ライフサイエンスコーパス: PMD

1 PMD has the potential to direct an Ab response at high r

2 PMD is highly heritable, but few genetic determinants ha

3 PMD is located adjacent and medial to the nucleus prepos

4 PMD may thereby lead to cell growth or hypertrophy respo

5 PMD measurements do not include amino acid backbone frag

6 PMDs are hypervariable in methylation level, size and di

7 PMDs are the discrete convolution of the mass distributi

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

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

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

11 9% of all 184 patients first evaluated for a PMD during the study period.

12 White), 1004 (15.4%) met the criteria for a PMD.

13 Additionally, PMD integrates several data analysis tools and provides

14 xtraction cohort, 13 patients had adjunctive PMD (age 59.4 +/- 14.0 years, vegetation size 2.1 +/- 0.

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

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

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

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

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

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

21 rimination (CMD) scores were calculated, and PMD index was created using the combination of HRL and C

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

23 d between elevated IFI27 gene expression and PMD, but not between IFI27 and secondary mitochondrial d

24 eractions (P < 0.05) between nulliparity and PMD/NDA, age at menarche and area of dense tissue, and b

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

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

27 At 1 month postoperatively, RNFL and PMD had improved by 38% and 4%, respectively.

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

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

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

31 Area PMD was composed of architectonically distinguishable ca

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

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

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

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

36 We assessed PMD using a computer-assisted method.

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

38 Associations between PMDs and total QOL score were evaluated using linear reg

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

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

41 mutations, overdosage of the gene can cause PMD.

42 ently as a major genetic abnormality causing PMD.

43 Classical PMD mutations correlate with accumulation of PLP in the

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

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

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

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

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

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

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

51 is classification, new lesions do not define PMD per se; rather, PMD requires an increase in the sum

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

53 ility that microbes play a role in degrading PMD.

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

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

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

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

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

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

60 40 patients with psychotic major depression (PMD); 26 patients with non-psychotic major depression (N

61 women who develop perimenopausal depression (PMD) are at an increased risk of cardiovascular and all-

62 hdrawal theory of perimenopausal depression (PMD).

63 a method, called protect, modify, deprotect (PMD), to generate immunogenic proteins aimed to direct a

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

65 s were changes in perimetric mean deviation (PMD) on Humphrey Visual Field Analyzer in both eyes.

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

67 al of 67 748 women with clinically diagnosed PMDs and 338 740 matched unaffected women were included,

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

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

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

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

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

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

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

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

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

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

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

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

80 Pelizaeus-Merzbacher disease (PMD) is an X-linked leukodystrophy caused by mutations i

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

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

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

84 leukodystrophy Pelizaeus-Merzbacher disease (PMD)(1,2).

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

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

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

88 ssociated with Pelizaeus-Merzbacher disease (PMD).

89 sociation with Pelizaeus-Merzbacher disease (PMD).

90 leukodystrophy Pelizaeus-Merzbacher disease (PMD).

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

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

93 re considered progressive metabolic disease (PMD).

94 Adult primary mitochondrial diseases (PMDs) frequently exhibit neurological manifestations tha

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

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

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

98 Although premenstrual disorders (PMDs) end at menopause, it is unclear whether they are a

99 e than two-thirds of premenstrual disorders (PMDs), including premenstrual syndrome and premenstrual

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

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

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

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

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

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

106 erlap with DNA partially methylated domains (PMDs) and occupy developmental gene promoters.

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

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

109 ests itself in partially methylated domains (PMDs) which extend up to megabases.

110 ally occurs at partially methylated domains (PMDs).

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

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

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

114 sing pretreatment partition model dosimetry (PMD).

115 of the potential risks induced by excessive PMD use.

116 However, existing PMDs cannot measure objects having discontinuous specula

117 increase in TdT labeling with more extended PMDs.

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

119 11.4 to 30.8% for SCC, and 10.5 to 33.5% for PMD.

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

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

122 t provide a general therapeutic strategy for PMD(1,3-5).

123 ession could be developed as a treatment for PMD in humans.

124 for premenstrual dysphoric disorder and for PMDs with symptom onset before 20 years of age and remai

125 ed cells and cancers have shown evidence for PMDs.

126 durance exercise regimen in mouse models for PMDs harboring distinct mitochondrial mutations.

127 clinical transition of genetic therapies for PMDs is feasible.

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

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

130 gligible as they are generally excluded from PMDs.

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

132 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,

133 1 had CMR, 15 had PMR, 2 had SMD, and 1 had PMD at week 1, whereas before surgery 1 patient had CMR,

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

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

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

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

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

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

140 mon mechanism by which duplications arise in PMD.

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

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

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

144 ficant overlap in genes that were changed in PMD regardless of experimental condition.

145 myelination is rescued by iron chelation in PMD pre-clinical models.

