ライフサイエンスコーパス: PMD

1 PMD is highly heritable, but few genetic determinants ha

2 PMD is located adjacent and medial to the nucleus prepos

3 PMD is now freely available at www.proteinmicroarray.cn.

4 PMD may thereby lead to cell growth or hypertrophy respo

5 PMD measurements do not include amino acid backbone frag

6 PMDs are the discrete convolution of the mass distributi

7 PMDs cover up to 40% of the genome and are associated wi

8 d within N-HMDs (neuronal HMDs, defined as a PMD in IMR90 but HMD in SH-SY5Y) were significantly enri

9 ke of endogenous serum albumin was used as a PMD marker.

10 9% of all 184 patients first evaluated for a PMD during the study period.

11 Additionally, PMD integrates several data analysis tools and provides

12 Adjusted PMD was higher by 1.5% per minor allele (P(ACT) = 0.04).

13 cally significantly associated with adjusted PMD (P(ACT) < 0.05) for nulliparous women.

14 For nulliparous women, adjusted PMD was higher by 8.6% per minor allele (P(ACT) = 0.003;

15 Although PMD is a rare monogenic disease, hundreds of mutations i

16 ts were elicited from PMDc and PMV, although PMD stimulation elicited mainly shoulder and elbow movem

17 Among PMD patients, the ACTH 24-hour mean was significantly (P

18 atively correlated with higher cortisol, and PMD patients had higher cortisol than did NPMDs and HCs.

19 nkeys, and galagos share a number of PMV and PMD connections, suggesting preservation of a common sen

20 Both the PMV and PMD had connections with the primary motor cortex (M1),

21 ion showed strong variation for TMD, SCC and PMD in both generations (F10 and F9).

22 -nucleotide polymorphisms (SNP) of TGFB1 and PMD and their interaction with parity, adjusting for age

23 ation between genetic variation in TGFB1 and PMD using a cross-sectional study of 2,038 women who wer

24 Area PMD was composed of architectonically distinguishable ca

25 imary motor area (M1), dorsal premotor area (PMD), ventral premotor area (PMV), supplementary motor a

26 ary motor cortex (M1), dorsal premotor area (PMD), ventral premotor area (PMV), supplementary motor a

27 from the dorsal and ventral premotor areas (PMD, PMV), the caudal and rostral divisions of primary m

28 ultrastructural release reaction defined as PMD produced primarily by TPA and in part by FMLP establ

29 We assessed PMD using a computer-assisted method.

30 in both cell types and found that autosomal PMDs can be >9 Mb in length and cover 41% of the IMR90 g

31 d 4 new PLP1 point mutations that cause both PMD and peripheral neuropathy, three of which truncate P

32 aB into the nucleus may also be regulated by PMD, based on a quantitative correlation similar to that

33 mutations, overdosage of the gene can cause PMD.

34 ently as a major genetic abnormality causing PMD.

35 Classical PMD mutations correlate with accumulation of PLP in the

36 On the other hand, connatal PMD mutations lead to the accumulation of both mutant PL

37 at human SH-SY5Y neuronal cells also contain PMDs.

38 ior parietal cortex, cingulate motor cortex, PMD, and PMV.

39 embrane damage (TMD), plasmamembrane damage (PMD), and SPAD chlorophyll content (SCC), which are indi

40 we constructed Protein Microarray Database (PMD), which is specifically designed for archiving and a

41 Plastic marine debris (PMD) collected at multiple locations in the North Atlant

42 his enzyme, phosphomevalonate decarboxylase (PMD), exhibits strong inhibition by 6-fluoromevalonate m

43 anufacturing, phase measuring deflectometry (PMD) has been widely studied for the measurement of the

44 ility that microbes play a role in degrading PMD.

45 n, a process termed piecemeal degranulation (PMD) and postulated to be effected by vesicular transpor

46 hermore, we confirmed that postmortem delay (PMD) does not affect TdT labeling within the limits used

47 Percent mammographic breast density (PMD) is a strong heritable risk factor for breast cancer

48 Percent mammographic density (PMD) adjusted for age and body mass index (BMI) is a str

49 en patients with psychotic major depression (PMD patients), 38 patients with nonpsychotic major depre

50 depression with psychotic major depression (PMD) and with nonpsychotic major depression (NPMD) and h

51 40 patients with psychotic major depression (PMD); 26 patients with non-psychotic major depression (N

52 hdrawal theory of perimenopausal depression (PMD).

53 for IIH and had a perimetric mean deviation (PMD) between -2 dB and -7 dB.

54 ye results (worse perimetric mean deviation [PMD]) were used for most analyses.

