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FM/ACFN and Ce-doped CFM/ACFN low-temperature catalysts are prepared by an impregnation method that takes polyacrylonitrile-based activated carbon fiber modified with nitric acid as the carrier. The catalysts are characterized by X-ray diffraction, scanning electron microscopy, Fourier-transform infrared spectroscopy, and thermogravimetric analysis. The effects of temperature, oxygen, and sulfur dioxide on the adsorption and removal of NO by catalyst are studied by laboratory gas distribution. Results show that the addition of metal oxide can increase the ability of chemical adsorption of NO by ACFN by 2.5%, and the ability of catalytic reduction of NO can be increased by up to 14%. Under the condition of oxygen and ammonia as reducing agent at 250 °C, the ability of metal-oxide-loaded ACFN to catalyze the reduction of NO can reach up to 68%. The addition of Ce does not completely inhibit the decrease of the ability of the catalyst in treating NO under sulfur-containing conditions, but it can maintain the catalyst’s reducing ability at a relatively stable level, and the presence of SO2 will reduce the redox capacity of ACFN itself.

Different atmospheric pressure and ambient temperature of different altitude affect the dynamic performance of vehicle. Subject to laboratory conditions, this paper builds a simulation model of a commercial vehicle based on GT-Power software to study the dynamic performance of a commercial vehicle at different altitudes by acceleration time, maximum gradability and maximum speed of vehicle evidently. Advanced turbocharging technique was deemed to be effective measure to improve dynamic performance of vehicle.

To assess associations between breastfeeding and iron status at 9 months of age in 2 samples of Chinese infants.Associations between feeding at 9 months of age (breastfed as sole milk source, mixed fed, or formula fed) and iron deficiency anemia (IDA), iron deficiency, and iron sufficiency were determined in infants from Zhejiang (n = 142) and Hebei (n= 813) provinces. Iron deficiency was defined as body iron 0 mg/kg, and IDA as iron deficiency + hemoglobin 110 g/L. Multiple logistic regression assessed associations between feeding pattern and iron status.Breastfeeding was associated with iron status (P .001). In Zhejiang, 27.5% of breastfed infants had IDA compared with 0% of formula-fed infants. The odds of iron deficiency/IDA were increased in breastfed and mixed-fed infants compared with formula-fed infants: breastfed vs formula-fed OR, 28.8 (95% CI, 3.7-226.4) and mixed-fed vs formula-fed OR, 11.0 (95% CI, 1.2-103.2). In Hebei, 44.0% of breastfed infants had IDA compared with 2.8% of formula-fed infants. With covariable adjustment, odds of IDA were increased in breastfed and mixed-fed groups: breastfed vs formula-fed OR, 78.8 (95% CI, 27.2-228.1) and mixed-fed vs formula-fed OR, 21.0 (95% CI, 7.3-60.9).In both cohorts, the odds of iron deficiency/IDA at 9 months of age were increased in breastfed and mixed-fed infants, and iron deficiency/IDA was common. Although the benefits of breastfeeding are indisputable, these findings add to the evidence that breastfeeding in later infancy identifies infants at risk for iron deficiency/IDA in many settings. Protocols for detecting and preventing iron deficiency/IDA in breastfed infants are needed.ClinicalTrials.gov: NCT00642863 and NCT00613717.

