50 expression.

58 ith a neutralizing antibody can reverse 1,25-VD-mediated suppression of PCa cell adhesion to the endo

59 in mediating the anticancer effects of 1,25-VD.

60 calcemic synthetic analogue of vitamin D(3) (VD(3)) in the Apc(min) mouse.

61 e (DATS), allicin, 3-vinyl-4H-1,3-dithiin (3-VD), 2-vinyl-4H-1,2-dithiin (2-VD) and (E)- and (Z)-ajoe

62 Overall response rates were 73% (VD), 80% (VTD), and 70% (VMP).

63 for 2 months; D2 (n=22), animals were fed a VD-deficient AIN-93G diet and were kept under incandesce

64 eficiency were randomized into two groups, a VD group (n = 29) and a placebo group (n = 29).

65 weeks old were randomized to four groups: a VD(3)-treated group (n = 11) were given injections of 0.

66 rmal anterior neurite, which caused aberrant VD commissure patterning along the A/P axis.

67 uclear hormone receptor, to prevent aberrant VD synaptic wiring in later larval and adult stages.

68 In addition, VD anterior neurites had underextension defects in the V

69 Additionally, VD-iTreg cells suppressed the proliferation of target CD

70 of unc-55 in the DD mns causes them to adopt VD mn features.

71 rge) were lower after CD compared with after VD (pooled OR: 0.57; 95% CI: 0.50, 0.64; P < 0.00001) an

72 eriod, before binocular viewing was allowed, VD decreased and comitance improved.

73 Once binocular viewing was allowed, VD increased and comitance worsened.

74 , 75% sensitivity cutoff) were AIC 0.042 and VD 3.795.

75 a 50% sensitivity cutoff) were AIC 0.049 and VD 4.088, and the values associated with 25% underdiagno

76 , 25% sensitivity cutoff) were AIC 0.061 and VD 4.272, the values associated with 50% underdiagnosis

77 y varying the diagnostic cutoffs for AIC and VD.

78 rees tilt); and (3) changes in comitance and VD over time.

79 nously supplied acetylcholine improve DD and VD axon guidance.

80 r the circumferential guidance of the DD and VD motor neuron axons, which are neighbors of the AVM ax

81 ling of the postsynaptic apparatus in DD and VD neurons using targeted expression of the acetylcholin

82 which are divided into two subgroups: DD and VD.

83 id receptor antagonist, both RVD-Hpalpha and VD-Hpalpha function as agonists.

84 In addition, SD and VD were significantly lower in the DRL of subjects with

85 with circulating WBC samples for both VC and VD variants (r = 0.78 and 0.75, respectively).

86 s unassisted vaginal delivery (VD), assisted VD, elective CS, and emergency CS (defined by before or

87 on, there was a negative correlation between VD and log10 time since last seizure (r = -0.53, P < 0.0

88 identify a possible mechanistic link between VD and these salutary effects, the role of VD in control

89 model their synapses, whereas the later born VD neurons do not.

90 we observed that some postembryonically born VD neurons had a posterior neurite instead of a normal a

91 luding the recurrent mutations and canonical VD rearrangements, similar to the late primary response

92 ally, for an additional set of 74 compounds, VD(ss) predictions made using the computational model we

93 Computational VD(ss) predictions were, on average, 2.13-fold different

94 ACh mediates cutaneous VD through prostanoid and non-NO-, non-prostanoid-depend

95 re compared for SCN5A variants C (VC) and D (VD).

96 1,25 dihydroxyvitamin D (VD) has been shown to exert a number of beneficial effec

97 remodeling program is blocked in Ventral D (VD) GABAergic motor neurons by the COUP-TF (chicken oval

98 The dorsal D (DD) and ventral D (VD) motorneurons (mns), referred to collectively as the

99 N) classes, the dorsal D (DD) and ventral D (VD) neurons, extend axons along both the dorsal and vent

100 imed to evaluate the influence of vitamin D (VD) deficiency on cardiac metabolism, morphology, and fu

101 Vitamin D (VD) has immunomodulatory properties, but whether immune

102 s, conditions associated with low Vitamin D (VD) levels.

103 Vitamin D (VD) supplementation has been shown to reverse these proc

104 ch individual voxel, the VD absorbed dose, D(VD), calculated assuming uniform density, was corrected

105 The D(VD) calculations showed a good agreement with D(3DRD).

106 d dose values, D(3DRD), were compared with D(VD) and D(VDd), using the relative difference Delta(VD/3

107 ues, D(3DRD), were compared with D(VD) and D(VDd), using the relative difference Delta(VD/3DRD).

