ライフサイエンスコーパス: postmortem

1 ation and processing of donated specimens at postmortem.

2 An etiological diagnosis was established postmortem.

3 One case was diagnosed postmortem.

4 s were used to assess their biocompatibility postmortem.

5 ies of 5416 pseudophakic human eyes obtained postmortem, accessioned in our center between January 19

6 channels to human retinas, which allowed the postmortem activation of different cell types by near-in

7 ging-Alzheimer Association guidelines define postmortem AD neuropathologic changes as a composite sco

8 genomic autism ADNP mutation (c.2188C>T) in postmortem AD olfactory bulbs and hippocampi.

9 lated marmoset trait anxiety scores to their postmortem aHipp glutamate levels and showed that low gl

10 rs of CHI3L1-positive cells were observed in postmortem ALS motor cortex as compared with controls, a

11 Postmortem analyses confirmed the diagnosis of PD and de

12 etected in serum or cerebrospinal fluid, but postmortem analysis confirmed dengue virus in the brain

13 Postmortem analysis included next generation sequencing,

14 Postmortem analysis of pancreases from 68 Medalists was

15 Postmortem analysis of pancreata from Medalists revealed

16 Postmortem analysis revealed small grafts from PITX3-eGF

17 technologies are predictive simulations and postmortem analysis.

18 ls of cortico-cortical wiring established by postmortem anatomical studies and capitalises on cutting

19 among clinically normal older individuals at postmortem and can now be detected with in vivo neuroima

20 cribe and discuss recent evidence from human postmortem and clinical biomarker studies addressing the

21 Postmortem and imaging studies revealed remarkable stria

22 y infected with Mycobacterium bovis Detailed postmortem and immunohistochemical examinations of lesio

23 Postmortem and neuromodulation schizophrenia studies foc

24 CTE can only be confidently identified at postmortem and patients are often confused and anxious a

25 t being treated with rituximab was diagnosed postmortem and the pathology findings correlated with th

26 enia OR schizoaffective) AND (post-mortem OR postmortem) AND hippocampus.

27 the central nervous systems (CNS) of humans postmortem, and infection with HSV has been correlated w

28 Here we review genetic, genomic, cellular, postmortem, animal model, and cell model evidence that s

29 characterize MNW network failure in situ and postmortem are also discussed.

30 ng data in human brains to confirm the prior postmortem association of the long intergenic noncoding

31 rmalin-fixed spinal cord samples were imaged postmortem at a synchrotron radiation facility.

32 tron emission tomographic imaging as well as postmortem autoradiography in an independent sample with

33 Postmortem autoradiography results revealed lower expres

34 51 articles measured inflammatory markers in postmortem BD brain samples.

35 sensus regarding the inflammatory markers in postmortem BD brain samples.

36 molecules, and other inflammatory markers in postmortem BD brain samples.

37 rations that overlap with the upper range of postmortem blood concentrations in fentanyl-related deat

38 We examined the concentration of lactate in postmortem brain (dorsolateral prefrontal cortex) in sub

39 In 3 collections of human postmortem brain (n = 206) and 1 collection of blood sam

40 Postmortem brain analyses documented increased GAS5 expr

41 s been implicated in SZ by gene association, postmortem brain and animal studies.

42 case-control studies of human tissue (i.e., postmortem brain and bio-fluids) were considered: DNA me

43 Analyses of 93 samples from postmortem brain and blood found (i) the 4977 bp 'common

44 d from mouse models of stress and from human postmortem brain and genome-wide association studies ind

45 essed in peripheral blood, muscle biopsy, or postmortem brain at the level of enzyme activity or subu

46 Sorted neurons/glia from a fourth postmortem brain collection (n = 58) were used for valid

47 opathic ASD cases from controls across three postmortem brain data sets.

48 need for age stratification in schizophrenia postmortem brain gene expression studies.

49 ial candidate gene expression studies of the postmortem brain have evolved into genome wide profiling

50 tical layer-specific protein levels in human postmortem brain is highly desirable.

