Although the prevalence of Kashin-Beck disease (KBD) has decreased greatly since its discovery,the etiology and pathogenesis of the disease have always been one of the mysteries of the medical world.Facing the difficult situation in obtaining human samples of cartilage tissues and chondrocytes from such as KBD children,we should pay great attention to the spontaneous and induced animal models,and establish the disease model for KBD research using modern molecular biology techniques such as induced pluripotent stem cells,to reproduce the developing process of epiphyseal cartilage,growth plate cartilage and articular cartilage in KBD children,and to verify the high-risk environmental causing factors and specific biological mechanism of the cartilage necrosis and to develop targeted therapeutic drugs for KBD and to enhance the prevention and control levels of the disease.

Kashin-Beck disease(KBD) is an endemic and deforming osteochondropathy and its etiology remains unclear up to now.The prevalence of the disease is the severest in the western China and the effective methods for prevention and cure still need further study.This article summarized the progression and problems to be investigated for three main hypotheses of KBD by reviewing literature published at home and abroad.Integrating with his own research work and his team members,the author suggested that excessive apoptosis and dedifferentiation of chondrocytes besides classic chondrocytic necrosis in KBD growth plate and articular cartilage,differences of gene expression profiles in cartilage and peripheral blood mononuclear cells,proteomic markers and short tandem repeat polymorphism in KBD patients were significantly different from those of the healthy subjects from both KBD-areas and non KBD-areas,and those of osteoarthritis patients.The important objectives in the future are to understand ① the gene and proteomic markers for chondrocytic necrosis in KBD,② environmental factors that cause the damage to KBD chondrocytes,③ the way it selectively impairs chondrocytes in the deep zone of growth and joint cartilage by interacting with susceptible gene related to KBD,and ④ effective intervention methods.

Objective To review the progression of molecular biological mechanism on chondronecrosis in cartilage with Kashin-Beck disease (KBD) so as to promote the research work for pathogenesis of KBD. Methods The document analysis was used to compare the status quo of domestic and abroad research on KBD and osteoarthrosis. Results An aggregation in pedigrees with KBD was found, and an excessive chondrocyte apoptosis and de-differentiation was observed in cartilage from KBD patients except for chondronecrosis in deep zone. In contrast to osteoarthrosis, short tandem repeat, collagen gene in cartilage and gene chip were little known in KBD. Conclusion The pathogenesis of KBD should be further studied using modern biotechonology, such as short tandem repeat, cartilage collagen gene and gene chip.

BACKGROUND: This study investigated the effects of the intracoronary injection of nicorandil and tirofiban on myocardial perfusion and short-term prognosis in elderly patients with acute ST-segment elevation myocardial infarction (STEMI) after emergency percutaneous coronary intervention (PCI). METHODS: Seventy-eight STEMI patients with age >65 years who underwent emergency PCI were consecutively enrolled. These patients received conventional PCI and were randomly divided into a control group and a treatment group (n=39 per group). The control group received an intracoronary injection of tirofi ban followed by a maintenance infusion for 36 hours after surgery. The treatment group received intracoronary injection of tirofiban and nicorandil, and then intravenous infusion of tirofi ban and nicorandil 36 hours after surgery. The following parameters were measured: TIMI grade, corrected TIMI frame count (cTFC), TIMI myocardial perfusion grade (TMPG), STsegment resolution (STR) rate 2 hours post-operatively, resolution of ST-segment elevation (STR) at 2 hours postoperatively, peak level of serum CK-MB, left ventricular end diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) at 7–10 days postoperatively, and major adverse cardiac events (MACEs) in-hospital and within 30 days post-operatively. RESULTS: Compared with the control group, more patients in the treatment group had TIMI 3 and TMPG 3, and STR after PCI was significantly higher. The treatment group also had significantly lower cTFC, lower infarction relative artery (IRA), lower peak CK-MB, and no refl ow ratio after PCI. The treatment group had signifi cantly higher LVEDD and LVEF but lower incidence of MACEs than the control group. CONCLUSION: The intracoronary injection of nicorandil combined with tirofi ban can effectively improve myocardial reperfusion in elderly STEMI patients after emergency PCI and improve shortterm prognoses.