108 density, was corrected for density, giving D(VDd).

109 Vitamin D3 (VD), a hydrophobic micronutrient, was successfully incor

110 The ICP and DCP VD were not significantly lower in the glaucoma group.

111 ic rabbit portal vein (PV) and vas deferens (VD) smooth muscles.

112 therapy, 92 patients with clinically defined VD were randomly assigned to receive active or sham rTMS

113 teria for magnetic resonance imaging-defined VD.

114 very defined as unassisted vaginal delivery (VD), assisted VD, elective CS, and emergency CS (defined

115 reastfeeding compared with vaginal delivery (VD).

116 Delta(VD/3DRD) was less than 3.5%, except for the tumor of cas

117 elationship between voxel bin-averaged Delta(VD/3DRD) and density, rho: case 1 (Delta = -0.56rho + 0.

118 At the voxel level, density-binned Delta(VD/3DRD) and Delta(VDd/3DRD) were plotted against rho an

119 D(VDd), using the relative difference Delta(VD/3DRD).

120 At the voxel level, the Delta(VD/3DRD) range was 0%-14% for cases 1 and 2, and -3% to

121 vel, density-binned Delta(VD/3DRD) and Delta(VDd/3DRD) were plotted against rho and fitted with a lin

122 method with the Monte Carlo approach (Delta(VDd/3DRD) < 1.1%), but with a lesser extent for the tumo

123 At the voxel level, the Delta(VDd/3DRD) range decreased for the 3 clinical cases (case

124 ory evoked PSPs invade the ventral dendrite (VD), as well as the opposite where visual PSPs invade th

125 ogs and 6 dogs with ventricular denervation (VD).

126 The vessel density (VD), defined as the percentage area occupied by flow pix

127 (OCT-A) devices by comparing vessel density (VD), fractal dimension (FD), and foveal avascular zone (

128 ulate skeleton density (SD), vessel density (VD), fractal dimension (FD), and vessel diameter index (

129 Vessel density (VD), vessel length density (VLD), vessel diameter index

130 ways produce a transient, voltage-dependent (VD) inhibition of N channel function and involve direct

131 oupled receptors leads to voltage-dependent (VD) inhibition of N- and P/Q-type Ca(2+) channels via G-

132 Voltage-dependent (VD) inhibition of N-type Ca(2+) channels is mediated pri

133 The term vascular depression (VD) has been used to describe late-life depressive disor

134 talline lens thickness (LT), vitreous depth (VD), and axial length (AL), were measured and compared w

135 n, down); (2) changes in vertical deviation (VD) with head tilt (Delta 2-6 degrees with left versus r

136 amethasone (RD) or bortezomib-dexamethasone (VD) but it is changing rapidly for 2 reasons.

137 of induction with bortezomib-dexamethasone (VD; n = 168; intravenous bortezomib 1.3 mg/m(2), days 1,

138 egrated curvature (AIC) and venous diameter (VD).

139 rinsic neuron type, the ventricular dilator (VD) neuron, a highly organized and stereotyped branching

140 ges in the motoneurons: ventricular dilator (VD), PY, and LP.

141 ired performance on a visual discrimination (VD) task that was not adversely affected by MPTP adminis

142 ented with an outbreak of vesicular disease (VD) that was associated with an increase in neonatal mor

143 or the prediction of volume of distribution (VD) in humans for neutral and basic compounds.

144 lding values for the volume of distribution (VD) of the tracer in tissue.

145 acer influx (K1) and volume of distribution (VD).

146 ovided similar total volume-of-distribution (VD(T)) values for each studied region.

147 PN), quantified as a volume-of-distribution (VD), with interictal binding and with binding changes in

148 -AMT PET parameters (volume of distribution [VD], characterizing tracer transport, and unidirectional

149 t removal of the regulatory variable domain (VD) in Drp1 enhances formation of a functional Drp1-Mff

150 nction of the corresponding variable domain (VD, or insert B) of Drp1 is unknown.