51 cal MRI n = 4180) along with high-resolution postmortem brain microarray data from Allen Brain Atlas

52 ive paired helical filaments (PHFs) from the postmortem brain of a patient with Alzheimer's disease,

53 e in both models of depression as well as in postmortem brain of depressed individuals.

54 lyze publicly available expression data from postmortem brain regions across humans, chimpanzees, and

55 ated data from deep RNA-seq and GWAS of four postmortem brain regions from 30 subjects with AUD and 3

56 S mouse model DEGs with human idiopathic ASD postmortem brain RNA-sequencing data and found significa

57 levels, and microglia activation in the same postmortem brain sample.

58 applied to RNA-Seq data collected from human postmortem brain samples collected within the ROS/MAP an

59 We combined RNA-seq data from 537 postmortem brain samples from the CommonMind Consortium

60 ross 364 schizophrenia cases and 383 control postmortem brain samples from the CommonMind Consortium,

61 egation analysis and Southern blotting using postmortem brain samples from two affected individuals a

62 We compiled data from 1408 postmortem brain samples in 3 collections to identify se

63 es have shown evidence of inflammation in BD postmortem brain samples.

64 cortex, and primary visual cortex) in human postmortem brain samples.

65 Evidence from postmortem brain studies have indicated that early prena

66 reveal autism-specific signatures similar to postmortem brain studies, indicating a potential common

67 Human postmortem brain tissue and fibroblasts from subjects wi

68 We evaluated postmortem brain tissue for adaptive immune cells and im

69 rotein levels are significantly decreased in postmortem brain tissue from BD patients, as compared to

70 n a mouse alpha-synucleinopathy model and in postmortem brain tissue from patients with alpha-synucle

71 yelitis murine model of demyelination and in postmortem brain tissue of patients with AD.

72 Additionally, neurogranin expression in postmortem brain tissue was studied.

73 cleus (CN) and accumbens nucleus (NAC)) from postmortem brain tissue were compared between 6 OCD and

74 We hypothesized that in postmortem brain tissue, OXTR binding in the hippocampal

75 within individual cortical layers from human postmortem brain tissue, providing a powerful tool in th

76 monoacylglycerol lipase (MAGL) expression in postmortem brain tissue, such that regions with higher M

77 studies of MDD employed bulk homogenates of postmortem brain tissue, which obscures gene expression

78 alleles and higher C4A transcript levels in postmortem brain tissue.

79 publicly available RNA expression data from postmortem brain tissue.

80 and controls from both blood (N = 1132) and postmortem brain tissues (N = 61 samples from Brodmann A

81 We examined postmortem brain tissues from patients with sporadic dee

82 LRP4 was reduced in postmortem brain tissues of AD patients.

83 littermates as well as in mitochondria from postmortem brain tissues of unaffected individuals and H

84 We also used mitochondria isolated from postmortem brain tissues of unaffected individuals and H

85 Herein, we perform a meta-analysis of 8 PD postmortem brain transcriptome studies by employing a mu

86 association study (EWAS) of smoking in human postmortem brain, focusing on nucleus accumbens (NAc) as

87 rgic system, drawing upon studies from human postmortem brain, neuroimaging, and drug challenge inves

88 patiotemporal expression with respect to the postmortem brain.

89 specific functional genomic studies in human postmortem brain.

90 xpression was mostly unaltered in BD and SCZ postmortem brain.

91 human nervous system with evidence from both postmortem brains and detection in cerebrospinal fluid o

92 D are enriched in those downregulated in ASD postmortem brains and in genes harboring de novo mutatio

93 een investigated over the last century using postmortem brains but there has been little progress in

94 Sulfhydration of AKT was detected in the postmortem brains from AD patients; thus, it represents

95 genome-wide circRNA expression profiling in postmortem brains from individuals with ASD and controls

96 In postmortem brains from Veterans/military Servicemembers

97 Transcriptomic analyses of postmortem brains have begun to elucidate molecular abno

98 exhibits disturbed circadian rhythms in the postmortem brains of depressed patients.

99 ntal cortex and superior temporal gyrus from postmortem brains of individuals with and without schizo

100 Postmortem brains of mild cognitive impairment (MCI) rat

101 enveloping NA-containing neuritic plaques in postmortem brains of patients with AD.

