Journal: Annals of Neurosciences

Article Title: Cyclodextrin-enabled δ-Tocotrienol for Treating Stress and Memory Dysfunction: Molecular Insights, Biotechnological Applications and Biomanufacturing Implications

doi: 10.1177/09727531261479841

Figure Lengend Snippet: Primer Sequences Used for Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) and Quantitative Polymerase Chain Reaction (qPCR).

Article Snippet: Protein samples (20 μM) were resolved by SDS-PAGE, transferred to nitrocellulose membrane (Millipore) by electroblotting using a semidry transfer blotter and probed with antibodies including MAP2 (M3696; Sigma-Aldrich), PSD (MA1-046; Thermo Fisher Scientific), NeuF-H/NF-200 (N4142; Sigma-Aldrich), GFAP (G9269; Sigma-Aldrich), GAP43 (sc-17790; Santa Cruz), NCAM (sc-106; Santa Cruz), Vimentin (sc-6260; Santa Cruz), Survivin (71G4B7; Cell Signalling), Nestin (sc-23927; Santa Cruz) and Mortalin.

Techniques: Reverse Transcription, Polymerase Chain Reaction, Real-time Polymerase Chain Reaction, Sequencing

Journal: Frontiers in Pediatrics

Article Title: PROX1-associated lymphatic reprogramming signatures in pediatric adamantinomatous craniopharyngioma: a comparative study with adult cases

doi: 10.3389/fped.2026.1865684

Figure Lengend Snippet: Characterization of the pathological landscape and cellular distribution in pediatric ACP. (A) HE staining revealing typical histopathological abnormalities. (B) IHC staining delineating the topographic distribution of PROX1 within the pediatric ACP. (C) A conceptual model depicting the spatial organization of key neoplastic cell states, including Palisade-like epithelium (PE), Whorl-like epithelium (WE), Keratinized-like epithelium (KE) and Glial scar. (D) Comparative HE and IHC analysis defining the spatial relationship between PROX1 and Nestin expression. Scale bar, 500 µm.

Article Snippet: For IHC, primary antibodies against PROX1 (Rabbit mAb, ABclonal, Wuhan, China), Nestin (Rabbit mAb, ABclonal), CD34 (Rabbit PolymAb, ABclonal), and LYVE1 (Rabbit mAb, ABclonal) were employed, followed by incubation with appropriate secondary antibodies (Zhongshan Golden Bridge Biotechnology, Beijing, China).

Techniques: H&E Stain, Immunohistochemistry, Analysis, Expressing

Journal: Frontiers in Neuroscience

Article Title: A pH-responsive and self-healing CEC/PEG-(CHO) 2 hydrogel for controlled neuropeptide S delivery and endogenous neural repair after spinal cord injury

doi: 10.3389/fnins.2026.1933351

Figure Lengend Snippet: Phenotypic characterization of mouse NSPCs and the Pro-neurogenic effects of NPS loaded CEC/PEG-(CHO) 2 hydrogel scaffold In Vitro. (a) After 7 days in proliferation medium, isolated NSPCs formed neurospheres. Scale bar = 100 μm. (b–d) Neurospheres were positive for the NSPC markers Nestin, SOX2, and PAX6. Scale bar = 100 μm. (e–g) Quantification of Nestin + , SOX2 + , and PAX6 + cells. (h) Schematic diagram of NSPC isolation. (i) Schematic of the NSPC differentiation assay. (j) After 7 days of differentiation, immature neurons were immunostained for Tuj-1. Scale bar = 50 μm. (k) After 14 days, mature neurons were immunostained for MAP2. Scale bar = 50 μm. (l,m) Quantification of Tuj-1 + immature neurons (l) and MAP2 + mature neurons (m) . ** P < 0.01, *** P < 0.001. (n,o) qPCR analysis of transcription factors associated with neuronal differentiation at 7 (n) and 14 (o) days. * P < 0.05, ** P < 0.01, *** P < 0.001. (p) Schematic of the NSPC axon growth assay. (q) After 7 days in proliferation culture, axons were immunostained for GAP43. Scale bar = 200 μm. (r) Quantification of axon length. (s) qPCR analysis of transcription factors regulating axon growth. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The following primary antibodies were used: Nestin (rabbit, Proteintech, 1:400; NSPCs), SOX2 (rabbit, Proteintech, 1:400; NSPCs), PAX6 (rabbit, Proteintech, 1:400; NSPCs), TUJ1 (mouse, Proteintech, 1:400; immature neurons), MAP2 (mouse, Abcam, 1:400; mature neurons), GFAP (rat, Thermo Fisher, 1:400; astrocytes), GAP43 (rabbit, Proteintech, 1:400; axons), MMP-9 (rabbit, Abclonal, 1:400; secreted MMP-9), TNF-α (mouse, Proteintech, 1:400; pro-inflammatory cytokines), IL-10 (mouse, Proteintech, 1:400; anti-inflammatory cytokines), CD68 (rat, Abcam, 1:400; activated immune cells), CSPGs (mouse, Cell Signaling Technology, 1:400; glial scar), synaptophysin (SYP, rabbit, Proteintech, 1:400; presynaptic membranes), and cAMP (rabbit, Proteintech, 1:400; intracellular second messenger).

