Methods for Functional Physiological Phenotyping and High-Order Data Quantification.

This chapter presents the application of Plantarray, a high-throughput platform commercially available for noninvasive monitoring of plant functional physiology phenotyping (FPP). The platform continuously measures water flux in the soil-plant-atmosphere for each plant in dynamic environments. To better interpret the massive phenotypic data acquired with FPP, several quantitative analysis methods were demonstrated for various types of data. Simple mathematical models were utilized to fit characteristic parameters of plant transpiration response to drought stress. Additionally, ecophysiological models were employed to quantify the sensitivity of transpiration to radiation and vapor pressure deficit (VPD) as component traits and predict more complex higher-order traits. The established protocols provide a tangible tool for integrating FPP and model analysis to address complex traits.

A composite of Fe3O4@C and multilevel porous carbon as high-rate and long-life anode materials for lithium ion batteries.

The iron oxide-based anode materials are widely studied and reported due to their abundance, low cost, high energy density and environmental friendliness for lithium ion batteries (LIBs). However, the application of LIBs is always limited by the poor rate capability and stability. In order to tackle these issues, a novel material with carbon-encapsulated Fe3O4 nanorods stuck together by multilevel porous carbon (Fe3O4@C/PC) is prepared through directly carbonizing the Fe-based metal-organic framework under a nitrogen atmosphere. This novel material shows a high specific capacity and rate performance. The initial specific capacity can reach 1789 mAh g-1 at a current density of 0.1 A g-1, and the specific capacity still remains 1105.3 mAh g-1 and 783.5 mAh g-1 after 150 cycles at the current densities of 0.1 A g-1 and 1 A g-1, respectively. Even under a current density as high as 12 A g-1, the specific capacity can achieve 309 mAh g-1 after 2000 cycles with an average attenuation rate of 0.019% per cycle. Overall, the simple strategy, low cost and high capacity can make the practical application possible.

Chlorogenic acid improves ex vivo vessel function and protects endothelial cells against HOCl-induced oxidative damage, via increased production of nitric oxide and induction of Hmox-1.

Dietary polyphenols are potential contributors toward improved cardiovascular health. Coffee is one of the richest sources of dietary polyphenols in a coffee-drinking population, the most abundant form being chlorogenic acid (CGA). Endothelial dysfunction is an early and major risk factor for cardiovascular disease. Nitric oxide (NO) is a key factor in regulation of endothelial function. Heme oxygenase-1 (Hmox-1), an inducible isoform of heme oxygenase that is produced in response to stressors such as oxidative stress, may also play a role in vascular protection. The aim of this study was to investigate the effect of CGA on endothelial function with oxidant-induced damage in isolated aortic rings from C57BL mice. We further examine the mechanism by investigating cell viability, activation of eNOS and induction of Hmox-1 in human aortic endothelial cells (HAECs). We found that pretreatment of isolated aortic rings with 10-µM CGA-protected vessels against HOCl-induced endothelial dysfunction (P<0.05). Pretreatment of cultured HAECs with 10-µM CGA increased endothelial cell viability following exposure to HOCl (P<0.05). Moreover, CGA increased NO production in HAECs in a dose-dependent manner, peaking at 6 h (P<0.05). CGA at 5 µM and 10 µM increased eNOS dimerization at 6 h and induced Hmox-1 protein expression at 6 h and 24 h in HAECs. These results are consistent with the cardiovascular protective effects of coffee polyphenols and demonstrate that CGA can protect vessels and cultured endothelial cells against oxidant-induced damage. The mechanism behind the beneficial effect of CGA appears to be in part via increased production of NO and induction of Hmox-1.

The anti-malarial artemisinin inhibits pro-inflammatory cytokines via the NF-κB canonical signaling pathway in PMA-induced THP-1 monocytes.

Several kinds of sesquiterpene lactones have been proven to inhibit NF-κB and to retard atherosclerosis by reducing lesion size and changing plaque composition. The anti-malarial artemisinin (Art) is a pure sesquiterpene lactone extracted from the Chinese herb Artemisia annua (qinghao, sweet wormwood). In the present study, we demonstrate that artemisinin inhibits the secretion and the mRNA levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6 in a dose-dependent manner in phorbol 12-myristate 13-acetate (PMA)-induced THP-1 human monocytes. We also found that the NF-κB specific inhibitor, Bay 11-7082, inhibited the expression of these pro-inflammatory cytokines, suggesting that the NF-κB pathway may be involved in the decreased cytokine release. At all time-points (1-6 h), artemisinin impeded the phosphorylation of IKKα/ß, the phosphorylation and degradation of IκBα and the nuclear translocation of the NF-κB p65 subunit. Additionally, artemisinin inhibited the translocation of the NF-κB p65 subunit as demonstrated by confocal laser scanning microscopic analysis and by NF-κB binding assays. Our data indicate that artemisinin exerts an anti-inflammatory effect on PMA-induced THP-1 monocytes, suggesting the potential role of artemisinin in preventing the inflammatory progression of atherosclerosis.