102 hether the molecular epigenetic signature of postmortem brains of patients with SZ, SZA, and BP disor

103 nosine (A-to-I) editing in a large cohort of postmortem brains of people with ASD.

104 We identify genetic variants within the postmortem brains that map to the CPG2 promoter region,

105 is review, we describe key findings in human postmortem brains, cultured cells, and animal models of

106 of Shank3-deficient mice and autistic human postmortem brains.

107 antify identified pathologic features in the postmortem brains.

108 consistently observed to be abnormal in SCZ postmortem brains.

109 ates from biological samples including human postmortem brains.

110 eir vicinity to the DA presynaptic terminals postmortem caudate and putamen of 3 healthy individuals,

111 )R-D(2)R heteromers was next demonstrated in postmortem caudate nucleus from schizophrenic subjects,

112 (HD) mouse cortices and striata and in human postmortem caudate.

113 Complete autopsy, including postmortem computed tomography and histopathologic and v

114 Postmortem computed tomography revealed reticular infilt

115 s have been clinically diagnosed with CTE, a postmortem condition.

116 gene expression signatures from SCZ and ASD postmortem cortex to 1) organize genes into the developm

117 ons from homogenate prenatal and adult human postmortem cortex using poly(A)+ and Ribo-Zero library p

118 nates from Hdh(Q140) KI mice and in human HD postmortem cortex.

119 e profile cortical circRNAs expression in 35 postmortem cortical gray matter (BA46) schizophrenia and

120 Postmortem cortical pathology was left-lateralized in bo

121 et between patients with ASD and controls in postmortem cortical regions.

122 ing phenotypes track gene down-regulation in postmortem cortical samples of patients with depression.

123 Synapse density is reduced in postmortem cortical tissue from schizophrenia patients,

124 morphologically activated microglia (PAM) in postmortem cortical tissue is strongly associated with b

125 iation with advanced epigenetic age in three postmortem cortical tissue regions: dorsolateral and ven

126 ough expected from welding and inferred from postmortem cross sections of fusion zones, the direct vi

127 Postmortem cryptococcal meningitis and pulmonary cryptoc

128 Postmortem data documented AD neuropathology.

129 These postmortem data provide strong evidence for membrane tub

130 n addition, we use CBA+ to align in vivo and postmortem data.

131 Human postmortem datasets from depression and posttraumatic st

132 ally organic (chitinous or collagenous), and postmortem decay and taphonomic mineralization resulted

133 ional measurement poorly investigated due to postmortem degradation of synaptic receptors.

134 l loss and striatal neuropathological grade, postmortem delay, CAG repeat in the IT15 gene, or age at

135 c ecology as decay can result in significant postmortem delta(15)N enrichment.

136 Further, studies of human postmortem-derived tau filaments from different tauopath

137 or if tissues exhibit delta(15)N enrichment postmortem despite the importance of tissue stable isoto

138 Despite being a postmortem diagnosis, 108 players (2.8%) self-reported c

139 Postmortem DLPFC expression data analysis showed decreas

140 investigated in RNA sequencing data from 610 postmortem Dorso-Lateral Pre-Frontal Cortex (DLPFC) samp

141 ssenger RNA levels were also detected in the postmortem dorsolateral PFC of individuals with depressi

142 ined agonist-induced mGluR5 signaling in the postmortem dorsolateral prefrontal cortex (DLPFC) derive

143 ries of individuals with COVID-19 undergoing postmortem evaluation is provided, with 4 aims: (1) desc

144 Postmortem evaluations of two patients revealed the clas

145 henotypes associated with schizophrenia, and postmortem evidence indicates lower hippocampal alpha5-G

146 Finally, we provide postmortem evidence of Nurr1 expression in striatal neur

147 Postmortem examination of pancreases from 68 Medalists s

148 asive tissue sampling (MITS) is a simplified postmortem examination technique that has shown to be an

149 brain disorders or pathology in independent postmortem expression datasets and clinical cohorts.

150 ate to potentially confounding antemortem or postmortem factors are difficult to prove.

151 These preclinical and postmortem findings highlight a link between extracellul

152 pital anticoagulation (AC) with outcomes and postmortem findings.

