ライフサイエンスコーパス: postmortem

1 trics were determined from ablations excised postmortem.

2 currently only can be definitively diagnosed postmortem.

3 d to various degrees during 20 sec to 10 min postmortem.

4 lation of proteins is rapidly changed during postmortem.

5 n (TES) in a nonhuman primate brain pre- and postmortem.

6 was reduced by 50% in the brain with 40 sec postmortem, a regular time for tissue processing.

7 n brain extract from tau-transgenic mice and postmortem AD brain and added to a sensitive fluorescenc

8 ar-weight (HMW) species that is found in the postmortem AD brain and can be taken up by neurons and s

9 n of these transcriptomic results with human postmortem AD gene networks, differential expression and

10 Axonal loss was confirmed in postmortem AD optic nerves.

11 We also found a significant loss of mRGCs in postmortem AD retinal specimens (p = 0.003) across all a

12 and specifically mRGC loss and pathology in postmortem AD retinal specimens, associated with Abeta d

13 ysing BODIPY-FL casein to varying extents at postmortem aging meat pH (5.0-6.0).

14 ioral assays tested for functional outcomes, postmortem analyses assessed neuropathology, and brain a

15 Postmortem analyses confirmed the diagnosis of PD and de

16 Postmortem analyses demonstrated robust survival of midb

17 Postmortem analyses reveal robust Alzheimer disease and

18 Here we report the postmortem analysis of a patient with Parkinson's diseas

19 he hypothesis is difficult to reconcile with postmortem analysis of human brains and connectome-mappi

20 On postmortem analysis of the fetal brain, diffuse cerebral

21 an link transplantation, animal behavior and postmortem analysis to enable the identification of mech

22 In MDD, recent evidence from human postmortem and animal studies suggests a selective vulne

23 Postmortem and longitudinal data will be useful to asses

24 We used a combination of human postmortem and rodent studies to test the hypothesis tha

25 The eyes of the deceased babies were removed postmortem and were sent to the Florida Lions Ocular Pat

26 ase Center in August 2015 using clinical and postmortem autopsy data that had been collected between

27 Additionally, we performed postmortem autoradiography.

28 as to examine the correlation of in vivo and postmortem AV-1451 binding patterns in three autopsy-con

29 Using postmortem beta-amyloid immunohistochemistry data from 2

30 By using RNA sequencing in the postmortem bipolar disorder brain, an interesting profil

31 mulation of cytoplasmic TDP-43 aggregates in postmortem brain and spinal cord (SC), it has been sugge

32 ved decreased synaptosomal F-actin levels in postmortem brain from mild cognitive impairment and AD p

33 al models of PTSD, and review the human PTSD postmortem brain gene profiling studies performed to dat

34 vely correlated with pCREB expression in the postmortem brain of persons with AD.

35 firmed in further ADLD-1-TO tissues and in a postmortem brain sample, where lamin B1 was increased in

36 In postmortem brain samples from human alcoholics we found

37 METHOD: Postmortem brain samples from human subjects (N=78) and

38 cortical p11 protein levels were assessed in postmortem brain samples from PD patients and matched co

39 assays, and quantitative tau measurements in postmortem brain samples from two progressive supranucle

40 ping in chromatin extracted from hundreds of postmortem brain samples in cell-type-specific manner.

41 -6 were significantly increased in blood and postmortem brain samples of patients with suicidality co

42 ne levels in blood, cerebrospinal fluid, and postmortem brain samples of patients with suicidality.

