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Aim: Interleukin-1 beta (IL-1β) has been implicated as an extracellular signal in the initiation of apoptosis in neurons and oligodendrocytes after spinal cord injury (SCI). To further characterize the apoptotic cascade initiated by IL-1β after SCI, we examined the expression of IL-1β, p38 mitogen-activated protein kinase (p38 MAPK) and caspase-3 after SCI, and further investigated whether p38 MAPK was involved in neuron apoptosis induced by IL-1β. Methods: Adult rats were given contusion SCI at the T-10 vertebrae level with a weight-drop impactor (10 g weight dropped 25.0 mm). The expression levels of IL-1β, p38 MAPK and caspase-3 after SCI were assessed with Western blots, immunohistochemistry staining, and real time reverse transcription polymerase chain reactions (RT-PCR). Neuron apoptosis was assessed with the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) method. Results: Increased levels of IL-1β and p38 MAPK were observed soon after injury, with a peak in expression levels within 6 h of injury. By 24 h after injury, caspase-3 expression was markedly increased in the injured spinal cord. TUNEL-positive cells were first observed in the lesioned area 6 h after SCI. The largest number of TUNEL-positive cells was observed at 24 h post-SCI. Intrathecal injection of the IL-1 receptor antagonist IL-1Ra significantly reduced expression of p38 MAPK and caspase-3, and reduced the number of TUNEL-positive cells. Moreover, intrathecal injection of an inhibitor of p38 MAPK, SB203580, also significantly reduced the expression of caspase-3, and reduced the number of TUNEL-positive cells in the injured spinal cord. Conclusion: The p38MAPK signaling pathway plays an important role in IL-1β mediated induction of neuron apoptosis following SCI in rats. Key wordsapoptosis; interleukin-1; interleukin-1-receptor antagonist protein; p38 mitogenactivated protein kinase; spinal cord injury; TUNEL

Since surface electromyograghic (sEMG) signals are non-invasive and capable of reflecting humans' motion intention, they have been widely used for the motion recognition of upper limbs. However, limited research has been conducted for lower limbs, because the sEMGs of lower limbs are easily affected by body gravity and muscle jitter. In this paper, sEMG signals and accelerometer signals are acquired and fused to recognize the motion patterns of lower limbs. A curve fitting method based on median filtering is proposed to remove accelerometer noise. As for movement onset detection, an sEMG power spectral correlation coefficient method is used to detect the start and end points of active signals. Then, the time-domain features and wavelet coefficients of sEMG signals are extracted, and a dynamic time warping (DTW) distance is used for feature extraction of acceleration signals. At last, five lower limbs' motions are classified and recognized by using Gaussian kernel-based linear discriminant analysis (LDA) and support vector machine (SVM) respectively. The results prove that the fused feature-based classification outperforms the classification with only sEMG signals or accelerometer signals, and the fused feature can achieve 95% or higher recognition accuracy, demonstrating the validity of the proposed method.

The atlantodental interval has been usually used for the evaluation of atlantoaxial instability. However, the asymmetry of the lateral atlantodental interval is occasionally found in healthy individuals. Controversy therefore exists as to the clinical significance of this asymmetry in patients after trauma. The purpose of this study was to determine the normal range of atlantodental intervals in normal individuals using reformatted computed tomography. In this study, C1-C2 vertebrae were imaged in 230 adult patients by a Lightspeed Vct CT (General Electric, CT, USA) with a slice thickness of 0.625 mm. After reformatting the original images, the anterior atlantodental interval (AADI) and lateral atlantodental interval (LADI) were measured. The AADI was found to be 1.83 ± 0.46 mm (0.9-3.4 mm) in males and 1.63 ± 0.43 mm (0.5-3.2 mm) in females. The AADI was significantly greater in males than in females (p < 0.05). The 95% confidence interval for AADI was 1.75-1.90 mm in males and 1.54-1.72 mm in females. No statistically significant differences were found between males and females in the left and right LADI, and LADI asymmetry. The left LADI was found to be 3.38 ± 0.87 mm (1.7-6.0 mm), and the right LADI was 3.42 ± 0.84 mm (1.7-5.9 mm) in males, while the left LADI was 3.30 ± 0.73 mm (1.5-5.3 mm) and the right LADI was 3.37 ± 0.92 mm (1.7-5.9 mm) in females. The 95% confidence interval for left LADI was 3.23-3.52 and 2.94-3.25 mm, and for right LADI was 3.27-3.56 and 3.18-3.56 mm in males and females, respectively. The mean asymmetry of LADI was 0.76 ± 0.66 mm (0.0-3.5 mm) in males and 0.73 ± 0.70 mm (0.0-3.7 mm) in females. The 95% confidence interval for LADI asymmetry was 0.65-0.87 mm in males and 0.59-0.88 mm in females. Most of the population was found to have an asymmetry ranging between 0.1 and 2.0 mm. The current study shows that LADI asymmetry is common in patients without any cervical spine abnormalities. LADI asymmetry may be a normal anatomic variant and there is no evidence to confirm that LADI asymmetry is a sensitive or specific indicator of traumatic atlantoaxial instability. Radiologists and clinicians should be aware of this normal range of asymmetry when interpreting CT scans of the atlantoaxial region.

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