153 ffspring, a phenotype previously observed in postmortem frontal cortex of schizophrenic subjects.

154 ve study on AD, NDAN, and aged-matched human postmortem frontal cortices of either sex.

155 g RNA sequencing to reveal global changes in postmortem gene expression in liver tissues from 27 Ital

156 Postmortem gene expression is indicative of the cellular

157 82.37% with CD; 57.39% male) and the largest postmortem gene-expression sample of individuals with co

158 Postmortem genetic testing was undertaken in 24 of 202 (

159 Postmortem genetic testing yielded pathogenic variants i

160 Here, we explore the findings of human postmortem genomic studies of neuropsychiatric disorders

161 We then applied DroNc-seq to postmortem heart tissue to test its performance on heter

162 sequencing (average read depth 584x) in 111 postmortem hippocampal formation and matched blood sampl

163 We have evaluated our technique using postmortem histopathologic staining data from 52 older p

164 ified by multi-scale gene network studies of postmortem human AD brain.

165 pal AMPKalpha isoform expression patterns in postmortem human AD patients and AD model mice.

166 -d(6) was used to detect CB2 upregulation on postmortem human ALS spinal cord tissues.

167 In postmortem human AUD hippocampus, mRNA and IHC protein a

168 TF-binding sites in distinct populations of postmortem human brain cells and further our understandi

169 e, and overlapped with changes identified in postmortem human brain from SCZ and ASD patients.

170 ty-adjusted DLPFC RNA-Seq data from the LIBD Postmortem Human Brain Repository (90 controls, 74 schiz

171 ing for this 2 megabase genomic region using postmortem human brain samples.

172 letion microscopy (STED), to characterize in postmortem human brain tissue non-fibrillar Abeta struct

173 This study utilizes postmortem human brain tissue to investigate whether Pur

174 s assessed in autoradiographic studies using postmortem human brain tissues from healthy individuals

175 to rodent brain, (R)- (11)C-Me-NB1 showed in postmortem human brain tissues higher binding in the cor

176 of direct molecular characterization of the postmortem human brain, and provide a brief overview of

177 reased OPRM1 expression in the cerebellum of postmortem human brains (p = 4.7e-5).

178 ptomic, proteomic and epigenomic analyses of postmortem human brains to identify molecular pathways i

179 Our method uses small tissue blocks from postmortem human brains, immersion fixation, lipophilic

180 ation was also seen in the ischemic areas of postmortem human brains.

181 quential neuronal formation ("birthdate") in postmortem human cerebral cortex.

182 rt the first transcriptome sequencing of the postmortem human dorsal striatum comparing bipolar (18)

183 he tissue surface in normal and glaucomatous postmortem human eyes, and 1-um spherical AFM tips to pr

184 ouse, which we generated using bacTRAP, with postmortem human functional genomics and quantitative ge

185 validated in autoradiographic studies using postmortem human GluN2B-rich cortical and GluN2B-deficie

186 ies in brain slices from HD mouse models and postmortem human HD samples.

187 blish that the network pathology observed in postmortem human LOAD brain can be faithfully recapitula

188 Using postmortem human MS tissue, a preclinical nonhuman prima

189 tures and animal models of PD, as well as in postmortem human PD brains.

190 Finally, levels of miR-298 varied in postmortem human temporal lobe between AD patients and a

191 Ms on multiple isoforms of Tau isolated from postmortem human tissue from 49 AD and 42 control subjec

192 Siglec-8 ligands were found on postmortem human trachea and bronchi and on upper airway

193 etry for a comprehensive characterization of postmortem huMG (10(3) - 10(4) cells).

194 ricans and Caucasians (n = 38), and analyzed postmortem IL-9-related gene expression profiles in the

195 Ns, glia, and DG volume in whole hippocampus postmortem in four groups of drug-free, neuropathology-f

196 We used postmortem in situ magnetic resonance imaging (MRI) scan

197 essenger RNA expression was also upregulated postmortem in the nucleus accumbens of male human cocain

198 To translate postmortem information into clinical phenotypes, we iden

199 he variability across the studies, including postmortem interval, brain area studied, age at diagnosi

200 human subjects as well as a monkey model of postmortem interval.

