GIMMS NDVI database and geo-statistics were used to depict the spatial distribution and temporal stability of NDVI on the Mongolian Plateau. The results demonstrated that:(1) Regions of interest with high NDVI indices were distributed primarily in forested mountainous regions of the east and the north, areas with low NDVI indices were primarily distributed in the Gobi desert regions of the west and the southwest, and areas with moderate NDVI values were mainly distributed in a middle steppe strap from northwest to southeast. (2) The maximum NDVI values maintained for the past 22 years showed little variation. The average NDVI variance coefficient for the 22-year period was 15.2%. (3) NDVI distribution and vegetation cover showed spatial autocorrelations on a global scale. NDVI patterns from the vegetation cover also demonstrated anisotropy; a higher positive spatial correlation was indicated in a NW-SE direction, which suggested that vegetation cover in a NW-SE direction maintained increased integrity, and vegetation assemblage was mainly distributed in the same specific direction. (4) The NDVI spatial distribution was mainly controlled by structural factors, 88.7% of the total spatial variation was influenced by structural and 11.3% by random factors. And the global autocorrelation distance was 1178 km, and the average vegetation patch length (NW-SE) to width (NE-SW) ratio was approximately 2.4:1.0.
Abstract. In order to optimize surface CO 2 fluxes at grid scales, a regional surface CO 2 flux inversion system (Carbon Flux Inversion system and Community Multi-scale Air Quality, CFI-CMAQ) has been developed by applying the ensemble Kalman filter (EnKF) to constrain the CO 2 concentrations and applying the ensemble Kalman smoother (EnKS) to optimize the surface CO 2 fluxes. The smoothing operator is associated with the atmospheric transport model to constitute a persistence dynamical model to forecast the surface CO 2 flux scaling factors. In this implementation, the "signalto-noise" problem can be avoided; plus, any useful observed information achieved by the current assimilation cycle can be transferred into the next assimilation cycle. Thus, the surface CO 2 fluxes can be optimized as a whole at the grid scale in CFI-CMAQ. The performance of CFI-CMAQ was quantitatively evaluated through a set of Observing System Simulation Experiments (OSSEs) by assimilating CO 2 retrievals from GOSAT (Greenhouse Gases Observing Satellite). The results showed that the CO 2 concentration assimilation using EnKF could constrain the CO 2 concentration effectively, illustrating that the simultaneous assimilation of CO 2 concentrations can provide convincing CO 2 initial analysis fields for CO 2 flux inversion. In addition, the CO 2 flux optimization using EnKS demonstrated that CFI-CMAQ could, in general, reproduce true fluxes at grid scales with acceptable bias. Two further sets of numerical experiments were conducted to investigate the sensitivities of the inflation factor of scaling factors and the smoother window. The results showed that the ability of CFI-CMAQ to optimize CO 2 fluxes greatly relied on the choice of the inflation factor. However, the smoother window had a slight influence on the optimized results. CFI-CMAQ performed very well even with a short lag-window (e.g. 3 days).
Cryptotanshinone (CPT), a diterpene quinone isolated from Salvia miltiorrhiza, is recently reported to have obvious anticancer activities against diverse cancer cells. However, the effect and regulatory mechanism of CPT remain unclear in human chronic myeloid leukemia (CML) cells. In this study, we investigated the antiproliferative activity of CPT on the multidrug resistant CML cells K562/ADM. Our results demonstrated that CPT decreased the cell viability of K562/ADM cells by inducing cell cycle arrest and apoptosis through suppressing the expression of cyclin D1 and Bcl-2. Further studies indicated that CPT mainly functions at post-transcriptional levels, suggesting the involvement of eukaryotic initiation factor 4E (eIF4E). CPT significantly reduced the expression and activity of eIF4E in K562/ADM cells. Overexpression of eIF4E obvious conferred resistance to the CPT antiproliferation and proapoptotic activity as well as the cyclin D1 and Bcl-2 expressions. Knockdown of eIF4E significantly reduced the inhibitory effect of CPT in K562/ADM, confirming the participation of eIF4E during CPT function process. More importantly, the relative inhibitory efficiency of CPT positively correlated with the reductions on eIF4E in primary CML specimens. These results demonstrated that CPT played antitumor roles in K562/ADM cells by inhibiting the eIF4E regulatory system. Our results provide a novel anticancer mechanism of CPT in human CML cells.
β,β-Dimethylacrylshikonin, one of the active components in the root extracts of Lithospermum erythrorhizon, posses antitumor activity. In this study, we discussed the molecular mechanisms of β,β-dimethylacrylshikonin in the apoptosis of SGC-7901 cells. β,β-Dimethylacrylshikonin reduced the cell viability of SGC-7901 cells in a dose- and time-dependent manner and induced cell apoptosis. β,β-Dimethylacrylshikonin treatment in SGC-7901 cells down-regulated the expression of XIAP, cIAP-2, and Bcl-2 and up-regulated the expression of Bak and Bax and caused the loss of mitochondrial membrane potential and release of cytochrome c. Additionally, β,β-dimethylacrylshikonin treatment led to activation of caspases-9, 8 and 3, and cleavage of poly (ADP-ribose) polymerase (PARP), which was abolished by pretreatment with the pan-caspase inhibitor Z-VAD-FMK. β,β-Dimethylacrylshikonin induced phosphorylation of extracellular signal-regulated kinase (ERK) in SGC-7901 cells. U0126, a specific MEK inhibitor, blocked the ERK activation by β,β-dimethylacrylshikonin and abrogated β,β-dimethylacrylshikonin -induced apoptosis. Our results demonstrated that β,β-dimethylacrylshikonin inhibited growth of gastric cancer SGC-7901 cells by inducing ERK signaling pathway, and provided a clue for preclinical and clinical evaluation of β,β-dimethylacrylshikonin for gastric cancer therapy.
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