ライフサイエンスコーパス: MPS

1 MPS can accurately describe polymicrobial specimens when

2 MPS decreased the extent of staining; the degree of its

3 MPS I is currently treated with hematopoietic stem cell

4 MPS IH is characterized by a broad spectrum of clinical

5 MPS models representing the major absorption, metabolism

6 MPS typically segregates as an autosomal-recessive disor

7 MPS VII is due to deficiency in beta-glucuronidase (beta

8 MPS was greater in the males than in the females in the

9 MPS-I and -II groups were further subdivided according t

10 d O ( approximately 1.35 +/- 0.1% day(-1) ), MPS increased in response to RET only in Y (3 weeks, Y:

11 atient samples (MPS-I n = 18, MPS-II n = 12, MPS-VI n = 6, control n = 20).

12 ion cohort of patient samples (MPS-I n = 18, MPS-II n = 12, MPS-VI n = 6, control n = 20).

13 Such 1D MPS was also observed in dendrites, but the extent to wh

14 We observed that the 1D MPS exists in a substantial fraction of dendritic region

15 and dendrites than the development of the 1D MPS in axons.

16 This 1D MPS structure was initially observed in axons and exists

17 ncluding 3-mercaptopropyltrimethoxysilane (3-MPS), N-gamma-Maleimidobutyryl-oxysuccinimide ester (GMB

18 simple multiparametric scoring function (AB-MPS) was devised that correlated preclinical PK results

19 For patients with abnormal MPS results, at a 50% reduction there was a significant

20 lly automated computer analysis of NC and AC MPS data is equivalent for per-patient and can be superi

21 racerebroventricularly to the brain of adult MPS IIIB mice, four times over 2 wk.

22 ys (interquartile range: 6 to 31 days) after MPS.

23 3D myocardial perfusion CMR and MPS agreed in 38 of the 45 patients for the detection of

24 cally significant difference between CMR and MPS strategies.

25 CSF than in serum collected from healthy and MPS IIIA-affected children.

26 Linear, as opposed to branched, MOS and MPS were preferentially extracted under all conditions t

27 4, which, over time, decreased basal RNA and MPS in a dose-dependent manner (correlation of RNA and M

28 ose-dependent manner (correlation of RNA and MPS, r(2) = 0.98), even though it had no effect on the a

29 = 85); basiliximab (BAS)/EVR (N = 102); BAS/MPS (N = 101).

30 inical or subclinical WHAE (r-ATG/EVR vs BAS/MPS hazard ratio 1.30; BAS/EVR vs BAS/MPS hazard ratio 1

31 vs BAS/MPS hazard ratio 1.30; BAS/EVR vs BAS/MPS hazard ratio 1.73, P = 0.028).

32 vs 42% vs 26%, P = 0.014) compared with BAS/MPS, respectively.

33 3% vs 7% vs 4%, P = 0.025) compared with BAS/MPS, respectively.

34 CS group) or HMP (WI-HMP group) using Belzer-MPS solution.

35 FJPS), fruit juice (FJPS) and milk beverage (MPS), were stored at 4, 24, or 37 degrees C and analysed

36 and the trisomy 20 were detected blindly by MPS, including a microdeletion as small as 300 kb.

37 omosomal abnormality was not demonstrated by MPS.

38 the abnormal neurite overgrowth exhibited by MPS neurons.

39 ble to obtain a fetal molecular karyotype by MPS of maternal plasma cfDNA that is equivalent to a chr

40 ith likelihood of CAD < 5%) were obtained by MPS with AC.

41 DNA coding for beta-glu (GUSB) in the canine MPS VII cornea.

42 ntrols, improved the pathology in the canine MPS VII cornea.

43 Pharmacological studies using the cardiac MPS show half maximal inhibitory/effective concentration

44 ontrast, two of the mutations found to cause MPS in this study occurred in the tail domain.

45 Given that the best characterized MPS-I murine model is an immunocompetent mouse, we here

46 or the quantification precision of clinical MPS.

