Journal: Neuron

Article Title: Functional ultrasound imaging of the human spinal cord.

doi: 10.1016/j.neuron.2024.02.012

Figure Lengend Snippet: Figure 1. Surgical procedure, fUSI acquisition, and epidural ESCS protocols (A) Patients undergo a T10 partial laminectomy for standard-of-care implantation of an epidural electrical spinal cord stimulator (Penta model 3228), under general anesthesia. A 15 MHz functional ultrasound probe (inner) is inserted into a sterilized cover to reduce the level of microbial contamination. The probe is mounted onto a retractor surgical arm and inserted into the lamina for fUSI. (B) X-ray confirmation of the position of the epidural leads. (C) Baseline fUSI images were continuously acquired for 3 min (n = 4 patients) or 30 s (n = 2), followed by 10 (or 5 in two patients) consecutive cycles of 30 s stimulation ON and 30 s stimulation OFF, and finished with 2 min of washout acquisition (i.e., stimulation OFF). (D) Electrical stimulation parameters. Red color represents the number of patients and the total number of stimulation cycles in sessions that include both fUSI acquisition with both low (i.e., 3.0 mA) and high (i.e., 4.5 mA) current-amplitude stimulation.

Article Snippet: Functional ultrasound imaging set-up Weutilized a fully featured commercial functional ultrasound acquisition system, Iconeus One (Iconeus, Paris, France) to acquire fUSI spinal cord images via a transducer probe inserted through laminar openings (Figure 1A).

Techniques: Functional Assay

Journal: Neuron

Article Title: Functional ultrasound imaging of the human spinal cord.

doi: 10.1016/j.neuron.2024.02.012

Figure Lengend Snippet: Figure 2. Functional ultrasound imaging of the spinal cord in a transverse plane (A) Schematic representation of spinal cord fUSI through a laminar window and cross section of spinal cord anatomy. The green area illustrates the approximate FOV of fUSI acquisition in patient P1. (B–G) Power Doppler-based ultrafast ultrasound image showing the transverse section of the spinal cords of patients. The FOV captures part of the anatomical vascularization of the spinal cord with the dorsal surface highlighted with white dashed lines (and dura in patient P2).

Article Snippet: Functional ultrasound imaging set-up Weutilized a fully featured commercial functional ultrasound acquisition system, Iconeus One (Iconeus, Paris, France) to acquire fUSI spinal cord images via a transducer probe inserted through laminar openings (Figure 1A).

Techniques: Functional Assay, Imaging

Journal: bioRxiv

Article Title: Dual-action nanoconjugate for overcoming r-tPA-resistant clots

doi: 10.64898/2026.05.13.725039

Figure Lengend Snippet: A. Schematic representation of the experimental design. Briefly, we used functional Ultrasound (fUS) imaging to quantify reperfusion in the ischemic area. Before inducing the IS, a 5-min acquisition was performed to have the baseline (T0) cerebral blood volume (CBV) of the mice. Then IS was induced by applying AlCl 3 on the MCA for 5 minutes. 15 minutes after, a 45-minute acquisition began to follow any changes in the CBV in the ischemic area. 5 minutes after the beginning of the 45-minutes acquisition, one of the treatments: IO@PDA (2mg/kg); DNase (1.37 mg/kg); tPA (10 mg/kg); a combination of IO@PDA (2 mg/kg) + tPA (2.5 mg/kg) + DNase (1.37 mg/kg) and the IO@PDA@tPA@DNase conjugate (corresponding to 2.5 mg/kg tPA and 1.37 mg/kg DNase equivalency) was administered to the mice (corresponding to 20 minutes post ischemic events). B. CBV variation of the ipsilateral isocortex of IO@PDA-treated mice (percentage from baseline (T0), n=5, 2-way ANOVA, Multiple comparisons (T0 vs Tn+1), **** p < 0.0001). C. CBV variation of the ipsilateral isocortex DNase-treated mice (percentage from baseline (T0), n=6, 2-way ANOVA, Multiple comparisons (T0 vs Tn+1), **** p < 0.0001). D. CBV variation of the ipsilateral isocortex tPA-treated mice (percentage from baseline (T0), n=5, 2-way ANOVA, Multiple comparisons (T0 vs Tn+1), **** p < 0.0001). E. CBV variation of the ipsilateral isocortex IO@PDA + tPA + DNase-treated mice (percentage from baseline (T0), n=5, 2-way ANOVA, Multiple comparisons (T0 vs Tn+1), **** p < 0.0001). F. CBV variation of the ipsilateral isocortex IO@PDA@tPA@DNase-treated mice (percentage from baseline (T0), n=5, 2-way ANOVA, Multiple comparisons (T0 vs Tn+1), **** p < 0.0001). G. Representative images obtained during baseline (T0); 20 minutes and 60 minutes post IS for IO@PDA@tPA@DNase-treated mice.