151 [11C]DPN VD did not undergo systematic changes between time point

152 In both SRL and DRL, VD (P = 0.0010 and P = 0.0003, respectively), VLD (P < 0

153 effect of freeze-drying (FD), vacuum drying (VD), convective drying (CD), microwave-vacuum drying (MV

154 VDnd in studied brain regions exceeded VD(T) in muscles by a factor of 1.3.

155 The following blood products produced faint VD values: washed red blood cells (wRBCs), platelet-depl

156 ons studied showed the highest value for FMZ VD at the youngest age measured (2 years), and the value

157 The ontogeny data of FMZ VD from children may contribute to understanding regiona

158 ve correlation between somatic mutations for VD-related genes and the TGF-beta pathway.

159 ly dependent on the presence of a functional VD receptor response element located approximately 495 b

160 Furthermore, VD deficiency was related to increased cytokines release

161 sequence similarity to that of hemopressin (VD-Hpbeta).

162 was found to be flow-dependent, with higher VD at lower flow rates, and correlated with visually den

163 t VD/F of 0.41 L and the monkey, the highest VD/F of 392.95 L.

164 The simple allometric human VD/F and MLP-corrected Cl/F were 2311.51 L and 51.35 L/h

165 putational model described can predict human VD(ss) with an accuracy comparable to predictions requir

166 ompounds, and it was demonstrated that human VD(ss) values could be predicted, on average, within or

167 The serum levels of 25-hydroxy VD, TGF-beta1, TIMP-1, MMP2 and MMP9 were measured at ba

168 In VD class neurons, which normally do not remodel, the tra

169 In those regions where abnormalities in VD and FMZ activity images were not matched, the asymmet

170 and higher lactate dehydrogenase activity in VD-deficient animals.

171 actional shortening and ejection fraction in VD-deficient animals.

172 ts confirm the requirement for Gbetagamma in VD modulation and implicate Galpha(q)-GTP and Gbetagamma

173 such as pde-4 to keep the cAMP levels low in VD.

174 systemic pressor and heart rate responses in VD dogs suggest that cardiac nerves mitigate the respons

175 The reflectance compensation step in VD calculation significantly improved repeatability, nor

176 expressed in DD neurons but is repressed in VDs by UNC-55/COUP-TF.

177 so obtained in both permeabilized and intact VD.

178 and CPI-17 Thr(38), respectively, in intact VD while MYPT1 Thr(695) phosphorylation was insensitive

179 e were no significant differences in isotime VD/VT or transcutaneous Pco(2) among treatments.

180 nimals were fed an AIN-93G diet with 1000 IU VD/kg of chow and were kept under fluorescent light for

181 The mouse showed the lowest VD/F of 0.41 L and the monkey, the highest VD/F of 392.9

182 Among the overall macular VD parameters, the SVC VD had the best diagnostic accura

183 Mean VD, FD, and FAZ values between the instruments were comp

184 recise mechanisms through which ACh-mediated VD acts and whether those downstream mechanisms change w

185 athways contribute to exogenous ACh-mediated VD, and that both are attenuated with advanced age.

186 shed prostanoid contribution to ACh-mediated VD.

187 sting for reconstitution of agonist-mediated VD inhibition.

188 ine (ACh) plays a role in thermally mediated VD, the precise mechanisms through which ACh-mediated VD

189 ctions in both skeletal muscle mass and Mito(VD) have been reported following mountaineering expediti

190 al muscle mitochondrial volume density (Mito(VD)) over equivalent normoxic training.

191 lysed for mitochondrial volume density (Mito(VD)), capillarity, fibre types and respiratory capacity

192 determined that intermyofibrillar (IMF) Mito(VD) was augmented (P = 0.028) by 11.5 +/- 9.2% from Pre

193 study demonstrates that skeletal muscle Mito(VD) may increase with 28 days acclimation to 3454 m.

194 drial characteristics, with emphasis on Mito(VD), while minimizing changes in energy balance.

195 re was no change in subsarcolemmal (SS) Mito(VD).

196 As a result, total Mito(VD) (IMF + SS) was increased (P = 0.031) from 6.20 +/- 1

197 ons, capillary-to-fibre ratio and total Mito(VD) increased (P < 0.05) following ET (18 +/- 16 and 43

198 mum (ACD), 14 mum (AD), 13 mum (LT), 14 mum (VD), and 16 mum (AL).

