ライフサイエンスコーパス: MCD

1 MCD apparently evolved toward preventing the nonspecific

2 MCD catalyzes the unprecedented oxidation of an alpha-me

3 MCD feeding triggered steatosis, hepatic lipid storage,

4 MCD induction further potentiated the defects in insulin

5 MCD saturation magnetization data for valence-delocalize

6 MCD should be subdivided into HHV-8-associated MCD and H

7 MCD spectrum of the P(+) state in the DeltanifB beta-188

8 MCD was assumed when IMR>/=29.1 (75(th) percentile).

9 MCD-fed ATGL-KO mice, although partially protected from

10 Following 2 (MCD groups) or 3 (HFD groups) weeks of treatment with G4

11 KSHV microRNA sequences from 23 MCD patients and 7 patients with a newly described KSHV-

12 (n = 9) samples from 32 patients with HHV-8 MCD and compared them with patients with KS (n = 24) and

13 re markedly decreased in patients with HHV-8 MCD and were undetectable in 6 of them.

14 oreover, iNKT cells from patients with HHV-8 MCD displayed a proliferative defect after stimulation w

15 IL-6-deficient genetic background abrogated MCD-like phenotypes, indicating that endogenous mouse IL

16 Compared with other ACDs, MCD contains an approximately 170-residue-long N-termina

17 The mainstay of treatment for adult MCD, oral glucocorticoids, is based on two randomized co

18 nificant across subgroups (children, adults, MCD/MesGN, and FSGS; P<0.01).

19 s infusions of FGF21 for 4 weeks while on an MCD diet had reduced steatosis and peroxidative damage,

20 e recapitulated in aged mice treated with an MCD inhibitor (CBM-3001106), and these mice also demonst

21 d hemodynamics: abnormal CFR in 28 (52%) and MCD in 18 (33%).

22 methods, including UV-vis-NIR absorption and MCD spectroscopies, single-crystal X-ray structure deter

23 solute bioavailabilities obtained by DCH and MCD nasal administration were 6% and 15%, respectively.

24 trin microparticles loaded with DFO (DCH and MCD, respectively) were obtained by spray drying.

25 THF)5][Fe8Me12], which combined with EPR and MCD studies is shown to be consistent with Kochi's S = 1

26 between eruptive cherry hemangiomatosis and MCD.

27 y showed improvement of steatosis in HFD and MCD mice concomitant with reductions in hepatic triglyce

28 (LPC), which was detectable in both HFD and MCD mice, was reduced by UDCA-LPE.

29 UDCA-LPE ameliorated both HFD- and MCD-induced increases in alanine aminotransferase (ALT)

30 ith concomitant HHV8-associated lymphoma and MCD at relapse.

31 We fed mice custom MCS and MCD formulas containing 4 different carbohydrate-fat com

32 on of diffuse atherosclerotic narrowings and MCD.

33 ges in disposition were caused by ob/ob- and MCD diet-specific decreases in the kidney mRNA expressio

34 that recapitulates features seen in PEL and MCD by gene expression and cell phenotype analysis, allo

35 protein (vFLIP) in the initiation of PEL and MCD by specifically expressing vFLIP at different stages

36 KS, PEL, and MCD are largely incurable and poorly understood diseases

37 EPR, resonance Raman, and MCD spectroscopies have been used to determine the redox

38 hyl-beta-cyclodextrin (MCD), when STARD4 and MCD were overexpressed or injected into cells.

39 Both VSM and MCD measurements highlight the robustness of the complex

40 D should be subdivided into HHV-8-associated MCD and HHV-8-negative MCD or iMCD.

41 HHV-8-associated MCD may be considered as a single clinicopathological en

42 role in the pathogenesis of HHV-8-associated MCD.

43 HIV-associated MCD is a remitting-relapsing disease.

44 d KSHV viral load similar to KSHV-associated MCD.

