BACKGROUND: As a minimally invasive technology, percutaneous vertebroplasty is a safe and effective treatment for osteoporotic vertebral compression fractures.OBJECTIVE: To overview the research progress concerning the biomechanical properties, bone strength maintenance, bone absorption and degradation of bone filling materials used in percutaneous vertebroplasty.METHODS: The first author conducted a computer-based retrieval of CNKI, PubMed and Medline databases for relevant articles published from January 2005 to May 2016. The keywords were bone cement, bone filling materials, percutaneous vertebroplasty in English and Chinese, respectively.RESULTS AND CONCLUSION: Polymethyl methacrylate is not an ideal material for osteoporotic vertebral compression fractures. Calcium phosphate cement and calcium sulfate cement can replace the traditional polymethyl methacrylate; however, some problems still exist, such as poor effect of venography, incontrollable biological degradation rate, and lack of the evidence-based medicine about its long-term effect. Composite bone cement, as a good bone repair material, holds the advantages of various bone cements. As the composite bone cement has just been introduced in clinical practice, its long-term curative efficacy needs to be further studied.

Objective To observe the effects of Tianma Gouteng Yin (TGY) on the proliferation of myocardial fibroblasts of spontaneous hypertensive rat(SHR) stimulated by insulin. Methods The cardiac fibroblasts from one-day-old spontaneously hypertensive rat were primarily cultured and then sub-cultured to 3rd-6th generation,and were identified with light microscopy and immunohistochemical technique. The effect of serum containing TGY on the proliferation of cardiac fibroblasts of SHR treated with insulin was determined by MTT colorimetric assay and 3-H-TdR incorporation,and the cell cycle was analysised with flow cytometer. Results TGY inhibited the proliferation of cardiac fibroblasts induced by insulin. Insulin can stimulate the proliferation of fibroblasts by promoting the cell cycle transfer from G0/G1 period to S period and increasing the synthesis of cell DNA. Compared with the model group,the percentage of the cells at G0/G1 period was much higher,while the percentage of the cells at S period was much lower in TGY group. Conclusion TGY has the effect on inhibiting the proliferation of cardiac fibroblasts and inhibiting the cell cycle transfer from G0/G1 period to S period,which may be one of its therapeutic and protective mechanisms for hypertension and myocardial fibrosis in clinic.

Objective To understand characteristics and research status of literatures related to surgical site infec-tion(SSI)in China.Methods Literatures about SSI published between January 2000 and March 2016 were retrieved from China National Knowledge Infrastructure(CNKI),VIP database,Vanfang Database,and China Biology Medi-cine(CBM)database. Bibliometric method was adopted to analyze external and internal characteristics of literatures. Results A total of 1036 articles in Chinese were included,40(3.86% ),189(18.24% ),and 807(77.90% )were published in 2000-2005,2006-2010,and the first quarter of 2011-2016 respectively. Articles were mainly pub-lishedinChineseJournalofNosocomiology(n= 226,21.81% ),ChineseJournalofInfectionControl(n= 53, 5.12% ),andChineseJournalofDisinfection(n= 27,2.61% ). The research fields included risk factors(n= 277, 26.74% ),infection rates (n= 261,25.19% ),antimicrobial application (n= 208,20.08% ),and pathogens (n=153,14.77% );the infection rates were higher in general surgery and neurosurgery,the main pathogens were Esch-erichiacoli,Staphylococcusaureus,and Pseudomonasaeruginosa,risk factors mainly included the types of incision, duration of surgery,diabetes,age,and body mass index.Conclusion In recent years,articles about SSI research in-creases significantly,research in etiology and epidemiology has gained substantial achievement,but in the interven-tion and economics is still weak,suggesting that SSI research in economics,risk management,and behavioral aspects should be strengthened.