Article Snippet: All ultrasound imaging acquisitions were performed from bregma -3 mm to bregma +1 mm, both before and 15 minutes after stroke onset, using an ultrafast scanner (Iconeus One, Iconeus, France), the IcoScan acquisition software, and a dedicated ultrasound probe (Iconeus IcoPrime-4D MultiArray, 15 MHz, 256 elements, 100 μm pitch).

Techniques: Functional Assay, Imaging

Journal: The European journal of neuroscience

Article Title: Expression pattern of miR-146a, an inflammation-associated microRNA, in experimental and human temporal lobe epilepsy.

doi: 10.1111/j.1460-9568.2010.07122.x

Figure Lengend Snippet: Fig. 2. In situ hybridization analysis of miR-146a expression in hippocampal tissue of control rats and after induction of SE. (A, C, E, G) Control hippocampus showing neuronal miR-146a expression in the different hippocampal subfields, including pyramidal neurons of CA3 (C; insert in C) and CA1 (E; insert in E) regions, granule cells of the dentate gyrus (DG; G) and hilar neurons (G; insert in G: high-magnification of hilar neurons). gcl, granule cell layer. (B, D, F, H) Hippocampus 1 week post-SE showing increased miR-146a expression within the different hippocampal regions, including CA3 (D; insert in D: high-magnification of CA3), CA1 (F; insert in F: high-magnification of CA1) and DG (H). miR-146a expression was observed in both neuronal and glial cells; arrows in D, F (and insert in D) indicate positive pyramidal neurons of CA3 and CA1; positive glial cells (arrowheads in D, F and insert in D) were particularly abundant in regions of prominent gliosis (CA1, CA3 and the inner molecular layer, iml, of the DG). Insert in (H) shows a high-magnification of positive glial cells in the DG (iml). (I and J) In situ hybridization analysis of miR-146a expression in the hilar region of the hippocampus 1 week (I) and 3–4 months post-SE (J) showing increased expression in glial cells (arrows; insert in I). Sections are counterstained with haematoxylin. Inserts in (J): in situ hybridization and immunohistochemistry analysis showing in (a) absence of miR-146a (red) expression in lectin-positive microglial cells (blue) and in (b) colocalization with the astroglial marker glial fibrillary acidic protein (GFAP; purple) in astrocytes. Scale bars: 1250 lm (A and B); 70 lm (C–J); 35 lm (inserts in C, D, F and G); 20 lm (insert in E); 17 lm (inserts in H and I); 11 lm (insert in J). LT, long-term, 3–4 months after SE.

Article Snippet: For the double-staining, combining immunocytochemistry with in situ hybridization, sections were first processed for immunocytochemistry as previously described (Aronica et al., 2001a, 2003) with glial fibrillary acidic protein (GFAP; polyclonal rabbit; DAKO, Glostrup, Denmark; 1 : 4000), neuronal nuclear protein (NeuN; mouse clone MAB377; Chemicon, Temecula, CA, USA; 1 : 2000), HLA-DR [anti-human leukocyte antigen (HLA)-DP, DQ, DR (mouse clone CR3 ⁄ 43); DAKO, Glostrup, Denmark; 1 : 400], CFH (polyclonal goat; Quidel, San Diego, CA, USA; 1 : 100) or the biotinylated lectin Ricinus Communis Agglutinin I (RCA 120; Vector Laboratories, Burlingame, CA, USA; 1 : 500, for the visualization of microglial cells on rat tissue), using Fast Blue B salt (St Louis, MO, USA) or Vector Blue substrate (Vector Laboratories) as chromogen.

Techniques: In Situ Hybridization, Expressing, Control, Immunohistochemistry, Marker