ライフサイエンスコーパス: MPT

1 MPT cells become resistant to rapamycin after prolonged

2 MPT inhibitors, cyclosporin A (CsA), and NIM811 temporar

3 MPT is caused by the opening of permeability transition

4 MPT, observed in situ as Deltapsi(m) loss, was prevented

5 MPT-based portfolios can also have 21% less uncertainty

6 MPT-guided diversification can work to reduce the climat

7 ubling the screw speed when processing a 10% MPT formulation does not affect the solid state of the p

8 At a 10% MPT load, increasing the extrusion temperature does not

9 Second malignancies were observed in 18 MPT-T patients vs 14 mPR-R patients.

10 Thus, methenyl-dH(4)MPT accumulation inhibits H(4)F-dependent assimilation.

11 nt strain, predicted to reduce methenyl-dH(4)MPT accumulation, enhances growth on methylamine.

12 in its kinetic properties for methylene-dH(4)MPT and for methenyl-H(4)F during growth on single-carbo

13 Putative functions of these genes in dH(4)MPT biosynthesis are discussed.

14 Methenyl-dH(4)MPT is shown to be a competitive inhibitor of the reduct

15 size dH(4)MPT, and six were found to be dH(4)MPT negative.

16 cs of dephosphotetrahydromethanopterin (dH(4)MPT) biosynthesis.

17 te is dephosphotetrahydromethanopterin (dH(4)MPT) dependent, while the assimilation of carbon into bi

18 re dehydrogenases able to use methylene-dH(4)MPT, an intermediate in the oxidation of formaldehyde to

19 analyzed for the ability to synthesize dH(4)MPT, and six were found to be dH(4)MPT negative.

20 ts role in oxidative metabolism via the dH(4)MPT-dependent pathway and its apparent inability to repl

21 results in the accumulation of methenyl-dH(4)MPT.

22 ovide the first biochemical evidence for H(4)MPT biosynthesis genes in bacteria.

23 Thus the first two enzymes involved in H(4)MPT biosynthesis in the archaea are Fe(2+) dependent.

24 te synthase, the first committed step of H(4)MPT biosynthesis.

25 suggesting a role for these two genes in H(4)MPT biosynthesis.

26 R that is required for the final step of H(4)MPT biosynthesis.

27 plex (Fhc) generates formate from formyl-H(4)MPT in two consecutive reactions where MYFR acts as a ca

28 ethanogenesis, respectively via a methyl-H(4)MPT intermediate, constituting the third methanogenesis

29 ization of four mutants defective in the H(4)MPT pathway and place them into three different phenotyp

30 These results define the role of the H(4)MPT pathway as the primary formaldehyde oxidation and de

31 ght to be essential, indicating that the H(4)MPT pathway is not absolutely required during growth on

32 ates; however, mutants defective for the H(4)MPT pathway reveal a unique phenotype of being inhibited

33 Unlike mutants defective for the H(4)MPT pathway, the ftfL mutant strain does not exhibit phe

34 H(4)MPT was detectable in wild-type cells but not in strains

35 n bond before the appearance of methenyl-H(4)MPT(+) (MPT(+)).

36 hway depends on tetrahydromethanopterin (H(4)MPT) and methylofuran (MYFR), an analog of methanofuran

37 e 5,10-methenyl tetrahydromethanopterin (H(4)MPT) cyclohydrolase, was constructed in vitro and recomb

38 oped to measure tetrahydromethanopterin (H(4)MPT) levels in wild-type and mutant cells of Methylobact

39 pathway and the tetrahydromethanopterin (H(4)MPT) pathway, and both are required for growth on C(1) c

40 tions linked to tetrahydromethanopterin (H(4)MPT) were analyzed in a variety of proteobacteria and in

41 erin portion of tetrahydromethanopterin (H(4)MPT), a C(1) carrier coenzyme first identified in the me

42 ns defective in tetrahydromethanopterin (H(4)MPT)-dependent formaldehyde oxidation.

