目的 探索甲状旁腺激素相关肽（PTH rP）在大骨节病儿童及成人关节软骨中的表达及分布。方法 应用免疫组化方法比较正常儿童和成人与大骨节病儿童和成人关节软骨中PTH rP的表达。结果 ①大骨节病儿童关节软骨表层、中层、深层PTH rP阳性细胞表达率分别为30%、24% 和31%，中层、深层表达率比正常儿童明显增高（P<0.01）；②大骨节病成人关节软骨表、中、深层PTH rP阳性细胞表达率分别为54%、46% 和16%，各层细胞阳性表达率均明显高于正常组（P<0.01）。③大骨节病儿童与成人比较各层软骨细胞PTH rP的阳性表达差异均有显著意义（P<0.01），表现为表、中层成人高于儿童，深层儿童高于成人。结论 大骨节病患者关节软骨中PTH rP阳性表达率高于正常对照。

Objective To analyze the genetic polymorphism of 6 STR loci (D12S358, D12S1675, D12S1663, D12S1697, D12S1725 and D12S1613) on chromosome 12 in Chinese Han population. Methods EDTA-blood specimens were collected from 153 unrelated individuals of Chinese Han population in Shaanxi province. Allele and genotype frequencies for the 6 STR loci were estimated and statistical parameters of polymorphism were calculated. Re sults 8 alleles and 18 genotypes, 10 alleles and 17 genotypes, 9 alleles and 15 genotypes, 12alleles and 29 genotypes, 12 alleles and 31 genotypes, 8 alleles and 11 genotypes were observed at D12S358, D12S1675, D12S1663, D12S1697, D12S1725 and D12S1613, respectively. No deviations of the observed allele frequency from Hardy-weinberg equilibrium expectations were found for any of these loci. The Heterozygotes of these 6 loci were 78.89%, 66.10%, 54.95%, 79.10%, 71.98% and 59.48%, respectively. It indicated the high genetic polymorphism of the loci in Chinese Han population. Conclusion The 6 STR loci belonged to the genetic marker system of high discriminutesation and high information in Chinese Han population and can be used in the study of gene-related diseases.

Objective According to the distr ibution of low selenium areas, low nutrition state of the residents and the affecting cartilage growth and articular cartilage of Kashin-Beck Disease (KBD), the chondrocyte differen tiation and differential expression of collagen types i, II and X in articular cartilage from Chinese mini-pigs treated with low selenium were investigated in order to gain in sight in to the effects of these condition son chondrocyte differen tiation in KBD cartilage. Me thods Eleven male juvenile mini-pigs, aged from 4 weeks to 6 weeks after birth, were divided in to 3 groups. The Secontent in the diet of the "low Se" group was 0.035mg/kg diet, and 0.175mg/kg diet in the control. For Se-supplemented group 0.390mg Na2SeO3/kg diet was added. The con tent of Sein blood was assayed at the beginning and at the end of each experiment. Samples of articular cartilage were taken from the right femur condylus, and collagen types I, II and "in articular cartilage were analyzed by immunohistochem istry and in situ hybridization. Results ①All cartilage samples from juven ilem in i-pigs fed with low selenium dietrevealed areduction in type "collagen mRNA expression in the hypertrophic chondrocytes as shown by in situ hybridization, and reduced type "collagen depos ition in the lower hypertrophic zone as shown by immunohistochem istry. ②Addition of selenium to the dietrestored the type" collagen to normal level. ③Type collagen was evenly distr ibuted over the entire articular cartilage in all experimental and controlgroups. Type collagen mRNA signals weremost prominent in the upper articular layer as well as in the hypertrophic zone in all groups. Type collagen express ion was restricted to the zone of endochondraloss if ication in all experimental groups and the control. Conclusion　Low selen ium has an down-regulatoryrole on the syn thes is and deposition of collagen type "in hypertrophic chondrocytes in articular cartilage of mini-pigs. Supplement of the low Sediet with additional Serestored the signals of collagen type" to normal levels. These findings indicate that selenium deficiency may disturb chondrocyte differen tiation to hypertrophic cells in the growth plate, and worthy to be investigated further.

The relation ship of cause-result between low selen ium (Se) and Kashin-Beck disease (KBD) was probed by the prospective study of epidemiolog icalmethod with regarding low-Se as an exposure factor in this paper. 597 healthy children l ived in KBD areas with low, middle and high prevalence were divided in to the low-Se exposed group and the non-low-Se exposed group according to their Secontent in hair. The low-Se exposed group was divided in to three subgroups, such as Secontent in hair ≤ 110ng/g, 110ng/g<Secontent in hair≤150ng/g and 150ng/g<Secontent in hair ≤ 200ng/g, respectively. Six new cases of the total with KBD (incidence was 01574% person-year) were found in the low-Se exposed group during three years period of the investigation. No new case was found in the non low-Se exposed group. KBD incidence was notsign if icantly different between those two groups. Two new cases were found in children with Secontent in hair keptbelow 110ng/g during three years (inc idence: 1121% person-year). SMR in each group indicated that the new cases observed in the low-Se exposed group was remarkable lower than the new cases expected. It was not observed that the dose-respon serelation ship between low-Se and KBD, and was not supported that the low-Se was a predominant factor to cause KBD.

The purpose of the current study was to investigate the abnormal expression of Col X, PTHrP, TGF-β, bFGF, and VEGF in cartilage from patients with Kashin-Beck disease (KBD) to understand the pathogenesis of chondronecrosis in KBD. Articular cartilage and growth plate cartilage collected were divided into four groups: control children (8 samples, 5 cases), KBD children (19 samples, 9 cases), control adults (8 samples, 6 cases), and KBD adults (16 samples, 15 cases). The presence of PTHrP, TGF-β1, bFGF, VEGF, and collagen X in articular cartilage and in growth plate cartilage was analyzed by immunohistochemistry. Articular cartilage and growth plate were each divided in three zones, and the rate of positive cells was counted by light microscope for cytoplasmic and pericellular staining. Results showed that (1) in KBD children, Col X expression was lower in the deep zone of growth plate cartilage than in normal children; in articular cartilage of KBD adults, however, collagen X expression was higher in the middle zone compared to the controls; (2) staining for bFGF, PTHrP, TGF-β1, and VEGF in KBD adult patients was prominent in the chondrocyte clusters and the eroded surface of articular cartilage, and the percentage of chondrocyte staining was significantly higher than in control samples (t=3.64-10.34, df=12 for children and 19 for adults, P=0.002-0.0001); and (3) the enhanced PTHrP, TGF-β1, and VEGF staining in the deep and middle zone of KBD articular cartilage correlated with the high incidence of chondronecrosis in the middle zone (48.5% ± 10.2%) and deep zone (70.6%±27.0%) of adult KBD cartilage. In conclusion, Col X expression was reduced in areas of chondrocyte necrosis in the deep zone of KBD articular cartilage, indicating changes in terminal chondrocyte differentiation. PTHrP, TGF-β1, and VEGF expression was significantly altered and indicated degenerative changes in KBD cartilage, which initially resemble those occurring in osteoarthritis, but lead eventually to chondronecrosis, an event not observed in osteoarthritis.