Objective To study the relationship between pathological, immunohistochemical and ultrastructural changes of skeletal myodystrophy (SMD) and the development of the disease.Methods SMD tissue of 20 cases were routinely processed,the paraffin sections,the semi thin sections and the ultrasthin sections were observed by light microscopy and electron microscopy.Results 20 cases with SMD tissue were divided into three groups: Simple SMD for 8 cases, major changes were regional; Progressive SMD for 10 ca ses, the pathological changes were diffuse with large amount of degeneration of cell organs; SMD derived from nerve injury for 2 cases, pathological changes of the part controlled by the nerve were observed. While SMD was injured, myosin got deneration first.Conclusion The pathological and ultrastructure changes could be used to judge the progressive degree of myodystrophin. The amount of lost myosin could forecast the progression of the disease.

AIM: To study the effect of the overexpression of p16 on an anion exchange function of band 3 in HeLa cells. METHODS: The expression of p16 and band 3 in HeLa cells was detected by immunohistochemistry (IHC). The p16 cDNA was subcloned to plasmids pEGFP-C1 by PCR and identified by restriction enzyme digestion and sequencing, and then, the recombinant pEGFP-C1-p16 plasmids were transiently transfected into HeLa cells. The expression of fusion protein in HeLa cells was detected by fluorescence microscope. 6-methoxy-N-(3-sulfopropyl)-quinolinium(SPQ)fluorescent probes were used to detect the anion exchange function of band 3. RESULTS: P16 and band 3 were expressed in HeLa cells. The amplificated p16 cDNA sequence was the same as the report sequence. The transfective efficacy of pEGFP-C1-p16 was above 60%. The anion exchange function increased after the transfection of pEGFP-C1-p16 plasmids. CONCLUSION: p16 facilitates the anion exchange function of band 3 in HeLa cells.