43 pathway and the tetrahydromethanopterin (H(4)MPT)-linked pathway.

44 a precursor of both tetrahydrofolate and H(4)MPT, and afpA apparently encodes a novel dihydromethanop

45 anogenic Archaea and Bacteria possessing H(4)MPT-linked functions, orfY, orf1, and afpA were shown to

46 ted that the evolution of genes encoding H(4)MPT-linked reactions in Proteobacteria involved lateral

47 the enzymes involved in C(1) metabolism (H(4)MPT/H(4) F pathways, formate oxidation and serine cycle)

48 When extruding a formulation with a 40% MPT concentration, the broadening of MPT peaks indicates

49 Per-protocol response rates were 63.6% (MPT-T) and 59.9% (mPR-R) (P = .557).

50 active MPT synthase and 4117 A(2) for active MPT synthase.

51 for the binding of MoaD-SH to MoaE in active MPT synthase.

52 The multi-redox active MPT undergoes four chemically and electrochemically reve

53 l killing was prevented by cyclosporin A, an MPT blocker, and by pancaspase and caspase 3 inhibition,

54 llapse in Deltapsi(m) is a consequence of an MPT and that the timing of the victorin-induced MPT is p

55 itochondrial depolarization, cell death, and MPT were detected by intravital confocal/multiphoton mic

56 se results suggest that NAD(+) depletion and MPT are necessary intermediary steps linking PARP-1 acti

57 , mitochondrial membrane depolarization, and MPT.

58 in, a common intermediate in both folate and MPT biosynthesis.

59 d increased mitochondrial ROS production and MPT.

60 ROS and MPT have been implicated in myocardial stunning associat

61 used them to investigate the role of ROS and MPT in cell death caused by t-butylhydroperoxide (tBHP)

62 leading to the formation of precursor Z and MPT, respectively.

63 a combination chemical and physical barrier MPT.

64 peak shifts indicating interactions between MPT and the carrier) between sections 5 and 6, due to fo

65 teria, this form is modified to form the bis-MPT guanine dinucleotide cofactor with two MPT units coo

66 ria depolarization by more than 60%, blocked MPT onset, and prevented cell death.

67 olar concentrations of cyclosporin A blocked MPT and cell death, suggesting that MPT is a necessary s

68 Blocking MPT diminished p53 translocation and apoptosis.

69 hondrial membrane potential and blocked both MPT and cell death.

70 We used BU.MPT cells, a mouse kidney epithelial cell line, as our p

71 sulfur- and metal-free precursor Z to MPT by MPT synthase involves the transfer of sulfur atoms from

72 moters to regulate transcription and control MPT.

73 0.7 Ma, very different from the conventional MPT characteristics.

74 Cultured MPT cells exposed to rapamycin for 7 days were approxima

75 The redox active 1,3,5-triazine derivative (MPT) was used as a guest to study host-guest, charge tra

76 an existing bioenergetics model to describe MPT induction under a variety of conditions.

77 t C-7 and C-9 of the pterin ring distinguish MPT from all other pterin-containing natural products.

78 We exposed MPT cells to 0.2 dynes/cm(2) FSS for 3 h and performed c

79 ochondria subjected to conditions that favor MPT.

80 e >/=3 nonhematologic toxicity was 59.5% for MPT-T vs 40.0% for mPR-R (P = .001).

81 phosphorus ratios, time-dependent assays for MPT and MGD detection, and determination of the numbers

82 des the three basic necessary conditions for MPT: a high calcium load, alkaline matrix pH and circums

83 gets and evaluate potential therapeutics for MPT mitigation.

