Bone Resorption ; China ; Cytokines ; physiology ; Diphosphonates ; pharmacology ; Estrogens ; pharmacology ; Humans ; Jaw ; drug effects ; metabolism

Objective The objective of this study was to determine the effect of curative chemotherapy regimen on breast cancer cells and its mechanism.Methods A tumor-bearing mouse model was established and routine dose of capecitabine was given as a conventional chemotherapy group.Continuous low-dose capecitabine chemotherapy was used as a radiotherapy group and no chemotherapy was used as a control group.The expression of microvessel density(MVD),vascular endothelial growth factor(VEGF)and thrombospondin 1(TSP-1)were measured by flow cytometry.The percentage of myeloid-derived suppressor cells(MDSCs),NK cells and macrophages in the program was observed.The tumor size and blood leukocyte count were measured after chemotherapy.Results MVD and VEGF in the radiotherapy group were significantly decreased and TSP-1 was significantly increased in comparison with the conventional chemotherapy group(P<0.05).The proportion of MDSCs in the radiotherapy group was significantly decreased,the proportion of NK cells and macrophages were significantly increased when compared to the conventional chemotherapy group(P<0.05).The tumor volume was no difference between the control and chemotherapy groups(P>0.05).However,the white blood cell count in the radiotherapy group was significantly higher than that in the conventional chemotherapy group(P<0.05).Conclusion Capecitabine chemotherapy at continuous low-dose inhibits neovascularization and adjusts the proportion of immune cells to suppress tumor formation.Thus,this chemotherapy could reduce side effects caused by chemotherapy and improve the quality of life.

Adult ; Causality ; Death, Sudden ; epidemiology ; Female ; Herbicides ; poisoning ; Humans ; Male ; Middle Aged ; Paraquat ; poisoning ; Retrospective Studies ; Young Adult

Animals ; Bone Regeneration ; Bone Resorption ; Cells, Cultured ; Disease Models, Animal ; Humans ; Jaw ; metabolism ; Osteoblasts ; Osteoclasts

Objective To understand the molecular epidemiology characteristics and its drug resistance of methicillin-resistant Staphylococcus aureus (MRSA) in the urban area of Jilin and to provide important basis for guiding the clinical medication and prevention of the MRSA infection. Methods One hundred and three strains of MRSA from July 2013 to July 2014 in the urban area of Jilin were selected. The polymerase chain reaction (PCR) technology and multiple polymerase chain reaction were used to detect mecA gene and Staphylococcus chromosomal cassette mec typing (SCCmec) genotype of MRSA. The drug sensitivity test for 13 kinds of clinical common antibacterial drugs were detected by using the K-B method. And the source of the strains were analyzed. Results The results of SCCmec genotype of MRSA showed that SCCmecⅢtype were 62 strains, accounting for 60.2%;SCCmecⅡtype were 39 strains, accounting for 37.9%; failing to parting were 2 strains,accounting for 1.9%. Drug susceptibility test results showed that all of 103 MRSA strains were resistant to cefoxitin, cefazolin, penicillin and benzene, and drug resistance rate was 100.0%. The resistant rate to erythromycin, levofloxacin, ciprofloxacin, tetracycline, gentamicin and rifampin were 96.1%, 93.2%, 95.1%, 91.3%, 90.3%and 55.3%receptively;the resistant rate to sulfamethoxazolewas was only 1.9%;and the resistant strains to vancomycin and teicoplanin were not detected. The top three department of the distribution of the strains source were department of neurosurgery (31.1%), ICU (19.4%) and burn plastic surgery (17.5%). Conclusions The SCCmecⅢtype is the main MRSA epidemic strains, and SCCmec type II is a minor epidemic strainin the urban area of Jilin. The antibiotic resistance of MRSA is a serious problem with multiple drug resistance, but MRSA is sensitive to vancomycin and teicoplanin.

