Spinal cord injury (SCI) is lead to locomotor impairment because of neurological damage after following trauma. Quercetin (Que) has been confirmed to have a neuro-protective effect during nerve damage processes. The purpose of this study was to determine the roles of Que in functional recovery, cavity formation, astrocyte activation, and nerve regeneration following SCI. Sprague-Dawley rats were randomly divided into three groups: Sham group, SCI group, and Que + SCI group. A rat model of SCI was made at T10 using the modified Allen's method. In the Que + SCI group, animals underwent laminectomy and were then intraperitoneally injected with 20 mg/kg Que for 7 days. Locomotor function was determined with the Basso, Beattie, Bresnahan (BBB) scores at 1, 3, 5, and 7 days post-injury. At 7 days post-injury, somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) were recorded. Hematoxylin-Eosin (HE) staining was used to investigate cavity formation. Astrocyte activation was assayed by immunohistochemistry staining with an antibody specific for glial fibrillary acidic protein (GFAP), as well as the expression of GFAP and S100β. Axons were stained using an antibody specific for neurofilament 200 (NF200) and 5-hydroxytryptamine (5-HT). In addition, the protein level of BDNF, p-JNK2, and p-STAT3 was detected using Western blot. Que promoted locomotor function and electrophysiological recovery, reduced cavity formation, contributed to astrocyte activation and axonal regeneration after acute SCI. Moreover, Que up-regulated the expression of BDNF, but reduced p-JNK2 and p-STAT3 expression after acute SCI. Taken together, Que promoted locomotor and electrophysiological functional recovery, astrocyte activation and axonal regeneration after acute SCI, possibly through BDNF and JAK2/STAT3 signaling pathways.
Hip fracture is a worldwide medical problem with devastating consequences. Older adults are at higher risk for complications and have more mobility limitation. The aim of this study was to assess the impact of delay in out-of-bed functional exercise on one-year mortality and functional outcomes for elderly patients with hip fracture in China. 1,022 cases of patients with hip fracture who were older than 75 were involved in this retrospective cohort study between 2007 and 2017. One-year mortality, follow up Activities of Daily Living (ADL) score, and Harris hip score were collected. Patients with hip fracture experienced an average of 2.9 days of in-bed functional exercise, 41.4% (n = 423) taken out-of-bed functional exercise within 2 days. A Cox proportional regression model showed that after adjustment for age, sex, cardiovascular disease, and urinary disease, delayed out-of-bed functional exercise (> 2 days) associated with higher one-year mortality (OR = 1.38, 95% confidence interval [CI]: 1.09 to 1.69). Ordinary least squares regression showed that delayed out-of-bed functional exercise associated with worsen ADL scores at 1-month (difference of-3.9 points, 95% CI:-6.4 to-1.7), although the long term ADL scores did not have increased. In addition, there were no associations between out-of-bed functional exercise timing and the Harris hip score at 12 months. In conclusion, in elderly patients with hip fracture in China, delayed out-of-bed functional exercise was not associated with improved Harris hip score, but it was associated with worsen ADL capacities at 1-month postoperatively and higher one-year mortality. The present study emphasizes the benefit of early out-of-bed exercise on the majority of elderly patients with hip fracture.
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