84 ontrast, protection of the mitochondria from MPT favors apoptosis of M. tuberculosis-infected macroph

85 nd step is catalyzed by the heterotetrameric MPT synthase protein consisting of two large (MoaE) and

86 Taken together, here we presented how MPT-SURF analysis of nuclear chromatin granules defines

87 d upon formation of the subunit interface in MPT synthase was estimated to be 2378 A(2) for inactive

88 role of c-Jun N-terminal kinase 2 (JNK2) in MPT-induced liver injury.

89 of the interaction between MoaE and MoaD in MPT synthase using a H/D exchange and matrix-assisted la

90 e was estimated to be 2378 A(2) for inactive MPT synthase and 4117 A(2) for active MPT synthase.

91 for the binding of MoaD to MoaE in inactive MPT synthase and a dissociation constant of 2.6 +/- 0.9

92 alcein into mitochondria after MHX indicated MPT onset.

93 +) depletion is necessary for PARP-1-induced MPT, NAD(+) was restored to near-normal levels after PAR

94 In addition, they inhibited 3NP-induced MPT in isolated mitochondria and prevented mitochondrial

95 me inactivation is observed for Ca2+-induced MPT.

96 reased susceptibility to the calcium-induced MPT in liver mitochondria isolated from a knock-in HD mo

97 The manganese-induced MPT in astrocytes was blocked by pretreatment with antio

98 The mutant huntingtin protein-induced MPT pore opening was accompanied by a significant releas

99 and that the timing of the victorin-induced MPT is poised to influence the cell death response.

100 t can scavenge mitochondrial ROS and inhibit MPT, suggesting that it may protect against ischemic ren

101 Exogenous H(2)O(2) inhibited MPT, because of its activation of PKCepsilon, with an IC

102 he K(+) ionophore valinomycin also inhibited MPT opening and that this inhibition required reactive o

103 s of PKG or protein kinase C (PKC) inhibited MPT opening.

104 ased mitochondrial ROS production, inhibited MPT and swelling, and prevented cytochrome c release ind

105 Heat shock inhibited MPT pore opening induced by 50 microm CaCl(2) plus 5 mic

106 r 3 to 6 hours followed by a CsA-insensitive MPT 9 to 16 hours after acetaminophen.

107 )-independent and cyclosporin A-insensitive) MPT pore opening induced by higher doses of HgCl(2) and

108 /kg, n = 7), a calcineurin inhibitor lacking MPT activity, followed in 30 min by LPS.

109 rmeability transition pore complex, to limit MPT induction is the general mechanism of cardiomyocyte

110 suggested the distinctness of CypD-mediated MPT from RIPK1/RIPK3-mediated necroptosis.

111 Methanopterin (MPT) and its analogs are coenzymes required for methanog

112 opy enabled identification of a novel bis-Mo-MPT intermediate on MobA prior to nucleotide attachment.

113 ddition of Mg-GTP to MobA loaded with bis-Mo-MPT resulted in formation and release of the final bis-M

114 n, which involves 1) the formation of bis-Mo-MPT, 2) the addition of two GMP units to form bis-MGD on

115 s via a dithiolene function, thus forming Mo-MPT.

116 of the fragments of the Mo-molybdopterin (MO-MPT) binding site and nitrate reduction active site and

117 d tungsten are coordinated by molybdopterin (MPT), a tricyclic pyranopterin containing a cis-dithiole

118 MOCS2A, the small subunit of molybdopterin (MPT) synthase.

119 basic form comprises a single molybdopterin (MPT) unit, which binds a molybdenum ion bearing three ox

120 The molybdopterin (MPT) synthase complex in Escherichia coli consists of tw

121 rom a pyranopterindithiolate (molybdopterin, MPT) cofactor.

122 onths, from 32.7 months (MP) to 39.3 months (MPT).

123 Overall survival was 52.6 months (MPT-T) vs 47.7 months (mPR-R) (P = .476).

124 efore the appearance of methenyl-H(4)MPT(+) (MPT(+)).