Adult ; Endocarditis ; complications ; microbiology ; Female ; Humans ; Pulmonary Embolism ; etiology ; Pulmonary Valve ; microbiology

Adult ; Chromium Alloys ; adverse effects ; Crowns ; adverse effects ; Female ; Foreign Bodies ; etiology ; Foreign-Body Reaction ; Gingiva ; surgery ; Gingival Hyperplasia ; etiology ; surgery ; Gingivectomy ; Humans ; Metal Ceramic Alloys ; adverse effects

Adult ; Dimethylformamide ; adverse effects ; Glutathione ; blood ; Humans ; Male ; Methanol ; adverse effects ; Nitric Oxide ; blood ; Occupational Exposure ; Oxygen ; metabolism ; Superoxide Dismutase ; blood ; Surveys and Questionnaires ; Toluene ; adverse effects

Objective:To investigate the effect of genistein,a soybean-derived isoflavone,on thestimulating effect on bone resorption of IL-1?.Methods:The osteoclasts(OCs)were isolated with themethods of Yu Shifeng.The rat calvaria were cultured as an organ.The cells in the experiment weregrown in four respectively:Control(without genistein or IL-1?),10~(-6) mol/L genistein,10 ?g/L IL-1?and 10~(-6) mol/L genistein+10 ?g/L IL-1?.The area of bone resorption,the concentration of Ca~(2+) in thesupernatant liquid of OCs cultures and mice calvaria were tested.The contents of acid phosphatase(ACP)were also examined by biochemistry method.The index of bone resorption was counted as the ra-tio of the experiment average and control ones,which indicated the increase in bone resorption when itwas above 1.0.Results:The area of bone resorption of 10~(-6) mol/L genistein+10 ?g/L IL-1? increasedcompared with that of 10~(-6) mol/L genistein,while the concentration of Ca~(2+) in the supernatant liquid ofOCs cultures decreased significantly.The index of bone resorption of 10~(-6) mol/L genistein+10 ?g/L IL-1? lied between 10~(-6) mol/L genistein and 10 ?g/L IL-1?.In the organ culture,there was no differencein the content of ACP among all the groups,The index of bone resorption of 10~(-6) mol/L genistein+10?g/L IL-1? was below that of 10?g/L IL-1?,but both were above 1.0.The index of bone resorptionwas below 1.0 in the group of 10~(-6) mol/L genistein.Conclusion:Genistein can suppress obviously thebone resorption simulated by single IL-1?.

Objective Getting the robust exogenous gene expression vector under the control of porcine insulin promoter, and to lay the foundation for pancreaticβ-cells specific transgene expressing pigs.Method Using porcine insu-lin promoter ( PIP, 1500 bp of the 5′UTR from the porcine INS gene including the first exon and the first intron) to con-struct expression vector, the HindIII restriction site which connected the sequences of PIP and EGFP was designed before ATG, named PIP-HindIII-EGFP.Considering that the different location of restriction site may affect the expression efficien-cy of the transgene, we optimized the expression vector.Firstly the HindIII restriction site was deleted to realize the seam-less connection of PIP and EGFP,the vector was named PIP-EGFP.Also we mutated the 3′intron splicing acceptor site( SA) of the first intron into HindIII restriction site, named as PIP-SA( M)-EGFP.Three different EGFP expression vectors were respectively transfected MIN-6 mouse pancreatic β-cells, pig ear fibroblasts and kidney cells.The transfected cells were cultured for 48 h and harvested for RT-PCR, flow cytometry and Western blot analysis, to analyze and compare the expres-sion efficiency of vectors.Results After transfection,green fluorescence was observed only in MIN-6 mouse pancreaticβ-cells.RT-PCR analysis and product sequencing showed that the three expression vectors did have different stability with in-tron splicing.The PIP-HindIII-EGFP construct and PIP-EGFP vector produced two kinds of mRNA with the first intron spliced and no spliced, indicating the instability of intron splicing.Mutation of the PIP splice site would cause the first in-tron not spliced, while flow cytometry and Western blot displayed that the mutation induced a most efficient expression of the downstream gene.Conclusions A robust and specific β-cells expression vector has been successfully generated by mutating the intron splicing acceptor site of the porcine insulin promoter.It provides the foundation for preparation of pigs with pancreaticβ-cells specifically expressing the transgene.