Objective To dynamically monitor the humoral immune parameters in the blood and cerebrospinal fluid and analyze the relationship between immunity and disease development and recovery after brain injury to explore the clinical effect of naloxone combined with mild hypothermia on the treatment of brain injury.Methods One hundred patients with severe craniocerebral injury admitted to our hospital from January 2008 to December 2008,were prospectively studied and equally divided into treatment group and control group.The control group was given conventional therapy,while the treatment group was given naloxone combined with mild hypothermia besides conventional therapy.We detected the changes of the contents of IgG,IgA,IgM,complement c3 and albumin in the blood and cerebrospinal fluid on the 4th,14th,and 21st d of injury.Then we compared the differences between the humoral immune parameters and both the clinical infection rates and the disability grades in the 2 groups.Results No statistical significance in the immune indexes of blood and the IgM content of cerebrospinal fluid was found between the control group and the treatment group (P>0.05),while statistical significances in the changes of the contents of IgG,IgA,IgM and albumin in the cerebrospinal fluid,the clinical infection rates and the disability grades were found between the 2 groups (P<0.05).The positive rate of complement c3 in the cerebrospinal fluid was statistically significant between the 2 groups on the 4th d of injury (P<0.05).Conclusion Naloxone combined with mild hypothermia has definite curative effect and no obvious adverse reaction in treating patients with craniocerebral injury,may resulting from the humoral regulation of naloxone.
Key words:
Craniocerebral injury; Monitoring,immunologic; Naloxone; Pharmacotherapy
MicroRNA (miR)‑27b has been reported to participate in glioma. However, a detailed role of miR‑27b and the underlying mechanism remain largely unknown. The present study found that the expression of miR‑27b was significantly increased in glioma tissues compared with normal adjacent tissues. In addition, miR‑27b was also upregulated in the U87, U251 and SHG44 glioma cell lines compared with normal human astrocytes. Sprouty homolog 2 (Spry2), which has been reported to be associated with invasive glioma, was identified as a novel target of miR‑27b in U251 glioma cells, and the protein expression of Spry2 was negatively regulated by miR‑27b in U251 cells. Additionally, inhibition of miR‑27b and upregulation of Spry2 suppressed glioma cell invasion, while downregulation of Spry2 reversed the suppressive effect of miR‑27b inhibition on glioma cell invasion. These data suggest that miR‑27b may promote glioma cell invasion through direct inhibition of Spry2 expression. The data also suggest that miR‑27b may become a promising molecular target for inhibiting the invasion and metastasis of glioma.
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