199 when fmi-1 was expressed exclusively in non-VD neighboring neurons, suggesting a cell nonautonomous

200 DD, but not VD, MNs reverse their cellular polarity in a development

201 1,25(OH)(2)VD(3) binds the nuclear VD receptor (VDR) that binds target DNA sequences known

202 re validated clinically, where an absence of VD supplementation was associated with low TGF-beta path

203 Our analyses of VD deprivation (VDD) in in vivo models of liver tumor fo

204 echanisms capable of altering the balance of VD and VI inhibition in chick dorsal root ganglion neuro

205 However, potential contributions of VD to liver tumor progression in the context of TGF-beta

206 Upon correction of VD levels, TGF-beta1 and TIMP-1 levels were decreased, a

207 A dataset of VD values for 384 drugs in humans was used to train a hy

208 The axon and synaptic defects of VD neurons could be rescued when fmi-1 was expressed exc

209 This study sought to determine the effect of VD supplementation on serum fibrotic markers in chronic

210 ot syntaxin-1B) shifts the ratio in favor of VD inhibition by potentiating the VD effects of Gbetagam

211 hich is essential for inhibitory function of VD-iTreg cells.

212 and left ventricular mass after 4 months of VD deficiency.

213 The ratio of VD:VI inhibition differs significantly among cell types,

214 reduced (42.3% compared to 86.1%) release of VD in simulated gastric fluid and an increased (36.0% co

215 n VD and these salutary effects, the role of VD in controlling the activity and expression of the typ

216 postpartum and compared outcomes after CD or VD, including foreign language publications, were identi

217 ew agents (except pomalidomide) to the RD or VD regimens were superior to the double combinations in

218 DH (3D-RD), and a DK approach (VoxelDose, or VD).

219 MP did not appear to offer an advantage over VD in transplantation-ineligible patients with myeloma t

220 arameters described, is then used to predict VD(ss) via the Oie-Tozer equation.

221 e the ruggedness of the method in predicting VD through the Oie-Tozer equation, via the use of severa

222 nts that broadly inhibit caspase activity, Q-VD-OPH and Z-VAD(OMe)-FMK, effectively inhibited virus-i

223 The combination of doxorubicin and Q-VD-OPH caused an increased expression of p21/WAF1 and se

224 M-54 or a combination of necrostatin-1 and q-VD-OPh.

225 However, Q-VD-OPh, a potent inhibitor of caspase activity provided

226 The pan-caspase inhibitor (Q-VD-OPH) greatly reduced doxorubicin-induced caspase-3 ac

227 ed by the broad-spectrum caspase inhibitor Q-VD-OPh and was associated with both caspase-3 and caspas

228 tion of the nonselective caspase inhibitor Q-VD-OPH in vivo.

229 e-9) or treated with the caspase inhibitor Q-VD-OPh increased viability but failed to increase clonog

230 ially or completely rescued with inhibitor Q-VD-OPh or Ro32-0432.

231 n be impaired by the pan-caspase inhibitor q-VD-OPh.

232 ombination with the pan-caspase inhibitor, Q-VD-OPH, elicited a strong reduction of cell viability th

233 nstruments are not interchangeable regarding VD, FD, and FAZ for both the superficial and deep capill

234 Macular retinal VD, ganglion cell complex (GCC) thickness, and visual fi

235 aucoma group, the SVC and all-plexus retinal VD (mean +/- standard deviation: 47.2%+/-7.1% and 73.5%+

236 The SD, VD, and FD of the parafoveal capillaries were lower in u

237 Subsequent supplementing VD led to restoration of TGF-beta member expression with

238 Reflectance-compensated SVC VD measurement by PR-OCTA detected glaucoma with high ac

239 e glaucoma participants, the hemispheric SVC VD values were highly correlated with the corresponding

240 g the overall macular VD parameters, the SVC VD had the best diagnostic accuracy as measured by the a

241 dverse events were more common with VTD than VD or VMP.

242 at least some of the beneficial effects that VD exerts on cardiovascular function.

243 this study provides additional evidence that VD plays an important role in the reversal of hepatic fi

244 Our data indicate that VD deficiency is associated with energetic metabolic cha

245 The VD images, which allow visualization of a quantitative m

246 The VD of wRBCs increased incrementally as increasing concen

247 on increased, the SEC became denser, and the VD level also increased until a plateau level was reache

248 he analogue (36% decrease; P < 0.05) and the VD(3) groups (46%; P < 0.001).

249 ng set of 384, the model was recast, and the VD(ss) values for each of the subsets were predicted.

250 that binds target DNA sequences known as the VD response element (VDRE).

