Polymorphism of the (CCTTT)n repeat, a short tandem repeats (STR) located in promoter region of the inducible nitric oxide synthase (iNOS) gene, was analyzed in a total of 316 Chinese healthy subjects. Twelve alleles and forty-nine genotypes were identified. Three alleles that had not been reported previously, namely 17-repeats, 18-repeats and 19-repeats, were found in Chinese population. Mendelian inheritance of the allele in a family composed of three generations was determined. Some of the observed allele frequency of this STR locus in Chinese differed significantly from that of Caucasians in England.

Objective： To investigate the in vivo inhibitory role ofoncostatin M on the melanoma growth as well as the potential application of OSM in the gene-radiotherapy for melanoma. Methods： The OSM expression vector (pO) and the OSM radiation-inducible expression vector (pEO), in which the regulatory sequence of Egr-1 gene (Egr-1R) was linked upstream to OSM cDNA, were used to transfect mouse B16 melanoma cells, respectively. OSM secreting cells (pO-17 and pEO-1) selected and then inoculated substaneously into C57BL/6 mice. A comparison of tumor weight after cells inoculation and an investigation on inhibition rate of tumors after treatment with localized 60Co γ-ray irradiation were taken. Results： The in vivo tumor weight of pO-17 and pEO-1 cells was drastically reduced compared to either B16 or pCI-neo-transfected cells in the same period of twenty days after cells inoculation. It was further observed that pEO-1 cells, but not pO-17, demonstrated an increase of 42.4% in the inhibition rate of tumor when tumors were treated with 20Gy of 60Co γ-ray irradiation twice. Conclusion： The in vivo growth of melanoma could be controlled by OSM secreted from OSM gene-modified cells. The activated Egr-1R by radiation could enhance the expression of OSM and thereby impose an aggravated damage on tumors in vivo, namely brining a dual inhibitory effect of gene and radiation on tumors.

To establish a method for quantitative assessment of mixed hematopoietic chimerism by competitive polymerase chain reaction after nonmyeloablative allogeneic stem cell transplantation　(NAST) using highly polymorphic short tandem repeats (STRs). The feasibility of this assay and the accuracy of quantitative results were tested using serial DNA mixtures of unrelated individuals. 2　patients receiving NAST were analyzed by this method. Chromosome　was analyzed simultaneously. The results showed a linear correlation between the DNA added and the proportion found. Comparison of values obtained with chromosome　analysis showed an excellent correlation with the STR-PCR results. Taken together, this novel approach allows a rapid, sensitive, versatile, less blood , even with minuscule numbers of cells,and also sex unlimited.

The study was done to study was done to investigate the inhibitory role of oncostatin M (OSM) on the melanoma growth as well as the potential application of OSM in the gene-radiotherapy for melanoma in vivo. The human OSM cDNA was inserted into the EcoR I-Xba I site of the vector pCI-neo to form the OSM expression vector (pO). The radiation-inducible OSM expression vector (pEO) was constructed by substituting the CMV promoter in pCI-neo with the regulatory sequence of Egr-1 gene (Egr-1R). The constructs pO and pEO were transfected into mouse B-16 melanoma cells, respectively, and then the OSM secreting cells (pO17 and pEO-1) were selected by anti-h OSM antibldy. An investigation on the tumor weight and comparisons of the inhibition rates between irradiated and non-irradiated tumors were taken. Results showed that the in vivo tumor weights of pO17 and pEO-1 cells were drastically reduced compared to either B-16 or B-neo cells as controls in the same period of twenty days after cells had been inoculated subcustaneously into C57BL/6 mice. It was further observed that for pEO-1 cells, but not for pO-17, there was an increase of 42.3% in the inhibition rate of tumor when tumors were treated with 20Gy of \+\{60\}Co γ ray radiation. Firstly, the in vivo growth of tumor could be controlled by OSM secreted from OSM gene-modified cells. Secondarily Egr-1R sequence linked upstream to OSM gene could be activated by irradiation and enhance the expression of OSM, and thereby impose an aggravated damage on tumors in vivo , i.e. a gene-radiotherapy effect.

By using a 672 bp length catalase gene fragment as probe which had been amplified from D. radiodurans genome DNA by degenerate primers PCR reaction and bioimformatical analysis, two complete coding sequences of the catalase were determined from the database of D. radiodurans genome, which were then designated as kat A and kat B gene. The kat A and kat B gene were 2 277 bp and 1 611 bp long, encoding 758 and 536 amino acids, respectively. The kat B gene was cloned into pKK223-3 expressing vector and transformed into the E. coli UM2, a catalase-deficient mutant. Staining of non-denatured PAGE for catalase activity demonstrated that kat B gene inserted into pKK223-3 encoded a catalase that co-migrated with the CatB found in D. radiodurans cell lysates. It was also observed that expression of kat B gene in E. coli UM2 could restore the resistance to H2O2 at low concentration. Fig 4, Ref 10