OBJECTIVE:To investigate clinical efficacy of cerebroventricular perfusion and intrathecal perfusion of vancomy-cin assisting with continuous drainage in the treatment of intracranial infection secondary to traumatic brain injury,and its effects on cerebrospinal fluid indexes and intracranial pressure. METHODS:One hundred and eighty patients with intracranial infection secondary to traumatic brain injury selected from Sanya Hospital of TCM during Jan. 2012 to Jun. 2015 were randomly divided into control group and observation group according to lottery,with 90 cases in each group. They were given cerebroventricular perfu-sion and intrathecal perfusion of vancomycin(20 mg dissolved in 5 mL normal saline)in cella lateralis and lumbar cisterna respec-tively combined with continuous drainage,q12 h. Both groups received treatment for 7 d.Clinical efficacy,the time of infection con-trol were compared between 2 groups as well as body temperature,intracranial pressure and cerebrospinal fluid indexes before and after treatment,and the occurrence of ADR. RESULTS:After treatment,total response rate of observation group (95.56%) was significantly higher than that of control group (77.78%),with statistical significance (P<0.05). The time of infection control in observation group [(9.67 ± 1.10)d] was significantly shorter than in control group [(11.84 ± 1.29)d],with statistical significance (P<0.05). Body temperature,intracranial pressure,cerebrospinal fluid protein and leukocyte of 2 groups were significantly lower than before treatment;cerebrospinal fluid glucose level was increased significantly compared to before treatment;above indexes of observation group were significantly better than those of control group,with statistical significance(P<0.05).There was no statisti-cal significance in the incidence of ADR between 2 groups(P>0.05). CONCLUSIONS:The intrathecal perfusion of vancomycin as-sisting with continuous drainage in the treatment of intracranial infection secondary to traumatic brain injury can effectively speed up the rehabilitation process,reduce the body temperature and intracranial pressure,and is helpful to improve the relevant cerebro-spinal fluid indexes. Therapeutic efficacy of it is better than that of cerebroventricular perfusion.

Dysfunction of the Hippo pathway enables cells to evade contact inhibition and provides advantages for cancerous overgrowth. However, for a significant portion of human cancer, how Hippo signaling is perturbed remains unknown. To answer this question, we performed a genome-wide screening for genes that affect the Hippo pathway in Drosophila and cross-referenced the hit genes with human cancer genome. In our screen, Prosap was identified as a novel regulator of the Hippo pathway that potently affects tissue growth. Interestingly, a mammalian homolog of Prosap, SHANK2, is the most frequently amplified gene on 11q13, a major tumor amplicon in human cancer. Gene amplification profile in this 11q13 amplicon clearly indicates selective pressure for SHANK2 amplification. More importantly, across the human cancer genome, SHANK2 is the most frequently amplified gene that is not located within the Myc amplicon. Further studies in multiple human cell lines confirmed that SHANK2 overexpression causes deregulation of Hippo signaling through competitive binding for a LATS1 activator, and as a potential oncogene, SHANK2 promotes cellular transformation and tumor formation in vivo. In cancer cell lines with deregulated Hippo pathway, depletion of SHANK2 restores Hippo signaling and ceases cellular proliferation. Taken together, these results suggest that SHANK2 is an evolutionarily conserved Hippo pathway regulator, commonly amplified in human cancer and potently promotes cancer. Our study for the first time illustrated oncogenic function of SHANK2, one of the most frequently amplified gene in human cancer. Furthermore, given that in normal adult tissues, SHANK2's expression is largely restricted to the nervous system, SHANK2 may represent an interesting target for anticancer therapy.