251 ns, an anterior neurite that will become the VD axon extends along the anteroposterior (A/P) axis in

252 Phosphorylation of a PKA site bordering the VD disassembled the filamentous DeltaVD mutant and accel

253 in the area defined as abnormal in both the VD and the FMZ activity images.

254 The cdh-4 is expressed by the VD neurons and seems to function in the same genetic pat

255 ificantly higher than those derived from the VD images (P = 0.01).

256 re, on average, 2.13-fold different from the VD(ss) predictions from animal data.

257 y hemodynamic responses were enhanced in the VD dogs.

258 P2 and MMP9 were significantly higher in the VD group than in the placebo group.

259 9 levels were significantly increased in the VD group.

260 NC-55 is a nuclear receptor expressed in the VD mns that is necessary for generating features that di

261 t are expressed in the DD mns but not in the VD mns.

262 The organization of branching seen in the VD neuron may play a critical role in the electrotonic a

263 hythm and suppressed spike discharges in the VD neuron.

264 in the VNC, we did not observe FMI-1 in the VD neurons themselves, suggesting that fmi-1 might be wo

265 th auditory PSPs being more prominent in the VD than visual PSPs in the LD.

266 growth rate were significantly lower in the VD(3) group (26%, P < 0.001, and 27%, P < 0.001, respect

267 In contrast, serum calcium in the VD(3) group was significantly elevated (P < or =0.001) a

268 and C-terminal alpha-helical segments in the VD-replacing linker converted Drp1 from constitutively a

269 In unc-55 mutants, the VD mns adopt the DD mn synaptic pattern and peptide expr

270 sttranslational modifications in or near the VD alter the conformation of a membrane-proximal oligome

271 Specifically, we show the morphology of the VD neuron consists of a single primary neurite that proj

272 early all secondary neurite branching of the VD neuron is from the subprimary neurites.

273 During the early development of the VD neurons, an anterior neurite that will become the VD

274 nown details of the early development of the VD neurons, indicating that the neurite defects arose du

275 s, but whether immune cell expression of the VD receptor (VDR) impacts costimulatory blockade induced

276 onsistent with an autoinhibitory role of the VD, we identified Arg-376 in the Drp1 stalk domain as ne

277 ment resulted in complete elimination of the VD-dependent induction of the NPR-A gene promoter but di

278 es expressed in the proximal segments of the VD.

279 n favor of VD inhibition by potentiating the VD effects of Gbetagamma.

280 l approach is described that can predict the VD(ss) of new compounds in humans, with an accuracy of w

281 attractive for prospectively predicting the VD of new chemical entities in humans.

282 We replaced the VD of Drp1 with a panel of linker sequences of varying l

283 ary structure composition and found that the VD is dispensable for mitochondrial recruitment, associa

284 (1)gamma(2) were tonically inhibited via the VD pathway.

285 For each individual voxel, the VD absorbed dose, D(VD), calculated assuming uniform den

286 This element was associated with the VD receptor/retinoid X receptor complex in vitro.

287 expression in 1,25(OH)(2)VD(3)-induced Treg (VD-iTreg) cells is critical for the inhibitory function

288 ontaining either three (RVD-Hpalpha) or two (VD-Hpalpha) additional amino acids, as well as a beta-he

289 , it is not expressed in the ventral D-type (VD) GABAergic motorneurons, which are defective in fmi-1

290 iated with ASD when compared with unassisted VD.

291 ional lumen volume (V(VD)) were related by V(VD)=1.06 V(C)-0.01 mL (r=0.99).

292 video densitometric regional lumen volume (V(VD)) were related by V(VD)=1.06 V(C)-0.01 mL (r=0.99).

293 Thermoregulatory cutaneous vasodilatation (VD) is attenuated in aged skin.

294 The videodensity (VD) of whole blood was found to be flow-dependent, with

295 inhibition of MLCP while the phasic visceral VD, which has a low CPI-17 concentration, probably utili

296 defects in the VNC in fmi-1 animals, whereas VD commissure growth along the dorsoventral (D/V) axis o

297 Fifty-four CHC patients with VD deficiency were randomized into two groups, a VD grou

298 ficacy of rTMS among geriatric patients with VD.

299 might also be effective among patients with VD.

300 ow-up, median progression-free survival with VD, VTD, and VMP was 14.7, 15.4, and 17.3 months, respec