ObjectiveTo investigate the effects and molecular mechanism of simvastatin in liver fibrosis model of non-alcoholic fatty liver disease (NAFLD) in vivo and hepatic stellate cell in vitro.MethodsFirstly,the rat liver fibrosis model of NAFLD was established by high-fat diet administration and intervened with simvastatin.The expression of endothelial nitric oxide synthase (eNOS),inducible nitric oxide synthase (iNOS) and Collagen Ⅰ at mRNA and protein level were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot.Secondly,quiescent phenotype of LX-2 cell line was induced by promoting adipocyte differentiation medium in vitro,and then the quiescent phenotype of LX-2 cell were treated with transforming growth factor β1(TGF-β1),Nitroso-L-arginine methyl ester (L-NAME) which was NOS inhibitor,simvastatin,TGFβ1 with simvastatin,and L-NAME with simvastatin separately.The changes of eNOS,iNOS,αsmooth muscle actin (α-SMA) and Collagen Ⅰexpressions at mRNA and protein level were determined by RT-PCR and Western blot.ResultsAs modeling time extended,the expressions of eNOS in rat's liver tissue of model group at mRNA and protein level decreased gradually,however the expression of iNOS and Collagen Ⅰ at mRNA and protein level increased gradually,compared with normal control group and the differences were statistically significant (P ＜0.05 and 0.01).By 24weeks,the expressions of eNOS in rat's liver tissue of simvastatin group at mRNA and protein level were increased,the expression of iNOS at mRNA and protein level were decreased and the expression of Collagen Ⅰ at mRNA and protein level were decreased (all P ＜0.05).The expression of eNOS in rat's liver tissue of model group negatively correlated with the expression of Collagen Ⅰ at mRNA and protein level (all P ＜0.01).The expression of iNOS positively correlated with that of Collagen Ⅰ at mRNA and protein level (all P ＜0.01).In LX-2 cell culture,L-NAME inhibited the activation of LX-2,reduced eNOS and iNOS expression and increased α-SMA and CollagenⅠexpression,consistent with the role of TGF-β1.Simvastatin could directly increase the eNOS expression both in quiescent and activated LX-2 cells,decrease iNOS expression,maintain quiescent phenotype and inhibit its activation.ConclusionsSimvastatin ameliorated the genesis and progression of liver fibrosis by increasing eNOS expression in LX-2 cells and reducing iNOS,α-SMA and Collagen Ⅰ expression.

The megakaryocyte and platelet lineage may be one of the major sites of human cytomegalovirus (HCMV) infection. However, whether HCMV aggravates apoptosis in normal megakaryocytes was not well investigated. Megakaryocytic cell line CHRF-288-11 and HCMV AD 169 strain were co-cultured in this study. PCR was used to detect the direct infection of the cells by HCMV IEA expression. The apoptotic cells were analyzed by morphologic observation, DNA ladder formation, annexin V/PI and PI assay with flow cytometry. The results showed that HCMV significantly inhibited the growth of CHRF cells in three different concentrations of viral infection groups (10(-3), 10(-2), 10(-1)). The viability levels in each infection groups were 77%, 73% and 68% respectively after incubation for 7 days, compared with 98% in the control group. Using annexin V/PI with flow cytometry, it was shown that the percentages of apoptotic cells viral infection in groups (10(-3), 10(-2), 10(-1)) were (21.3 +/- 2.49)%, (25.8 +/- 3.65)% and (31.4 +/- 3.91)% at 7 days after infection, while the control was (3.68 +/- 1.47)%. The apoptotic cells were further confirmed by morphologic observation and DNA ladder formation. Furthermore, PCR detection also showed the direct infection by identification of HCMV IEA expression in CHRF cells. This study suggested that HCMV could directly infect megakaryocytes and aggravated apoptosis in HCMV-infected megakaryocytes.
Apoptosis ; Cell Survival ; Cells, Cultured ; Cytomegalovirus ; pathogenicity ; DNA, Viral ; analysis ; Humans ; Megakaryocytes ; cytology ; virology ; Polymerase Chain Reaction

OBJECTIVETo analyze the complications of percutaneous kyphoplasty except bone leakge for the treatment of osteoporotic thoracolumbar vertebral compression fractures.

METHODSFrom October 2008 to October 2012,178 patients with 224 osteoporotic vertebral compression fractures were treated with percutaneous kyphoplasty under local anethsia. There were 72 males and 106 females,ranging in age from 58 to 92 years old,with an average of 75.3 years,including 93 thoracic vertebrae and 131 lumbar vertebrae. The complications except bone cement leakage were analyzed during operation and after operation.

RESULTSAll operations were successful and all patients were followed up from 12 to 60 months with an average of 26.2 months. No death was found. Bone cement leakage occurred in 27 cases, about 15.1% in 178 cases; and complications except bone cement leakage occurred in 15 cases. There was 1 case with cardiac arrest,was completely recovery by cardiopulmonary resuscitation (CPR) immediately; and 1 case with temporary absence of breathing,was recovery after treatment. There were 3 cases with fall of blood pressure and slower of heart rate; 1 case with intestinal obstruction; 2 cases with local hematoma and 1 case with intercostal neuralgia. Vertebral body fractures of 2 cases were split by bone cement and the fractures of adjacent body occurred in 4 cases.

CONCLUSIONIt's uncommon complication except bone cement leakge in treatment of osteoporotic thoracolumbar vertebral compression fractures with percutaneous kyphoplasty. The complication of cardiopulmonary system is a high risk in surgery; and cytotoxicity of bone cement,nervous reflex,fat embolism and alteration of intravertebral pressure may be main reasons.

