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Health care workers have higher risk of influenza infection because of their occupational exposure to infected patients. Infection of the health care workers may not only result in the increasing risk of the nosocomial infection and family transmission, but also disrupt the health services due to absence from work. Health care workers were recommended as a priority group of influenza vaccinationin more than 40 countries and regions in the world. In recent years, domestic surveys show that the influenza vaccine coverage among health care workers was low. This paper outlines the current status and related policies of influenza vaccination among health care workers in China and global. Additionally, we analyzed and discussed the proper immunization strategy of influenza vaccine for medical staff in China.
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Objective@#To investigate the effects and the underlying mechanism of DS2, a newly synthetic analog of natural ent-kaurane diterpenoid, on the proliferation and migration capabilities of human gastric cancer cells.@*Methods@#MTT assay, colony formation assay and flow cytometry were used to measure the effects of DS2 on growth, apoptosis and cell cycle of several human gastric cancer cell lines. The function of DS2 in the migration was further detected by wound healing and transwell assays. The expression of migration related proteins were determined by western blot.@*Results@#DS2 inhibited the growth of MGC-803, SGC-7901 and HGC-27 cells in a dose dependent manner. After treatment of DS2 at a concentration of 6.25 μmol/L for 24 h, the survival rates of MGC-803, SGC-7901 and HGC-27 cells were 53.87±3.05%, 55.91±6.97% and 32.41±2.64%, respectively. However, for the normal gastric epithelial cell GES-1, no obvious growth inhibition was observed. In addition, DS2 caused significant G2/M arrest and induced apoptosis in MGC-803 cells. Furthermore, compared with the negative control, the colony formation, wound healing rate as well as the number of migrating cells of MGC-803 were significantly decreased in a dose dependent manner after DS2 treatment. DS2 induced the expression of E-cadherin, whereas β-catenin and N-cadherin levels were downregulated in MGC-803.@*Conclusion@#The new compound DS2 has a strong anti-cancer activity, and this study will help us to design and synthesize better diterpenoids derivatives.
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This study aims to learn drug resistance situation of four first-line anti TB drugs among 251 Mycobacterium tuberculosis isolates from Qinghai and to explore their relationships with genotypes by Spoligotyping,so as to provide basis for effective prevention of tuberculosis.Isolates of 251 M.tuberculosis were tested susceptibilities of four first-line drugs including isoniazid (INH),rifampicin (RFP),streptomycin(SM) and ethambutol (EMB) by using conventional proportion method and genotyped by Spoligotyping.Relationship between drug resistance and genotypes was analyzed statistically.Results showed the total drug resistance rate was 56.2％ (141/251) among 251 M.tuberculosis isolates.Resistance rates of four first-line drugs were 43.0％ (108/251) for INH,37.1％ (93/251) for RFP,39.0％ (98/251) for SM,27.9％ (70/251) for EMB respectively.Rate of multidrug-resistant TB (MDR TB) was 31.5％ (79/251).All 251 isolates of M.tuberculosis were typed by spoligotyping.The 185 (73.7 ％) were Beijing genotypes and 66 (26.3.％) were non-Beijing genotypes,and no statistical association was found with drug resistance.This paper concludes that isolates of M.tuberculosis prevail in Qinghai have both high rates of drug resistance and MDR and dominant isolates are Beijing genotypes by spoligotyping.
