AIM: To study apoptosis and the involved genes in malignant transformation of gastric carcinoma. METHODS: Apoptotic cell and apoptotic regulating gene p53,bcl-2,c-myc were detected in 46 cases with gastric carcinomas, 20 cases with precancerous lesions and 24 cases with normal mucosa in situ using TdT-mediated dUTP-biotin nick end labeling (TUNEL) technique and immunohistochemical stain. RESULTS: Apoptotic index in precancerous lesion(intestinal metaplasia and dysplasia) and gastric carcinoma were significantly higher than that in normal mucosa( P

Purpose To investigate the relationship between Epstein-Barr virus (EBV) and lymphoepithelioma-like carcinoma (LELC) of the parotid gland and detect the gene expression products of EBV harbouring in LELC cells. Methods Thirty-two parotid LELCs were collected from the Departments of Pathology, Sun Yat-sen University of Medical Sciences, Guangzhou, China during the period of January 1986 and December 1995. All the 32 formalin-fixed paraffin-embedded blocks had been consecutively re-sectioned again. Immunohistochemical and in situ nucleic acid hybridization methods for detection of EBV gene encoded products were performed. Results (1) 32 LELCs were found out of 125 parotid gland carcinomas, the frequency was 25.6% (32/125). (2) All of the 32 specimens contained a variable number of EBNA-1 and EBERs positive neoplastic cells. (3) Twenty-seven out of 32 specimens (27/32, 84.4%) had a portion of carcinoma cells expressing LMP-1. (4) No ZEBRA positive cell could be found. (5) EA-D, VCA and MA positivity rates for these 32 parotid LELCs reached to 71.9%(23/32), 68.8%(22/32), and 12.5%(4/32), respectively. Conclusions (1) The parotid gland LELC is frequently to be seen in Guangzhou locale of China, where is a high-incidence area of nasopharyngeal carcinoma (NPC). The parotid gland LELC and NPC are co-prevalent in Guangzhou locale. (2) This disease is also consistently associated with EBV infection. (3) The EBV infection of the parotid gland LELCs is essentially the type of latency Ⅱ, expressing EBNA-1, EBERs and LMP-1. (4) The latent infected EBV harbouring in LELC cells could in part be switched over to lytic cycle, producing EA-D, VCA or/and MA.

AIM: To investigate the distribution and clonal expansion of TCR V? subfamily T cells in patients with acute monoblastic leukemia (M5). METHODS:The CDR3 of TCR V? 24 subfamily genes were amplified in peripheral blood mononuclear cells from 9 cases with M5 using RT-PCR and the PCR products were further labeled with fluorescent and analyzed by genescan technique for the CDR3 size, to evaluate clonality of the detectable TCR V? T cells. RESULTS:Only 1-10 V? subfamily T cells were identified in M5 cases. Genescan analysis showed that oligoclonal (clonal expansion) T cells were found in some V? subfamilies from 8 cases with M5, V? 2 oligoclonal T cells were identified in six cases, whereas V? 7- or V? 9 clonal expansion T cells were detected in the other two cases, respectively. In addition, except V? 2, V? 7 or V? 21 oligoclonal T cells could be detected in two cases, respectively. CONCLUSION:The skew distribution and clonal expansion of TCR V? subfamily T cells could be found in patients with M5. It may be a specific anti-leukemia immune response with which the host T cells were activated by the leukemia-associated-antigen. The clonal expansion T cells were tendentious in V? 2, which may be related to the M5 leukemia cells associated antigen.

Objective To investigate the protective effects on the renal allografts from brain dead (BD) donor rats pretreated with bone marrow mesenchymal stem cells (MSCs).Method Three groups [normal transplant group (G1).BD transplant group (G2),and MSCs pretreated + BD transplant group (G3)] were set up.Male F344 rats served as donors and male Lewis rats as recipients.In G1,kidneys from F344 donor rats were implanted into Lewis recipients.In G2,kidneys from F344 BD donor rats were engrafted into Lewis recipients.In G3,after BD was established in F344 rats,MSCs were given intravenously to the rats.The kidneys harvested 6 h later were transplanted to Lewis recipients.Cyclosporine was intromuscularly given daily to the recipient rats for 10 days.Right kidneys were resected from recipients on day 10.Creatinine level was examined on day 14,21,28,and 35.Renal allografts harvested on day 35 were pathologically detected.The irnmunochemistry expression of interleukin (IL)-1β and tumor necrotic factor (TNF)-α in renal allograft tissue was tested.Result Serum creatinine levels in G2 were remarkably higher than those in G1 and G3 (P＜0.01) on day 14,21,28,and 35 postoperatively.The creatinine levels on the above mentioned time points had no statistically significant difference between G3 and G1 except on day 21.Postoperative pathological changes in G2 of both pronounced infiltration of mononuclear cells and tubular epithelia[inflammation were notably increased in renal allografts as compared with those in G1 and G3.There was no obvious difference between G1 and G3 in infiltrated mononuclear cells and tubular epithelial inflammation.Positive expression levels of both IL-1β and TNF-α in glomerular,tubular and interstitial epithelial cells were statistically enhanced in G2 as compared with those in G1 and G3 (H =7.210,P =0.027),while there was no statistically significant difference in the expression of both IL-1[β and TNF-α between G1 and G3.Conclusion Brain dead donor rats pretreated with bone marrow MSCs might reduce renal allograft injury via decreasing both inflammatory cell infiltration and IL-1β and TNF-α expression.