EPO promotes axonal sprouting via upregulating GDF10.

Erythropoietin (EPO) has an exact neuroprotective effect on stroke. However, it remains unknown whether it participates in axonal sprouting after neuron damage. Growth and differentiation factor 10 (GDF10) has been shown to be a trigger of axonal sprouting after stroke. Hence, it was hypothesized that EPO promotes axonal sprouting mainly through GDF10. In the present in vitro experiment, it was found that EPO could promote axonal sprouting and GDF10 expression in a dose-dependent manner. The knockdown of GDF10 using siRNA abolished the effect of EPO-mediated axonal sprouting, indicating that GDF10 is the executor of EPO-mediated axonal sprouting. The treatment of neurons with nuclear factor-kappaB (NF-κB) inhibitor JSH-23 could inhibit the accumulation of NF-κB phospho-p65 (p-p65) in the nucleus, the upregualtion of GDF10 and extending of axonal length. Furthermore, the addition of Janus kinase 2 (JAK2) inhibitor CEP-33779 or phosphoinositide 3-kinase (PI3K) inhibitor LY294002 to the culture medium also blocked the nuclear translocation of p-p65, the expression of GDF10, and axonal sprouting, suggesting that EPO induces axonal sprouting via activating cellular JAK2 and PI3K signaling. Impeding JAK2 signaling with CEP-33779 can suppress the phosphorylation of PI3K, and this confirms that the upstream of PI3K signaling is JAK2. These present results provide a novel insight into the role of EPO and the molecular mechanism of axonal sprouting, which is beneficial for the development of novel approaches for neurological recovery after brain injury, including stroke.

[Analysis of pathogen isolated from lower respiratory tract in coalminer's pneumoconiosis patients complicated with infection].

OBJECTIVE: To investigate the composition and resistance of main pathogens isolated form Lower respiratory tract in coalminer's pneumoconiosis patients complicated with infection to provide the basis for clinical treatment. METHOD: Coalminer's pneumoconiosis patients complicated with infection during 2009 to 2010 were divided into mechanical ventilation group and non mechanical ventilation group. Specimens were obtained from lower respiratory tract by fibrobronchoscopy with protected specimen brush in patients of both groups to perform isolation, culture, identification and susceptibility test of pathogen. RESULT: Total 111 patients were enrolled, 36 of them in mechanical ventilation group and 75 patients in non mechanical ventilation group. The pathogenic bacteria detection rate of patients in mechanical ventilation group was significantly higher than that of patients in non mechanical ventilation group (88.9% vs. 46.7%, P < 0.01). In non mechanical ventilation group, Mycobacterium tuberculosis was detected in 3 patients, and 27 strains of G- bacilli, 3 strains of G+ coccus, and 2 strains of fungus; and 26 strains of G- bacilli, 3 strains of G+ coccus, and 3 strains of fungus were detected in mechanical ventilation group. There was no significant difference in term of strains between the two groups (P > 0.05). Rate of resistance to main antibiotics of patients in mechanical ventilation group was higher than that of patients in non mechanical ventilation group. CONCLUSION: Resistance of pathogenic bacteria isolated from lower respiratory tract was severe in coalminer's pneumoconiosis patients complicated with infection, which was higher in patients treated with mechanical ventilation than patients without mechanical ventilation. Mycobacterium tuberculosis and fungal infection and increasing resistance prompted that clinicians must attach importance to rational drug use and keep to monitoring bacterial resistance.