43 determined with and without nalbuphine, and postmortem brain samples were subjected to Western blot

44 her transcriptional levels of PCDH17 mRNA in postmortem brain samples, which is consistent with incre

45 Loss of M1R has been found in postmortem brain tissue for several neuropsychiatric dis

46 lum of experimental MSUD animals, as well as postmortem brain tissue from a child that died of leucin

47 ssion in Alexander disease model mice and in postmortem brain tissue from Alexander disease patients,

48 ssed in demyelinated white matter lesions of postmortem brain tissue from human subjects with multipl

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

50 , SV2C expression is dramatically altered in postmortem brain tissue from PD cases but not in Alzheim

51 This linkage was also observed in postmortem brain tissue from subjects with mild cognitiv

52 Postmortem brain tissue samples from AD patients, transg

53 Postmortem brain tissue specimens were collected from in

54 With the use of postmortem brain tissue, mouse models of defeat stress,

55 alable to non-human primate brains and human postmortem brain tissues, and can visualize neuronal pro

56 mouse cerebral cortex and spinal cord, human postmortem brain, and glioma biopsy specimens.

57 orrelated with RNA polymerase II activity in postmortem brain, and pharmacologic modulation of RNA po

58 molecules in isolated neuronal nuclei from a postmortem brain, generating 3227 sets of single-neuron

59 stem, a rodent depression model, and a human postmortem brain, we investigated the role of a brain-en

60 ed with lower D2 short isoform expression in postmortem brain.

61 the neuronal and nonneuronal nuclei from the postmortem brain.

62 by deep sequencing (ChIP-seq) datasets from postmortem brains are needed.

63 diseases are diagnosed definitively only in postmortem brains by the presence of key misfolded and a

64 CpG loci) in the orbital frontal cortices of postmortem brains from 22 younger (age <42 years) and 22

65 and GAL peptide by RIA of the GAL system in postmortem brains from depressed persons who had committ

66 ssion of GluN2C subunit has been reported in postmortem brains from schizophrenia patients.

67 By injecting pathological tau extracted from postmortem brains of AD (AD-tau), progressive supranucle

68 d its expression and activity are reduced in postmortem brains of AD patients.

69 nt study, we first reevaluated the pH of the postmortem brains of patients with schizophrenia and bip

70 molecular changes similar to changes seen in postmortem brains of patients with SZ.

71 al targeting; and its levels are elevated in postmortem brains of schizophrenics.

72 creased mitochondrial calcium uptake, and in postmortem brains of sporadic PD/PDD patients of both se

73 Furthermore, qRT-PCR analysis of the AD postmortem brains with different Braak stages also showe

74 We further validated miRNA data using AD postmortem brains, amyloid precursor protein transgenic

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

76 In a different set of postmortem brains, p11 mRNA expression was measured in d

77 cortex and substantia nigra of control human postmortem brains, using the 454 GS FLX Titanium pyroseq

78 By comparative analysis in human postmortem brains, we found that ubiquitin immunoreactiv

79 ates from biological samples including human postmortem brains.

80 lates of CTE reflect the current reliance on postmortem case series investigations.

81 enetic risk factors for BD, are increased in postmortem cerebellar tissue from BD patients, as well a

82 te mortem CSF phosphorylated tau levels with postmortem cerebral tau pathology in FTLD (Beta = 1.3; 9

83 ys an important role in spoilage of fish and postmortem changes in fish tissue are due to the breakdo

84 s inevitably limited by advanced disease and postmortem changes.

85 nd basilar membrane vibrations are absent in postmortem cochleae.

86 A postmortem cohort of pathologically confirmed MS (n = 47

87 s of STZ-rats and in human diabetic retinas (postmortem) compared with their respective controls.

88 erse basilar membrane tuning in the passive, postmortem condition.

89 tween October 2008 and November 2015 who had postmortem confirmed sCJD and compare these features wit

90 .20 x 10(-7)) and PPDPF (P=1.13 x 10(-6)) in postmortem cortex tissue; EFNA1 (P=7.26 x 10(-9)), RNU4A

91 regions in adulthood, which we validate with postmortem cytoarchitectonic measurements.

92 veloped a computational method that compares postmortem damage patterns of a test dataset with bona f

93 in vivo findings align very closely with the postmortem data and provide evidence for vulnerability a

94 similar to those shown in the limited human postmortem data available.

