Study Design. To evaluate the effect of p38 pathway on spinal cord injury (SCI), a rat model of SCI was performed. Objective. We determined the effect of p38 on SCI and SCI related inflammation, apoptosis, and autophagy. Summary of Background Data. SCI is a severe clinical problem worldwide. It is difficult to prevent cell necroptosis and promote the survival of residual neurons after SCI. p38, a class of mitogen-activated protein kinases, its effect on SCI and SCI related inflammation, apoptosis, and autophagy have not been studied very well. Methods. The rats were randomly divided into the following four groups: the sham-operated (sham) group, the SCI group, the SCI + vehicle group, and the SCI + SB203580 (10 mg/kg) group. The p38 inhibitor SB203580 was administered by oral (10 mg/kg/d) gavage once per day for 14 days. Neurological recovery was assessed using the Basso, Beattie, and Bresnahan locomotion rating scale. Apoptosis, autophagy, and inflammation related proteins were measured by enzyme-linked immunosorbent assay kits or western blotting. Results. Our results showed that p38 was upregulated after SCI from day 3, which was paralleled with the levels of its proteins ATF-2, suggesting an increase in p38 activity. Our results showed administration of SB203580 attenuated histopathology and promoted locomotion recovery in rats after SCI. SB203580 administration significantly inhibited inflammatory cytokines levels as well as the inflammation signaling pathway. SB203580 administration also modulated the apoptosis and autophagy signaling pathway. Conclusion. Our findings suggest that p38 inhibitor SB203580 treatment alleviates secondary SCI by inhibiting inflammation and apoptosis, thereby promoting neurological and locomoter functional recovery, thus suggest the important role of p38 in neuronal protection after SCI. Level of Evidence: N/A
Aims and objectives To examine the serial mediating effect of executive function and attentional bias in the relationship between frailty and depressive symptoms. Background Although the role of frailty in predicting depression has been well documented, the underlying mechanisms remain unclear. Design A cross‐sectional study was conducted with 667 older inpatients aged 60–90 years in the internal medicine wards of a hospital in China. Methods Attentional bias, frailty and depressive symptoms were assessed using the Attention to Positive and Negative Information Scale, the Physical Frailty Phenotype and the 5‐item Geriatric Depression Scale. Executive function was measured using 3 tests, including digital backward, category Verbal Fluency Test and Trail Making Test. The study followed the STROBE guideline. Results The latent profile analysis (LPA) identified four patterns of attentional bias, namely “no positive bias & no negative bias” (class 1, 9.3%), “minor positive bias & no negative bias” (class 2, 48.0%), “major positive bias & minor negative bias” (class 3, 25.6%) and “major positive bias & no negative bias” (class 4, 17.1%). Regression analysis found that frailty was associated with depressive symptoms. Frailty was also negatively associated with executive function, which was a protective factor for attentional bias class 1, 2 and 3 with reference to class 4. Attentional bias class 1 and 2 but not class 3 was associated with depressive symptoms with reference to class 4. The joint significance test confirmed executive function and attentional bias as serial mediators linking frailty to depressive symptoms. Discussion Unlike robust older adults who have the age‐related positivity effect, frail older adults have attentional bias deficits due to executive dysfunction, and consequently experience clinically relevant depressive symptoms. Relevance to clinical practice Healthcare providers should take executive function training and attentional bias regulation into consideration to reduce the detrimental effects of frailty on emotional well‐being.
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