201 otocol and suitability on tissue with longer postmortem intervals should facilitate higher-powered st

202 prior studies using tissue with much shorter postmortem intervals.

203 mpted humanitarian euthanasia and a detailed postmortem investigation to assess whether a COVID-19-li

204 ype of sudden death without explanation upon postmortem investigation.

205 hods enable increasingly detailed volumetric postmortem investigations of human neuroanatomy for diag

206 ing this method on tissue that is up to 28 h postmortem is comparable to prior studies using tissue w

207 Obtaining a blood sample within 24 h postmortem is mandatory.

208 We examined the postmortem kidneys from 42 patients who died of COVID-19

209 g minimally invasive tissue sampling (MITS), postmortem laboratory and pathology testing, verbal auto

210 We examined postmortem lens tissue from individuals with and without

211 ectly identified as tissues originating from postmortem livers.

212 Here we analyzed postmortem lung specimens from four patients who succumb

213 Human postmortem lung tissue and human lung epithelial cell li

214 TRPV4 levels were measured in postmortem lung tissue from ventilated and nonventilated

215 from immunolabeled vertical sections of six postmortem male and female human donor retinas and image

216 erms of formal deposition of the body versus postmortem manipulation versus surface abandonment.

217 In a functional mixed effects model, postmortem markers (Alzheimer disease pathology, Lewy bo

218 a neuropathologic examination to quantify 9 postmortem markers of common neurodegenerative and cereb

219 rabbits with cavitary TB and confirmed using postmortem mass spectrometry.

220 utilized tg340-PRNP129MM mice infected with postmortem material from sCJD patients of the most susce

221 Usually, postmortem measurement is too late to save the product o

222 reviously demonstrated synaptic changes with postmortem methods.

223 we validated that NM-MRI signal intensity in postmortem midbrain specimens correlated with regional N

224 pillaries and neurons was investigated using postmortem midbrain tissues of young (25-38 years) and e

225 nsulin, we assessed insulin signaling in the postmortem middle frontal gyrus cortex.

226 Postmortem minimally invasive tissue sampling (MITS) is

227 human samples obtained opportunistically or postmortem, mostly from adults.

228 te-of-the-art human histology (BigBrain) and postmortem MRI (50 um).

229 ual folia from multicontrast high-resolution postmortem MRI scans.

230 Transcriptome analyses of postmortem mRNA from a tissue fragment may determine uni

231 nance-based measurements of infarct size and postmortem myocardial pathology (n=33).

232 N5-related molecular changes were reduced in postmortem NAc from antidepressant-treated subjects.

233 criptional profiling of vGAT and gephyrin in postmortem NAc samples from a cohort of healthy controls

234 In the population who underwent postmortem neuropathologic evaluation, 68% of extracorpo

235 ncing were performed on three patients, with postmortem neuropathologic examination for one patient.

236 Postmortem neuropathology of five TIA1 mutations carrier

237 udy provides evidence that cDCD LT following postmortem NRP can be safely and effectively performed i

238 biquitinated protein levels were elevated in postmortem OFC in schizophrenia compared to controls (p

239 ination, and proteasome activities in frozen postmortem OFC tissue from 76 (38 schizophrenia, 38 cont

240 than seen with clinical use but overlap with postmortem overdose concentrations.

241 Although postmortem pathologic changes consistent with chronic tr

242 of coronavirus disease 2019 (COVID-19) with postmortem pathology observations.

243 t anatomic distributions of left-lateralized postmortem pathology that relate to antemortem structura

244 Postmortem pathology was inversely associated with antem

245 yzed laterality and regional distribution of postmortem pathology, quantified using a validated digit

246 ell as in patient-specific motor neurons and postmortem patient spinal cord.

247 porate measures of cortical gene expression, postmortem patient transcriptional data, depression geno

248 We investigated p11 levels in postmortem PD brains and assessed whether peripheral p11

249 Consistently, SNpc of postmortem PD patients shows a significant population of

250 found to be pathological when isolated from postmortem PD patients' substantia nigra; and (b) leucin

251 Since 2010, 60 postmortem pediatric brain tumor donations from 26 insti

252 time quaking-induced conversion (RT-QuIC) in postmortem PNS samples from 14 subjects.

