Fig 2: Validation of proteomic analysis.a Table representing the detection (green for attractive molecules, magenta for repulsive molecules) or the absence of detection (grey) of guidance ligands in each brain target. b Table representing the detection (green for attractive molecules, magenta for repulsive molecules) or the absence of detection (grey) of guidance receptors in each brain target. c Table summarizing the type of cells expressing the guidance molecules of interest. d Epifluorescence images of NCAM1 immunofluorescent labelling in the adult chiasm, SCN, LGN and SCol (co-labelled with CTB). d’ Confocal images of NCAM1 and different cell populations markers (GFAP, Iba1, Olig2, NeuN) in the adult intact chiasm, SCN, dLGN, vLGN and SCol. e Epifluorescence images of Ephrin-B3 immunofluorescent labelling in the adult LGN (co-labelled with CTB). e’ Confocal images of Ephrin-B3 and different cell populations markers (GFAP, Iba1, Olig2, NeuN) in the adult intact dLGN and vLGN. f Epifluorescence images of Sema4D immunofluorescent labelling in the adult chiasm and LGN (co-labelled with CTB). f’ Confocal images of Sema4D and different cell populations markers (GFAP, Iba1, Olig2, NeuN) in the adult intact chiasm, dLGN and vLGN. g Epifluorescence images of Sema7A immunofluorescent labelling in the adult intact LGN (co-labelled with CTB). g’ Confocal images of Sema7A and different cell populations markers (GFAP, Iba1, Olig2 and NeuN) in the adult intact dLGN and vLGN. h Epifluorescence images of CSPG4 immunofluorescent labelling in the adult intact LGN (co-labelled with CTB). h’ Confocal images of CSPG4 and different cell populations markers (GFAP, Iba1, Olig2 and NeuN) in the adult intact dLGN and vLGN. d, e, f, g, h scale bar: 200 µm. d’, e’, f’, g’, h’: scale bar: 50 µm. All images are representative of N = 3 biologically independent animals.

Fig 3: High CD56(+)CD107a(+) NK cells in the ascites led to favorable prognosis for serous OvCa patients(A) After EpCAM-magnetic bead isolation, the EpCAM(–) cells were stained with anti-CD56 and anti-CD107a to detect activated NK cells [CD56(+)CD107a(+)] through flow cytometry. (B) The ascetic CD56(+)CD107a(+) activated NK cells were significantly and positively correlated with CTC mHSP70 expression (R2 = 0.5582; p = 0.0009) and Tx-01 binding (R2 = 0.7221; p < 0.0001). (C) Activated NK cells [CD56(+)CD107a(+)] were significantly associated with PFS (p = 0.04).

Fig 4: The guidance map is established during innervation of the developing visual target regions.a Schematic drawing showing in utero injection of mouse embryo eye at E15.5 and postnatal eye injection. Experimental design and timeline, and representative epifluorescent images of CTB-labelled dLGN at the different time points. For P2 to P14 time-points: one day before sample collection, one eye of mouse pups was injected intravitreally with CTB-555. For P0 time-point: 6 h before sample collection, one eye of mouse pups was injected intravitreally with CTB-555. b–f Epifluorescent images of immunofluorescent labelling of b CSPG4, c NCAM1, d NrCAM, e Sema7A and, f Ephrin-B3 in the developing dLGN (co-labelled with CTB, marked with white dashed lines on coronal sections). Scale bar: 100 µm. All images are representative of N = 3 biologically independent animals.

Fig 5: KOR agonist inhibits Ca2+ overload and improves synaptic plasticity in amyloid precursor protein/presenilin-1 mice. (A) ELISA analysis demonstrated the Glu concentration of mice in each group. (B) Western blot analysis of NMDAR, CaMKII, p-CaMKII, CREB and p-CREB expression levels of mice in each group. (C) Golgi-Cox staining of brain tissue samples. Scale bar, 10 µm. (D) Western blot analysis demonstrating NCAM, NR2B, GluR1, PSD95 and SYN expression levels of mice in each group. *P<0.05 vs. Control group; #P<0.05 vs. AD group. Experiments were performed in triplicate and repeated three times. KOR, κ-opioid receptor; Glu, glutamate; NMDAR, N-methyl-D-aspartate receptor; CaMKII, calcium/calmodulin-dependent protein kinase II; p, phosphorylated; CREB, cyclic adenosine monophosphate response element binding protein; NCAM, neural cell adhesion molecule; NR2B, N-methyl D-aspartate receptor subtype 2B; GluR1, glutamate receptor 1; PSD95, postsynaptic density protein 95; SYN, α-synuclein; AD, Alzheimer's disease.