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A higher diet quality has been associated with lower environmental impacts, but not consistently. Considering the cultural diversity of dietary habits and the heterogeneity of socioeconomic development in China, we aimed to evaluate the association between diet quality and environmental impacts across demographic subgroups and regions. This study used dietary consumption data from the China Health Nutrition Survey 2011. Diet quality was measured with the Chinese Healthy Eating Index 2016 (CHEI2016). Diet-related environmental impact (Greenhouse Gas Emissions (GHGE), Total Water Use (TWU), and Land Use (LU)) were estimated using the Chinese Food Life Cycle Assessment Database. Multilevel regression models were used to quantify the association of the CHEI2016 score and the diet-related environmental impacts across heterogeneous population subgroups. A one-standard deviation increase in CHEI2016 score was associated with an increase of 9.7% in GHGE, 9.1% in TWU, and 6.4% in LU. This occurs because increasing the consumption of under-consumed foods (dairy products and fruit), partially offsets the environmental benefits of reduced meat consumption. Demographic subgroups characterized by either higher educated or a higher income exhibited a larger proportion of animal-based foods within their diet, consequently leading to higher diet-related environmental impacts. When expressed per standard deviation increase in CHEI2016, the dietary environmental impacts rose fastest in the Metropolitan area and slowest in the Northeast. Diets with higher CHEI2016 scores are associated with higher diet-related environmental impacts among Chinese adults but this varies per region. The development of sustainable diet strategies needs to account for potential trade-off between the health and environmental goals, and dietary habits of consumers in different regions and subpopulations. [ABSTRACT FROM AUTHOR]

Over the past decade or two, the concept has emerged of using multiple types of weak interactions simultaneously to enhance the mechanical properties of elastomers. These weak interactions include physical entanglements, hydrogen bonds, metal-coordination bonds, dynamic covalent bonds, and ionic bonds. The combination of entanglements and ionic bonding has been minimally explored and is particularly exciting because of the broad application space for polyelectrolytes. In this work, a constitutive model framework is developed to describe the response of elastomers with both ionic bonds and entanglements. We formulate a micromechanical model that couples together chain stretching, ionic bond slipping, and entanglement evolution. The ionic bonds provide toughness by enabling plastic deformation in comparison to covalently crosslinked material and add strength compared to a linear polymer. Evolution of the entanglement density is taken as a key mechanism that can govern stiffness, toughness, and self-recovery in elastomers. The model is used to match bulk polyelectrolytes with different fractions of ionic components under a variety of loading histories. The variations in material parameters are then used to help understand the relative importance of different governing mechanisms in the bulk polymers. We show that the theoretical framework can explain our experimental uniaxial tensile experimental results for polyelectrolytes. This model can help to design better material with high stiffness and toughness. We expect that our model can be extended to explain the mechanical behavior of other polyelectrolytes and other soft materials with a wide range of dynamic bonds. • Model entanglement evolution driven by shear stress and chain diffusion. • Ionic bonds found to provide strength and dissipate energy without stiffness loss. • Establishes constitutive model coupling entanglement and ionic crosslink effects. [ABSTRACT FROM AUTHOR]

This paper introduced a laboratory study on quantifying the impact of display angles 0.0°–90.0° on the legibility of Sans-Serif 5 × 5 Capitalized Letters C, D, E, F, H, K, N, P, R, U, V, and Z, commonly used for acuity tests. This study addressed three issues not tackled in the previous studies, including (a) extremely large incident angles 82.8°–90°, (b) multiple letters other than a single letter E previously used, and (c) the interference of people's normal reading habit on legibility evaluation. A total of 20 young college students with Snellen acuity 20/20 or better and normal color vision participated in this experiment. They were asked to read viewing materials presented at 15 display angles. This study derived two equations and modified an existing legibility index to correct the interference of people's normal reading habit on legibility evaluation at extreme oblique display angles. [ABSTRACT FROM AUTHOR]

Abstract: Text is often viewed not perpendicularly to its display. With nine assumptions, this study developed a new equation for estimating the legibility of a single letter E viewed at different display angles. This equation examines viewing distance, text height, strokewidth, Snellen acuity, background luminance, luminance contrast, and incident angle. This equation was derived from the existing Howett''s equation based on a constant-solid-angle hypothesis tested in a lighting laboratory by reading letter ‘E’s using 20 young human subjects. The hypothesis holds when the incident angle 0° ≤ ξ ≤ 65.7°, but fails when 65.7° < ξ ≤ 82.8° (the maximum angle tested). Another ambient-light hypothesis was also tested in the same laboratory using 20 young subjects to verify the negligible influence (less than 9%) of ambient light on legibility of text. The new equation was accordingly improved to help ergonomists and other professionals create and maintain legible displays. [Copyright &y& Elsevier]