55 clinical symptoms associated with different PMDs, many similarities in their mechanism suggest that

56 This paper presents a new direct PMD (DPMD) method that measures the full-field 3D shape

57 leukodystrophy Pelizaeus-Merzbacher disease (PMD) as well as in three mouse models of this disease an

58 Pelizaeus-Merzbacher disease (PMD) is a dysmyelinating disease caused by mutations, de

59 Pelizaeus-Merzbacher disease (PMD) is a dysmyelinating disease resulting from mutation

60 Pelizaeus-Merzbacher disease (PMD) is a genomic disorder most commonly arising from ge

61 Pelizaeus-Merzbacher disease (PMD) is a hypomyelinating leukodystrophy caused by mutat

62 Pelizaeus-Merzbacher disease (PMD) is a leukodystrophy linked to the proteolipid prote

63 Pelizaeus-Merzbacher disease (PMD) is a myelin disorder of the CNS that arises from bo

64 Pelizaeus-Merzbacher disease (PMD) is a pediatric disease of myelin in the central ner

65 Pelizaeus-Merzbacher disease (PMD) is an X-linked disorder characterized by dysmyelina

66 Pelizaeus-Merzbacher disease (PMD) is an X-linked dysmyelinating disorder caused most

67 Pelizaeus-Merzbacher disease (PMD) is an X-linked, dysmyelinating disorder of the CNS.

68 ng from severe Pelizaeus-Merzbacher disease (PMD) to uncomplicated HSP type 2.

69 severe form of Pelizaeus-Merzbacher disease (PMD) who have three, and in one case, five copies of the

70 LP1/DM20 cause Pelizaeus-Merzbacher Disease (PMD), a leukodystrophy, and in some instances, a periphe

71 proteins cause Pelizaeus-Merzbacher disease (PMD), an X-linked dysmyelinating neuropathy.

72 is allelic to Pelizaeus-Merzbacher disease (PMD), with both conditions resulting from mutations in t

73 ssociated with Pelizaeus-Merzbacher disease (PMD).

74 leukodystrophy Pelizaeus-Merzbacher disease (PMD).

75 sociation with Pelizaeus-Merzbacher disease (PMD).

76 ), and 2 with progressive metabolic disease (PMD).

77 se (SMD), and progressive metabolic disease (PMD).

78 ntral event in protein misfolding disorders (PMDs) is the accumulation of a misfolded form of a natur

79 are termed primary mitochondrial disorders (PMDs), and the use of nutritional interventions is routi

80 Psychogenic movement disorders (PMDs) may be difficult to differentiate from organic abn

81 effects where polarization mode dispersion (PMD) degrades entanglement.

82 asic theory of polarization mode dispersion (PMD) in optical fibers.

83 Sublethal plasma membrane disruption (PMD) is an established mechanism for signaling in severa

84 now report that plasma membrane disruption (PMD) is quantitatively correlated on a cell-by-cell basi

85 e suitability of peptide mass distributions (PMDs) as an alternative to amino acid label measurements

86 convoluted into peptide mass distributions (PMDs) during protein synthesis.

87 , primarily at partially methylated domains (PMDs) in normal breast cells.

88 revealed large partially methylated domains (PMDs) in some human cell lines.

89 he genome with partially methylated domains (PMDs, <70% average methylation), in contrast to the rest

90 -horseradish peroxidase (WGA-HRP) in dorsal (PMD) and ventral (PMV) premotor areas of owl monkeys.

91 an brain, the nucleus paramedianus dorsalis (PMD).

92 sing pretreatment partition model dosimetry (PMD).

93 However, existing PMDs cannot measure objects having discontinuous specula

94 increase in TdT labeling with more extended PMDs.

95 timulation and was associated with extensive PMD and no morphologic evidence of recovery.

96 11.4 to 30.8% for SCC, and 10.5 to 33.5% for PMD.

97 Associations were identified for PMD on chromosomes 7A, 2B and 1D, SCC on 6A, 7A, 1B and

98 of infinitesimal rotation, and the rules for PMD vector concatenation.

99 ed cells and cancers have shown evidence for PMDs.

100 structure data from PDB; mutation data from PMD; BLAST homology data from NCBI NR; and proteins foun

101 hypomethylated but smaller and distinct from PMDs, with some being hypermethylated in placenta compar

102 ntified peptides to peptides identified from PMDs using unlabeled E. coli protein.

103 1 had CMR, 22 had PMR, 3 had SMD, and 1 had PMD at week 1, whereas 1 had CMR, 22 had PMR, 2 had SMD,

104 1 had CMR, 15 had PMR, 2 had SMD, and 1 had PMD at week 1, whereas before surgery 1 patient had CMR,

105 h PERCIST, 34 had PMR, 20 had SMD, and 7 had PMD as their BOmR.

106 criteria, 38 had PMR, 16 had SMD, and 7 had PMD as their BOmR.

