Abstract.The original Gash analytical model and the sparse Gash's model were combined to simulate rainfall interception losses from the top-and sub-canopy layers in Shaoshan evergreen forest located in central-south China in 2003. The total estimated interception loss from the two canopy layers was 334.1 mm with an overestimation of 39.8 mm or 13.5% of the total measured interception (294.3 mm). The simulated interception losses of the top-and sub-canopy suggested that the simulated interception losses in the stages of "during storms" and "after storms" were in good agreement with the published ones. Both the original Gash model and the sparse model overestimated the interception losses, but the sparse model gave more accurate estimates than the original Gash model.

Endothelial progenitor cells (EPCs) have been reported to replace the damaged endothelial cells to repair the injured or dead endothelium. However, EPC senescence might lead to the failure in EPC function. Thus, developing an in‐depth understanding of the mechanism of EPC senescence might provide novel strategies for related vascular disorders’ treatments. Herein, nicotinamide phosphoribosyltransferase (NAMPT) overexpression could increase cell proliferation and suppress cell senescence in EPCs. miR‐223 directly bound to the 3′‐untranslated region of NAMPT to inhibit its expression, therefore modulating EPC proliferation and senescence through NAMPT and phosphoinositide 3‐kinase (PI3K)/protein kinase B (AKT) signaling. Long noncoding RNA (lncRNA) GAS5 sponges miR‐223, consequently downregulating miR‐223 expression. GAS5 knockdown inhibited EPC proliferation and promoted senescence. GAS5 might serve as a competing endogenous RNA for miR‐223 to counteract miR‐223‐mediated suppression on NAMPT, thus regulating EPC proliferation and senescence via the PI3K/AKT signaling pathway. In summary, our findings provide a solid experimental basis for understanding the role and mechanism of lncRNA GAS5/miR‐223/NAMPT axis in EPC proliferation and senescence.

The Notch signaling pathway participates in pulmonary artery smooth muscle cell (PASMC) proliferation and apoptosis. Astragaloside IV (AS-IV) is an effective antiproliferative treatment for vascular diseases. The present study aimed to investigate the protective effects and mechanisms underlying AS-IV on hypoxia-induced PASMC proliferation and pulmonary vascular remodeling in pulmonary arterial hypertension (PAH) model rats. Rats were divided into the following four groups: i) normoxia; ii) hypoxia (10% O 2); iii) treatment, hypoxia + intragastrical administration of AS-IV (2 mg/kg) daily for 28 days; and iv) DAPT, hypoxia + AS-IV treatment + subcutaneous administration of DAPT (10 mg/kg) three times daily. The effects of AS-IV treatment on the development of hypoxia-induced PAH, right ventricle (RV) hypertrophy and pulmonary vascular remodeling were examined. Furthermore, PASMCs were treated with 20 µmol/l AS-IV under hypoxic conditions for 48 h. To determine the effect of Notch signaling in vascular remodeling and the potential mechanisms underlying AS-IV treatment, 5 mmol/l γ-secretase inhibitor [N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT)] was used. Cell viability and apoptosis were determined by performing the MTT assay and flow cytometry, respectively. Immunohistochemistry was conducted to detect the expression of proliferating cell nuclear antigen (PCNA). Moreover, the mRNA and protein expression levels of Notch-3, Jagged-1, hes family bHLH transcription factor 5 (Hes-5) and PCNA were measured via reverse transcription-quantitative PCR and western blotting, respectively. Compared with the normoxic group, hypoxia-induced PAH model rats displayed characteristics of PAH and RV hypertrophy, whereas AS-IV treatment alleviated PAH and prevented RV hypertrophy. AS-IV also inhibited hypoxia-induced pulmonary vascular remodeling, as indicated by reduced wall thickness and increased lumen diameter of pulmonary arterioles, and decreased muscularization of distal pulmonary vasculature in hypoxia-induced PAH model rats. Compared with normoxia, hypoxia promoted PASMC proliferation in vitro, whereas AS-IV treatment inhibited hypoxia-induced PASMC proliferation by downregulating PCNA expression in vitro and in vivo. In hypoxia-treated PAH model rats and cultured PASMCs, AS-IV treatment reduced the expression levels of Jagged-1, Notch-3 and Hes-5. Furthermore, Notch signaling inhibition via DAPT significantly inhibited the pulmonary vascular remodeling effect of AS-IV in vitro and in vivo. Collectively, the results indicated that AS-IV effectively reversed hypoxia-induced pulmonary vascular remodeling and PASMC proliferation via the Notch signaling pathway. Therefore, the present study provided novel insights into the mechanism underlying the use of AS-IV for treatment of vascular diseases, such as PAH.

The effects of Weak acids (WA) on the canopy leaching and uptake processes are evaluated by comparing the leached base cations or the absorbed protons while including and excluding WA, e.g. the WA-included method and the WA-excluded method. The seasonal WA throughfall flux is even larger than twice the bulk precipitation flux except summer, which not only partly agrees with the conclusion that the total deposition of WA equals twice the bulk or dry deposition flux in European Intensive Monitoring plots (level II), but also indicates the significant canopy leaching of WA in Shaoshan forest. The seasonal canopy leaching of base cations in association with WA accounts for 6-30% of the total base cations in throughfall, with an annual mean of 23%, which is slightly higher than the 15% at the Speulder forest in The Netherlands. The canopy exchange capacity of H + to NH + 4 is closed to 6.0 while neglecting the WA exchange, which probably supports the assumption that the exchange capacity of H + is six times that of NH + 4 . Simultaneously, we suggest that the WA is competitive to a certain extent with protons to leach base cations of plant tissues during the canopy exchange processes.

The aim of the present study was to determine the ferulic acid (FA) content of Radix Angelicae Sinensis (AS), Danggui-Buxue-Tang (DBT) and Danggui-Sini-Tang (DST) using the same ultra performance liquid chromatography system and method. FA was eluted using an Acquity BEH C18 column (100×2.1 mm inner diameter; 1.7 μm). A mobile phase of methanol and 0.5% acetic acid was used and a flow rate of 0.3 ml/min was selected. The calibration curve exhibited a good linear regression (R2=0.9997). The inter- and intra-day precision measurements of FA ranged between 0.27 and 3.03% and the recovery ranged between 98.44 and 101.64% with relative standard deviation (RSD) values ≤4.73%. The method was reliable and simple. The results of the chromatographic analyses indicate that the FA contents of the DBT and DST decoctions were increased compared with that of AS due to the presence of other herbs.