Colorectal cancer (CRC), the third most frequent occurred cancer, is associated with high mortality and extremely poor prognosis. Ginsenoside Rg3 (Rg3), one of the pharmacologically active components of traditional Chinese herbal medicine Panax ginseng , exerts antitumor effects against several types of cancer growth, including colorectal cancer. However, the detailed molecular mechanisms and particularly the signaling pathways that are decisive in this process are not yet fully elucidated. The present study was carried out to determine the antitumor effects of Rg3 using human colorectal cells in vitro and Xenograft tumor model of human colon cancer in vivo. We found that Rg3 effectively suppressed the proliferation of cancer cells in three human colorectal cancer cell lines (HCT116, HT29, SW480). In addition, intraperitoneal injection of Rg3 for 3 weeks significantly inhibited the growth of xenografts in nude mice. Furthermore, we determined the potential underlying mechanisms for these actions. Treatment with Rg3 significantly inhibited the transactivation of C/EBPβ and NF-κB, as well as the association of C/EBPβ with p65-NFκB in nucleus. However, when SW-480 cells were co-transfected with C/EBPβ, or pretreatment with TNFα, Rg3 failed to inhibit tumor growth. Taken together, our results revealed a robust anti-tumor effect of Rg3, which is mediated by inhibition of C/EBPβ/NF-κB signaling. [ABSTRACT FROM AUTHOR]

Light aromatics are important organic building blocks in the chemical industry which can be produced by catalytic fast pyrolysis (CFP) of biomass. In this work, wet torrefaction pretreatment (WTP) was employed to improve the quality of bamboo by synergistic effect of deoxygenation and demineralization. Then, CFP was employed to produce bio-aromatics by using zeolite (e.g. HZSM-5, HY, Al-MCM-41, and USY) as catalyst. Results showed that WTP temperature (180–260 °C) had more significant influence on the mass yields of torrefied products compared to WTP duration (30–150 min). The maximum deoxygenation rate was 49.36% at WTP conditions of 260 °C and 150 min, and the maximum demineralization rate followed the order of 96.29% (K) > 94.54% (Na) > 90.33% (Mg) > 89.22% (Ca). Among the five types of zeolite catalyst tested, HZSM-5 (25) was the best catalyst to obtain bio-aromatics due to its unique pore size and reasonable acidity. The maximum yield of aromatics (25.46 ×107 a.u./mg) was obtained at the WTP temperature of 220 °C, biomass-to-catalyst ratio of 3:1, and CFP temperature of 850 °C. Toluene was the more favored monocyclic aromatic hydrocarbon formed during CFP compared to xylene and benzene. [Display omitted] • Novel approach (WTP coupled with CFP) was developed to produce bio-aromatics. • Synergistic deoxygenation and deminerization of WTP was investigated. • Maximum deoxygenation and deminerization rates by WTP were 49.36% and over 90%, respectively. • Optimal operation parameters of WTP and CFP were investigated. • Toluene was more favorable to be formed than xylene and benzene. [ABSTRACT FROM AUTHOR]