107 had CMR, 16 had PMR, 2 had SMD, and none had PMD.

108 enotype similar to the pattern seen in human PMD patients with duplications.

109 We identified PMD in eight human brainstems, but found some variabilit

110 In PMD, users can easily browse and search the entire datab

111 mon mechanism by which duplications arise in PMD.

112 Cells in PMD are also immunoreactive to nNOS, and immunoreactivit

113 Cells in PMD are not immunoreactive for either calbindin or parva

114 d primary outcome variable was the change in PMD from baseline to month 6 in the most affected eye, a

115 g genes that are also commonly duplicated in PMD patients.

116 rearrangement that resembles those found in PMD patients.

117 The mean improvement in PMD was greater with acetazolamide (1.43 dB, from -3.53

118 Injections in PMD labeled neurons across a mediolateral belt of poster

119 f the PLP gene are the commonest mutation in PMD.

120 st report of more than two copies of PLP1 in PMD patients and clearly demonstrates that severe clinic

121 ur current analysis of junction sequences in PMD patients confirms the occurrence of simple tandem PL

122 trongly correlated with clinical severity in PMD, potentially reflecting the functional contribution

123 RNA-seq analysis confirmed that genes in PMDs are repressed in placenta.

124 r nutritional interventions commonly used in PMDs, including micronutrients, metabolic agents, signal

125 l systems are important tools to investigate PMD metabolic mechanisms and therapeutic strategies.

126 Thirteen patients from 11 Japanese PMD families were determined to have PLP duplications.

127 es were enriched within PMDs and the largest PMD observed in SH-SY5Y cells marked a 10 Mb cluster of

128 1 region and defined several novel LCRs (LCR-PMDs).

129 is analysis using probes adjacent to the LCR-PMDs detected unique recombination-specific junction fra

130 12 patients, enabled us to associate the LCR-PMDs with breakpoint regions, and revealed rearrangement

131 Other connections were with M1, PMD, and frontal cortex and sparsely with somatosensory

132 the duplication commonly present with a mild PMD phenotype.

133 hesis that accounts for pathogenesis in most PMD patients and animal models of this disease and, more

134 irected migration, and neurodifferentiation (PMD) in the damaged adult central nervous system would h

135 Approximately 60% of PMD cases result from genomic duplications of a region o

136 Investigating the molecular basis of PMD in patients and animal models is furthering our unde

137 hat the brain contains stem cells capable of PMD in response to an exogenously administered growth fa

138 Since duplications are a major cause of PMD, we propose that interphase FISH is a reliable metho

139 These observations enabled classification of PMD subgroups by cell-intrinsic phenotypes and identifie

140 Comparisons of PMD and PMV connectivity with the cortex of the lateral

141 associated with the morphologic continuum of PMD-->anaphylactic degranulation (characterized by extru

142 oligomers correlates with the development of PMD.

143 of PLP1 gene copy number in the diagnosis of PMD and carrier detection.

144 nt implications for molecular diagnostics of PMD.

145 anning the genetic and clinical diversity of PMD-including point mutations and duplication, triplicat

146 ons and suggest that disparate etiologies of PMD could require specific treatment approaches for subs

147 th, which is the primary clinical feature of PMD.

148 Distinguishing features of PMD include pleiotropy and a range of disease severities

149 Women with a history of PMD should be alert to the risk of recurrent depression

150 We investigated the in vivo induction of PMD in the forebrain of the adult rat by using a combina

151 that oligodendrocytes in an animal model of PMD, the msd mouse, accumulate Plp gene products in the

152 odulates pathogenesis in the mouse models of PMD; however, this protein exhibits antiapoptotic activi

153 odendrocytes contributes to the pathology of PMD.

154 When the population of PMD-affected cells in injured monolayers was selectively

155 connections of M1 and the caudal portion of PMD (PMDc) were with homotopic sites, and the major call

156 llosal connections of the rostral portion of PMD (PMDr), SMA, and FEF were with homotopic sites and a

157 trices, the definition and representation of PMD vectors, the laws of infinitesimal rotation, and the

158 In a second unrelated family with signs of PMD, cytogenetic analysis showed a pericentric inversion

159 Stimulation of PMD elicited movements of the hindlimb, forelimb, neck a

160 These sequence-based structures of PMD-associated CNVs further support the role of DNA repl

161 tron 3 in families with clinical symptoms of PMD who did not have coding-region mutations revealed mu

162 requirements for the unique deconvolution of PMDs into amino acid mass distributions (AAMDs), the inf

163 Deconvolution of PMDs of the storage protein beta-conglycinin of soybean

164 nown normal tissue showing clear evidence of PMDs.

165 rise the prevalence and clinical features of PMDs resembling tics during the last 3.5 years in our ce

166 computationally map the genomic locations of PMDs in both cell types and found that autosomal PMDs ca

167 to understand the origin and progression of PMDs.