95 Postmortem data indicate that tau pathology in the trans

96 We present postmortem data showing that CIT is critical to building

97 c tractography was performed on high-quality postmortem diffusion imaging scans from two Old World mo

98 re affected by warming-induced bleaching and postmortem dissolution, but the finding here that ACC pa

99 uman brain regions correlated with the known postmortem distribution of 5-HT1A receptors.

100 by fluorescence-activated cell sorting from postmortem DLPFC of 36 PDS and 26 age-matched controls.

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

102 real-time polymerase chain reaction in human postmortem dorsolateral prefrontal cortex from 286 nonps

103 real-time polymerase chain reaction in human postmortem dorsolateral prefrontal cortex from 286 nonps

104 ned by sequencing of poly-A RNA derived from postmortem dorsolateral prefrontal cortex from people wi

105 creening, risk stratification approaches and postmortem evaluation, and identification of modifiable

106 us was born at term and euthanized on day 3: postmortem examination confirmed the patency of the sten

107 Postmortem examination identified infectious virus for u

108 012, through November 11, 2014, we conducted postmortem examination of the eyes of 23 infants and chi

109 viral vectors in vivo has generally required postmortem examination of tissue.

110 hilic Muller cell foot processes swelling in postmortem examination of young infant eyes, a potential

111 On postmortem examination, FACS-based enumeration of intrac

112 A postmortem examination, including a histological assessm

113 H relative to those of healthy controls upon postmortem examination, it remains controversial whether

114 of the most reliable alterations observed at postmortem examination.

115 uminescence emission measurements along with postmortem examination.

116 n Aging-Reagan criteria following a standard postmortem examination.

117 from radiologically confirmed pneumonia and postmortem examinations.

118 In a postmortem expression analysis of 33 individuals affecte

119 This step will enable further engineering of postmortem facial grafts, thereby offering new perspecti

120 gan dose measurements were obtained in eight postmortem female subjects.

121 protein kinase C (PKCdelta) was increased in postmortem fibroblasts from Medalists, fibroblasts from

122 We present postmortem findings in 10 patients with survival times r

123 Here, we present recent postmortem findings on the alterations in this system in

124 Consistent with human postmortem findings, we found that Kal9-P2255T protein l

125 )H]sulpiride) binding in the dorsal striatum postmortem from matched suicides and controls.

126 We obtained written informed consent postmortem from the next of kin.

127 er maps in brains obtained opportunistically postmortem from wild sea lions with and without chronic

128 Expression of AQP4 was analyzed in postmortem frontal cortex of cognitively healthy and his

129 We provide an overview of postmortem GABAergic perturbations in the brain affected

130 Postmortem genetic testing for heritable cardiovascular

131 Targeted postmortem genetic testing of the 4 major channelopathy-

132 Postmortem hippocampal subfield tissue (CA3, CA1) from s

133 g individuals with schizophrenia in vivo and postmortem hippocampal tissue in vitro.

134 Postmortem histochemical staining showed absence of neur

135 We describe an autolytic postmortem histologic artifact of eosinophilic Muller ce

136 tegrated with electrophysiologic testing and postmortem histology.

137 Findings were verified at postmortem histopathologic and/or autoradiographic exami

138 1 subjects who underwent in vivo imaging and postmortem histopathology for Abeta plaques, and the thi

139 We found that necroptosis was activated in postmortem human AD brains, positively correlated with B

140 Postmortem human AD cortex shows profound reductions of

141 A similar association was supported by postmortem human brain analyses.

142 Both gene expression profiling in postmortem human brain and studies using animal models h

143 on of the regional PET binding measures with postmortem human brain autoradiography outcomes showed a

144 and non-neuronal nuclei isolated from frozen postmortem human brain by fluorescence-activated nuclear

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

146 y published observation of increased urea in postmortem human brain from HD cases.