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OBJECTIVE To investigate the toxicological effect of patulin(PAT)on the growth of human normal liver cells L-02 and its possible mechanisms. METHODS After cells were treated with PAT 1.25, 2.5,5,10 and 20μmol·L-1 for 24 or 48 h,cell viability was examined using MTT assay. L-02 cells were treated with PAT 5 and 10 μmol · L- 1 for 24 h ,respectively. Cytomorphology and mitochondrial membrane potential (MMP) were observed under a fluorescence microscope. Apoptosis,MMP and reactive oxygen species (ROS)were analyzed by flow cytometry. Mitochondria apoptosis pathways were detected by Western blotting. RESULTS PAT exhibited a strong inhibitory effect on L-02 in a concentration-dependent and time-dependent manner. IC50 of PAT treatment for 24 or 48 h was 6.61 and 2.78 μmol · L-1,respectively. MMP was decreased,while the percentage of low MMP cells increased from(9.2±2.3)%in controls to(23.4±4.5)%( PAT 5μmol·L-1)and(47.1±5.5)%(PAT 10μmol·L-1), respectively. Compared to untreated cells,the early apoptosis population increased from(3.8±1.1)%to(29.8±4.5)%( PAT 5μmol·L-1)and (24.1±6.2)%(PAT 10μmol·L-1)(P<0.01),respectively. Further?more,the accumulation of ROS was also observed. The effect of PAT on ROS and cell viabilities could be attenuated by glutathione. CONCLUSION PAT can significantly inhibit the growth of L-02 and induce apoptosis via ROS-dependent mitochondria pathways.
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Aim To investigate Jaridonin′s selective killing of cancer cells and explore the related molecular mechanism. Methods After treatment by Jaridonin for 24 h, the effect of Jaridonin on the cell viability was examined using MTT assay. The effect of Jaridonin on cytomorphology and mitochondrial membrane poten-tial (Δψm) was observed by a fluorescence microsco-py. The apoptosis of cell lines treated with Jaridonin, as well as the level of reactive oxygen species ( ROS ) was analyzed by flow cytometry. Expression of the pro-teins related with mitochondria apoptosis pathways was detected by Western blot. Results Jaridonin caused strong antiproliferative and apoptotic effects on MGC-803 cells, but there were not remarkable effects on GES-1 cells. Furthermore, the expression of Bax was up-regulated, and the release of cytochrome c from mi-tochondria to cytosol was also promoted in MGC-803 cells treated by Jaridonin. The cleavage of caspase-3 in MGC-803 cells was also observed. Jaridonin increased persistently intracellular levels of ROS in MGC-803 cells, whereas the level of ROS in GES-1 rose in the first stage, and then decreased, and dropped to the basic level after 6 h. More interestingly, Jaridonin-in-duced ROS accumulation and the inhibition of MGC-803 cell proliferation were almost completely attenuated in the presence of GSH. Conclusions Jaridonin se-lectively kills cancer cells and induces apoptosis in MGC-803 through ROS-mediated mitochondrial dam-age.
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<p><b>OBJECTIVE</b>To investigate the variable number tandem repeats (VNTR) genetic polymorphisms, genotyping and distribution pattern of clinical Mycobacterium (M.) tuberculosis isolates from Qinghai province.</p><p><b>METHODS</b>The clinical M. tuberculosis strains isolated from the patients with tuberculosis and related background data were collected from Qinghai Provincial Center for Disease Control and Prevention from 2009 to 2012. Genotyping was conducted by using multiple locus VNTR analysis (MLVA). Genomic DNA was extracted and 15 VNTR loci were amplified with PCR and the PCR products were detected with gel electrophoresis. The VNTR diversity and clusters of genotyping were analyzed with BioNumerics (Version 5.0).</p><p><b>RESULTS</b>A total of 251 clinical M. tuberculosis isolates were analyzed with 15 VNTR loci showing that there were great genetic diversity in these isolates. Six of the 15 VNTR loci, showed that the Hunter-Gaston index (HGI) were higher than 0.6, in which the highest resolution was MIRU26. The clusters of genotyping showed that these isolates could be categorized into four gene clusters and 238 genotypes. The four gene clusters accounted for 4.9%, 91.9%, 1.6% and 1.6% of the clinical isolates, respectively.</p><p><b>CONCLUSION</b>The results showed that there is great variety of VNTR genetic polymorphisms in clinical M. tuberculosis isolates in Qinghai province.</p>
