Histological observation of a gelatin sponge transplant loaded with bone marrow-derived mesenchymal stem cells combined with platelet-rich plasma in repairing an annulus defect - Fig 2

<p>The exposure of annulus fibrosus after decompression of the lamina, (A) sham group, arrow showing annulus fibrosus. (B)injury group,arrow showing a 1 × 1 cm defect of annulus fibrosus. (C)therapeutic group,arrow showing complexes including BMSCs, PRP,and Gelatin sponges.</p

HE staining score for each group (x ± s, n = 90).

<p>HE staining score for each group (x ± s, n = 90).</p

Quantitative analysis of type II collagen staining for each group (x ± s, n = 90).

<p>Quantitative analysis of type II collagen staining for each group (x ± s, n = 90).</p

Masson staining score for each group (x ± s, n = 90).

<p>Masson staining score for each group (x ± s, n = 90).</p

Masson staining in each group after 3,6,12 weeks.

<p>(A-C) Masson staining in the sharm group after 3,6,12 weeks (×100). (D-F) Masson staining in the injury group after 3,6,12 weeks (×100). (G-I) Masson staining in the therapeutic group after 3,6,12 weeks (×100). Blue arrows:mature bone trabecular.Black arrows:muscle fiber connective tissue.</p

Results of HE staining in each group after 3,6,12 weeks.

<p>(A-C) HE staining in the sharm group after 3,6,12 weeks (×100). (D-F) HE staining in the injury group after 3,6,12 weeks (×100). (G-I) HE staining in the therapeutic groupafter 3,6,12 weeks (×100).Blue arrows:collagen and matrix.Black arrows:cartilage cells.</p

AB-PAS staining in each group after 3,6,12 weeks.

<p>(A-C) AB-PAS staining in the sharm group after 3,6,12 weeks (×100). (D-F) AB-PAS staining in the injury group after 3,6,12 weeks (×100). (G-I) AB-PAS staining in the therapeutic groupafter 3,6,12 weeks (×100). Black arrows:cartilage cells.</p

Additional file 1: Figure S1. of C-C motif chemokine ligand 20 regulates neuroinflammation following spinal cord injury via Th17 cell recruitment

Animal model of contusion SCI. (A) The localization of T10 by X-ray. (B) Skin preparation. (C) Skin incision. (D) The exposure of T10. (E) The exposure of the spinal cord. (F) Contusion injury. (G) Observation after SCI. (H) Suture the incision. (DOCX 2344 kb

Additional file 3: Figure S2. of C-C motif chemokine ligand 20 regulates neuroinflammation following spinal cord injury via Th17 cell recruitment

The temporal profile (from 0 h to 28 days post-injury) of IL-17A mRNA expression in the spinal cord. IL-17A, as determined by qRT-PCR, shows that SCI leads to increased IL-17A mRNA level in the spinal cord, especially at 14 days post-SCI. + P < 0.05, compared with the sham group. (DOCX 168 kb

Correlation study between facet joint cartilage and intervertebral discs in early lumbar vertebral degeneration using T2, T2* and T1ρ mapping

<div><p>Recent advancements in magnetic resonance imaging have allowed for the early detection of biochemical changes in intervertebral discs and articular cartilage. Here, we assessed the feasibility of axial T2, T2* and T1ρ mapping of the lumbar facet joints (LFJs) to determine correlations between cartilage and intervertebral discs (IVDs) in early lumbar vertebral degeneration. We recruited 22 volunteers and examined 202 LFJs and 101 IVDs with morphological (sagittal and axial FSE T2-weighted imaging) and axial biochemical (T2, T2* and T1ρ mapping) sequences using a 3.0T MRI scanner. IVDs were graded using the Pfirrmann system. Mapping values of LFJs were recorded according to the degeneration grades of IVDs at the same level. The feasibility of T2, T2* and T1ρ in IVDs and LFJs were analyzed by comparing these mapping values across subjects with different rates of degeneration using Kruskal-Wallis tests. A Pearson’s correlation analysis was used to compare T2, T2* and T1ρ values of discs and LFJs. We found excellent reproducibility in the T2, T2* and T1ρ values for the nucleus pulposus (NP), anterior and posterior annulus fibrosus (PAF), and LFJ cartilage (intraclass correlation coefficients 0.806–0.955). T2, T2* and T1ρ mapping (all <i>P</i><0.01) had good Pfirrmann grade performances in the NP with IVD degeneration. LFJ T2* values were significantly different between grades I and IV (<i>P</i>_L = 0.032, <i>P</i>_R = 0.026), as were T1ρ values between grades II and III (<i>P</i>_L = 0.002, <i>P</i>_R = 0.006) and grades III and IV (<i>P</i>_L = 0.006, <i>P</i>_R = 0.001). Correlations were moderately negative for T1ρ values between LFJ cartilage and NP (<i>r</i>_L = −0.574, <i>r</i>_R = −0.551), and between LFJ cartilage and PAF (<i>r</i>_L = −0.551, <i>r</i>_R = −0.499). T1ρ values of LFJ cartilage was weakly correlated with T2 (<i>r</i> = 0.007) and T2* (<i>r</i> = −0.158) values. Overall, we show that axial T1ρ effectively assesses early LFJ cartilage degeneration. Using T1ρ analysis, we propose a link between LFJ degeneration and IVD NP or PAF changes.</p></div