147 expression data that were acquired from both postmortem human brain regions (BP case/control: 45/50)

148 We used postmortem human brain specimens from a homogeneous Euro

149 ion rates (>3x) across two large independent postmortem human brain studies of schizophrenia and also

150 ation production; and 3) results from recent postmortem human brain studies providing additional mole

151 ions call for studies that combine data from postmortem human brain tissue and animal models, assess

152 Nuclear transcriptomes can be obtained from postmortem human brain tissue stored at -80 degrees C, m

153 pression, paralleling the elevations seen in postmortem human brain tissue.

154 pression quantitative trait loci analysis of postmortem human brain tissues revealed an association b

155 Extending that finding, we demonstrate that postmortem human brain urea levels are elevated in a lar

156 The amygdala from 32 postmortem human brains (7-46 years of age) were stained

157 cular profiles across the cerebral cortex of postmortem human brains (n = 6).

158 nd reduced Nrf2 levels have been reported in postmortem human brains and animal models of AD.

159 nstrate that alphaS aggregates isolated from postmortem human brains with diffuse Lewy body disease (

160 cumbens shell (NAcSh) and caudate nucleus in postmortem human brains.

161 ng genome-wide DNA methylation data from 740 postmortem human brains.

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

163 Postmortem human donor eyes were obtained with ethical a

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

165 fection and cardiovascular diseases, we used postmortem human heart tissues obtained from HIV-infecte

166 Postmortem human hippocampus tissue samples were obtaine

167 lutamate transporters (vGLUT1 and vGLUT2) in postmortem human SN in schizophrenia subjects (n=13) and

168 ate of the T1/T2-weighted ratio by combining postmortem imaging and histopathology in 9 multiple scle

169 Additionally, postmortem imaging by SPECT was performed.

170 alysis of the T1/T2-weighted ratio values of postmortem imaging yielded a strong correlation with den

171 We performed a series of postmortem immunohistochemical and immunofluorescent sta

172 Postmortem implications in muscle softening and melanisa

173 In this MRI-histological study, postmortem in situ scans were acquired from 6 cadavers w

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

175 between in vivo [F-18]-AV-1541 retention and postmortem in vitro binding and tau measures in these ca

176 Our studies of postmortem infant human brains revealed a collection of

177 identification, body fluid characterization, postmortem interval estimation, and biocrimes involving

178 en when a few potential confounding factors (postmortem interval, age, and history of antipsychotic u

179 were drug naive with the same agonal state, postmortem interval, and age within each strain.

180 y control participants matched for age, sex, postmortem interval, and other potential confounds from

181 These findings were not explained by postmortem interval, antipsychotic medication, or other

182 gists as a new source of data for estimating postmortem interval.

183 nce, particularly in the areas of estimating postmortem intervals (PMIs), locating clandestine graves

184 of 27 human corpses from criminal cases with postmortem intervals between 3.5-240 hours.

185 imeframe for the implementation of potential postmortem interventions that could be applied to improv

186 ssigned an undetermined cause of death after postmortem investigation and autopsy.

187 ype of sudden death without explanation upon postmortem investigation.

188 Postmortem investigations were conducted in the cingulat

189 Postmortem kidney specimen were taken for histological e

190 mplementing findings in the rodent and human postmortem literatures.

191 l-like receptor 3 expression was analyzed in postmortem lung samples from patients with lung contusio

192 In postmortem material, opsins were found to be expressed i

193 prefrontal cortex and dentate gyrus of human postmortem MDD patients.

194 tomography and X-ray computed tomography, to postmortem measurements of colonic immune cell infiltrat

195 anaerobes, Clostridium spp., in the internal postmortem microbial communities.

196 We first examined the levels of Grx1 in postmortem midbrain samples from PD patients, and observ

197 We studied postmortem mRGCs by immunohistochemistry in retinas, and

198 itochondrial respiration in gray matter from postmortem MS and control cortical samples.

199 myelinated and demyelinated hippocampi from postmortem MS brains.