45 or laboratory findings that were present at MCD diagnosis predicted subsequent relapse, and the medi

46 rate attenuated hepatic inflammation in both MCD-fed and LPS-treated ATGL-KO mice.

47 In contrast, disruption of caveolae by MCD treatment or Cav-3 knockdown abolished the protectio

48 ent 2Cu2 in solution was now investigated by MCD and EPR spectroscopy.

49 Circular dichroism (CD) and magnetic CD (MCD) studies demonstrate that chloride binding triggers

50 Using circular dichroism (CD), magnetic CD (MCD), and variable-temperature, variable-field (VTVH) MC

51 n (Abs)/circular dichroism (CD)/magnetic CD (MCD)/variable temperature, variable field (VTVH) MCD spe

52 From CD, MCD, and VTVH MCD, p-anisidine addition is found to mini

53 Abs/CD/MCD/VTVH MCD data exhibit 12 transitions that are assign

54 een characterized using UV-vis absorption/CD/MCD, EPR, Mossbauer, and resonance Raman spectroscopies.

55 A comprehensive MCD spectral analysis coupled with a molecular field mod

56 of a subsequent lymph node biopsy confirmed MCD.

57 ffered symptomatic, histologically confirmed MCD relapse.

58 Mice fed the custom MCD formulas developed varying degrees of hepatic steato

59 lesterol with 5 mm methyl-beta-cyclodextrin (MCD) caused a substantial increase in the rate of agonis

60 le sterol carrier, methyl-beta-cyclodextrin (MCD), when STARD4 and MCD were overexpressed or injected

61 Interestingly, STARD4 and cytosolic MCD act similarly by increasing the rate of transfer of

62 In comparison with DCH, MCD enhanced the in vitro DFO permeation across lipophil

63 ice deficient for malonyl CoA decarboxylase (MCD(-/-)), a mouse model of reduced fat oxidation, were

64 Malonyl-CoA decarboxylase (MCD) has been a target of investigation because it reduc

65 ates and inhibits malonyl CoA decarboxylase (MCD), an enzyme that produces acetyl CoA from malonyl Co

66 to acetyl-CoA by malonyl-CoA decarboxylase (MCD; EC 4.1.1.9) is an essential facet in the regulation

67 e by feeding a methionine-choline deficient (MCD) diet up to 8 weeks.

68 re we used the methionine-choline deficient (MCD) model of NASH to characterize the possible involvem

69 rticularly the methionine-choline deficient (MCD) model, profound changes are seen in redox enzymes a

70 llenged with a methionine-choline-deficient (MCD) diet as a nutritional model of NASH or lipopolysacc

71 chow or a methionine and choline-deficient (MCD) diet for 1 week were divided into 4 groups: control

72 mice received a methionin-choline-deficient (MCD) diet for up to 11 weeks, which induced advanced non

73 ) or fed a methionine and choline-deficient (MCD) diet to induce experimental NASH and underwent MR i

74 ced by CCl4 or methionine-choline-deficient (MCD) diet, liver injury and fibrosis were attenuated in

75 feeding mice a methionine-choline-deficient (MCD) diet, the degree of liver damage is related to diet

76 using the methionine and choline-deficient (MCD) diet, which depletes methyl groups and results in a

77 ed by the methionine- and choline-deficient (MCD) diet, which was reasoned to be due to increased hep

78 (ALD) and methionine and choline-deficient (MCD) diet-induced liver injury.

79 ouse models of methionine choline-deficient (MCD) diet-induced NASH and high-fat diet-induced NASH, w

80 diet or a methionine- and choline-deficient (MCD) diet.

81 ere fed with a methionine-choline-deficient (MCD) diet.

82 r starting the methionine/choline-deficient (MCD) diet.

83 uced by a methionine- and choline-deficient (MCD) diet.

84 m mice given a methionine-choline-deficient (MCD) diet.