Aged ; Aged, 80 and over ; Female ; Fractures, Compression ; surgery ; Humans ; Kyphoplasty ; adverse effects ; Lumbar Vertebrae ; injuries ; surgery ; Male ; Middle Aged ; Osteoporotic Fractures ; surgery ; Postoperative Complications ; etiology ; Spinal Fractures ; surgery ; Thoracic Vertebrae ; injuries ; surgery

Background: Previous study has found that ursolic acid (UA) inhibited the proliferation of gastric cancer cells by the down-regulation of cyclooxygenase-2 (COX-2) expression.However,its molecular mechanism is not fully clear.Aims: To investigate the role of adenosine monophosphate-activated protein kinase (AMPK)/signal transducer and activator of transcription 3 (STAT3)/COX-2 signaling pathway in UA-mediated inhibition of gastric cancer cells proliferation.Methods: AMPK-pLVX,AMPK-shRNA,STAT3-pLVX,STAT3-shRNA plasmids were constructed,and then were transfected into human gastric cancer cell lines SGC-7901 and MKN-45,respectively.Gastric cancer cells were cultured with different concentrations of UA for different times.The expressions of phosphorylated AMPK (p-AMPK),phosphorylated STAT3 (p-STAT3) and COX-2 were measured by Western blotting,and cell proliferation was detected by CCK-8 assay.Results: UA dose-and time-dependently increased p-AMPK expression,inhibited p-STAT3 and COX-2 expressions in SGC-7901 and MKN-45 cells.Knockdown of AMPK blocked UA-induced inhibition of STAT3 phosphorylation and COX-2 expression.Overexpression of STAT3 blocked UA-induced down-regulation of COX-2 expression.Knockdown of AMPK and overexpression of STAT3 blocked UA-induced inhibition of proliferation of gastric cancer cells.Conclusions: UA may inhibit the proliferation of gastric cancer cells via down-regulation of COX-2 expression through AMPK/STAT3 pathway.

Melittin exhibits high antibacterial potency against drug-resistant bacteria. However, the clinical utility of melittin is limited by its serious hemolytic activity. Thus, the need for developing novel melittin analogues with high antimicrobial activity and low hemolytic activity has grown. We designed, synthesized, and evaluated 20 novel melittin analogues with varying hydrophobic, polar or positively charged amino acids. The results showed that 8 compounds had antimicrobial activity (MIC: 1-4 μg·mL^-1) against gram-positive pathogens equal to or better than that of melittin, and 16 compounds had low hemolytic activity (HC₅₀ ≥ 11.9 μg·mL^-1). Compounds 13 (MIC: 2-4 μg·mL^-1) and 15 (MIC: 1-2 μg·mL^-1) showed equal or better antimicrobial activity against both susceptible and resistant strains of Staphylococcus aureus and Enterococcus faecium compared to melittin (MIC: 4 μg·mL^-1). Compound 13 (HC₅₀: 24.0 ± 4.3 μg·mL^-1) displayed noticeably decreased hemolytic activity compared to melittin (HC₅₀: 5.3 ± 0.4 μg·mL^-1). This work established a base for further study on the structure-activity relationships and structure-toxicity relationships of melittin.

Accidents, Occupational ; statistics & numerical data ; China ; epidemiology ; Humans

OBJECTIVETo observe the effects of tetramethylpyrazine (TMP) on tissue factor (TF) expression induced by thrombin in human umbilical vein endothelium derived cell line ECV304.

METHODSThe changes in the total cellular procoagulant activity (PCA) of ECV304 cells exposed to thrombin were observed with one-stage clotting assay. TF mRNA expression in the exposed cells was examined using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR).

RESULTSECV304 cells stimulated with increasing concentrations of thrombin (1.25-20 U/ml) showed a gradual increase of PCA (r=0.9602, P<0.01). The application of FVII-deficient plasma and the monoclonal antibody of TF confirmed that the PCA of the cells mediated by TF activity. TMP at 125-1000 microg/ml alone did not affect TF expression in ECV304 cells (P>0.20), TMP administered 30 min prior to thrombin exposure showed a significant concentration-dependent inhibitory effect on the increments of PCA (r=-0.9644, P<0.01) and TF mRNA expression (r=-0.9576, P<0.05) in ECV304 cells, and 1000 microg/ml TMP produced the strongest effect. In ECV304 cells stimulated with thrombin for 4, 6, 8, 10 and 12 h, TMP administration significantly inhibited the thrombin-induced PCA, and the effect was especially obvious at 8 h following thrombin exposure (P<0.05).

CONCLUSIONThrombin induces TF expression in vascular endothelial cells, and this effect can be inhibited by TMP at the mRNA level.

Animals ; Cell Line ; Dose-Response Relationship, Drug ; Endothelial Cells ; cytology ; drug effects ; metabolism ; Gene Expression Regulation ; drug effects ; Humans ; Pyrazines ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Thrombin ; pharmacology ; Thromboplastin ; genetics ; metabolism ; Time Factors