125 8 kcal/mol lower than that in the absence of MPT+, a result that explains why the isotopic H2/D2O exc

126 t is essential for the catalytic activity of MPT synthase.

127 /H(2)O exchange take place as the arrival of MPT(+) triggers the breaking of the strong Fe-H(delta-).

128 (3) Only upon the arrival of MPT(+) with its strong hydride affinity can D(2)/H(2)O e

129 h a 40% MPT concentration, the broadening of MPT peaks indicates melting of MPT between sections 2 an

130 d 668 patients between nine 4-week cycles of MPT followed by thalidomide maintenance until disease pr

131 ion-free survival (PFS) hazard ratio (HR) of MPT-T/mPR-R </=0.82.

132 lted in mitoK(ATP)-independent inhibition of MPT opening, whereas activation of PKCepsilon by PKG or

133 se caused mitoK(ATP)-dependent inhibition of MPT opening.

134 ow that cyclosporin A (CsA), an inhibitor of MPT, protects the mitochondria from release of cytochrom

135 As a guest, the host-guest interaction of MPT was studied with two macrocyclic cucurbit[7,8]uril (

136 broadening of MPT peaks indicates melting of MPT between sections 2 and 3, caused by the first kneadi

137 e barrier for H2 cleavage in the presence of MPT+ is 18 kcal/mol lower than that in the absence of MP

138 Hmd is strictly dependent on the presence of MPT+.

139 ng must ultimately involve the prevention of MPT.

140 n essential component and a key regulator of MPT induction.

141 Use of MPT-T or mPR-R in elderly patients with untreated MM dem

142 rates (partial response or better was 59% on MPT and 37% on MP).

143 Median PFS was 21 months on MPT-T and 18.7 months on mPR-R (HR, 0.84; 95% confidence

144 l permeability transition (MPT)-dependent or MPT-independent mechanisms.

145 Moreover, we used our MPT-SURF analysis to study the apparent mechanical prope

146 MPR-R has no advantage over MPT-T concerning efficacy.

147 utations confirmed that Vp15 encodes a plant MPT synthase small subunit (ZmCNX7).

148 cene (LPT, 2.5 to 3 Ma) and mid-Pleistocene (MPT, 1.2 to 0.85 Ma) climate transitions.

149 eet dynamics and that longer and deeper post-MPT ice ages were sustained by carbon cycle feedbacks re

150 Its recovery into the post-MPT 100-thousand-year world is characterized by continue

151 ted and the activities of the four predicted MPT-containing enzymes were assayed in the presence of m

152 n after MHX, at least in part, by preventing MPT onset and subsequent compromised energy supply and p

153 In conclusion, NO prevents MPT-dependent necrotic killing of ischemic hepatocytes a

154 predicted to contain a metal binding pterin (MPT), with the metal being either molybdenum or tungsten

155 8 patients were randomly assigned to receive MPT-T, and 319 received MPR-R.

156 ed cortical neurons had a delayed or reduced MPT as compared with astrocytes.

157 t-D+TPEN, and rOx production did not require MPT or caspase activation.

158 The MPT inhibitor sanglifehrin A reversed MPT markers and increased respiration in LM7 and 143B ce

159 clusion, after acetaminophen a CsA-sensitive MPT occurred after 3 to 6 hours followed by a CsA-insens

160 ngs suggest that the development of specific MPT inhibitors may be an interesting therapeutic avenue

161 In summary, these results support MPT as an upstream target for pharmacologic intervention

162 Metoprolol tartrate (MPT) concentration (10 and 40% in Eudragit RSPO), extrus

163 itiated, multipurpose prevention technology (MPT) that simultaneously reduces their risk of acquiring

164 l (LTD) nuclei of the mesopontine tegmentum (MPT).