47 Under postabsorptive conditions, MPS and LPB were equivalent between groups, whereas insu

48 Moreover, D2O heralds promise for coupling MPS and muscle mass and providing insight into the contr

49 E), provide guidance for physically coupling MPS, and offer an approach to coupling MPS with distinct

50 pling MPS, and offer an approach to coupling MPS with distinct media and perfusion requirements.

51 Compared to culture, MPS allowed for triple the number of bacterial identific

52 Measurements of cumulative MPS, the sum synthesis over an extended period, using de

53 However, current MPS typically lack integrated sensors and their fabricat

54 pared with a normal result (risk difference: MPS 20 per 100 patients tested [95% CI, 0.11-0.29], DSE

55 en identified, the genetic basis of dominant MPS remains unknown.

56 w ranges of MOS, lower DP MPS, and higher DP MPS were obtained through repetitive 70%-ethanol extract

57 th relatively narrow ranges of MOS, lower DP MPS, and higher DP MPS were obtained through repetitive

58 e mycophenolic acid absorption as well as EC-MPS.

59 orption of SRL and mycophenolic acid from EC-MPS were similar.

60 al symptoms with mycophenolate mofetil or EC-MPS in combination with Tac and cyclosporin, but this wa

61 ac), enteric-coated mycophenolate sodium (EC-MPS) and sirolimus (SRL) in oral dosage forms was well-p

62 ttenuation of MPB without robustly enhancing MPS or NPB.

63 mutations establish the molecular basis for MPS IV A and for the larger MPS family of diseases.

64 The mean ischemic burden for MPS and CMR was similar (7.5+/-8.9% versus 6.8+/-9.5%, r

65 d stress and rest scores were calculated for MPS and CMR using a 17-segment model and expressed as a

66 group x time interactions) were detected for MPS or cell signaling.

67 male, 52% prior known CAD) over 8 months for MPS (72%), STE (24%), and CCTA (5%).

68 elopment of next generation therapeutics for MPS.

69 easibility of enzyme replacement therapy for MPS IIIB.

70 This study explores a potential therapy for MPS-I at a very early stage in life and represents a nov

71 We treated four MPS I cats at 3-5 mo of age with an adeno-associated vir

72 Additional studies in cultured neurons from MPS I mice showed that elevated spermine was essential f

73 Electroretinogram (ERG) was recorded from MPS IIIB and wild-type (WT) mice at the age of 28 and 46

74 tification of HS in 5 muL urine samples from MPS patients and healthy controls.

75 ECT images were analyzed to calculate global MPS defect size and regional defect size for 3 coronary

76 For the first time, we document greater MPS and mitochondrial biogenesis during SIT in males tha

77 Over 1.5-4.5 h, MPS remained increased above baseline after all treatmen

78 In this study, five human MPS models were evaluated for functional coupling, defin

79 e studies demonstrate the potential of human MPS for multi-organ toxicity and absorption, distributio

80 Patients with mucopolysaccharidosis type I (MPS I), a genetic deficiency of the lysosomal enzyme alp

81 patients with mucopolysaccharidosis type I (MPS I).

82 his concept in mucopolysaccharidosis type I (MPS IH; Hurler syndrome), a lysosomal storage disorder c

83 Mucopolysaccharidosis type I (MPS-I) is a progressive multi-system disorder caused by

84 rler syndrome (mucopolysaccharidosis type I [MPS I]).

85 Mucopolysaccharidosis type IIIA (MPS IIIA) is an autosomic recessive LSD caused by a defi

86 ndrome Type B or Mucopolysaccharidosis IIIB (MPS IIIB) is a neurodegenerative autosomal recessive lys

87 Mucopolysaccharidosis type IIIB (MPS IIIB, Sanfilippo syndrome type B) is a lysosomal sto

88 In MPS I patients, elevated CSF spermine was restricted to

89 spleen with complete metabolic correction in MPS I mice.