Objective: The occurrence characteristic of Kashin-Beck Disease (KBD) in pedigrees ascertained on the basis of one proband was estimated. Methods: A total of 255 individuals in 40 pedigrees were collected from areas in the Shaanxi Province. Results: (1) Parents and siblings of index cases have a 3-4 times higher risk than a randam unrelated individual. The odds ratio for disease is higher in mothers than in fathers of index cases; (2) Prevalence in relatives of index cases (Kr = 59.2%) greatly exceeds population prevalence (K = 17.5%); (3) Kr increases with sibship size; (4) There is no significant difference of Kr for male and female siblings of index cases. Also, population prevalence is not sex-specific. Conclusion: In conjunction with invironmental agents, genetics may play an important role in KBD etiology.

Objective To analyze the allele frequencies of 5 short tandem repeat(STR)loci(D12S313,D12S304,D12S1640,D12S1708 and D12S1583)on chromosome 12 among Kashin-Beck disease(KBD)patients and the control population living in the area suffered from KBD.Methods Fifty KBD patient8 and 50 non-KBD patients were chosen in endemic afea of Shaanxi Province,5 STR loci on chromosome 12 were genotyped by the technology of polymerase chain reacfion(PCR)and capillary electmphoresis.The pelymorphisms of STR in these popIllations were analyzed.The allele and genotype frequencies of each STR in the corresponding groups were caleulated and compared. Results In KBD group,the 5 STR loci had 8,6,7,5 and 11 types ofalleles and 17,11,15,8 and 28 genotypes, respectively;while in the control group,the number of aUele types of 5 STR loci were 6,8,6,4 and 10,the number of genotype of those loci were 13,21,14,8 and 23,respectively The allele frequence of D12S304 locus was statiBtically significant between KBD patients and controls(P<0.05),especially for the 319 bp allele(P<0.006 25). Conclusion There is an association between D12S304 locus and KBD.The 319 bp allele might play the key role.

Objective To survey the relationship between myocardial damage of chronic and latent Keshan disease with A360P missense mutation in desmin gene exon6. Methods By clinical epidemiology method,30 cases had been collected randomly among chronic Keshan disease patients and 30 cases equally among healthy adults (inner control groups) in Diantou town,Huangling county,Shaanxi province,a Keshan disease area,and 30 cases among health adults(outer control group) in Chang'an district,Xian city,a normal area. Genome DNA had been extracted from 90 blood samples. Different restriction sites had been analyzed by the methods of PCR,digested by restriction endonuclease and electrophoresis. By virtue of Bsp1286 Ⅰ enzyme,122 bp and 60 bp strap could be found in control group from exnn4,showing that Bsp1286 Ⅰ enzyme was active. By virtue of Bsp1286 Ⅰ enzyme,desmin gene exon6 was digested to 184 bp and 66 bp strip when A360P missense mutation site exited in exon6. Results One hundred and twenty two bp and 60 bp strap could be found in control group from exon4 digested by Bsp1286 Ⅰ ,which showed Bsp1286 Ⅰ enzyme was active. Two hundred and fifty bp strips can only be found in digest products of exon6. One hundred and eighty-four and 66 bp strips which were the products of DNA digested by Bsp1286 Ⅰ could not be found. A360P missense mutation site of desmin gene exon6 had not been found among chronic and latent Keshan disease patients and tow control groups in Keshan disease area and in normal area. Conclusions A360P missense mutation site of desmin gene exon6 has not been found among chronic and latent Keshan disease patients. A360P missense mutation of desmin gene exon6 probably is not predisposing genes of chronic Keshan disease.

Animals ; Antitussive Agents ; pharmacology ; Drug Evaluation, Preclinical ; methods ; Female ; Male ; Mice

Objective To investigate two techniques and outcome in repairing facial concave deficits.Methods Eleven patients with facial concave deformity were included in this study:nine were treated with autologous fat granule injection,1,3 and 5 patients were given fat granules injection fourth,twice and once,respectivly.The other 2 patients were repaired with homolateral temporal fascia flap.Results The implantation by using autologous fat granules in all 9 patients showed excellent results.Homolateral temporal fascia flaps were used in 2 cases,one of which was formed hematoma after operation and scavenged thereafter.All the patients had satisfactory results.Conclusion Both approaches well rehabilitate patients' facial contour,and thus are capable of repairing moderate or minimal facial concave deficit and worth recommendation.

The discovery of microRNAs (miRNAs) has introduced a new paradigm into gene regulatory systems. Since inception, computational methods have been an invaluable tool complementing experimental approaches, and many discoveries have been obtained through combination of experimental and computational approaches. The knowledge that has been accumulated about the principles of miRNAs and target recognition were reviewed. The currently available computational methodologies and software for prediction of miRNA and their target genes also have been discussed.