Highlights • IL-2 promotes sorafenib-mediated apoptosis in Huh7 cells. • IL-2 in combination with sorafenib interrupts mitochondrial metabolism. • Mitochondrial fragmentation is augmented by IL-2 in the presence of sorafenib. Abstract Sorafenib is a standard targeted drug used to treat hepatocellular carcinoma (HCC). Notably, cytokine has been found to further enhance the therapeutic effectiveness of the targeted drug. Thereby, the aim of this study is to verify whether cytokine IL-2 could increase the anti-cancer effects of sorafenib on liver cancer in vitro. Huh7 cells were used in the present study and the cell apoptosis and migration were determined in response to sorafenib treatment. Then, siRNA and pathway blocker were used to determine the molecular mechanisms by which IL-2 enhance the therapeutic effectiveness of Huh7 liver cancer cell in vitro. The data in our study illustrated that sorafenib treatment induced apoptosis in Huh7 liver cancer cell in vitro, an effect that was accompanied with a drop in cell proliferation and migration. Biological investigation demonstrated that IL-2 supplementation further augmented the pro-apoptotic effects of sorafenib in vitro. At the molecular levels, the combination of IL-2 and sorafenib impaired mitochondrial respiratory function, reduced mitochondrial potential, promoted mitochondrial ROS overloading and activated mitochondrial apoptotic pathway. Meanwhile, we found that IL-2 supplementation induced mitochondrial stress via activating mitochondrial fragmentation in a manner dependent on MAPK-JNK signalling pathway and TAZ protein. Blockade of the JNK signalling pathway and/or knockdown of TAZ could abrogate the inhibitor effects of IL-2/sorafenib on liver cancer survival, growth and mobility. Collectively, these data indicated that IL-2 supplementation could further augment the anti-cancer effectiveness of sorafenib via activating mitochondrial fragmentation in a manner dependent on MAPK-JNK signalling pathway and TAZ protein. This finding identifies mitochondrial stress and the JNK-Hippo pathway as the potential targets to treat liver cancer. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) is becoming a major hepatic disease in the Western world. The hallmark feature of NAFLD is steatosis, the accumulation of hepatic triacylglycerol (TG), which results from the disruption of metabolic pathways, one of which is de novo lipogenesis (DNL). RRR-α-tocopherol (αT) can reduce steatosis in animals and NAFLD patients through a yet-unknown mechanism. We aimed to identify the mechanism by which αT decreases liver TG and whether its antioxidant (AO) effect is required for this effect. HepG2 cells cultivated under high glucose medium (25 mmol/L) had a 19% increase in lipid accumulation and 2-fold increase in expression of fatty acid synthase (FASN), a key enzyme in DNL, which were reversed by αT to control levels in a dose dependent manner (25-100 µmol/L, 48h). Similarly, 100 µmol/L of αT decreased incorporation of 14 C glucose into lipids by 24%. We confirmed this effect in vivo in plasma samples from NAFLD patients (n=21), obtained before and after 4 weeks of αT supplementation (NCT01792115). Liver TG, measured by 1 H-magnetic resonance spectroscopy, decreased in 55% of the patients. The lipogenic index, the ratio of C16:0/C18:2n6 in VLDL, reflects hepatic DNL. Patients with reduction in liver TG after 4 weeks of αT also had a significant reduction in the lipogenic index compared to non-responders (p=0.01). To address if αT reduces DNL through its AO function we synthesized methoxy-αT (m-αT), a lipid-soluble αT derivate lacking the AO function and compared it to αT, trolox (water-soluble αT analogue with AO capacity), and probucol (lipid-soluble AO). In our lipogenic HepG2 model, αT, m-αT, trolox and probucol decreased lipid content by max. 18, 0, 0 and 13%, respectively. Thus, our data indicates that αT reduces hepatic DNL in vitro and in vivo through a mechanism that is likely dependent on its antioxidative activity in the lipid compartment. [ABSTRACT FROM AUTHOR]

Large tumor suppressor 2 (LATS2), an important mediator of the cell apoptotic response pathway, has been linked to the progression of several cancers. Here, we described the molecular feature of LATS2 as a novel antitumor factor in liver cancer cells in vitro. Western blotting was used to detect the expression of LATS2 and its downstream factors. ELISA, immunofluorescence, and flow cytometry were used to evaluate the alterations of mitochondrial function in response to LATS2 overexpression. Adenovirus-loaded LATS2 and siRNA against DRP1 were transfected into liver cancer cells to overexpress LATS2 and knockdown DRP1 expression, respectively. The results of the present study demonstrated that overexpression of LATS2 was closely associated with more liver cancer cell death. Mechanistically, LATS2 overexpression increased the expression of DRP1, and DRP1 elevated mitochondrial division, an effect that was accompanied by mitochondrial dysfunction, including mitochondrial membrane potential reduction, mitochondrial respiratory complex downregulation, mitochondrial cyt-c release into the nucleus and mitochondrial oxidative injury. Moreover, LATS2 overexpression also initiated mitochondrial apoptosis, and this process was highly dependent on DRP1-related mitochondrial division. Molecular investigations demonstrated that LATS2 modulated DRP1 expression via the Wnt/β-catenin pathway. Inhibition of the Wnt/β-catenin pathway pregented LATS2-mediated DRP1 upregulation, ultimately sustaining mitochondrial function and cell viability in the presence of LATS2 overexpression. Altogether, the above data identify LATS2-Wnt/β-catenin/DRP1/mitochondrial division as a novel anticancer signaling pathway promoting cancer cell death, which might be an attractive therapeutic target for the treatment of hepatocellular carcinoma. [ABSTRACT FROM AUTHOR]