Diffusion tensor imaging predicting neurological repair of spinal cord injury with transplanting collagen/chitosan scaffold binding bFGF.

Prognosis and treatment evaluation of spinal cord injury (SCI) are still in the long-term research stage. Prognostic factors for SCI treatment need effective biomarker to assess therapeutic effect. Quantitative diffusion tensor imaging (DTI) may become a potential indicators for assessing SCI repair. However, its correlation with the results of locomotor function recovery and tissue repair has not been carefully studied. The aim of this study was to use quantitative DTI to predict neurological repair of SCI with transplanting collagen/chitosan scaffold binding basic fibroblast growth factor (bFGF). To achieve our research goals, T10 complete transection SCI model was established. Then collagen/chitosan mixture adsorbed with bFGF (CCS/bFGF) were implanted into rats with SCI. At 8 weeks after modeling, implanting CCS/bFGF demonstrated more significant improvements in locomotor function according to Basso-Beattie-Bresnahan (BBB) score, inclined-grid climbing test, and electrophysiological examinations. DTI was carried out to evaluate the repair of axons by diffusion tensor tractgraphy (DTT), fractional anisotropy (FA) and apparent diffusion coefficient (ADC), a numerical measure of relative white matter from the rostral to the caudal. Parallel to locomotor function recovery, the CCS/bFGF group could significantly promote the regeneration of nerve fibers tracts according to DTT, magnetic resonance imaging (MRI), Bielschowsky's silver staining and immunofluorescence staining. Positive correlations between imaging and locomotor function or histology were found at all locations from the rostral to the caudal (P < 0.0001). These results demonstrated that DTI might be used as an effective predictor for evaluating neurological repair after SCI in experimental trails and clinical cases.

Modulation of mitogen­activated protein kinase attenuates sepsis­induced acute lung injury in acute respiratory distress syndrome rats.

Sepsis is the most important predisposing cause inducing acute respiratory distress syndrome (ARDS); however, the mechanism of sepsis leading to the development of ARDS remains to be elucidated. Suppression of the mitogen­activated protein kinase (MAPK) signal by blocking the phosphorylation of Jun N­terminal kinase (JNK) and p38 in lung tissues could alleviate acute lung injury induced by sepsis. MAPK signaling may have a crucial role in development of the sepsis­induced acute lung injury. The specific inhibitors of JNK and p38 MAPK, SP600125 and SB203580, were administrated by intragastric injection 4 h before induction of ARDS after cecal ligation and puncture (CLP). Rats were sacrificed at 1, 6 or 24 h after CLP challenge. The histological evaluation, lung water content, and biochemical analysis were performed. The results revealed that the JNK and p38 MAPK inhibitor improved lung permeability, attenuated system inflammation, further alleviated the lung injury induced by sepsis. In conclusion, JNK and p38 MAPK signaling are essential for the development of ARDS following sepsis. Further studies are needed to illuminate the detailed mechanisms of JNK and p38 MAPK signaling in sepsis­induced ARDS.