85 placed on methionine- and choline-deficient (MCD), high-fat, or control diets for 8-16 weeks.

86 (2S)-methylsuccinyl-CoA dehydrogenase (MCD) belongs to the family of FAD-dependent acyl-CoA deh

87 Myocardial microvascular density (MCD) in aFGF-NP+UTMD group was up to 35n/hpf, much highe

88 with malformations in cortical development (MCD) or spinal muscular atrophy with lower extremity pre

89 se of malformations of cortical development (MCD), typically lissencephaly, pachygyria and polymicrog

90 Malformations of cortical development (MCDs) compose a diverse range of disorders that are comm

91 ) are malformations of cortical development (MCDs) that are highly associated with medication-resista

92 Since 2003, 49 patients with newly diagnosed MCD have been treated with rituximab with (n = 14) or wi

93 We show that magnetic circular dichroism (MCD) of sun's ultraviolet C light by oxygen in Archaean

94 absorption and magnetic circular dichroism (MCD) spectra show weak ligand-field transitions between

95 e Mossbauer and magnetic circular dichroism (MCD) spectroscopies of well-defined and in situ formed m

96 absorption, and magnetic circular dichroism (MCD) spectroscopies show that CuZ degrees is a 1-hole (i

97 absorption and magnetic circular dichroism (MCD) spectroscopies.

98 absorption, and magnetic circular dichroism (MCD) spectroscopies.

99 crystals using magnetic circular dichroism (MCD) spectroscopy and SQUID magnetometry.

100 ble-temperature magnetic circular dichroism (MCD) spectroscopy to experimentally evaluate this excite

101 s on the use of magnetic circular dichroism (MCD) spectroscopy to validate the results of TD-DFT calc

102 absorption, and magnetic circular dichroism (MCD) spectroscopy, coupled with DFT and highly correlate

103 estigated using Magnetic Circular Dichroism (MCD) spectroscopy.

104 Magnetic circular dichroism (MCD) spectrum of the P-cluster in the oxidized DeltanifB

105 esonance (EPR), magnetic circular dichroism (MCD), and nuclear magnetic resonance (NMR) spectroscopic

106 dichroism (CD), magnetic circular dichroism (MCD), and variable temperature variable field (VTVH) MCD

107 dichroism (CD), magnetic circular dichroism (MCD), and variable-temperature, variable-field (VTVH) MC

108 susceptibility, magnetic circular dichroism (MCD), and X-ray magnetic circular dichroism (XMCD) measu

109 s ((119)Sn-NMR, magnetic circular dichroism (MCD), electron paramagnetic resonance (EPR), SQUID, UV-v

110 divided into 4 groups: control (chow diet), MCD diet, chow diet plus G49, and M+G49 (MCD diet plus G

111 ding sign of multicentric Castleman disease (MCD) and other lymphoproliferative diseases.

112 V-associated multicentric Castleman disease (MCD) as a distinct lymphoproliferative disorder.

113 )-associated multicentric Castleman disease (MCD) is a lymphoproliferative inflammatory disorder comm

114 )-associated multicentric Castleman disease (MCD) is a polyclonal B-cell lymphoproliferative disorder

115 V-associated multicentric Castleman disease (MCD) is associated with a high risk of developing non-Ho

116 a (PEL), and multicentric Castleman disease (MCD) patients.

117 oma (KS) and multicentric Castleman disease (MCD), a life-threatening, virally induced B-cell lymphop

118 a subset of multicentric Castleman disease (MCD).

119 ma cell-type multicentric Castleman disease (MCD).

120 ma (PEL) and multicentric Castleman disease (MCD).

121 Minimal change disease (MCD) is the etiology of 10%-25% of cases of nephrotic sy

122 ephrotic syndrome of minimal change disease (MCD), mesangial proliferative GN (MesGN), or FSGS may be

123 uria are features of minimal-change disease (MCD).

