BACKGROUND:After spinal cord injury, endogenous neural stem cel s are activated to proliferate and migrate to repair damaged tissue. As a clinical medicine, methylprednisolone shows a lot of functions, but its effects on endogenous neural stem cel s are stil unknown.
OBJECTIVE:To explore the effects of methylprednisolone on the proliferation and migration of endogenous neural stem cel s after spinal cord injury.
METHODS:Seventy-five Sprague-Dawley rats were used to make animal models of T10 complete paraplegia using Al en’s method, and randomized into methylprednisolone, normal saline and model groups. Rats in these three groups were given intraperitoneal injection of 1 g/L methylprednisolone solution at a dose of 30 mg/kg for 10 minutes and at a dose of 5.4 mg/kg/h for 23 hours, given intraperitoneal injection of normal saline at the same dose and given no treatment, respectively. Neurological and motor functions were assessed by somatosensory evoked potential and Basso Beattie Bresnahan scores at 7, 14, 21, 28 days after spinal cord injury. BrdU and Nestin staining of the injured spinal cord segment was conducted.
RESULTS AND CONCLUSION:A large amount of BrdU-and Nestin-positive cel s were visible in al the groups, and the number of these cel s reached the peach at 14 days after spinal cord injury. Methylprednisolone was found to inhibit BrdU-, Nestin-or double-positive cel s, indicating methylprednisolone can inhibit the proliferation and migration of endogenous neural stem cel s. The results of Basso Beattie Bresnahan scores showed no notable improvement in the motor function of the limbs. Methylprednisolone also showed no significant effects on the motor evoked potential latency, but promoted nerve conduction recovery. Al these findings indicate that methylprednisolone has some hindering effects on spinal cord repair by inhibiting the proliferation and migration of endogenous neural stem cel s after spinal cord injury.

Objective To investigate the clinical features of acute traumatic subdural hematomas (SDH) in infants and discuss the treatment methods. Methods The clinical features of 48 infants under three years old with acute traumatic SDH admitted from 2002 to 2008 were retrospectively analyzed.Results There were 31 infants under one year old (65%). The most popular injury cause was accidental fall in 37 patients (77%). Of all patients, 12 patients (25%) had disturbance of consciousness,eight ( 17% ) had convulsion and eight ( 17% ) were combined with skull fractures. The treatment methods included craniotomy and evacuation of the blood clot in 18 patients ( including 13 patients underwent instant operation after admission ), burr hole craniotomy and external drainage of the chronic subdural hematoma in seven and conservative management in 23 with small subdural hematomas. All patients obtained good outcome except that two patients had motor dysfunction and one death. Conclusions The incidence of acute traumatic SDH in infants is high, especially in infants under one year old. It is easy to be disregarded at early stage and may deteriorate to chronic subdural hematoma or hydropsy. Early diagnosis and active surgical treatment may attain sound prognosis.

Objective To investigate the expressions of fatty acid-binding protein 5 (FABP5)and dihydroli-poamide dehydrogenase(DLD)in skin lesions of symmetrical acrokeratoderma(SAK), and to explore their significance. Methods Biopsy specimens were obtained from skin lesions on the wrists and perilesional skin of 9 patients with SAK, and from normal skin in the wrists of 9 healthy volunteers (control group). Reverse transcription PCR (RT-PCR)and immunohistochemical staining were performed to measure the expressions of FABP5 and DLD in these specimens. Results RT-PCR showed no significant differences in the mRNA expressions of FABP5 or DLD between lesional, perilesional and normal control skin specimens(both P > 0.05). Immunohistochemically, there was a significant increase in the extent and intensity of staining for FABP5 in SAK lesions. Concretely speaking, FABP5 was strongly expressed in the stratum corneum, granular and spinous layers in SAK lesions, but weakly expressed in the stratum corneum, granular and spinous layers in perilesional skin, and only in spinous and basal layers in normal control skin. The expression of DLD decreased in SAK lesions, and was observed only in the stratum corneum and spinous layer in a few cases of SAK. However, the full-thickness epidermis stained positive for DLD in perilesional skin, with the nuclei and cytoplasm both stained deep brown. Conclusion The overexpression of FABP5 in SAK lesions may participate in dysdifferentiation of keratinocytes, while the down-regulation of DLD expression suggests an imbalance in energy metabolism.