Background and purpose. Gastric stromal tumor (GST) is the most common mesenchymal tumor of the gastrointestinal tract and most often arises in the stomach. In the past, surgery was the only effective treatment. The diagnosis and treatment of GST has been revolutionized over the past, since expression of the receptor tyrosine kinase KIT (CD117) was shown to occur on these tumors, the outcome of GST treatment has dramatically been improved. This study focused on the therapeutic experience of GST and analyzed the pathological features and prognostic factors of GST in our center. Methods: All the 26 cases underwent surgical resection and three of them were treated over 6 months with imatinib 400 mg/d. The clinical pathological and follow-up data of 26 patients with GST admitted in our hospital between Jan. 2000 and Dec. 2008 were analyzed retrospectively. Results. All the cases underwent curative resections, including palliative liver resection in 3 patients with liver metastasis. Recurrence occured on 6 patients, including 1 case with low risk group, 1 case with intermediate risk group, 4 cases with high risk group. Tumor size ranged from 2 to 15 cm with the mean of 5.5 cm. The immunohistochemistry results revealed that the positive rates of CD117, CD34 and Vimentin were 92.3%, 80.8% and 96.2% respectively. After operation, three patients accepted imatinib mesylate therapy over 6 months. Two of them were alive, but one had liver metastasis. The follow-up period ranged from 4 to 36 months (median: 28 months). Four cases were lost. The 1-, 3-year overall survival rates of 26 cases were 96.2% and 84.6%. Conclusion: Tumor size, location, mitosis and immunohistochemical data are important variables to evaluate GST behavior and prognosis. Surgical resection is the main therapy for GST and targeted therapy will improve the prognosis.

Objective:To investigate the expression characteristics of high mobility group box 1 protein (HMGB1) in rat models of deafferentation pain induced by posterior root injury of spinal nerves, and its relation with neuroinflammation.Methods:Sixty SD rats were divided into a blank control group ( n=10) and a model group ( n=50) according to random number table method. Neuropathic pain rat models in the model group were established by cutting the posterior root of C 5-T 1 spinal nerve, while rats in the control group were performed the same operation without cutting the posterior root of C 5-T 1 spinal nerve. Three, 7, 10, 14, and 21 d after modeling, behavioral changes, including spontaneous pain scale scores, mechanical antagonistic pain threshold, and autophagy scale scores, were evaluated in the two groups of rats. Immunohistochemical staining was used to detect the HMGB1, ionized calcium binding adapter molecule 1 (IBA-1) and phosphorylated nuclear factor κB (pNF-κB) positive cells in the spinal cord of the two groups. Western blotting was used to detect the protein expressions of HMGB1, toll-like receptor (TLR)2 and pNF-κB in the spinal cord of the two groups. Results:(1) The scores of spontaneous pain scale and autophagy scale 14 and 21 d after modeling were significantly higher than those 3, 7 and 10 d after modeling ( P<0.05), and those 21 d after modeling were significantly higher than those 14 d after modeling ( P<0.05). (2) Immunohistochemical staining showed that HMGB1, IBA-1 and pNF-κB all expressed in the spinal cord tissues of rats in the model group 3 d after modeling, and the number of positive cells in the dorsal horn of the spinal cord on the injured side became larger with prolongation of exposure time, and that was obviously larger as compared with that on the opposite side; in the spinal cord tissues of the blank control group, the number of positive cells in the spinal dorsal horn area was small, and there was no significant difference in the number of positive cells in the spinal dorsal horn area on both sides. (3) Western blotting showed that, as compared with those in the blank control group, HMGB1, TLR2 and pNF-κB protein expressions in the spinal cord tissues of the model group were significantly increased 3, 7, 10, 14 and 21 d after modeling ( P<0.05), and which showed an increasing trend with prolongation of exposure time. Conclusion:The gradual increase in HMGB1 expression in the local spinal cord of rats with deafferentation pain leads to HMGB1/TLR2/NF-κB pathway high expression and activation of microglia cells, which induces the occurrence of local neuroinflammation in the spinal cord and eventually results in pain behavioral changes.