165 at 33 degrees C (male producing temperature: MPT) yields male offspring, whereas incubation temperatu

166 n of melphalan, prednisone, and thalidomide (MPT) is considered standard therapy for newly diagnosed

167 ared melphalan, prednisone, and thalidomide (MPT-T) with melphalan, prednisone, and lenalidomide (mPR

168 ombination melphalan-prednisone-thalidomide (MPT) is considered a standard therapy for patients with

169 prednisone alone (MP) and with thalidomide (MPT).

170 e of cytochrome c occurred much earlier than MPT; hence, the former is unlikely to be a consequence o

171 ility to MPT, increasing the likelihood that MPT will occur on reperfusion (the MPT trigger phase).

172 el was corroborated and used to predict that MPT in an acidic environment is mitigated by an increase

173 blocked MPT and cell death, suggesting that MPT is a necessary step linking PARP-1 activation to cel

174 The MPT containing enzymes nitrate reductase, sulphite oxida

175 The MPT group included more advanced eyes (P < 0.001) and ha

176 The MPT group required less laser and cryotherapy after trea

177 The MPT induction model was able to reproduce the expected b

178 The MPT inhibitor sanglifehrin A reversed MPT markers and in

179 The MPT ocean circulation crisis facilitated the coeval draw

180 The MPT then induces ATP depletion-dependent necrosis or cas

181 tely 43 to approximately 75 muatm across the MPT, mainly because of lower glacial CO2 levels.

182 ced terrestrial vegetation change across the MPT.

183 of the RIPK1 inhibitor necrostatin-1 and the MPT inhibitor sanglifehrin A confirmed the results with

184 h manganese acetate (10-100 microM), and the MPT was assessed by changes in the mitochondrial membran

185 ing, the shift to 100,000-year cycles at the MPT is more likely to be a response to an additional cha

186 lacial CO(2) levels, similar to those at the MPT, lead to the local decline of C(3) grasses under con

187 Because the MPT is a cell death-inducing phenomenon, we hypothesized

188 Minocycline blocked the MPT by decreasing mitochondrial Ca(2+) uptake, whereas N

189 and NIM811 but not tetracycline blocked the MPT.

190 7), a calcineurin inhibitor that blocks the MPT, or tacrolimus (FK506, 0.1 mg/kg, n = 7), a calcineu

191 crotic cell death after reperfusion, but the MPT is also implicated in apoptosis.

192 that apoptotic signaling is initiated by the MPT and further amplified by downstream caspases, probab

193 mohaline circulation (THC) system during the MPT between marine isotope stages (MISs) 25 and 21 at ~9

194 nor CO2 change in isolation can explain the MPT.

195 Following the MPT high-amplitude lake level variations dominate the re

196 with a previously proposed mechanism for the MPT synthase reaction.

197 approved (FDA-approved) drugs identified the MPT antagonist tigecycline (TIG) as a potent inhibitor o

198 estimated a better globe salvage rate in the MPT group (66%) compared with the MA group (58%, P = 0.0

199 lar acetylcholine transporter (VAchT) in the MPT of rat brain to identify the potential sites for M2R

200 east grade 3 was significantly higher in the MPT-T arm: 16% vs 2% in MPR-R, resulting in a significan

201 holinergic and noncholinergic neurons in the MPT.

202 rons and astrocytes to manganese induces the MPT.

203 Instead, the MPT promotes caspase-and ATP-dependent apoptosis.

204 During ischemia (the MPT priming phase), factors such as intracellular Ca2+ a

205 amine methyl ester to visualize onset of the MPT and mitochondrial depolarization, respectively.

206 optotic effect of CypD is independent of the MPT but is due to its interaction with some key apoptosi

207 Induction of the MPT by manganese and associated mitochondrial dysfunctio

208 ng atmospheric CO2 levels as a driver of the MPT has proven difficult with available observations.

209 The framework of the MPT induction model includes the potential states of the

210 This difference is a result of the MPT+ triggering the pyridone to provide electron density

211 f autophagy proteins, prevented onset of the MPT, and decreased cell death after reoxygenation.