253 mmary, our findings in 1983 samples of human postmortem prefrontal cortex show that coexpression of a

254 data generated from 27 321 nuclei from human postmortem prefrontal cortical tissue.

255 as adult (N = 207; 57 active smokers) human postmortem prefrontal cortices.

256 % of attempts respectively), irrespective of postmortem processing time.

257 In human postmortem retinas and vitreous from donors with DR, we

258 We generated transcriptional profiles of postmortem retinas from 453 controls and cases at distin

259 expression networks in two prefrontal cortex postmortem RNA sequencing datasets (n = 688) and replica

260 specific molecular profiles in schizophrenia postmortem samples compared with controls, implicating a

261 it is difficult to observe IAV particles in postmortem samples from patients with seasonal influenza

262 We applied this method to frozen postmortem samples of human cerebral cortex and retina a

263 ale gene expression and genotype analyses in postmortem samples of two frontal cortical brain regions

264 After 2 and 4 weeks, postmortem samples were analyzed by microcomputed tomogr

265 ng or tonsil swab samples harvested prior to postmortem showed less within-sample variability of VP1

266 eloped TaqMan Array Cards (TACs) for testing postmortem specimens (blood, cerebrospinal fluid, lung t

267 ibular endorgan, the utricular macula, using postmortem specimens from individuals with documented no

268 investigated the degree of synaptic loss in postmortem spinal cords (18 chronic MS, 8 healthy contro

269 hared between murine models of ALS and human postmortem spinal cords.

270 Postmortem studies are a particularly important avenue f

271 In contrast, postmortem studies are well suited to explore subfield a

272 Several recent postmortem studies have made important contributions to

273 We selected case-control postmortem studies in schizophrenia quantifying synaptic

274 Prior ex vivo histological postmortem studies of autism spectrum disorder (ASD) hav

275 Here, we review the results of recent postmortem studies of ET and attempt to place these find

276 ophrenia's pathophysiology is still unclear, postmortem studies point toward a dysfunction of cortica

277 rom tissue biopsies, case reports, and small postmortem studies restricted to the lung and specific o

278 An independent postmortem study found no differential gene expression i

279 efined SCDs autopsied in the POST SCD study (Postmortem Systematic Investigation of SCD) to determine

280 sociation of ante mortem CSF tau levels with postmortem tau pathology adjusting for demographics.

281 elated with digital histology measurement of postmortem tau pathology averaged from three cerebral re

282 At postmortem there was extensive myocardial infarction wit

283 Postmortem tissue analyses can only imply dynamic struct

284 Postmortem tissue and clinical data were provided by the

285 ced pluripotent stem cell (iPSC) neurons and postmortem tissue and mediates a protective shift from p

286 MITS included postmortem tissue biopsies of brain, liver, and lung for

287 Postmortem tissue derived from depressed suicide brain s

288 Our findings highlight the importance of postmortem tissue donations as an invaluable resource to

289 ds over the course of disease, as well as of postmortem tissue from ALS patients, to characterize the

290 CatD-positive-layer III neurons accrued from postmortem tissue obtained from the Rush Religious Order

291 es of four prefrontal cortex subregions from postmortem tissue of people with PTSD demonstrate extens

292 JCV DNA isolated from postmortem tissue samples identified a novel 12bp insert

293 ynaptic and postsynaptic structures in human postmortem tissue that is accurate, rapid, and relativel

294 noid signaling (from Allen Human Brain Atlas postmortem tissue) were associated with spatial patterns

295 erved within degenerating regions of patient postmortem tissue.

296 central nervous system (CNS) and peripheral postmortem tissues from seven adult-onset and one juveni

297 ere increased in brain lysates obtained from postmortem tissues of individuals with PD and DLB compar

298 ate analysis of synaptic structures in human postmortem tissues.

299 A postmortem, virological analysis of multiple organs, suc

300 Purpose To evaluate the viability of postmortem x-ray phase-contrast micro-CT to provide tiss