1.Relationship between N-acetyltransferase-2 alleles polymorphism and type 2 diabetes mellitus
Chinese Journal of Postgraduates of Medicine 2012;(31):14-17
Objective To explore the relationship between N-acetyltransferase-2(NAT2)alleles polymorphism and type 2 diabetes mellitus(T2DM).Methods Polymerase chain reaction and sequence determination technique were used to identify NAT2 alleles in 174 patients with T2DM(T2DM group)and 174 unrelated healthy individuals(control group).Results Compared with control group,the allelic frequency of NAT2 mutation was no significant difference in T21DM group(x2=7.38,P>0.05).The frequencies of the NAT2 genotypes(Wt/Wt,Wt/M1,Wt/M2,Wt/M3,M1/M1,M1/M2,M1/M3,M2/M2,M2/M3,M3/M3)were 39.08%(68/174),3.45%(6/174),22.99%(40/174),14.94%(26/174),0.57%(1/174),2.30%(4/174),1.15%(2/174),4.60%(8/174),9.20%(16/174),1.72%(3/174)and 44.83%(78/174),2.60%(8/174),27.59%(48/174),17.24%(30/174),0.57%(1/174),0.57%(1/174),0.57%(1/174),1.15%(21174),2.30%(4/174),0.57%(1/174)respectively,and significant differences showed between T2DM group and control group(x2=13.92,P<0.01).The proportion of fast acetylate in T2DM group was significantly higher than that in control group[94.25%(164/174)vs.80.46%(140/174)],and the propoaion of slow acetylate in T2DM group was significantly lower than that in control group[5.75%(10/174)vs.19.54%(34/174)](P<0.05),The risk of T2DM in people who were fast acetylate had 3.98 times(95% CI:1.90-8.35)more than that in people who were slow acetylate.Conclusion It shows that the fast acetylate may be one of the genetic factors that influencing the susceptibility to T2DM,and slow acetylate may be one of the protecting factors.
2.Progress in surgical treatment of unstable sacral fractures
Chinese Journal of Orthopaedic Trauma 2017;19(2):180-184
Treatment of sacral fractures,unstable ones in particular,has attracted more and more attention.Despite numerous classification systems for sacral fractures,the commonly used ones are Denis and Tile classifications.Stable sacral fractures deserve conservative treatment,but unstable ones should be treated surgically,by operative reduction,internal fixation to reconstruct stability of the pelvis,and prevention or relief of nerve compression.There are many methods of internal fixation for unstable sacral fractures,and each has its own advantages and disadvantages.This review summarizes the progress in surgical treatment of unstable sacral fractures and makes comments on the latest surgical strategies.
3.Effect of hypoxia on chemotaxis of rat polymorphonuclear leukocytes
Chinese Journal of Pathophysiology 1986;0(03):-
AIM: To explore the effect of acute and chronic hypoxia on the chemotaxis of polymorphonuclear leukocytes(PMNs) of rats.METHODS: Serum and PMNs were separated from rats under normoxia, acute hypoxia and chronic hypoxia condition,and cell aspiration technology system was used to determine the chemotactic migration of pseudopod of PMNs induced by serum as chemotactic factor.RESULTS: Induced by autoserum,the length of pseudopod of PMNs migrated into micropipette [(1.200?0.178)?m,(1.094?0.164)?m ]under acute hypoxic and chronic hypoxic condition was significantly longer than the corresponding value for control[(0.914?0.156)?m,P
4.Mechanism of sodium selenite-mediated death of human colon cancer HCT116 cell line
Gang ZHENG ; Zhaoxia GAO ; Haibin SONG
Chinese Journal of Postgraduates of Medicine 2013;36(z1):1-3
Objective To investigate the inhibition mechanism of sodium selenite on HCT116 cells.Methods In the present study,we explored the cytotoxicity induced by sodium selenite and the underlying mechanism by MTS assay,WesternBlot,and small RNA interference technique.Results It was found that the sodium selenite at 5uM concentration could indeed reduce the viability of colon cancer cell line HCT116 by a large margin through increasing the generation of reactive oxygen species (ROS),and that the increased levels of ROS could activate c-Jun Nh2-terninal kinase 1 (JNK1).Additionally,knockdown expression of JNK1 or p53 by using RNAi attenuated the cytotoxicity induced by sodium selenite,indicating that both of JNK1 and p53 are required in the process of cell death induced by sodium selenite.Conclusion The sodium selenite could induces cell death in HCT116 through oxidative stress by involvement of JNK1 and p53,both of which play a critical role in toxicity of sodium selenite.
5.Perspective of biosimilars: A brief comment on immunogenicity of human insulin biosimilars based on viewing of severe adverse events of epoetin α and roferon A
Yongyi GAO ; Gang HAN ; Xiujun LI
Chinese Journal of Endocrinology and Metabolism 2013;29(8):637-641
A number of biosimilars will be soon marketing due to the expiration of patent protection of their originators.Unlike classical chemical drugs,biotherapeutics are proteins with large and complex molecules produced by biological high-tech with sophisticated manufactural procedures.This leads to the difficulties of the copy of biosimilars from their originators,and the almost inevitable distinctions between the two products.Thus biosimilars are only similar but not identical to their reference drugs in terms of stracture,action,and safety.It is important for physicians to understand these differences before using biosimilars.Optimal management by a national regulatory authority with rigorous standards is very important in all aspects of authorization of the development,production,marketing,and postmarketing surveillances for biosimilars.