212 CsA delayed these changes, indicative of the MPT, to approximately 11 hours after acetaminophen admin

213 release from mitochondria independent of the MPT.

214 losporin A, consistent with induction of the MPT.

215 Quantification of the MPT/molybdenum and molybdenum/phosphorus ratios, time-de

216 poptosis and delayed but did not prevent the MPT.

217 hood that MPT will occur on reperfusion (the MPT trigger phase).

218 osis, suggesting that apoptosis requires the MPT, and that caspase activation is downstream to the MP

219 Our data suggest that the MPT may play a role in suppression of mitochondrial func

220 Model simulations further reveal that the MPT transition likely reflects decreased sensitivity of

221 Instead, we infer that the MPT was initiated by a change in ice sheet dynamics and

222 Our results suggest that the MPT was initiated by an abrupt increase in Antarctic ice

223 re became increasingly glaciated through the MPT.

224 Thus, the MPT is a common mechanism responsible for both necrosis

225 a proton while transferring a hydride to the MPT+.

226 that caspase activation is downstream to the MPT.

227 l for investigators to use to understand the MPT induction phenomenon, explore alternative hypotheses

228 mitochondria, which is not mediated via the MPT.

229 increased mitochondrial dysfunction via the MPT.

230 me inactivation linearly correlates with the MPT onset and propagation.

231 d the pathway that links mitoK(ATP) with the MPT.

232 We adapt Modern Portfolio Theory (MPT) to optimal spatial targeting of conservation activi

233 e crystal structures of non-thiocarboxylated MPT synthase from Staphylococcus aureus in its apo form

234 protein catalyzes the nucleotide addition to MPT, but the mechanism of the biosynthesis of the bis-MG

235 alyses showed that RB1-E2F complexes bind to MPT gene promoters to regulate transcription and control

236 al autophagy, and this subsequently leads to MPT-dependent hepatocyte death after A/R.

237 or 72 weeks (18 cycles; 541 patients), or to MPT for 72 weeks (547 patients).

238 s lenalidomide-dexamethasone was superior to MPT for all secondary efficacy end points, including ove

239 ely increase mitochondrial susceptibility to MPT, increasing the likelihood that MPT will occur on re

240 of the sulfur- and metal-free precursor Z to MPT by MPT synthase involves the transfer of sulfur atom

241 The combination of melphalan plus topotecan (MPT) was used to treat 149 patients and 158 eyes for a t

242 isease progression or unacceptable toxicity (MPT-T) and the same MP regimen with thalidomide being re

243 Here, we use multiple-particle tracking (MPT) microrheology and traction force cytometry to probe

244 By using multiple particle tracking (MPT) technique on chromatin granules, we designed a SURF

245 microscopy, and multiple particle tracking (MPT) to investigate the intracellular trafficking of hig

246 r environment by multiple particle tracking (MPT).

247 iated mitochondrial permeability transition (MPT) and receptor-interacting protein kinase (RIPK)1-med

248 n and mitochondrial permeability transition (MPT) are sequential and necessary steps in PARP-1-mediat

249 e the mitochondrial permeability transition (MPT) as a key factor in acetaminophen-induced necrotic a

250 f the mitochondrial permeability transition (MPT) can initiate necrotic cell death after reperfusion,

251 r the mitochondrial permeability transition (MPT) in cardiomyocytes and that cell survival is steeply

252 ty to mitochondrial permeability transition (MPT) induction that may contribute significantly to HD p

253 Mitochondrial permeability transition (MPT) is a highly regulated complex phenomenon that is a

254 The mitochondrial permeability transition (MPT) is a marker of impaired mitochondrial function that

255 The mitochondrial permeability transition (MPT) mediates hepatic necrosis after ischemia and reperf

256 duced mitochondrial permeability transition (MPT) pore opening in isolated mouse liver mitochondria,

257 f the mitochondrial permeability transition (MPT) pore, resulting in mitochondrial depolarization, de

258 ng of mitochondrial permeability transition (MPT) pores, mitochondria from heat-preconditioned rat li

259 f the mitochondrial permeability transition (MPT) process], z-VAD (a pan-caspase inhibitor) and inhib

260 d the mitochondrial permeability transition (MPT) were assessed in isolated rat liver mitochondria.