124 cells from multicentric Castleman's disease (MCD) and Kaposi's sarcoma (KS) lesions, suggesting that

125 Multicentric Castleman's disease (MCD) describes a heterogeneous group of disorders involv

126 coma (KS), multicentric Castleman's disease (MCD), and primary effusion lymphoma (PEL).

127 coma (KS), multicentric Castleman's disease (MCD), and primary effusion lymphoma (PEL).

128 oma (PEL), multicentric Castleman's disease (MCD), and the inflammation-driven neoplasm Kaposi's sarc

129 t focus in multicentric Castleman's disease (MCD), nature of the surgical approach (resective vs diag

130 (PEL), and multicentric Castleman's disease (MCD).

131 (PEL), and multicentric Castleman's disease (MCD).

132 (PEL) and multicentric Castleman's disease (MCD).

133 phoma, and multicentric Castleman's disease (MCD).

134 (PEL), and multicentric Castleman's disease (MCD).

135 the treatment of motor conversion disorder (MCD).

136 cellularly located mature C-terminal domain (MCD) of FHA to achieve its proper conformation.

137 etella lacking the mature C-terminal domain (MCD), suggesting the direct interaction between AC domai

138 arrowings, and microcirculatory dysfunction (MCD) contribute to limit myocardial flow.

139 Mice lacking SIRT4 display elevated MCD activity and decreased malonyl CoA in skeletal muscl

140 ified according to a new imaging/embryologic MCD classification system.

141 ations and thereby assignments of low-energy MCD bands associated with the Fe-Fe interaction.

142 ignals, we unambiguously assign a low-energy MCD feature of [Mn(IV)(O)(N4py)](2+) as the (4)E excited

143 Importantly, mice fed MCD starch-palmitate accumulated as much hepatic palmita

144 ulated as much hepatic palmitate as mice fed MCD sucrose-oleate, yet their degree of liver injury was

145 By contrast, mice fed MCD sucrose-palmitate developed severe liver injury, wor

146 tty acid oxidation were suppressed following MCD induction.

147 e expressing a muscle specific transgene for MCD (Tg-fMCD(Skel)) stabilized posttranslationally by th

148 luster of 5 KSHV sequences, including 2 from MCD patients.

149 t), MCD diet, chow diet plus G49, and M+G49 (MCD diet plus G49).

150 An HF/MCD diet and hyperleptinemia increase hepatic endocannab

151 Both in HF/MCD-Zucker and HF/MCD+leptin lean rats, significant hepatic fibrogenesis a

152 a high fat/methionine-choline-deficient (HF/MCD) diet with and without exogenous administration of r

153 Both in HF/MCD-Zucker and HF/MCD+leptin lean rats, significant hepa

154 sociated multicentric Castleman disease (HIV MCD) is a rare lymphoproliferative disorder, the inciden

155 diagnosis, management, and prognosis of HIV MCD.

156 nclusions regarding optimal treatment of HIV MCD.

157 sociated multicentric Castleman disease (HIV+MCD) with rituximab-based approaches has dramatically im

158 cohort of 84 patients with biopsy-proven HIV+MCD were treated with risk-stratified rituximab-based th

159 Four patients (5%) died of refractory HIV+MCD and 80 achieved clinical remission.

160 es to predict factors associated with an HIV-MCD attack.

161 sociated multicentric Castleman disease (HIV-MCD) is a rare lymphoproliferative disorder caused by in

162 Rituximab is effective in HIV-MCD, but its impact on NHL incidence remains unknown.

163 ents were identified with a diagnosis of HIV-MCD for the present study.

164 dividuals with a histologic diagnosis of HIV-MCD, we performed univariate and multivariate analyses t

165 isome has been investigated by docking human MCD onto the peroxisomal import protein peroxin 5, which

166 t regulator of lipid homeostasis, identifies MCD as a SIRT4 target, and deepens our understanding of

167 which we propose referring to as idiopathic MCD (iMCD).