6.Construction of tissue-engineered bone using a xenogenic deproteinized bone scaffold for spinal intertransverse fusion
Gang LI ; Chunyang GAO ; Lianjin JIN
Chinese Journal of Tissue Engineering Research 2009;13(38):7459-7463
BACKGROUND:Xenogenic deproteinized bone is generally collected and has unique biological properties;however,its immunogen hopes be resolved so as to discover a new type of bone graft material.OBJECTIVE:To explore the performance of xenogenic deproteinized bone scaffold for tissue-engineered bone and the effect on spinal intertransverse fusion in goats.DESIGN,TIME AND SETTING:An in vivo cell-scaffold study was performed at the Key Laboratory of Fibrotic Biotherapy of Heilongjiang Province between February and October 2008.MATERIALS:Twelve healthy male goats aged 6-8 months were provided by Animal Center of Mudanjiang Medical College.METHODS:Cancellous bone at distal femur of adult swine was obtained to prepare xenogenic deproteinized bone scaffold using physical and chemical methods.Effects of the scaffold on morphology,structure,component,biomechanical property,and biological behavior of seed cells were detected and analyzed.Bone marrow was extracted from ilium of goat and gradient-centrifuged to obtain the third-passaged bone marrow mesenchyme stern cells (BMSCs).A certain quantity of autologous BMSCs and recombinant human bone morphogenetic protein 2 (rhBMP-2) were plated onto the scaffold to achieve tissue-engineeried bone.Models of bilateral L3,4 intertransverse bone graft were established on 12 goats.Tissue-engineeried bone was implanted into the left side in a repairing group,while the same volume of autologous ilium was implanted into the right side in a control group.MAIN OUTCOME MEASURES:X-ray examination and histological detection were performed at 4,8,and 12 weeks after implantation.RESULTS:Deproteinization-treated cancellous bone exhibited a spatial grid structure of variously sized,crossing and opening pores,composing hydroxyapatite and collagen.The pore diameter was 200-500 μm,and porosity was about 60%.Mechanical property and cell compatibility were well.X-ray examination demonstrated that at 4 weeks after implantation,some or even lateral intertransverse bridging regions were unclear,and material density in the repairing group was lower than control group;at 8 weeks after implantation,interspace between up and down bridging was shrunk,and a great quantity of calluses were successively formed;at 12 weeks after implantation,complete confluence was observed,and the density in the repairing group was closed to that in the control group.Histological detection indicated that at 4 weeks after implantation,new bone was multidrop-formed in the repairing group;at 8 weeks after implantation,bone tissue like the islet shape was passed through the whole implanted materials;at 12 weeks after implantation,woven bones arranged across,medullary cavity was formed,and osteogenic activity in the repairing group was closed to that in the control group.On the other hand,at 4 weeks after implantation,a large quantity of new bones were formed in the control group;at 8 weeks after implantation,a great quantity of collagen fibers were observed,and osteogenesis was clear in marginal region;at 12 weeks after implantation,fibrous tissues were reduced,and osteogenesis was active.CONCLUSION:BMSCs and rhBMP-2 incubated on xenogenic deproteinized cancellous bone is an ideal tissue-engineeried bone scaffold,characterizing by an excellent histocompatibility and a strong osteogenesis,based on in vitro X-ray diffraction analysis,mechanical test,and in vivo osteogenesis experiment.
9.Treatment of intractable port-wine stains
Rong YIN ; Lin GAO ; Gang WANG
Chinese Journal of Dermatology 2016;(3):222-225
Port-wine stains(PWS)are a common congenital capillary malformation. The lesions of PWS appear to gradually darken in color and thicken with age, and even progress into nodules in late stage. Based on the principles of selective photothermolysis, pulsed dye laser (PDL)has become a standard treatment for PWS. However, for some intractable PWS, single PDL treatment shows unsatisfactory and even no effects. Considering this state, the authors summarize multiple treatment strategies for intractable PWS with thick or nodular lesions, providing a reference for their treatment.
10.Roles and mechanism of inflammation in intracranial aneurysm formation and rupture
Pengfei YAO ; Gang CHENG ; Chen GAO
International Journal of Cerebrovascular Diseases 2016;24(3):275-278
Inflammation is involved in the pathogenesis of many vascular disorders. Hemodynamics cause the activation of inflammatory factors in the vascular wal , resulting in dysfunction of vascular endothelial cels and vascular smooth muscle cels, activating vascular wal inflammatory cascade. Inflammatory cels, especialy macrophage infiltration and secretion of enzymes gradualy weaken the vessel wal to form aneurysm, and even cause aneurysm rupture. Therefore, inflammation plays a key role in the formation and rupture of intracranial aneurysms.