Techniques: In Vitro, Isolation, Differentiation Assay, Analysis, Growth Assay

Journal: Frontiers in Neuroscience

Article Title: A pH-responsive and self-healing CEC/PEG-(CHO) 2 hydrogel for controlled neuropeptide S delivery and endogenous neural repair after spinal cord injury

doi: 10.3389/fnins.2026.1933351

Figure Lengend Snippet: The functional scaffold enhanced neuronal differentiation and myelination of endogenous NSPCs after SCI. (a,b) At 7 days post injury, the functional scaffold recruited endogenous Nestin + NSPCs to the lesion site and promoted their differentiation into newly generated Tuj-1 + neurons. Scale bar = 500 μm. (c,d) At 6 weeks post injury, the functional scaffold promoted neural regeneration and myelination in the lesion area, with increased MAP2 + mature neurons and MBP + /Tuj-1 + co-localization. Scale bar = 500 μm. (e,f) Quantification of Nestin + and Tuj-1 + cells. * P < 0.05, ** P < 0.01, *** P < 0.001. Groups (left to right): control, scaffold, NPS, functional scaffold and NPSR-KO. (g,h) Quantification of MAP2 and MBP fluorescence intensity. * P < 0.05, ** P < 0.01, *** P < 0.001. Groups (left to right): control, scaffold, NPS, functional scaffold and NPSR-KO. (i) Quantification of SYP expression in MAP2 + cells. * P < 0.05, ** P < 0.01, *** P < 0.001. Groups (left to right): control, scaffold, NPS, functional scaffold and NPSR-KO. (j) At 6 weeks, SYP/MAP2 double-positive cells were evident at the lesion site in the functional scaffold group. Scale bar = 50 μm. (k) Nissl staining revealed no residual scaffold material at the lesion site at 6 weeks post implantation, indicating complete degradation. Scale bar = 500 μm.

Article Snippet: The following primary antibodies were used: Nestin (rabbit, Proteintech, 1:400; NSPCs), SOX2 (rabbit, Proteintech, 1:400; NSPCs), PAX6 (rabbit, Proteintech, 1:400; NSPCs), TUJ1 (mouse, Proteintech, 1:400; immature neurons), MAP2 (mouse, Abcam, 1:400; mature neurons), GFAP (rat, Thermo Fisher, 1:400; astrocytes), GAP43 (rabbit, Proteintech, 1:400; axons), MMP-9 (rabbit, Abclonal, 1:400; secreted MMP-9), TNF-α (mouse, Proteintech, 1:400; pro-inflammatory cytokines), IL-10 (mouse, Proteintech, 1:400; anti-inflammatory cytokines), CD68 (rat, Abcam, 1:400; activated immune cells), CSPGs (mouse, Cell Signaling Technology, 1:400; glial scar), synaptophysin (SYP, rabbit, Proteintech, 1:400; presynaptic membranes), and cAMP (rabbit, Proteintech, 1:400; intracellular second messenger).

Techniques: Functional Assay, Generated, Control, Fluorescence, Expressing, Staining

Journal: eBioMedicine

Article Title: Microcephaly-like phenotype triggered by novel reassortant and prototypic Oropouche virus strains in brain organoids

doi: 10.1016/j.ebiom.2026.106408

Figure Lengend Snippet: OROV infects human NSCs and modulates neurodevelopment. (A) Representative immunofluorescence images of hiPSC-derived NSCs at 24 hpi following infection with OROV strains BeAn19991 or RJ (LVM-2024), stained for OROV (green), nestin (red), and DAPI (blue). (B) Quantification of OROV-positive hiPSC-derived NSCs by immunofluorescence. Cells were stained with anti-OROV (green), anti-Nestin (red), and DAPI (blue). Scale bars = 100 μm. (C) OROV RNA quantification in conditioned medium of NSCs infected at a MOI 0.1 for 24 h. Data represent mean ± SEM from three independent experiments. Statistical significance was determined by one-way ANOVA followed by Tukey's multiple comparisons test. (D) Venn diagrams showing differentially expressed genes (DEGs) in NSCs infected with BeAn19991 or RJ (LVM-2024) compared to mock. (E) Gene Set Enrichment Analysis (GSEA) of shared DEGs. NES: normalised enrichment score; dot size reflects –log(padj). Data from three independent transcriptomic experiments. (F) Volcano plot comparing RJ (LVM-2024) to BeAn19991. Differentially expressed genes above the defined threshold are indicated in red.