168 The increased severity of NASH in immunized MCD-fed mice involved liver recruitment and the T helper

169 al features of the most common and important MCDs.

170 In MCD mice, we observed a significant decrease in HP DHA t

171 In MCD-fed WT mice, hepatic AnxA1 increased in parallel wit

172 ating the features seen in infected cells in MCD.

173 ic expression of proinflammatory cytokine in MCD-fed mice.

174 e degree of hepatic fibrosis was enhanced in MCD-fed AnxA1 KO mice, an effect associated with augment

175 models and decreased lipid hydroperoxides in MCD mice.

176 ro functional results in cells maintained in MCD medium.

177 Decreased fat oxidation in MCD(-/-) mice resulted in the accumulation of lipid inte

178 treatment improves the hepatic phenotype in MCD- or LPS-challenged ATGL-knockout (KO) mice.

179 between hepatic gene expression profiles in MCD diet-fed wild-type and untreated Lrh-1(-/-) mice sug

180 Inducing MCD activity >5-fold in skeletal muscle over two weeks d

181 KSHV-MCD activity is associated with (18)F-FDG PET abnormalit

182 KSHV-MCD activity was associated with hypermetabolic symmetri

183 None developed KSHV-MCD; 6 died with median survival from KICS diagnosis 13.

184 ociated multicentric Castleman disease (KSHV-MCD) is a lymphoproliferative disorder, most commonly se

185 ociated multicentric Castleman disease (KSHV-MCD) is characterized by severe inflammatory symptoms ca

186 (PEL), and a form of Castleman disease (KSHV-MCD).

187 ) and hIL-6, and other cytokines during KSHV-MCD flare and remission in 21 patients with 34 flares an

188 cytokine syndrome (KICS) distinct from KSHV-MCD was reported.

189 geted therapy have improved outcomes in KSHV-MCD, and decreased need for cytotoxic chemotherapy.

190 ough rituximab has reported activity in KSHV-MCD, its use is often associated with KS progression.

191 immunofluorescence staining of involved KSHV-MCD lymph nodes reveals that most plasmablasts expressin

192 Using NCI KSHV-MCD response criteria, major clinical and biochemical re

193 plications for the development of novel KSHV-MCD therapies targeting IL-6 and its downstream signalin

194 ed understanding of the pathogenesis of KSHV-MCD and KSHV-associated inflammatory cytokine syndrome i

195 is is a key step in the pathogenesis of KSHV-MCD and other KSHV-induced diseases.

196 n important step in the pathogenesis of KSHV-MCD and PEL.

197 ons for the diagnosis and monitoring of KSHV-MCD and shed light on its pathobiologic mechanism.

198 ur understanding of the pathogenesis of KSHV-MCD has increased in recent years and improved therapies

199 The pathogenesis of KSHV-MCD is attributed to proliferation of KSHV-infected B ce

200 We show that a number of KSHV-MCD lymph node plasmablasts express vIL-6 but do not hav

201 ducing plasmablasts from lymph nodes of KSHV-MCD patients coexpress XBP-1s.

202 Within a natural history study of KSHV-MCD, we prospectively evaluated rituximab 375 mg/m(2) co

203 ed plasmablasts is a central feature of KSHV-MCD.

204 R-Dox is effective in symptomatic KSHV-MCD and may be useful in patients with concurrent KS.

205 HIV-infected patients with symptomatic KSHV-MCD received high-dose zidovudine (600 mg orally every 6

206 6 can independently or together lead to KSHV-MCD flares, and suggests that vIL-6 and hIL-6 may jointl

207 lasts from lymph nodes of patients with KSHV-MCD express vIL-6 but not ORF45, a KSHV lytic gene.

208 aphy (PET) findings in 27 patients with KSHV-MCD.

209 conformation of the extracellularly located MCD.