90 amplitudes were significantly diminished in MPS IIIB compared to WT mice.

91 arkers for central nervous system disease in MPS patients would facilitate the evaluation of new agen

92 ghts into the pathogenesis of CNS disease in MPS patients, and support the use of spermine as a new b

93 glycosaminoglycan and beta-hexosaminidase in MPS I mice 5 mo after moderate yet sustained delivery of

94 es are reported, they can be incorporated in MPS models to maximize phenotype prediction.

95 F heparan sulfate and a 3-8 fold increase in MPS-IH specific non-reducing ends, I0S0 and I0S6.

96 sponses to nutrition, fed-state increases in MPS ( approximately 50-75%; P < 0.001) were identical in

97 ormal brain IDUA activities were obtained in MPS I mice, and IDUAe1 protein was detected in neurons a

98 rotein Heg1 was significantly raised only in MPS-VI.

99 eviously observed in this animal model or in MPS I patients treated with current therapies.

100 e corrects both CNS and somatic pathology in MPS IIIA mice.

101 suggest that inflammation may play a role in MPS pathophysiology.

102 rcise efficacy in addition to effect size in MPS per se, i.e. while 'mixed' MPS increases similarly w

103 f testing the therapeutic efficacy of UCB in MPS-I mice transplanted at birth, we first defined the f

104 ulin and amino acid administration increased MPS in only healthy-weight subjects and was associated w

105 MB induces acute muscle anabolism (increased MPS and reduced MPB) albeit perhaps via distinct, and/or

106 +/- 0.08%/d), the T leg exhibited increased MPS at 0-3 wk (1.6 +/- 0.01%/d), but not at 3-6 wk (1.29

107 protein dose (25 g) at stimulating increased MPS rates when supplemented with a high (5.0 g total leu

108 ients who had undergone clinically indicated MPS underwent rest and adenosine stress 3D myocardial pe

109 EGFC receptor, VEGFR3, selectively inhibited MPS-driven increases in cutaneous lymphatic capillary de

110 ar Cardiology guidelines for (99m)Tc-labeled MPS is highly feasible while retaining short imaging pro

111 ecular basis for MPS IV A and for the larger MPS family of diseases.

112 It is unclear whether this local MPS response to osmotic stress is important to systemic

113 saccharides (MOS), and maltopolysaccharides (MPS).

114 Lean mass, MPS, LPB and strength were not different but work output

115 Ultra-low-dose (<190 MBq) MPS even with short imaging times (<6 min) is feasible u

116 h serial muscle biopsies was used to measure MPS under baseline fasted and postprandial conditions in

117 lated with 3-mercaptopropyltrimethoxysilane (MPS) encapsulation.

118 0.05) in all disease groups apart from mild MPS-I and -II.

119 ffect size in MPS per se, i.e. while 'mixed' MPS increases similarly with endurance and RE, increases

120 -mer peptide targeting the MARCKS PSD motif (MPS peptide), we were able to suppress tumor growth and

121 in, we show that deletion of TonEBP in mouse MPS cells prevents the VEGFC response to a high-salt die

122 was elevated in neuropathic subtypes of MPS (MPS I, II, IIIA, IIIB), but not in subtypes in which cog

123 The mucopolysaccharidoses (MPS) are lysosomal storage disorders that result from de

124 The mucopolysaccharidoses (MPS) are rare genetic disorders marked by severe somatic

125 otably several of the mucopolysaccharidoses (MPS).

126 Mucopolysaccharidosis (MPS) type-IH is a lysosomal storage disease that results

127 s diseases, including mucopolysaccharidosis (MPS) type VII.

128 ofiling the burden of mucopolysaccharidosis (MPS) disease at baseline and during therapy.

