To investigate the common mutation patterns of hereditary nonpolyposis colorectal cancer(HNPCC) genes.MethodsUsing PCR-agarose electrophoresis and PCR-SSCP to screen the hMSH2, hMLH1 genes mutation of 9 HNPCC patients and 4 family members. ResultsAbnormal shifting of PCR productions was identified in 7 patients and 2 HNPCC family members out of 9 different families. ConclusionPCR-agarose and PCR-SSCP are simple, rapid , sensitive, economic and specific methods that can be used to detect HNPCC gene hMSH2, hMLH1 mutations.

To study the clinical application of molecular diagnosis in cutaneous T-cell lymphoma (CTCL),the polymerase chain reaction Was used to detect the rearrangements of T-cell receptor (TCR)gene in 60 patients with cutaneous lymphocytic infiltrates.The result showed that dominant clonal TCR-? or ? gene rearrangements were detected in 36/40 CTCL,4/6 suspected mycosis fun- goldes/S?zary syndrome,1/1 lymphomatoid papulosis.No dominant clonal TCR-? or ? gene rearrange- ments were detected in 2 patients with CBCL,1 patient with lymphocytoma cutis,8 patient with benign lymphocytic infiltrates of skin and 2 normal controls.This study demonstrates that the method is help- ful for the lineage determination,clonality and early diagnosis of CTCL.

Objective: To investigate the expression of co-stimulatory molecule CD86 and inducible costimulator(ICOS) in the intestinal mucosa of Crohn disease (CD) and to exlpore its pathologic significance. Methods: Expression of co-stimulator CD86 and ICOS was examined by immunohistoehemistry on paraffin embedded tissue from patients with CD (30 cases) and normal controls (20 cases). The subsets of lamina propria mononuclear cells (LPMC) were also analysed via immunostaining for CD4, CD8 and CD20. Results: Increased amount of CD86 or ICOS positive LPMC was observed in the lesional area of CD when compared with the essentially normal area of CD and normal controls (q = 9. 23 ,P ＜0. 01 and q =5. 46 ,P＜0. 01). In addition, the expression of CD86 or ICOS was higher in intestinal epithelium of CD than that in normal controls (H = 24. 93, P＜0. 01 and H = 4. 66, P＜0. 01 ) , whereas no significant difference was seen between the diseased and the essentially normal area of CD. The amount of CD4 or CD8 positive lymphocytes in lamina propria, epithelium and small vascular walls was also significantly increased in CD than that in normal controls (P＜0. 05 or P＜0. 01). Conclusion: Increased amount of CD86 or ICOS positive LPMC and enterocytes in CD suggests that co-stimulatory molecules may play a role in the pathogenesis of CD. The enterocytes may act as non-specific antigen presenting cells in the process of cellular immunity activation in CD.

Ojective To study the pathological changes of testis tissue in SARS patients.Methods Tissue specimens were studied by HE staining、TUNEL and immunohistochemistry(IHC).Results SARS patients showed that widespead germ cells destruction,few or no spermatozoon in the seminiferous epithelium and the lumen,thickened basement membrane、 peritubular fibrosis、 vascular congestion and leukocytes infiltration.The apoptotic seminiferous cells increased significantly(P

AIM: In order to explore the pathogenesis of ulcerative colitis (UC), an experimental colitis in mouse was induced by the hapten dinitrochlorobenzene (DNCB), and the activity of leukocyte migration inhibitory factor (LMIF) was measured at the same time. METHODS: 67 BALB/c mice were randomly divided into control (60% ethanol) and DNCB groups. After they were sensitized by smearing 3.3% DNCB on the abdominal skin, they were challenged with DNCB at concentration of 0.1%, 0.2% and 0.4% respectively by instillation once a day. The weight, stool viscosity and hematochezia were observed and accumulated as disease active index (DAI) score. The pathological changes in colon tissue were judged macropathologically and by means of microscope. LMIF activity was determined by the absorbance (A) of migrated leukocytes. RESULTS: Compared to control group, the increases in DAI accumulate score, pathologic score, and LMIF activity in DNCB groups were observed. CONCLUSION: Mouse colitis was induced by DNCB, which was accompanied by an increase in LMIF activity. [