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1.
Huan Jing Ke Xue ; 44(10): 5400-5409, 2023 Oct 08.
Artigo em Zh | MEDLINE | ID: mdl-37827758

RESUMO

In recent years, the ozone (O3) volume fraction in the Beijing-Tianjin-Hebei Region in summer have remained high, light to moderate pollution occurs frequently, and research on related response mechanisms is urgently needed. This study applied the WRF-Chem model to simulate the change in ozone volume fraction in this region by setting 13 precursor emission scenarios in a representative month in the summer of 2018. The results revealed that VOC-sensitivity and no-sensitivity regimes commonly occurred in the Beijing-Tianjin-Hebei Region in July, and the VOC-sensitivity regimes were mainly accumulated in the central Beijing-Tianjin-Hebei Region, with a north-to-south zonal distribution and an area share of 15.60%-26.59%. The relative response intensity (RRI) of O3 volume fraction to precursor emissions in urban areas had large spatial variability, with RRI_VOC and RRI_NOx in the ranges of 0.03-0.16 and -0.40-0.03, respectively. The higher the latitude of urban areas, the more dramatic were the RRI values, indicating a more significant regional transport influence. The lower RRI_NOx values in urban areas with high intensity of precursor emissions implied a negative dependence of RRI_NOx on local NO2 concentrations; however, RRI_VOC was not significantly correlated with NO2levels and was more dependent on the relative abundance of precursors (VOCs:NOx). The ratio of RRI_VOC to RRI_NOx showed negative values in majority of the cities; therefore, collaborative VOCs emission reduction is necessary to suppress the deterioration of O3 volume fraction. The absolute value of this ratio was much lower in cities with high industrialization and urbanization than in ordinary small and medium-sized cities, implying that the demand for collaborative VOCs emission reduction in these cities will be higher. However, even under 50% reduction of precursors, the improvement in O3 volume fraction was limited in regional cities, and the combined prevention in neighboring cities remains important.

2.
Zhonghua Xue Ye Xue Za Zhi ; 34(11): 941-5, 2013 Nov.
Artigo em Zh | MEDLINE | ID: mdl-24294849

RESUMO

OBJECTIVE: To investigate the down-regulated TRAF6 gene expression and its effects on proliferation and apoptosis in multiple myeloma (MM) cells. METHODS: Detection of TRAF6 expression were conducted by RT-PCR and Western blot in MM cell lines of KM3, U266, RPMI8226 and primary cells from patients. RPMI8226 cell lines were transfected with siRNA of TRAF6. The efficiency of transfection was identified by using of fluorescence microscope, RT-PCR, and Western blot. The levels of proliferation were analyzed by CCK-8 method under the different concentrations of siRNA. Apoptosis rate were detected with Hoechst33258/PI double staining by flow cytometry. Apoptosis related proteins Bcl-2, BAX, and NF-κB signal pathway were observed before and after siRNA transfection by Western blot. RESULTS: The levels of TRAF6 mRNA and protein in MM cell lines, especially in primary myeloma cells, were significantly higher than those in controls. After transfected with 50 nmol/L siRNA in RPMI8226 cells, the relative level of TRAF6 mRNA (0.49±0.24) was significantly lower than that in non-transfected group (1.87±0.23) and idling group (1.74±0.35). The proliferation rate of siRNA transfected cells decreased with dose dependence (P<0.01). The apoptosis rates increased from 11.20% (before transfection) to 51.82% (after transfection), accompanied by down-regulated Bcl-2 protein, NF-κB signal pathway (p-p65 and p52), and up-regulated BAX protein. CONCLUSION: TRAF6 expression was high in myeloma cells. TRAF6 siRNA could inhibit proliferation of myeloma cells and induce apoptosis mediated by NF-κB classical and alternative pathway in myeloma cells.


Assuntos
Mieloma Múltiplo/metabolismo , Mieloma Múltiplo/patologia , Fator 6 Associado a Receptor de TNF/metabolismo , Estudos de Casos e Controles , Proliferação de Células , Regulação para Baixo , Feminino , Expressão Gênica , Humanos , Masculino , Fator 6 Associado a Receptor de TNF/genética , Células Tumorais Cultivadas
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