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.

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.

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 screen the optimal formula and preparation process of vitamin B1 ( VB1 ) sustained-release tablets. Methods:The single-factor tests were used to investigate the type of filler, type and amount of matrix material hydroxypropyl methycel-lulose(HPMC), type and amount of retarder, tablet weight and core hardness. The orthogonal tests were used to investigate the amount of HPMC and ethyl cellulose( EC) and the core hardness. Results:The optimum formula was as follows:HPMC accounted for 50% of the tablet weight, EC accounted for 20%, the filler was lactose, the tablet weight was 200 mg and the tablet core hardness was 50 N. Conclusion:The prepared sustained-release tablets have significant controlled-release property, which provides reference for the devel-opment of new dosage form for VB1 .

[Objective]To prove the feasibility of using the distance between sagittal plane of the spinal process and the enter point to individualize the placing of pedicle screw.[Method]Thirty spine specimen were collected and divided into two groups,data were measured,such as the width of the pedicle,distance between the enter point and anterior border of the vertebra,distance between sagittal plane of the spinal process and the enter point,angle from the longitudinal axis of the pedicle to sagittal axis of the vertebra,angle from the longitudinal axis of the pedicle to vertical line of the operating table.In group one the pedicle screws were placed with the help of the distance between sagittal plane of the spinal process and the enter point,the other by the method advised by Ebraheim.CT scan was applied to evaluate the place of the screws,according to the perforation extent,they were classified into 4 grades:A=totally in the pedicle;B=perforation extent4mm.[Result]The individualized group showed much lower perforation rate than the traditional method group in T3~10,and similar in T1,T2,T11,12.[Conclusion]It can obviously improve the accuracy of the pedicle screw placement to use the distance between sagittal plane of the spinal process and the enter point to localize the enter point,especially when anatomic landmark such as articulationes zygapophysiales and transverse process change.

Objective:To explore the effects of survivin antisense RNA on apoptosis in pancreatic cancer cell Panc-1.Methods:survivin antisense RNA was transferred into pancreatic cancer cell Panc-1 by lipofection.The opposite livability on Panc-1 cell line were assayed with MTT test.Expression of survivin detected by RT-PCR.Apoptosis was detected by DNA gel electrophoresis.Results:survivin antisense RNA obviously inhibited the Panc-1 cell growth(P

Objective To investigate the effect of lysostaphin on golden staphylococcal bacteria in vitro and on acestoma tissue.Methods Effects of lysostaphin on golden staphylococcal bacteria,Candida albicans and P.aeruginosa were detected by drug sensitivity test.Quantitative analysis of bacteria was used to detect the effect of lysostaphin on golden staphylococcal bacteria in 29 cases of 10%-30% TBSA.Results Most golden staphylococcal bacteria,as well as Candida albicans could be killed by lysostaphin.Lysostaphin had little effect on P.aeruginosa.Eighty-nine percent bacteria could be killed by lysostaphin after gauze with lysostaphin had been used for over 3 d,indicating lysostaphin may control bacteria quantity and improve survival rate of skin graft on granulation tissue.Gauze with lysostaphin contained biological enzymes and it had no systemic side effects.Conclusion Gauze with lysostaphin may be available on controlling golden staphylococcal bacteria as well as Candida albicans in burnt patients.Lysostaphin is effective in controlling residual trauma infected by golden staphylococcal bacteria.

Aim This study was designed to investigate the effects of pravastatin,a potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor,on vascular smooth muscle cells (VSMCs) proliferation and leukocyte-endothelial cell adhesion induced by lysophosphatidylcholine (LPC).Methods Cultured VSMCs from rabbit thoracic aorta were incubated with various concentrations of LPC in the absence or presence of different concentrations of pravastatin. MTT was used to evaluate the proliferation of VSMCs. We determined the effects of LPC and pravastatin on neutrophil K562 adhesion to endothelial cells ECV304 by directly counting non-adhesive K562 cells.Results Incubation of VSMCs with LPC (1～10 ?mol?L -1) stimulated proliferation of VSMCs in a time- and dose-dependent manner,while pravastatin (0.3～1 mmol?L -1) treatment prevented the proliferation of VSMCs caused by LPC. Moreover, incubation of ECV304 with 3 ?mol ? L -1 LPC for 12 h significantly enhanced K562 cells adhesion to endothelial cells, whereas pretreatment with pravastatin reduced leukocyte-endothelial cell adhesion. Conclusion These results suggest that pravastatin can antagonize the effects of VSMCs proliferation and leukocyte-endothelial cell adhesion induced by LPC.