RESUMO
Cumulative evidence has indicated that celastrol may suppress cancer growth; however, the underlying mechanism requires further investigation. In the present study, A549 cells were treated with various concentrations of celastrol. Lung cancer cell proliferation was evaluated using an MTT assay and observed under a microscope. Cell apoptosis was detected by Annexin V fluorescein isothiocyanate/propidium iodide double-labeled flow cytometry. The results demonstrated that celastrol suppressed proliferation and induced apoptosis in a dose-independent manner. Celastrol may also decrease the phosphorylation levels of signal transducer and activator of transcription 3 (STAT3) and the B cell lymphoma-2 (Bcl-2)/Bcl-2 associated C protein (Bax) ratio. As microRNA (miR-24 and miR-181b) were predicated to target STAT3, STAT3 activation was inhibited in miR-24-or miR-181b-treated A549 cells compared with the control treatment. The ratio of Bcl-2/Bax was further reduced in miR-24 or miR-181b-treated A549 cells. The results were further confirmed by detecting in another lung adenocarcinoma cell line, LTEP-a-2. In summary, the results of the present study demonstrated that celastrol treatment suppressed the proliferation and induced apoptosis by regulating the expression levels of miR-24 and miR-181b.
RESUMO
The present study aimed to investigate the association between brain natriuretic peptide (BNP) levels and the prognosis of patients with left ventricular (LV) diastolic dysfunction. A total of 708 inpatients with cardiovascular disease (mean age, 66 years; 395 males and 313 females) were grouped according to initial BNP and were followed-up for 20-51 months (average, 30.86 months) until endpoint events occurred. Endpoints were defined as mortality or readmission due to cardiovascular disease, or mortality due to any other reason. A total of 67 and 77 events were reported in the BNP ≤80 pg/ml and BNP >80 pg/ml groups, respectively. The occurrence rate of the endpoint was significantly higher in the BNP >80 pg/ml group, as compared with the BNP ≤80 pg/ml group (26.28 vs. 16.14%; relative risk=1.63). Furthermore, the durations of patient survival were significantly shorter in the BNP >80 pg/ml group, as compared with the BNP ≤80 pg/ml group (P=0.0006), and patient survival decreased as BNP levels rose (P=0.0074). Among the 708 patients, 677 underwent echocardiographic detection at the same time. No significant correlation was detected between BNP levels and survival time in 178 patients with normal LV diastolic function [mitral Doppler flow, early diastolic (E)/late diastolic (A)>1] (P=0.2165); whereas a negative correlation was determined in 499 patients with LVD dysfunction (E/A≤1) (Spearman's rho=-0.0899; P=0.0447). The prognoses of patients with elevated BNP levels were correspondingly worse in the present study and these correlations were demonstrated to be significant in patients with LV diastolic dysfunction. Therefore, BNP levels may be used to predict the prognosis of patients with cardiovascular disease.
RESUMO
Verticillium wilt, caused by Verticillium dahliae, is an important disease of cotton worldwide. Isolates of V. dahliae can be characterized as race 1 or race 2 based on the responses of differential cultivars of tomato and lettuce, or as defoliating or nondefoliating based on symptom expression in cotton. To investigate the frequency and distribution of races and defoliation phenotypes of cotton-associated V. dahliae, 317 isolates from China, Israel, Turkey, and the United States were tested by polymerase chain reaction (PCR) using defoliating, nondefoliating, and race 1- and race 2-specific primers DF/DR, NDF/NDR, VdAve1F/VdAve1R, and VdR2F/VdR2R, respectively. Of the total, 97.2% of isolates genotyped as defoliating were also characterized as race 2, while 90.8% of isolates genotyped as nondefoliating were also genotyped as race 1. To verify these results, three cotton cultivars-'FM 2484B2F' (highly resistant), '98M-2983' (highly susceptible), and 'CA4002' (partially resistant)-used as differentials were each inoculated with 10 isolates characterized by PCR: six defoliating/race 2 strains (GH1005, GH1021, HN, XJ2008, XJ592, and reference strain Ls17) and four nondefoliating/race 1 strains (GH1015, GH1016, GH1020, and reference strain Ls16). All defoliating/race 2 isolates except for Ls17 caused defoliation on 98M-2983 and CA4002. Isolate Ls17 caused defoliation on 98M-2983 only. The nondefoliating/race 1 isolates caused Verticillium wilt symptoms devoid of defoliation on 98M-2983. The greenhouse assays confirmed the molecular identification of race and defoliation phenotype. Although the existence of races has not been previously established among V. dahliae isolates from cotton, the long-established nondefoliating and defoliating population structure corresponded with V. dahliae races 1 and 2, respectively.
RESUMO
To confirm the inactivating effect of chito-oligosaccharides on Tobacco mosaic virus (TMV) par ticles in vitro, the difference of TMV pathogenicity was evaluated according to the decrease of local lesion numbers after inoculating with TMV mixed with chito-oligosaccharides (DP3-10) in Nicotiana glutinosa, and the virion structural change was studied by transmission electron microscopy after mixed with chito-oligosaccharides. In the range of tested concentrations of chito-oligosaccharides (100-1000 microg /mL), the numbers of local lesions were strongly reduced with over 30% decrement, and the 88.4% reduction gained at the concentration of 600g /mL. It revealed that treatment with chito-oligosaccharide solution of 300-500 microg /mL directly broke TMV particles into tiny pieces of 50-150nm long, and that treatment with solutions of 600-1000 microg/mL caused virus particle agglomerated. The data presented here suggested that chito-oligosaccharides exerted strong inactivating effect on plant virus in vitro.