129 n in a mouse model of mucopolysaccharidosis (MPS) type I, one of the most common lysosomal storage di

130 Using a murine MPS I model, we demonstrated that megakaryocyte/platelet

131 of neutralizing mAbs to these CSFs on murine MPS populations in the steady-state and during acute inf

132 Myofibrillar MPS (mean +/- SD) increased (P < 0.05) above 0 g whey pr

133 endurance and RE, increases in myofibrillar MPS are specific to RE, prophetic of adaptation (i.e. hy

134 Postabsorptive rates of myofibrillar MPS and whole-body rates of phenylalanine oxidation and

135 tion of postabsorptive rates of myofibrillar MPS in rested and exercised muscle of ~80-kg resistance-

136 tion of postabsorptive rates of myofibrillar MPS to increasing amounts of whey protein at rest and af

137 nsplantation in busulfan-conditioned newborn MPS-I mice.

138 is that transplanting normal BM into newborn MPS I mice soon after birth can prevent skeletal dysplas

139 For patients with normal MPS results, there were no differences in defect size, L

140 commented on the implications of this novel MPS classification in solid organ transplantation.

141 o a prolonged (6-36 h) elevation (30-50%) of MPS that was fully blocked by rapamycin at 6 h but only

142 ficantly improves the diagnostic accuracy of MPS and can significantly outperform visual assessment b

143 describes the discovery of new biomarkers of MPS that represent disease pathology and allows the stra

144 Blunting of MPS in the obese men was offset by an apparent decline i

145 andial LGD in obese subjects and blunting of MPS responses to amino acids suggest that obesity in old

146 zed 1-28 d later and compared with brains of MPS IIIB mice that received vehicle alone or control (he

147 Urine samples from a small cohort of MPS-I, -II, and -VI patients (n = 12) were analyzed usin

148 Heparan sulfate from the cerebral cortex of MPS IIIA mice showed enhanced ability to increase glutam

149 The time course of MPS responses to exercise and the influence of training

150 potentially useful for clinical diagnosis of MPS.

151 tive tissue are typical clinical features of MPS due to disruption of the extracellular matrix.

152 distinguish the severe neurological form of MPS-II from the milder non-neurological form.

153 , developmental requirements and function of MPS cells are beginning to solve this problem in an obje

154 ments for the neurological manifestations of MPS has been hindered by the lack of objective measures

155 Markers of MPS disease pathology are needed to determine disease se

156 l fluid (CSF) samples from a canine model of MPS I revealed a marked elevation of the polyamine, sper

157 sing the naturally occurring feline model of MPS I, we tested liver-directed gene therapy as a means

158 et of behavioral changes in a mouse model of MPS IIIA.

159 e progression using the established model of MPS IIIB, the B6.129S6-Naglu(tm1Efn)/J mouse line.

160 urodevelopment, we examined murine models of MPS IIIA, which lack the enzyme sulfamidase.

161 activity was increased in visceral organs of MPS-I animals, glycosaminoglycans storage was reduced, a

162 nit cell parameters, and atomic positions of MPS.

163 We observed the presence of MPS in all of the tested neuronal types cultured from mo

164 The properties of MPS materials are reviewed in terms of their ability to

165 In the postprandial period, rates of MPS were increased above baseline over 0-1.5 h in all tr

166 ales and females would have similar rates of MPS, mitochondrial biogenesis, and synthesis of individu

167 e pathology and allows the stratification of MPS-II patients according to disease severity.

168 mine was elevated in neuropathic subtypes of MPS (MPS I, II, IIIA, IIIB), but not in subtypes in whic

169 life markedly reduces signs and symptoms of MPS I before they appear.

170 A simple synthesis of MPS is detailed which produces relatively pure product i

171 lation of this approach for the treatment of MPS IIIA and other LSDs with CNS involvement.

172 The cone a- and b-waves of MPS IIIB mice were not significantly different from thos

173 We anticipate the widespread adoption of MPSs for drug screening and disease modeling.

174 The 6 patients in whom the placement of MPSs failed were retreated with a fully cover self-expan

175 we studied the effect of HMB or Leu alone on MPS (by tracer incorporation into myofibrils), and for H

176 Large scale reactors based on MPS will require continuous flow systems where the prope

177 reports of the immobilisation of enzymes on MPS have been described, their use as biocatalytic suppo

178 revascularization and inducible ischemia on MPS realize no survival benefit from repeat revasculariz

179 =32 ml/m(2); however, myocardial ischemia on MPS was not a predictor.