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

147 Gene networks dysregulated in PMD included inflammatory response, early/late E2-respon

148 cant differences in transcript expression in PMD in all experimental conditions, and significant over

149 rearrangement that resembles those found in PMD patients.

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

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

152 rs and molecular targets for intervention in PMD.

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

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

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

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

157 insic to DHEA metabolism, was upregulated in PMD across experimental conditions (F((1,45)) = 19.93, p

158 erential behavioral responsivity to E2-WD in PMD reflects intrinsic differences in cellular gene expr

159 uently, the benefit of endurance exercise in PMDs strongly depends on the underlying mutation, althou

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

161 rehensively show that loss of methylation in PMDs occurs in a large fraction of the genome and repres

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

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

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

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

166 1 region and defined several novel LCRs (LCR-PMDs).

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

168 12 patients, enabled us to associate the LCR-PMDs with breakpoint regions, and revealed rearrangement

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

170 Mean PMDs improved over 6 months in deficit-trained patients

171 the duplication commonly present with a mild PMD phenotype.

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

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

174 ections to the dorsal premammillary nucleus (PMD).

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

176 ny attractive targets for the application of PMD.

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

178 ting that ISG upregulation is a biomarker of PMD.

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

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

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

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

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

184 oligomers correlates with the development of PMD.

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

186 nt implications for molecular diagnostics of PMD.

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

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

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

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

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

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

193 (LSS) is the most frequent manifestation of PMD in children, but may also present in adults.

194 We developed an in vitro model of PMD with lymphoblastoid cell lines (LCLs) derived from p

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

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

197 odendrocytes contributes to the pathology of PMD.

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

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

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

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

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

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

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

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

206 te lysozyme, then demonstrate the utility of PMD using influenza virus hemagglutinin (HA).

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

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

209 The genomic distribution of PMDs reports tissue-of-origin and may represent tissue-s

210 However, the distribution of PMDs within and between tumor types, and their effects o

211 nown normal tissue showing clear evidence of PMDs.

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

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

214 to understand the origin and progression of PMDs.

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

216 years was associated with increased risk of PMDs (confounding-adjusted relative risk, 1.09 per unit

217 n the vulnerability to, and consequences of, PMD.

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

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

220 LCLs from women with past PMD (n = 8) or control women (n = 9) were cultured in th

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

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

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

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

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

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

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

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

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

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

231 ew lesions do not define PMD per se; rather, PMD requires an increase in the sum of SULpeak by 30%.

232 Here, we review PMD disease mechanisms and outline rationale for therape

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

234 p1(jp)) point-mutation mouse model of severe PMD, increased myelination and restored nerve conduction

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

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

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

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

239 a substantial fraction of cell-type-specific PMDs and DMRs identified here in esophageal cancer are a

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

241 n with PND were at higher risk of subsequent PMDs (HR 1.81, 95% CI [1.74,1.88]; p < 0.001).

242 this progress, many patients with suspected PMD remain without a genetic diagnosis, which restricts

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

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

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

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

247 Our data suggest that PMD should not be defined by the appearance of new lesio

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

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

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

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

252 The PMD and PMV were only weakly interconnected.

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

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

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

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

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

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

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

260 Here, we use the PMD mouse model Jimpy to determine the impact of the int

261 Antisera from guinea pigs immunized with the PMD-modified HA show increased cross-reactivity with HAs

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

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

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

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

266 es in E2 at the cellular level contribute to PMD.

267 NMT1 ubiquitin signaling axis contributes to PMD formation in cancers.

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

269 estimates if fluxes were directly fitted to PMDs.

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

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

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

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

274 We validate PMD using a well-characterized antigen, hen egg white ly

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

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

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

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

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

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

281 biosynthesis have recently been linked with PMD.

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

283 uptake occurred more often in patients with PMD (n = 24) by imPERCIST5 than in those with stable met

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

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

286 ignaling is frequently seen in patients with PMD suggesting that interferon dysregulation is a contri

287 blood samples from a cohort of patients with PMD.

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

289 cular disease, was upregulated in women with PMD, but most so after E2-WD (p < 1.55 x 10(-5)).

290 Adulthood adiposity has been associated with PMDs; however, the association with childhood and adoles

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

292 erved in a small proportion of patients with PMDs.

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

294 ), 367 deaths were observed among women with PMDs (rate, 8.4 deaths per 10 000 person-years; 95% CI,

295 age 45 years) was reported by 17 women with PMDs and 12 women without PMDs.

296 Compared with unaffected women, women with PMDs had increased risk of death due to nonnatural cause

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

298 958 deaths were observed among women without PMDs (rate, 9.1 deaths per 10 000 person-years; 95% CI,

299 d by 17 women with PMDs and 12 women without PMDs.

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