Purpose To study the reversal effect on multidrug resistance (MDR) by TNF-α gene combined with verapamil (VRP) or tamoxifen (TAM). Methods By using recombinant retrovirus vector, TNF-α gene was transfected into multidrug-resistant human breast cancer cell line MCF7/ADR. The TNF-α secreting cell clone MCF7/ADR-TNF was obtained by G418 screening. The integrating and secreting of TNF-α were analyzed by PCR and ELISA. MTT assay and formula"I = d/D1 + d/D2" were used to evaluate the reversal effect of multidmg resistance with TNF-α gene combined with verapamil or tamoxifen. ResultsThe level of TNF-α secreted by MCF7/ADR-TNF was 1 737 pg/ml (106cells/48 h). Compared with control,the resistance to ADR of MCF7/ADR-TNF was reversed by 1.6 times. The reversal effect produced by combination of TNF-α gene and VRP was antagonistic. The combination of TNF-α gene and TAM produced synergic effect (interaction index I = 0.64). ConclusionsTNF-α gene combined with TAM has synergic effect on reversing MDR.

OBJECTIVETo investigate the application of Chinese guideline for the diagnosis and treatment of chronic rhinosinusitis (2008, Nanchang) on a national scale.

METHODSThe contents of the guideline and its relevant applied indicators were designed into an initial questionnaire and, after a pre-survey, revised into a formal questionnaire. Then a stratified sampling was selected out of otolaryngology practitioners in the different level hospitals across the country. After a uniform training, the investigators were sent to these different hospitals to conduct questionnaire survey by face to face interview with otolaryngology respondents. Based on the summarized data, statistical analyses on the awareness and practice status of the guideline, together with their influencing factors, were made. SPSS 16.0 software was used to analyze the data.

RESULTSIssuing and withdrawing questionnaires were performed from December 2012 to June 2013 and 1 240 respondents in 350 hospitals from 30 different provinces, municipalities or autonomous regions were effectively investigated. An average awareness and practice rate of 48.7% and 40.8% upon the guideline was acquired, respectively. There was a significant correlation (r = 0.280, P = 0.000) between the two indicators. With linear regression, county-level hospitals, junior practitioners, non-rhino professionals were the risk factors of poor guideline adherence. In addition, respondents form western region showed lower awareness and practice rate than that of ones from central and eastern region.

CONCLUSIONThe adherence on Chinese guideline for the diagnosis and treatment of chronic rhinosinusitis is nationally low, so popularization of activities should be urgently strengthened, especially in focus areas, focus hospitals, and focus groups.

Chronic Disease ; therapy ; Guideline Adherence ; Humans ; Practice Guidelines as Topic ; Risk Factors ; Sinusitis ; therapy ; Surveys and Questionnaires

Porphyromonas gingivalis (P. gingivalis), a key pathogen in periodontitis, has been shown to accelerate the progression of atherosclerosis (AS). However, the definite mechanisms remain elusive. Emerging evidence supports an association between mitochondrial dysfunction and AS. In our study, the impact of P. gingivalis on mitochondrial dysfunction and the potential mechanism were investigated. The mitochondrial morphology of EA.hy926 cells infected with P. gingivalis was assessed by transmission electron microscopy, mitochondrial staining, and quantitative analysis of the mitochondrial network. Fluorescence staining and flow cytometry analysis were performed to determine mitochondrial reactive oxygen species (mtROS) and mitochondrial membrane potential (MMP) levels. Cellular ATP production was examined by a luminescence assay kit. The expression of key fusion and fission proteins was evaluated by western blot and immunofluorescence. Mdivi-1, a specific Drp1 inhibitor, was used to elucidate the role of Drp1 in mitochondrial dysfunction. Our findings showed that P. gingivalis infection induced mitochondrial fragmentation, increased the mtROS levels, and decreased the MMP and ATP concentration in vascular endothelial cells. We observed upregulation of Drp1 (Ser616) phosphorylation and translocation of Drp1 to mitochondria. Mdivi-1 blocked the mitochondrial fragmentation and dysfunction induced by P. gingivalis. Collectively, these results revealed that P. gingivalis infection promoted mitochondrial fragmentation and dysfunction, which was dependent on Drp1. Mitochondrial dysfunction may represent the mechanism by which P. gingivalis exacerbates atherosclerotic lesions.
Endothelial Cells ; Mitochondria ; Mitochondrial Dynamics ; Porphyromonas gingivalis

Humans ; Critical Illness ; Critical Care ; Intensive Care Units ; Surveys and Questionnaires