180 o guided care based on the results of CMR or MPS testing.

181 Total POP contents followed the order MPS>>FJPS>MFJPS.

182 howed additional material of unknown origin, MPS identified both the translocation breakpoint and the

183 Our MPS is able to keep human induced pluripotent stem cell

184 one/CsA (P/CsA; n=7), or prednisolone/MPS (P/MPS; n=9).

185 ith P/EVL but not after switch to P/CsA or P/MPS.

186 rically, children with the severe phenotype, MPS-IH (Hurler syndrome) develop progressive neurodegene

187 Bed rest decreased postabsorptive MPS by 30% +/- 9% (CON group) and by 10% +/- 10% (LEU gr

188 ednisolone/CsA (P/CsA; n=7), or prednisolone/MPS (P/MPS; n=9).

189 es in which cognitive function is preserved (MPS IVA, VI).

190 e taken at 3 and 6 wk to temporally quantify MPS via gas chromatography:pyrolysis:isotope ratio mass

191 Whereas several mutations causing recessive MPS have been identified, the genetic basis of dominant

192 axonomy (Yukl et al., 2002), and the related MPS questionnaire, on a nursing sample.

193 tandard leadership taxonomy, and the related MPS questionnaire, on a nursing sample.

194 ristics, type of previous revascularization, MPS data, and propensity scores, only age and hyperchole

195 ntaining up to 37.5% of encapsulated roasted MPS pea starch not only provided high SDS and RS fractio

196 at predicting cardiovascular mortality (RRR, MPS, 0.89; 95% CI, 0.38-2.10; P = 0.78; DSE, 1.09; 95% C

197 5% CI, 0.12-10.05; P = 0.93), and MACE (RRR: MPS, 1.09; 95% CI, 0.64-1.86; P = 0.74; DSE, 1.56; 95% C

198 nown crystal structure of Magnus' pink salt (MPS), [Pt(NH3)4][PtCl4], study the isomeric Magnus' gree

199 larger validation cohort of patient samples (MPS-I n = 18, MPS-II n = 12, MPS-VI n = 6, control n = 2

200 ram and a myocardial perfusion scintigraphy (MPS) at inclusion.

201 chemia on myocardial perfusion scintigraphy (MPS) is commonly used to risk-stratify patients with cor

202 s, stress myocardial perfusion scintigraphy (MPS) is widely used to identify ischemia in patients wit

203 abnormal myocardial perfusion scintigraphy (MPS), dobutamine stress echocardiography (DSE) or corona

204 tings for myocardial perfusion scintigraphy (MPS), stress echocardiography (STE), or coronary compute

205 re, but here we use a multi-polygenic score (MPS) approach to increase predictive power by exploiting

206 in the field of massive parallel sequencing (MPS) is about to bring this technology within reach for

207 but targeted massively parallel sequencing (MPS) of 1,034 genes encoding known mitochondrial protein

208 We used massively parallel sequencing (MPS) of the 16S rRNA gene to characterize microbial comm

209 Massively parallel sequencing (MPS) technologies including custom, targeted gene panels

210 CR assays and massively parallel sequencing (MPS) to identify a novel RNA virus belonging to the orde

211 Massively parallel sequencing (MPS) was performed with 25-mer tags at approximately 10(

212 Rest-stress (99m)Tc-sestamibi MPS studies (n = 995; 650 consecutive cases with coronar

213 ein 7 concentrations were elevated in severe MPS I and II groups.

214 ite its strong presence in the axonal shaft, MPS is disrupted in most presynaptic boutons but is pres

215 Mesoporous silicates (MPS) are attractive materials for the immobilisation of

216 orm a membrane-associated periodic skeleton (MPS) in neurons.

