[Clinicopathologic features of delayed radiation-induced brain injury after radiotherapy for brain tumor].

OBJECTIVE: To study the clinicopathologic features of delayed radiation-induced brain injury after radiotherapy for brain tumor. METHODS: The clinical, histopathologic and immunohistochemical features of 9 cases with delayed radiation-induced injury were evaluated. RESULTS: The disease occurred from 6 months to 12 years after radiotherapy and often presented with headache and muscle weakness. Magnetic resonance imaging showed peripheral enhancing lesions with slight mass effect and surrounding edema. Microscopically, the major changes included coagulative necrosis, fibrinoid necrosis of vessels, vascular hyalinization with luminal stenosis and peripheral reactive gliosis. Immunostaining for hypoxia-inducible factors 1α was positive in reactive astrocytes. CONCLUSIONS: Delayed radiation-induced brain injury is a relatively common complication of radiation therapy. The lesion was frequently misdiagnosed as brain tumor. Correct diagnosis relies on clinical, radiologic and pathologic correlation.

Effects of puerarin on receptor for advanced glycation end products in nephridial tissue of streptozotocin-induced diabetic rats.

To explore the effects of puerarin on mRNA expression of advanced glycation end products (AGE) specIfic cellular receptor (RAGE) in renal cortex of diabetic rats induced by streptozotocin (STZ). We induced Diabetic rats by an intraperitoneal injection of STZ in Sprague-Dawley (SD) rats. 30 male SD rats were randomly divided into 3 groups, diabetes adding puerarin group (DP group, n = 11, intraperitoneal injection of puerarin 100 mg/kg d), Diabetes group (D group, n = 11) and normal control group (C group, n = 8). The body weight (BW) and blood glucose (BG) were measured every 2 weeks. eight weeks later, all rats were sacrificed and the expression of RAGE mRNA was detected in renal cortex by reverse transcription-polymerase chain reaction (RT-PCR), respectively, and renal AGEs content was determined by fluorescence microscopy. Compared with those of control group, the BW and BG were lower in DP group and D group at 8th week (P < 0.01). RAGE/beta-actin ratio were 0.263 +/- 0.023, 0.435 +/- 0.010, 0.141 +/- 0.045, respectively, in DP group, D group and C group, and there was significant difference between every two groups (P < 0.01). The renal AGEs fluorescence intensity of DP group was weaker than D group, stronger than C group. Puerarin can protect the renal tissue from the impairment of hyperglycemia and AGE by decreasing AGEs contents and inhibiting of the expression of RAGE mRNA in the kidney.

[Amplification and specific expression of T-bet gene in nasal NK/T cell lymphoma].

OBJECTIVE: To investigate the specific genetic alterations in nasal NK/T cell lymphoma (N-NK/T-L) and the significance thereof. METHODS: Restriction landmark genomic scanning (RLGS) was performed on the specimen of a case of N-NK/T-L and the peripheral blood leukocytes of the same case. The RLGS image was analyzed with the Virtual genome scan (VGS) software so as to discover abnormality of T-bet gene. The discovered abnormal gene underwent cloning and preparation of probes. Southern blotting and dot blotting were performed on 3 cases of fresh N-NK/T-L tumor tissues and the genome of the case of peripheral blood lymphocytes. The expression of the T-bet (T-box expressed in T cell) gene in the tissue sections of 20 cases of N-NK/T-L, 17 cases of B cell lymphoma (BCL), 3 cases of normal spleen, and 5 cases of chronic nasopharyngitis was detected by in situ hybridization. RESULTS: RLGS combined with VGS revealed a genomic alteration in the T-bet gene and consequent Southern and dot blotting confirmed this genomic alteration in the N-NK/T-L cells. In situ hybridization showed that the T-bet mRNA expression rate of the N-NK/T-L cells was 90.0% (18/20), significantly higher than that of the BCL (11.8%, 2/17, P < 0.01). T-bet mRNA expression was not detected in the normal spleen and chronic nasopharyngitis tissues. CONCLUSION: The amplification and over-expression of the T-bet gene may play a role in the development of N-NK/T-L. The potential value of over-expression of T-bet gene in diagnosis of N-NK/T-L is worth further investigating.