210 temperature magnetic circular dichroism (LT MCD) spectroscopy in combination with quantum-chemical c

211 0.68 mug/mL (DCH) to 14.37 +/- 1.69 mug/mL (MCD) 30 min after insufflation of microparticles.

212 Moreover, MCD were able to promote the DFO permeation across monol

213 It is almost always multicentric (MCD) and linked to human herpesvirus 8 (HHV-8).

214 .77 +/- 0.06 mum (DCH) to 3.47 +/- 0.05 mum (MCD); the aerodynamic diameters were about 1.1 mum and t

215 The in vivo role of muscle MCD expression in the development of insulin resistance

216 into HHV-8-associated MCD and HHV-8-negative MCD or iMCD.

217 ma concentrations were 4.8-fold higher in ob/MCD mice compared with WT/control.

218 ct1 mRNA expression was only decreased in ob/MCD mice.

219 esulted in a full assignment of the observed MCD and electronic absorption bands, a detailed understa

220 respectively, through direct calculations of MCD spectra and independent determination of the MCD C-t

221 sequencing tubulin genes in large cohorts of MCD patients has detected tubulin mutations in only 1-13

222 changes demonstrated by CM in the course of MCD.

223 coronary narrowings with variable degrees of MCD.

224 al growths, for the potential development of MCD and other lymphoproliferative diseases.

225 n Unit (years 2007-2011) with a diagnosis of MCD were included.

226 ct variant cluster consisting exclusively of MCD and KICS patients in all trees.

227 showed the classic histological features of MCD, and LANA-1 immunostaining identified HHV-8-infected

228 ven in the absence of pathologic findings of MCD, KSHV-infected patients may have inflammatory sympto

229 inations of 3 SNPs as putative indicators of MCD and KICS risk.

230 Induction of MCD in skeletal muscle resulted in a suppression of mito

231 Acute induction of MCD in the skeletal muscle of obese and glucose intolera

232 ensitivity were determined upon induction of MCD.

233 e dismutase 2 in muscle but not the liver of MCD(-/-) mice.

234 A and FK506 on proteinuria in a rat model of MCD induced by puromycin aminonucleoside (PAN) and in vi

235 evaluate the characteristics and outcomes of MCD patients admitted to a specialist neuropsychiatric i

236 the observed sequence variation and risk of MCD and KICS.

237 To determine the role of MCD in skeletal muscle of diet induced obese and insulin

238 herry hemangiomata is the presenting sign of MCD.

239 were able to shift substrate specificity of MCD toward succinyl-CoA through active-site mutagenesis.

240 Here we report the crystal structure of MCD at a resolution of 1.37 A.

241 mbination with chemotherapy for treatment of MCD.

242 Assignments are based on MCD/Abs intensity ratios, transition energies, polarizat

243 SL had a phenotype similar to the WT mice on MCD and LPS challenge.

244 inactivation of CES1 aggravated alcohol- or MCD diet-induced liver inflammation and liver injury, li

245 ucial role in protection against alcohol- or MCD diet-induced liver injury.

246 hat in addition to decreasing fat oxidation, MCD inhibition also has novel effects on protein acetyla

247 The structure of human peroxisomal MCD reveals a molecular tetramer that is best described

248 Only 1 patient died of relapsed MCD (at fifth relapse 9.4 years after initial diagnosis)

249 hose described in HIV-positive HHV-8-related MCD.

250 -8 and immune cells that cause HHV-8-related MCD.

251 The diabetes group showed similar results (MCD, CVF and cardiac myocyte apoptosis index) to other a

252 Here, we review MCD in adults with particular focus on the evidence for

253 d pathobiological characteristics of several MCDs have been recently elucidated.

254 Mice showed MCD-like abnormalities and immunological defects includi

255 Patients with severe, long-standing MCD can achieve significant improvements in functioning

256 Disrupting lipid rafts by statins MCD, and filipin recuperates ABCA1 phenotype and likely

257 The low-temperature MCD spectra of complex 1 exhibit three pseudo A-term sig

258 rs and demonstrate that variable-temperature MCD spectroscopy provides a means of detecting and inves

259 -NIR absorption, CD and variable-temperature MCD, and protein-film electrochemistry.