217 this membrane-associated periodic skeleton (MPS), it is important to address how prevalent this stru

218 losporine A (CsA), and mycophenolate sodium (MPS) for the first 6 months after transplantation follow

219 ng everolimus (EVR) or mycophenolate sodium (MPS).

220 acy of automatic myocardial perfusion SPECT (MPS) interpretation analysis for the prediction of coron

221 oncorrected (NC) myocardial perfusion SPECT (MPS) with the corresponding performance of experienced r

222 on exposure from myocardial perfusion SPECT (MPS).

223 Using the modulation power spectrum (MPS [4, 5]), a recently developed, neurally informed cha

224 y at a relatively late state in steady-state MPS development; in contrast, GM-CSF neutralization had

225 s were treated with multiple plastic stents (MPSs) with a success rate of 62.5% (10 patients).

226 ed using Yukl's Managerial Practices Survey (MPS) framework.

227 ucopolysaccharidosis type I-Hurler syndrome (MPS-IH) is a lysosomal storage disease characterized by

228 ucopolysaccharidosis type I-Hurler syndrome (MPS-IH), along with an analysis defining a path to bette

229 Multiple pterygium syndrome (MPS) is a phenotypically and genetically heterogeneous g

230 Sanfilippo syndrome, MPS IIIA-D, results from deficits in lysosomal enzymes t

231 me biogenesis, and muscle protein synthesis (MPS) and degradation.

232 between long-term muscle protein synthesis (MPS) and hypertrophic responses to RET.

233 dy that determined muscle protein synthesis (MPS) and leg protein breakdown (LPB) under postabsorptiv

234 osal, muscle myofibrillar protein synthesis (MPS) and leg protein breakdown (LPB) were measured durin

235 However, muscle protein synthesis (MPS) and mitochondrial biogenesis during SIT have not be

236 s (BCAAs) on myofibrillar protein synthesis (MPS) at rest and after exercise.

237 Muscle protein synthesis (MPS) fluctuates widely over the course of a day and is i

238 acute response of muscle protein synthesis (MPS) to protein ingestion in rested and exercised muscle

239 weeks to quantify muscle protein synthesis (MPS) via gas chromatography-pyrolysis-isotope ratio mass

240 Muscle protein synthesis (MPS) was measured using [1, 2-(13) C2 ] leucine with bre

241 ation and skeletal muscle protein synthesis (MPS), can protect skeletal muscle health during bed rest

242 g Leu, stimulated muscle protein synthesis (MPS; HMB +70% vs. Leu +110%).

243 present a cardiac microphysiological system (MPS) with the attributes required for an ideal in vitro

244 modulating the mononuclear phagocyte system (MPS) accumulation of polyion complexes.

245 Mononuclear phagocyte system (MPS) cells are recruited to the skin, sense the hyperton

246 The mononuclear phagocyte system (MPS) comprises monocytes, macrophages and dendritic cell

247 uptake by the mononuclear phagocyte system (MPS) in vivo with a long blood circulation half-life of

248 The mononuclear phagocyte system (MPS) is a family of functionally related cells including

249 posited in the mononuclear phagocyte system (MPS) such as the liver and spleen.

250 unction of the mononuclear phagocyte system (MPS).

251 y cells of the mononuclear phagocyte system (MPS).

252 Human microphysiological systems (MPS) can model these interactions and are predicted to d

253 Recently, microphysiological systems (MPS), also known as organs-on-chips, that recapitulate t

254 on of the gene to chromosome 19 and targeted MPS of the linkage region identified a homozygous c.3G>C

255 Rest-stress gated (99m)Tc MPS NC studies (n = 957) from 623 consecutive patients w

256 While 'basal' longer term MPS was identical between Y and O ( approximately 1.35 +

257 early stages of RET, reflecting longer-term MPS.

258 who had undergone stress (99m)Tc-tetrofosmin MPS were postprocessed.

259 rdial perfusion CMR with (99m)Tc-tetrofosmin MPS.