168 for the identification and quantification of PMDs for nonuniformly labeled samples is therefore lacki

169 de identification because prior knowledge on PMDs is used in all available peptide identification sof

170 ess the movements and coexistence with other PMDs and pseudoseizures were common in our patients.

171 asymptomatic postmenopausal women with past PMD responsive to hormone therapy (n = 26) and asymptoma

172 In women with past PMD that was previously responsive to hormone therapy, t

173 Women with past PMD who continued estradiol therapy and all women in the

174 Women with past PMD who were crossed over from estradiol to placebo expe

175 Using a hidden Markov model to map placental PMDs genome-wide and compare them to PMDs in other cell

176 lines, we found that genes within placental PMDs have tissue-specific functions.

177 e actually higher for genes within placental PMDs, despite the lower overall methylation of surroundi

178 TARE (41 resin, 36 glass) using pretreatment PMD.

179 for uHCC with (90)Y TARE using pretreatment PMD.

180 To produce PMD, we used a 50-g load from a spring activated in the

181 In transverse sections, PMD is oval with its long axis aligned with the dorsal b

182 the PMR group and 7.2 in the combined SMD + PMD group.

183 s 14.5 in the PMR group and 7.9 in the SMD + PMD group.

184 Genomic regions marked by cell line specific PMDs contain genes that are expressed in a tissue-specif

185 ions and clinical manifestations of specific PMDs are evaluated for their potential in determining pa

186 In the population studied, PMD and NPMD patients have distinct profiles of HPA axis

187 e was completely ablated, demonstrating that PMD is a requisite event.

188 We report here that PMD-linked mutations of PLP are associated with the acce

189 We propose that PMD, by allowing a flux of normally impermeant molecules

190 Together, our results show that PMD and breast cancer have a shared genetic basis that i

191 y 5 min of mechanical loading, suggests that PMD could promote uptake or release of signaling molecul

192 The territory that PMD occupies is included in PH in other species.

193 We found that PMDs cover 37% of the placental genome, are stable throu

194 These results suggest that PMDs are a developmentally dynamic feature of the methyl

195 The PMD and PMV were only weakly interconnected.

196 The PMD received inputs from more caudal portions of the cor

197 The PMD-SC projection assists in the participation of the SC

198 emarkably close in the animal models and the PMD cases, making them useful models for studying the me

199 states in an AlGaAs waveguide, aided by the PMD and without any compensation steps.

200 Pits visualized in the PMD surface conformed to bacterial shapes suggesting act

201 ave multiple subregions, we suggest that the PMD in human may be a further differentiation of PH and

202 he fluorinated analog also suggests that the PMD utilizes a reaction mechanism similar to that demons

203 a priori knowledge on metabolic fluxes, the PMDs are therefore unknown.

204 This PMD-dependent expression of fos protein did not require

205 not be explained by factors released through PMD, because cell injury conditioned medium failed to el

206 Thus, PMD represents the first member of a novel class of disp

207 cortex, overlapping the region projecting to PMD but centered more laterally.

208 estimates if fluxes were directly fitted to PMDs.

209 Similar to PMDs, polycomb-regulated regions are hypomethylated but

210 acental PMDs genome-wide and compare them to PMDs in other cell lines, we found that genes within pla

211 d as having either classical or transitional PMD rather than the more rare severe connatal form.

212 ntify a common pathogenic process underlying PMD have been complicated by an incomplete understanding

213 to changes in bone cell activity in part via PMD.

214 To explore whether PMD and breast cancer have a shared genetic basis, we id

215 .03) increased compared with controls, while PMD patients and the control group did not differ signif

216 wo new families in which males affected with PMD were found to have a copy of PLP on the short arm of

217 netic variants most strongly associated with PMD in a published meta-analysis of five genome-wide ass

218 and deletion rearrangements associated with PMD, and potentially other nonrecurrent rearrangements,

219 CMR, 33 with PMR, 4 with SMD, and none with PMD.

220 Patients with PMD and NPMD were outpatients recruited primarily by adv

221 we have evaluated a cohort of patients with PMD and PLP1 mutations for the presence of neuropathy.

222 NV breakpoint sequencing in 49 subjects with PMD-associated CNVs.

223 expressed in a tissue-specific manner, with PMDs being a mark of repressed transcription.

224 erved in a small proportion of patients with PMDs.

225 patients with Tourette syndrome, those with PMDs resembling tics were older: 36.3 versus 18.7 years

226 Autism candidate genes were enriched within PMDs and the largest PMD observed in SH-SY5Y cells marke

227 n the fifth percentile of controls had worse PMD (P = 0.001) than study eyes with RGCL in the fifth p