Objective: The worldwide prevalence of anemia is ~24.8%. Iron deficiency anemia is common in children and women and associated with sensory, motor, cognitive, language, and socioemotional deficits. Therefore, detection and early intervention strategies for anemia in infants are urgently needed. To prevent the occurrence of iron deficiency anemia, we aimed to identify risk factors associated with anemia in infants.Methods: This investigation involved a cross-sectional study of 6-months-old infants discharged between April 2014 and September 2017 from Peking University First Hospital. We assessed birth information, maternal age, and maternal educational level as well as data on feeding style, complementary foods and primary caregivers. The infants were assessed with the Denver Developmental Screening Test (DDST).Results: A total of 1,127 6-months-old infants were enrolled at the hospital. We found that the prevalence of anemia among infants in Beijing was ~11.8%. Premature infants had a higher rate of anemia than full-term infants (χ2 = 40.103, P < 0.001). Infants born in autumn or winter were at an elevated risk of developing anemia (χ2 = 22.949, P < 0.001). Birth weight had no effect on the rate of anemia in infants (χ2 = 0.023, P = 0.568). Infants who were exclusively breastfeeding had higher anemia rates than those who were fed formula (χ2 = 38.466, P < 0.001). Infants whose caregivers added no complementary foods had higher anemia rates (24.7%) than those whose caregivers added more than two kinds of complementary food (8.2%). The type of caregiver had no effect on the anemia rate in infants (χ2 = 0.031, P = 1.000).Conclusions: The following factors resulted in a higher prevalence of anemia in our study a gestational age at birth of

BACKGROUND: Previous trials of iron supplementation in infancy did not consider maternal iron supplementation. OBJECTIVE: This study assessed effects of iron supplementation in infancy and/or pregnancy on infant iron status illnesses and growth at 9 mo. METHODS: Enrollment occurred from December 2009 to June 2012 in Hebei China. Infants born to women in a pregnancy iron supplementation trial were randomly assigned 1:1 to iron [ approximately 1 mg Fe/(kg . d) as oral iron proteinsuccynilate] or placebo from 6 wk to 9 mo excluding infants with cord ferritin /=2 abnormal iron measures) or body iron 60% of infants still had ID at 9 mo. Receiving more bottles of iron in infancy was associated with better infant iron status at 9 mo but only among iron-supplemented infants whose mothers were also iron supplemented (i.e. the iron/iron group). There were no group differences in hospitalizations or illnesses and no adverse effects on growth overall or among infants who were iron sufficient at birth. CONCLUSIONS: Iron supplementation in Chinese infants reduced ID at 9 mo without adverse effects on growth or illness. Effects of iron supplementation in pregnancy were observed only when higher amounts of iron were distributed in infancy. This trial was registered at clinicaltrials.gov as NCT00613717. (c) 2016 American Society for Nutrition.

A series of thermal-insulating films are prepared by adding the corresponding new thermal insulating materials to polymethyl methacrylate (PMMA) by dissolution-condensation method. On the basis, the microstructure of the thermal barrier film, the corresponding infrared, ultraviolet blocking rate and visible light transmittance are tested by the infrared spectroscopy analyzer and solar film tester (LS183). The thermal-insulating properties of the film are tested by a self-built semi-closed hot box model. The results show that: When the molar ratio of Al to Si is 1:9, the composite material with 5 wt% modified potassium hexatitanate whiskers shows the best infrared radiation blocking performance and the lowest thermal conductivity reaches 0.06036 (W/(m·K)). Based on this, the heat-insulating film prepared with 12 wt% such new composite materials based PMMA exhibits the best heat-radiating resistance：The infrared blocking rate reaches 62.1%, and the ultraviolet blocking rate reaches 73.9%. And the maximum temperature difference can reach 5 °C at an ambient temperature of 40 °C.