200 Postmortem muscle samples were obtained from 1 additiona

201 he activity of calpains (mu and m) in eighty postmortem muscle samples.

202 -weighted magnetic resonance (MR) images and postmortem neuronal tissue samples from 13 patients who

203 review board approval, the authors compared postmortem neuronal tissue samples from five patients wh

204 regions of the ALS group that coincided with postmortem neuropathological stages.

205 Postmortem neuropathology of five TIA1 mutations carrier

206 est that numerous miRNAs are dysregulated in postmortem neuropathology of neuropsychiatric disorders,

207 Neither the postmortem nor the MRS studies directly address the phys

208 of disease mechanisms derived from detailed postmortem observations, however, a link between the two

209 However, nuclear PRMT1 was not stable postmortem obviating meaningful evaluation of ALS autops

210 thologic feature that can be demonstrated in postmortem ocular investigation of deceased children usi

211 n the biomedical studies, but the effects of postmortem on protein phosphorylation have not been rece

212 nalyses were performed with (123)I-PIP using postmortem orbitofrontal cortex from cognitively normal

213 Postmortem, organs were sampled for immunohistochemistry

214 within 6 months of initial evaluation; and a postmortem pathological diagnosis of PSP or CBD.

215 and temporal progression of tau pathology in postmortem patient brains.

216 ction, including brain involvement; however, postmortem PCR revealed Cunninghamella elegans, Lichthei

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

218 llular models of PD and by immunostaining of postmortem PD brains.

219 Ks was also found in a PD mouse model and in postmortem PD brains.

220 We examined postmortem PFC DNA methylomes of 16 male and seven femal

221 and GABRA1) with differential expression in postmortem PFC of male AUD subjects.

222 1 (SGK1) expression is down-regulated in the postmortem PFC of PTSD subjects.

223 During postmortem, phosphorylation of cAMP-dependent protein ki

224 We isolated single cholinergic neurons from postmortem PPNs of aged controls and PD patients.

225 predicts CNR1 prefrontal mRNA expression in postmortem prefrontal human tissue.

226 y nigrostriatal dopamine neuron loss and the postmortem presence of Lewy bodies, depositions of insol

227 had hematic fluid in their optical fibers at postmortem, presumably limiting NIr exposure and overall

228 We propose a relatively simple postmortem procedure to collect brain samples without pe

229 ssue slides and pathology reports, and fetal postmortem reports of all stillbirths.

230 In the postmortem sample, we observed up-regulation of SHANK1,

231 were then compared to results from ante- and postmortem samples (RAMALT, brainstem, and medial retrop

232 noprecipitation sequencing (ChIP-seq) on 257 postmortem samples from ASD and matched control brains.

233 ing results of 16S rRNA gene amplicons of 27 postmortem samples from cadavers demonstrated statistica

234 Subgenual anterior cingulate cortex postmortem samples from four MDD cohorts (single episode

235 s, and we analyzed Olig1 expression in human postmortem samples from neonates that suffered HI enceph

236 1451 in vitro binding assays to the study of postmortem samples from patients with a definite patholo

237 Postmortem samples from three brain structures regulatin

238 Postmortem samples were obtained from orbitofrontal cort

239 In human postmortem samples, there was an accumulation of phospho

240 nohistochemistry (IHC) analysis of ante- and postmortem samples.

241 nificant attention, particularly research in postmortem samples.

242 tumor uptake could be visualized with a 1-h postmortem scan.

243 n = 71) were collected as part of a national postmortem screening program between March 7 and July 20

244 Previously, these types of postmortem screenings have not been a feasible option fo

245 iple-label immunofluorescence was applied to postmortem sections of 10 IPD patients and 10 controls t

246 al analysis of myelin basic protein in human postmortem specimens confirmed a dramatic increase in my

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

248 s shifted from studies of lung aspirates and postmortem specimens intent on identifying pneumococcal

249 cted a histologic analysis of this region in postmortem specimens.