260 ysis of the signs of the experimental C-term MCD signals, we unambiguously assign a low-energy MCD fe

261 ed metabolic dysfunction, demonstrating that MCD inhibitors may have utility in the battle against ch

262 We found that MCD diet-fed, liver-specific LRH-1 knockout mice (Lrh-1(

263 These findings show that MCD and KICS patients frequently have unusual KSHV micro

264 The MCD diet increased hepatic levels of FGF21 messenger RNA

265 The MCD diet significantly increased plasma half-life and me

266 The MCD spectrum of biferrous MIOX shows two ligand field (L

267 ate that the diabetic ob/ob genotype and the MCD disease model alter kidney transporter expression an

268 direct interaction between AC domain and the MCD is required for the inhibitory effect.

269 ting the pathological changes induced by the MCD diet.

270 Wildtype mice (C57BLKS/J) fed the MCD or control diet were treated with SP600125; a c-Jun

271 e serum albumin (MDA-BSA) before feeding the MCD diet.

272 ity as carbohydrate-derived palmitate in the MCD model of fatty liver disease.

273 In the MCD model of steatohepatitis, carbohydrate-derived palmi

274 oxic when combined with dietary sugar in the MCD model, presumably by enhancing hepatic de novo lipog

275 spectra and independent determination of the MCD C-term signs from the corresponding electron donatin

276 Supplementation of the MCD diet with methionine revealed that the changes in se

277 identify sequences at the C-terminus of the MCD that are required for release of mature FHA from the

278 responses observed in wild-type mice on the MCD diet were also observed in Lrh-1(-/-) mice on a norm

279 nd hepatic regeneration ratio in mice on the MCD diet.

280 Based on the MCD structure, we were able to shift substrate specifici

281 Casp8 expression in hepatocytes reduced the MCD-dependent increase in apoptosis and decreased expres

282 In mice fed up to 8 weeks with the MCD diet the extension of liver injury and lobular infla

283 velop key features of human plasma cell-type MCD, including splenomegaly, multifocal lymphadenopathy,

284 18 cases and 12 HIV-negative HHV-8-unrelated MCD cases showed marked discrepancies.

285 Finally, vis-UV MCD spectra show an unusually high-energy Fe(II) --> alp

286 surgery in human immunodeficiency virus (-) MCD needs to be evaluated in prospective studies.

287 The VT MCD spectra of the enzymatic S = 2 Fe(IV) horizontal lin

288 VTVH MCD magnetization curves of unbound and MI-bound Fe(II)F

289 From CD, MCD, and VTVH MCD, p-anisidine addition is found to minimally perturb

290 Abs/CD/MCD/VTVH MCD data exhibit 12 transitions that are assigned as d-d

291 variable-temperature, variable-field (VTVH) MCD spectroscopies are used to determine the geometric a

292 /variable temperature, variable field (VTVH) MCD spectroscopies to obtain detailed insight into its g

293 variable-temperature, variable-field (VTVH) MCD spectroscopies, 4-AP is found to bind directly to th

294 d variable temperature variable field (VTVH) MCD spectroscopies.

295 variable-temperature, variable-field (VTVH) MCD studies of non-alpha-KG-containing forms and the con

296 tivity; NRVS focuses on the Fe(III), whereas MCD reflects the spin-allowed transitions mostly on the

297 recurrence in 10 children and 20 adults with MCD/MesGN (n=22) or FSGS who had suffered >/=2 recurrenc

298 ious loci were significantly associated with MCD and KICS risk.

299 dynein motility in vitro are associated with MCD.

300 entrations were slightly increased in the WT/MCD and ob/control groups, whereas plasma concentrations