Background and Purpose B cell lymphoma 2 (Bcl-2) is a central regulator of cell survival that is overexpressed in the majority of small-cell lung cancers (SCLC) and contributes to both malignant transformation and therapeutic resistance. The purpose of this work was to study the key factors that determine the sensitivity of SCLC cells to Bcl-2 homology domain-3 (BH3) mimetic S1 and the mechanism underlying the resistance of BH3 mimetics. Experimental Approaches Western blot was used to evaluate the contribution of Bcl-2 family members to the cellular response of SCLC cell lines to S1. Acquired resistant cells were derived from initially sensitive H1688 cells. Quantitative PCR and gene silencing were performed to investigate Bcl-2 up-regulation. Key Results A progressive increase in the relative levels of Bcl-2 and phosphorylated Bcl-2 (pBcl-2) characterized the increased de novo and acquired resistance of SCLC cell lines. Furthermore, acute treatment of S1 induced Bcl-2 expression and phosphorylation. We showed that BH3 mimetics, including S1 and ABT-737, induced endoplasmic reticulum (ER) stress and then activated MAPK/ERK pathway. The dual function of MAPK/ERK pathway in defining BH3 mimetics was illustrated; ERK1/2 activation leaded to Bcl-2 transcriptional up-regulation and sustained phosphorylation in naive and acquired resistant SCLC cells. pBcl-2 played a key role in creating resistance of S1 and ABT-737 not only by sequestrating pro-apoptotic proteins, but also sequestrating a positive feedback to promote ERK1/2 activation. Conclusions and Implications These results provide significant novel insights into the molecular mechanisms for crosstalk between ER stress and endogenously apoptotic pathways in SCLC following BH3 mimetics treatment.

B cell lymphoma 2 (Bcl-2) is a central regulator of cell survival that is overexpressed in the majority of small-cell lung cancers (SCLC) and contributes to both malignant transformation and therapeutic resistance. The purpose of this work was to study the key factors that determine the sensitivity of SCLC cells to Bcl-2 homology domain-3 (BH3) mimetic S1 and the mechanism underlying the resistance of BH3 mimetics.Western blot was used to evaluate the contribution of Bcl-2 family members to the cellular response of SCLC cell lines to S1. Acquired resistant cells were derived from initially sensitive H1688 cells. Quantitative PCR and gene silencing were performed to investigate Bcl-2 up-regulation.A progressive increase in the relative levels of Bcl-2 and phosphorylated Bcl-2 (pBcl-2) characterized the increased de novo and acquired resistance of SCLC cell lines. Furthermore, acute treatment of S1 induced Bcl-2 expression and phosphorylation. We showed that BH3 mimetics, including S1 and ABT-737, induced endoplasmic reticulum (ER) stress and then activated MAPK/ERK pathway. The dual function of MAPK/ERK pathway in defining BH3 mimetics was illustrated; ERK1/2 activation leaded to Bcl-2 transcriptional up-regulation and sustained phosphorylation in naïve and acquired resistant SCLC cells. pBcl-2 played a key role in creating resistance of S1 and ABT-737 not only by sequestrating pro-apoptotic proteins, but also sequestrating a positive feedback to promote ERK1/2 activation.These results provide significant novel insights into the molecular mechanisms for crosstalk between ER stress and endogenously apoptotic pathways in SCLC following BH3 mimetics treatment.

Drug resistance in chemotherapy for breast cancer is associated with high levels of P-glycoprotein (P-gp) as well as endoplasmic reticulum (ER) stress. In this paper, we aimed to evaluate the efficacy of a pan-BH3 mimetic S1 on drug-resistant MCF-7/ADR cells, and the roles of S1-induced ER stress in cell death. S1 exhibited greater and faster mitochondrial apoptosis in MCF-7/ADR cells than in MCF-7 cells. We demonstrated by Bax/Bak activation and cyrochrome c release that the p-glycprotein had little influence on S1 entering cells and hitting its targets in MCF-7/ADR cells. An IRE1-mediated ER stress response followed by c-Jun N-terminal kinase (JNK) and extracellular signal-regulated protein kinase (ERK) activation was specifically induced by S1 in MCF-7 cells, but not in MCF-7/ADR cells. Coimmunoprecipitation and western blotting analysis determined that ER stress played a protective role in S1-induced apoptosis by triggering Bcl-2 phosphorylation, which grabbed more pro-apoptotic proteins. The synergism effect of ERK inhibitor PD98059 with S1 confirmed the protective role of ER stress. Defective ER stress in MCF-7/ADR cells confers the more sensitivity toward S1.