261 f the mitochondrial permeability transition (MPT) with N-methyl-4-isoleucine cyclosporine (NIM811) im

262 duced mitochondrial permeability transition (MPT), an effect that was reversed by KT5823.

263 f the mitochondrial permeability transition (MPT), but not FK506, a calcineurin inhibitor, abolished

264 of a mitochondrial permeability transition (MPT), on a per cell basis, did not occur simultaneously

265 f the mitochondrial permeability transition (MPT), such as mitochondrial swelling, depolarization, an

266 n the mitochondrial permeability transition (MPT), which is associated with increased release of cyto

267 d via mitochondrial permeability transition (MPT)-dependent or MPT-independent mechanisms.

268 f the mitochondrial permeability transition (MPT).

269 h the mitochondrial permeability transition (MPT).

270 n and mitochondrial permeability transition (MPT).

271 o the mitochondrial permeability transition (MPT).

272 f the mitochondrial permeability transition (MPT).

273 f the mitochondrial permeability transition (MPT).

274 with mitochondrial permeability transition (MPT).

275 The mid-Pleistocene transition (MPT) is widely recognized as a shift in paleoclimatic pe

276 The mid-Pleistocene transition (MPT) marked a fundamental change in glacial-interglacial

277 observed at the Mid-Pleistocene Transition (MPT), consistent with far-field climate forcing, which s

278 d years ago, the mid-Pleistocene transition (MPT), when the dominant periodicity of climate cycles ch

279 ecline after the mid-Pleistocene transition (MPT, c.

280 During the Mid-Pleistocene Transition (MPT; 1,200-800 kya), Earth's orbitally paced ice age cyc

281 drial membrane permeability pore transition (MPT) and consequent cytochrome c release in these cells.

282 on of the mitochondrial protein translation (MPT) gene pathway relative to tumors harboring p53 delet

283 ased the Ca2+ threshold necessary to trigger MPT pore opening.

284 ulture filtrate proteins of M. tuberculosis, MPT 32, and the 81-kDa GlcB protein were detectable in p

285 Cultured mouse proximal tubular (MPT) cells were used to compare the antiproliferative ef

286 s study, we have used mouse proximal tubule (MPT) cells as a model to study the role of fluid shear s

287 s-MPT guanine dinucleotide cofactor with two MPT units coordinated at one molybdenum atom, which addi

288 Chinese Loess Plateau, we document a unique MPT reflecting terrestrial vegetation changes from a dom

289 We find that using MPT instead of simple diversification in the PPR can ach

290 continuous lenalidomide-dexamethasone versus MPT.

291 NP, and ROS mediate cytochrome c release via MPT.

292 or continuous lenalidomide-dexamethasone vs. MPT and 0.70 for continuous lenalidomide-dexamethasone v

293 tuberculosis, and this may be enhanced when MPT is stabilized.

294 of lenalidomide-dexamethasone, and 51% with MPT.

295 mitoK(ATP) and the other in association with MPT.

296 As compared with MPT, continuous lenalidomide-dexamethasone given until d

297 As compared with MPT, continuous lenalidomide-dexamethasone was associate

298 lidomide-dexamethasone, and 21.2 months with MPT (hazard ratio for the risk of progression or death,

299 er a median follow-up of 36 months, PFS with MPT-T was 20 months (95% confidence interval [CI], 18-23

300 tinuous lenalidomide-dexamethasone than with MPT (70% vs. 78%).

301 s H(2) capture and hydride formation without MPT(+) while the pyridone's special role involves the pr