China's state-owned forest enterprises have been important national timber production bases and their timber resources have been severely degraded during the past decades. About one-third of the state-owned forestland has been classified as commercial forestland, but no economic mechanisms have been laid out on governing timber plantations under market economy. This paper demonstrates the potential investment returns and analyzes factors that directly influence the returns of fast-growing poplar plantations in a state owned-forest enterprise, China Jilin Forest Industry Group (CJFIG), in northeastern China. We examined practically possible ranges of mean annual increment (MAI), general inflation rate, rate of forest fund, and interest rate in the study area. We then computed net present values (NPV), equivalent annual income (EAI) and internal rate of return (IRR) by using the minimum, medium, and maximum values of the each determinant above.

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BackgroundThis study aimed to investigate the inhibitory effect of blueberry anthocyanin (BBA) on Angiotensin II (Ang II)-induced apoptosis of human umbilical vein endothelial cells (HUVECs), and its regulation mechanisms involving Bax and Caspase 3.Material/MethodsHUVECs were first treated by different concentrations of Ang II (10−9, 10−8, 10−7, 10−6, 10−5, and 10−4 mol/L) and BBA (80, 40, 20, 10, 5, and 2.5 μg/ml). After 24 h and 48 h of treatment, MTT was performed to detect the viability of HUVECs. Then, HUVECs were randomly divided into the Ang II group (10−6 mol/L Ang II) and Ang II + BBA group (10−6 mol/L Ang II and 20 μg/ml BBA), and the apoptosis rate was detected by flow cytometry. Western blot analysis was performed to detect the expression of Bax and Caspase 3 in these 2 groups. During the whole process, HUVECs without any treatments served as the control group.ResultsThe cell viability of HUVECs was significantly reduced by Ang II in a time- and concentration-dependent manner (P<0.05), while BBA significantly elevated the cell viability of HUVECs until a peak of 20.0 μg/ml. The apoptosis rate of HUVECs was significantly increased by Ang II (P<0.01) and reduced by the BBA intervention (P<0.05). Ang II significantly elevated the expression of Bax and Caspase 3 in HUVECs, but their expression was significantly inhibited by BBA.ConclusionsBBA increased cell viability and reduced apoptosis rate of HUVECs induced by Ang II through Bax- and Caspase 3-dependent pathways.

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