Subject(s)
Humans , China , DNA, Bacterial , Genetics , Genetic Variation , Genotype , Minisatellite Repeats , Mycobacterium tuberculosis , Genetics , Polymerase Chain Reaction , Polymorphism, Genetic , Sequence Analysis, DNA , Tuberculosis , MicrobiologyABSTRACT
<p><b>OBJECTIVE</b>The aim of this study was to explore the molecular mechanism of apoptosis in esophageal cancer cells induced by Isodon rubescens.</p><p><b>METHODS</b>The DNA-damage effect of Jaridonin was detected by single cell gel electrophoresis (SCGE). The p53 protein was determined by Western blot. GSH assay kit was employed to determine the GSH content in human esophageal cancer EC-1 cells. Intracellular levels of hydrogen peroxide (H2O2) or superoxide (O(2).-) were determined using the redox-sensitive probes 2', 7'-dichlorodihydrofluorescein diacetate (DCF) or dihydroethidium (DHE), and the fluorescence signal was assayed by fluorescence microscopy and by flow cytometry.</p><p><b>RESULTS</b>Jaridonin induced DNA damage in EC-1 cells remarkably. The olive tail moments (OTM) of control and 20, 40 µmol/L Jaridonin were 3.2, 45.2 and 89.0, respectively. Compared with the control, the differences were significant (P < 0.01 for both). Jaridonin resulted in extensive p53 up-regulation in the EC-1 cells. More importantly, the p53 up-regulation occurred as early as 2 h after Jaridonin incubation, and in a time-dependent manner (P < 0.05). p53 siRNA transfection inhibited apoptosis in the EC-1 cells, and the Jaridonin-induced apoptosis rate was reduced from 38.5% to 8.8%. Intracellular level of H2O2 was increased by Jaridonin, whereas the level of O(2).- was barely changed. The GSH content in EC-1 cells was reduced from (10.3 ± 1.6) nmol/mg protein to (4.6 ± 2.1) nmol/mg protein after 20 µmol/L Jaridonin incubation for 8 h, and it was further reduced with the increase of Jaridonin concentration. Jaridonin induced DNA damage, H2O2 accumulation and apoptosis were significantly attenuated in the presence of GSH, but Jaridonin showed little effect on normal human liver L-02 cells.</p><p><b>CONCLUSIONS</b>Jaridonin selectively induces apoptosis in esophageal cancer EC-1 cells through H2O2-mediated DNA damage by depleting GSH.</p>
Subject(s)
Humans , Antineoplastic Agents , Pharmacology , Apoptosis , DNA Damage , Diterpenes, Kaurane , Pharmacology , Esophageal Neoplasms , Metabolism , Hydrogen Peroxide , Metabolism , Up-RegulationABSTRACT
BACKGROUND: There were disadvantages of animal models in the study of the relationship of muscle and skeleton. Recent study has been demonstrated the effect of Botulinum toxin type A to atrophy local muscle without influencing the surrounding muscle.OBJECTIVE: To construct a reasonable animal model of local muscle atrophy by local injection of Botulinum toxin type A.METHODS: Totally 25 male Wistar rats of 4 months were subjected to ketamine (0.2 mL/kg) and Sumianxin (0.2 mL/kg) by intramuscular injection. A 0.5-cm incision was made on the middle of dorsal femur to expose quadriceps femoris. Right quaddceps femods was injected with 2 Units (0.2 mL) of Botulinum toxin type A, and left quaddcaps femoris of the same rat with the same amount of saline as controls. At 1, 2, 4, 8, 8 weeks after injection, 5 rats were used to take gross observation and histological examination.RESULTS AND CONCLUSION: Gross observation of the muscle tissue showed that, compared with self-controlled group, the volume and weight of the quadriceps femods were decreased significantly (P < 0.01). The histological examination of muscle tissue showed the atrophy of the quadricaps femods from expedmental group was more obvious, the muscle fiber become thin,and the nuclei of the muscle fiber assemble together, with small distance betWeen muscle fibers. Weight of the quadricaps femods treated with Botulinum toxin type A was decreased at 1 and 2 weeks. The increase in weight of muscle was slow among muscle at 4, 6 and 8 weeks. The muscle weight showed an increased tendency in the saline side at vadous time points. Injecting Botulinum toxin type A into local muscle is a reasonable way to set up an experimental model of the atrophy of a destination muscle with strong practice, good repeatability, high stability, and may be used to examine the relationship of muscle and skeleton.