260 etter at predicting all-cause mortality than MPS (RRR, 0.69; 95% CI, 0.49-0.96; P = 0.03) and DSE (RR

261 Quantitative analyses show that MPS is preferentially formed in axons in all neuronal ty

262 The MPS approach predicted 10.9% variance in educational ach

263 The MPS approach should be useful in research with modest sa

264 resulting in the preferential loss among the MPS populations of a cycling, monocyte-derived inflammat

265 95% CI, 6.4%-11.6%; 42/481 patients) for the MPS group.

266 (17.7% [95% CI, 14.4%-21.4%]); and 78 in the MPS group (16.2% [95% CI, 13.0%-19.8%]).

267 roup, 2.5% in the CMR group, and 2.5% in the MPS group (adjusted hazard ratios: CMR group vs NICE gui

268 7.5%) in the CMR group, and 34 (7.1%) in the MPS group; adjusted odds ratio of unnecessary angiograph

269 neovascularization were also detected in the MPS IIIB retina.

270 In the MPS, short actin filaments, capped by actin-capping prot

271 decades, classification of the cells of the MPS has generated considerable controversy.

272 t a model consistent with the concept of the MPS in which local proliferation and monocyte recruitmen

273 study one demonstrated the relevance of the MPS leadership framework for nurses at hospital ward lev

274 tailor the surface functionalization of the MPS to suit a specific enzyme.

275 urprisingly, attenuation of MARCKS using the MPS (MARCKS phosphorylation site domain) peptide synergi

276 y two, self ratings of leadership (using the MPS) from 15 senior charge nurses (SCN) and upward ratin

277 % CI, 0.12-0.34, P < .001); CMR group vs the MPS group, 1.27 (95% CI, 0.79-2.03, P = .32).

278 yocardial perfusion CMR is an alternative to MPS for detecting the presence and rating the severity o

279 inflammatory-mediated mechanisms related to MPS diseases and perhaps lead to improved targeted thera

280 families affected by dominantly transmitted MPS characterized by pterygia, camptodactyly of the hand

281 s with previous revascularization undergoing MPS between January 1, 2005, and December 31, 2007, we i

282 that the developmental mechanism underlying MPS differs from that of other conditions and/or that ce

283 our series there were several failures using MPSs as a strategy for rescue endotherapy suggesting tha

284 roup, 1.37 [95% CI, 0.52-3.57]; CMR group vs MPS group, 0.95 [95% CI, 0.46-1.95]).

285 ificantly diminished at the 46 th week, when MPS IIIB mice showed a major loss of rods and rod bipola

286 Critically, whereas MPS remained unchanged in the UT leg (e.g., approximatel

287 onic interstitial fluid compartment in which MPS cells exert homeostatic and blood pressure-regulator

288 al and morphological changes associated with MPS IIIB disease progression using the established model

289 Cytokine analyses in CSF of children with MPS-IH showed significantly elevated inflammatory marker

290 port of CSF characteristics in children with MPS-IH.

291 clinical and subclinical WHAE compared with MPS.

292 BMT increases the life span of patients with MPS IH, musculoskeletal manifestations are only minimall

293 es on the long-term outcome of patients with MPS-IH after HCT are lacking.

294 rs of the long-term outcome of patients with MPS-IH after successful HCT.

295 The long-term prognosis of patients with MPS-IH receiving HCT can be improved by reducing the age

296 Two hundred seventeen patients with MPS-IH successfully engrafted with a median follow-up ag

297 e majority of the transplanted patients with MPS-IH, with high variability between patients.

298 ated the CSF of 25 consecutive patients with MPS-IH.

299 eover, the vertebral fusions in persons with MPS, coupled with evidence of MYH3 expression in bone, s

300 The phenotypic overlap among persons with MPS, coupled with physical findings distinct from other

301 ificant predictors of treatment failure with MPSs in refractory bile leaks.

302 s prohibit metallophilic interactions within MPS.