Article Snippet: Depending on the experiment, the following primary antibodies were used: anti-OROV (mouse polyclonal anti-OROV, ATCC, antibody, in-house, 1:1000), anti-Nestin (RRID: AB_2155426 , rabbit, Neuromics, 1:500), anti-MAP2 (RRID: AB_10982739 , rabbit, Invitrogen, 1:100) and anti-GFAP (RRID: AB_880202 , rabbit, Abcam, 1:250).

Techniques: Immunofluorescence, Derivative Assay, Infection, Staining

Journal: Molecular Therapy Oncology

Article Title: Targeted attack: Harnessing myelin-specific plasmolipin for suppression of neuroblastoma and glioblastoma

doi: 10.1016/j.omton.2026.201154

Figure Lengend Snippet: McERV-PTLVs specifically transduce cells of brain tumors induced by GSCs injection, leaving normal brain tissues untouched (A) Mice with intracranial tumor induced by GSCs were transduced with concentrated McERV-PTLVs encoding marker EGFP. Seven days after transduction, the brain was isolated, and first cut in coronal section by the injection holes was performed. (B) Fluorescence microscopy images representing the area of the first cut demonstrate the distribution of transduced cells expressing marker EGFP. Magnified images with signed white scale bar provided. White doted lines represent the EGFP-positive area. The small image at the left upper corner of the first picture is the coronal slice stained immunohistochemically with anti-nestin antibodies representing the tumor engraftment. (C) Control group of mice was injected with 1×PBS instead of GSCs and then with McERV-PTLVs. The brain of control mice was analyzed as written above. (D) Fluorescence microscopy images of the area of the first cut represent the absence of EGFP-positive cells. The scheme of the coronal section of caudate-putamen area, where injection holes were performed (marked with red-dotted square). The small image left from the first picture is the coronal slice stained immunohistochemically with anti-nestin antibodies representing the absence of tumor. (E) Mice with intracranial tumor induced by GSCs were transduced with concentrated VSVG-PTLVs encoding marker EGFP. Black-dotted arrow below represents the timescale. (F) The fluorescence microscopy images represent the more disseminated areas of EGFP-positive cells provided on several magnifications (pointed by white arrows). The small image at the left bottom corner of the first picture is the coronal slice stained immunohistochemically, with anti-nestin antibodies representing the tumor engraftment. (G) Images of hematoxylin/eosin staining (right column) and immunohistochemical staining of slices with anti-(human) nestin antibody. Black dotted line represents the area of tumor growth. The upper row samples obtained from mice injected with GSCs and McERV-PTLVs; middle row:1×PBS and McERV-PTLVs; bottom row: GSCs and VSVG-PTLVs. Black scale bars, 100 μm. (H) Fluorescence microscopy images of IF-stained slices obtained from mice with GSC-induced tumor and injected with McERV-PTLVs. DAPI: nuclei staining (blue); anti-(human) nestin mAb stained with Alexa 555 (Red) fluor-conjugated secondary Ab, EGFP: marker fluorescent protein indicates the cells transduced with McERV-PTLVs (the merged image of EGFP [green] and anti-nestin [red] pictures are represented). The white dotted line represents the nestin-positive area of tumor growth. (I) Fluorescence microscopy images of IF-stained slices obtained from mice of control group injected with 1×PBS and McERV PTLVs, representing the absence of nestin and EGFP-positive cells. (J) Fluorescence microscopy images of IF-stained slices obtained from mice with GSC-induced tumor and injected with VSVG-PTLVs. White scale bars on H, I, and J: 100 μm.

Article Snippet: For immunohistochemical assessments, an antibody specific to human nestin (R&D Systems GmbH, Wiesbaden-Nordenstadt, Germany) was used.

Techniques: Injection, Transduction, Marker, Isolation, Fluorescence, Microscopy, Expressing, Staining, Control, Immunohistochemical staining