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Published: 26 April 2025
Figure 1. Generation of the EOAD cell model. (A) Immunostaining of PSEN1 in the EOAD cell model. (B, C) Sanger sequencing of SH-SY5Y cells transfected with PSEN1 lentivirus (B) and PSEN1 M139I lentivirus (C). Scale bar: 100 μm. Abbreviations: EOAD, early-onset Alzheimer disease; PSEN1, presenilin 1.
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Published: 26 April 2025
Figure 3. The expression of NOTCH-1, NICD, Hes1, and miR-34a in the different groups. (A) The mRNA level of NOTCH-1. (B) Representative immunoblots of NOTCH-1, NICD, and Hes1 (original Western blot images in Figure S2 ). (C-E) Quantification of NOTCH-1 (C), NICD (D), and Hes1 levels (E). (F) Expression of mi
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Published: 26 April 2025
Figure 4. NOTCH-1 is the target gene of miR-34a. (A) The predicted miR-34a binding site of 3′UTR of NOTCH-1 by Targetscan ( www.targetscan.org ). (B) Dual-luciferase assay. Abbreviations: NC, negative control; NS, not significant; WT, wild type; MT, mutant type. n  = 3 independent experiments. ** P  < .01
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Published: 26 April 2025
Figure 5. The regulatory effect of miR-34a in the EOAD cell model. (A) The expression of miR-34a was determined in different groups by qRT-PCR. (B) Ratios of Aβ42/Aβ40 were detected by ELISA. (C, D) The mRNA levels of NOTCH-1 (C) and Hes1 (D) were assessed by qRT-PCR. (E) Representative immunoblots of NOTCH-1
Journal Article
Xuechun Sun and others
Journal of Neuropathology & Experimental Neurology, nlaf044, https://doi.org/10.1093/jnen/nlaf044
Published: 26 April 2025
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Published: 26 April 2025
Figure 2. Aβ42/40 ratios in the different groups. (A) mRNA levels of PSEN1. (B) Representative immunoblots of PSEN1 (original Western blot images in Figure S2 ). (C) Quantification of PSEN1 level. (D) Ratios of Aβ42/40 were detected by ELISA. Abbreviations: MT, mutant-type PSEN1; N, normal; NC, negative cont
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Published: 26 April 2025
Figure 6. miR-34a promotes cell proliferation and apoptosis in the EOAD cell model. (A) The OD value of the MTT assay. (B) Representative immunoblots of cleaved Caspase-3 (original Western blot images in Figure S2 ). (C) Quantification of cleaved Caspase-3 levels. (D) Flow cytometry analysis. (E) Quantificat
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Published: 25 April 2025
Figure 1 Histopathological findings of EGFR tv-positive cases. (A) Glioblastoma, IDH-wildtype. (B) Diffuse pediatric-type high-grade glioma, H3-wildtype and IDH-wildtype, RTK2A. (C) Astrocytoma, IDH-mutant, CNS WHO grade 4. (D) Diffuse glioma, IDH-mutant, NEC. (H&E; A, 400×; B-D, 200×).
Journal Article
David J Cook and others
Journal of Neuropathology & Experimental Neurology, nlaf041, https://doi.org/10.1093/jnen/nlaf041
Published: 25 April 2025
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Published: 24 April 2025
Figure 1. Experimental protocol. Animals were evaluated using the Garcia Neuroscore Scale (GNS) 1 day before the onset of ischemia (−24 h). On the day of surgery, unilateral middle cerebral artery occlusion (MCAO) was performed with simultaneous monitoring of CBF by laser Doppler flowmetry (LDF). The LDF acqu
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Published: 24 April 2025
Figure 2. Correcting for edema in MRI images accurately estimates lesion volume; Garcia Neuroscore Scale (GNS) values do not correspond to the corrected LV. (A) The left/right hemispheric ratio (L/R ratio) was used to estimate the swelling of the left hemisphere affected by acute ischemic stroke (AIS). Note t
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Published: 24 April 2025
Figure 3. A subgroup of mice exhibited a paradoxical relationship between small lesion volume and severe neurological deficit. (A) A representative mouse with a typical prognosis displays a low Garcia Neuroscore Scale (GNS) score over the course of 72 hours of survival (A2), and a large lesion volume as measu
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Published: 24 April 2025
Figure 1. Digital histology methods. Images and the digital detection overlay for representative regions immunostained for p-Tau (AT8) (A and B), p-Tau neurofibrillary tangles (AT8) (C and D), Aβ (NAB228) (E and F), and p-αSyn (81A) (G–J). For p-αSyn digital histology detections, a higher optical density thre
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Published: 24 April 2025
Figure 4. Cortical LVs show a linear relationship with neurological impairment 72 hours after stroke. (A) A representative axial (top) and coronal (bottom) T2 weighted sequence showing the semi-automated separation of cortical and subcortical infarcts. Light blue selection indicates cortical (red arrow), deep
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Published: 24 April 2025
Figure 2. Run-to-run variability in immunostaining protocols. Correlation plots comparing ln %Area Occupied (ln%AO) of p-Tau, p-Tau neurofibrillary tangles, Aβ, and p-αSyn pathology using serial sections and immunostained using manual methods and automated methods. * P  < .05, ** P  < .001.
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Published: 24 April 2025
Figure 5. Clinical cases of typical and atypical prognosis in patients with ischemic stroke. (A) Case 1: typical prognosis in a patient with a large infarct volume with severe residual symptoms. An 81-year-old female patient was admitted with aphasia and severe right-sided hemiparesis. The National Institutes
Journal Article
Réka Tóth and others
Journal of Neuropathology & Experimental Neurology, nlaf046, https://doi.org/10.1093/jnen/nlaf046
Published: 24 April 2025
Journal Article
Yongya Kim and others
Journal of Neuropathology & Experimental Neurology, nlaf047, https://doi.org/10.1093/jnen/nlaf047
Published: 24 April 2025
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Published: 24 April 2025
Figure 3. Bland-Altman plots. Differences in %lnAO for methodologically similar staining methods for p-Tau, p-Tau neurofibrillary tangles, Aβ, and p-αSyn pathology are plotted against the mean of these values. The dashed line represents the mean difference between the staining runs, and solid grey lines repre
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Published: 24 April 2025
Figure 4. Digital histology measures and traditional scales. (A) Ordinal scores for regional pathological severity compared to ln% area occupied (ln%AO). (B) Regional p-Tau ln%AO by Braak tau stage. (C) Regional p-Tau neurofibrillary tangle detection by Braak tau stage. (D) Regional Aβ ln%AO by Thal phase. (E