250 ution of galaninergic neurons was studied in postmortem spinal cord segments of 6 men and compared wi

251 d enhancement magnetic resonance imaging and postmortem staining.

252 and we identify cholinergic abnormalities in postmortem striatal tissue from DYT1 dystonia patients.

253 A long history of postmortem studies has provided significant insight into

254 Postmortem studies have consistently found lower levels

255 Postmortem studies have demonstrated considerable dendri

256 Postmortem studies have identified clear morphological c

257 Previous postmortem studies have long demonstrated that neurofibr

258 Postmortem studies have revealed a reduction in specific

259 Postmortem studies in schizophrenia reveal alterations i

260 Extant data from in vivo animal models and postmortem studies indicate that Alzheimer's disease (AD

261 Postmortem studies of DRS have reported abducens nerve h

262 Postmortem studies of patients with schizophrenia have r

263 Postmortem studies showed no difference in the corneal e

264 bodies (DLB) have been widely documented in postmortem studies, whereas in vivo studies are sparse,

265 Here, we report our postmortem study that demonstrates the use of benchtop X

266 gene expression studies of a large cohort of postmortem subjects, including subjects with MDD and con

267 in a mouse model of LB disease and in LBs of postmortem synucleinopathy brains.

268 Qualitative comparisons with postmortem tau are reported in 1 patient who died 9 mont

269 ence between in vivo (18) F-flortaucipir and postmortem tau neuropathology.

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

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

272 spinal fluid (CSF) tau levels correlate with postmortem tau pathology in frontotemporal lobar degener

273 We show that pre- vs. postmortem, TES-induced intracranial electric fields dif

274 hest sensitivity (69.8%) compared to that of postmortem testing, with a specificity of >93.9%.

275 Postmortem tissue and clinical data were provided by the

276 Loss of synaptosomal F-actin in human postmortem tissue correlates directly with decreased per

277 with a dedicated small-animal PET system and postmortem tissue counting in healthy rats.

278 Postmortem tissue counting of (18)F-FDS confirmed the hi

279 Postmortem tissue from 79 individuals was evaluated, inc

280 Central p11 levels are reduced in postmortem tissue from depressed individuals; however, p

281 a significantly disrupted nuclear lamina in postmortem tissue from human Alzheimer's disease brain.

282 s this question, we used Western blotting of postmortem tissue from human V1 (12 female, 18 male) cov

283 ptures the complexity of gene expression, in postmortem tissue from the anterior cingulate cortex fro

284 Postmortem tissue from the hippocampus and anterior orbi

285 nction are not well understood because human postmortem tissue offers only static descriptive data, a

286 Furthermore, immunostaining of human postmortem tissue revealed that a B-lymphocyte response

287 LCO-stained cores of beta-amyloid plaques in postmortem tissue sections from frontal, temporal, and o

288 Semiquantitative autoradiography studies on postmortem tissue sections of human Alzheimer's disease

289 Analysis of postmortem tissue suggested impaired axonal transport of

290 Additionally, postmortem tissue was analysed for CHIT1 expression.

291 terminal HTT fragments are also prevalent in postmortem tissue, and expression of some of these fragm

292 Because prior reports were based on postmortem tissue, it was unknown whether this anatomica

293 In an independent sample of human postmortem tissue, we investigated expression of protein

294 Postmortem tissues are widely being utilized in the biom

295 is study, we isolated and sequenced HIV from postmortem tissues from three HIV(+) cART(+) individuals

296 equences using single-genome sequencing from postmortem tissues of three HIV(+) cART-treated (cART(+)

297 would correspond to that of IHC analysis of postmortem tissues.

298 nd CSF from an AD transgenic mouse model and postmortem ventricular and antemortem lumbar CSF from AD

299 relative stability of histone modifications postmortem, we anticipate that the HAWAS approach will b

300 apitulating the deficit observed in patients postmortem, without any effect on GABAergic markers or o