Search

The released NOx during fuel combustion is one of the major air pollutants, directly related to acid rain and photochemical smog. At present, there is not an economical and effective method of inhibiting NOx emission from sintering flue gas. Therefore, controlling the conditions of fuel combustion is extremely required for the reduction in NOx. The current research investigated the effects of different combustion parameters on the formation of NOx for three type of coals. The formation of NOx decreased with increasing temperature and heating rate while it increased when oxygen content in an atmosphere increased. Anthracite coal replacement with coke up to 100 pct promoted a decrease in the formed NOx amount and XNO by 21 and 53 pct, respectively. The addition of CaO and FeO enhanced the conversion of nitrogen to NOx, especially at temperatures below 1273 K (1000 °C). Taking both the oxidation reaction to form NOx and reduction reaction of NOx to form N2 into account, the activation energy (EA) values of anthracite and coke were evaluated to be 2.2 and 3.6 kJ/mol, respectively. The combustion of semi-anthracite coal emitted the largest amount of NOx, but the anthracite coal containing less fuel-N than other coals showed the highest value of XNO, which indicates that nitrogen content in coal is not the major factor affecting the formation of NOx. The change in nitrogen functionality after combustion process might be the reason for the unpredicted results in the XNO. The pyrrolic-N in anthracite coal might be considered to be the major functional form that directly affects the conversion of nitrogen to NO.

OBJECTIVES: Polyunsaturated fatty acids (PUFA) such as n-3 PUFA, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and n-6 PUFA, arachidonic acid (AA) may mediate inflammatory responses. Vitamin B6 deficiency has been shown to alter plasma PUFA levels. This perturbation of PUFA metabolism in vitamin B6 deficiency measured by pyridoxal-5’-phosphate (PLP) may contribute to inflammation. Thus, we aimed to examine the associations of 1) dietary EPA + DHA, and vitamin B6 with plasma ratio of AA/(EPA + DHA) by PLP level, 2) plasma AA/(EPA + DHA) and PLP with C-reactive protein (CRP), a marker for inflammation, and 3) dietary EPA + DHA, and vitamin B6 with CRP level, using NHANES. METHODS: NHANES datasets (2003–2004) with subjects ≥20 years were analyzed, accounting for survey design and sample weights (n = 4486). The significance level was P < 0.05. Covariates were age, gender, ethnicity, BMI, smoking, alcohol, total energy, dietary supplements, physical activity, and NSAIDs, depending on analyses. Multiple linear regression assessed the association of dietary EPA + DHA, and vitamin B6 with plasma ratio of AA/(EPA + DHA) by PLP level (Low: 3 mg/L); then, dietary EPA + DHA, and B6 with CRP level. RESULTS: In the low PLP level, dietary EPA + DHA was negatively associated with plasma ratio of AA/(EPA + DHA) (B = ─5.29, SE = 0.84, P = < .0001), but B6 intake was not, whereas, in the high PLP level, both dietary EPA + DHA (B = ─2.99, SE = 0.53, P = < .0001) and dietary vitamin B6 (B = ─0.21, SE = 0.04, P = 0.0001) were inversely associated with plasma AA/(EPA + DHA). Further, low PLP level was associated with greater odds of moderate to high CRP level compared to high PLP level (adjusted OR (aOR): 2.8, 95% CI: 1.93–4.04, P = < .0001), but plasma AA/(EPA + DHA) was not. In addition, both dietary EPA + DHA (aOR: 0.5, 95% CI: 0.23–0.98, P = 0.04) and vitamin B6 (aOR: 0.8, 95% CI: 0.68–0.95, P = 0.009) were inversely associated with moderate to high CRP level. CONCLUSIONS: Our findings show that low plasma PLP level and low vitamin B6 intake are associated with inflammation, and the relationship may be through their effect on PUFA metabolism, suggesting that increased intake of vitamin B6 and EPA and DHA may protect against inflammation. FUNDING SOURCES: N/A.

An improved efficiency of non-fullerene acceptor-based organic solar cells based on PBDB-T : ITIC-m composites has been obtained by using post-additive soaking (PAS) treatments on pristine BHJ films. The PAS-treated BHJ films show improved carrier dynamics in charge transfer and transport, leading to increased photocurrent and fill factors in the photovoltaic devices, followed by a high power conversion efficiency of 12.3%, which is an increase of 28% compared to that of the control device. We found that this superior performance predominantly resulted from improved exciton dissociation and enhanced electron transport after photoexcitation of the ITIC-m phase.

The power conversion efficiency of perovskite solar cells has reached 23.3%. Although significant developments have been made through intensive studies, the stability issue is still challenging. Passivation of perovskite solar cells with a transparent polymer provides better stability; however, there are a few disadvantages of organic polymer such as low thermal stability, weak adhesion and the lack of water retention ability. In this work, we prepared a dual Parylene-F/C layer with 3- methacryloxypropyltrimethoxysilane, A-174, to combine the advantages of organic and inorganic materials. As a result, A-174 treated dual Parylene-F/C layer demonstrated improved passivation effects compared to a single Parylene layer due to the strong binding of Parylene and the water retention ability by SiO2 formed from A-174. This synergetic effects can be expanded to the combination of other organic materials and organosilane compounds.

Methylammonium lead halide (MAPbI3) perovskites are considered as promising materials owing to their excellent optical and electrical properties. However, perovskite materials suffer from degradation in air, which limits their practical applications. Here, we demonstrate successful passivation of the MAPbI3 photodetectors through monochloro-para-xylylene (Parylene-C) deposition. The time-dependent photocurrent characteristics were systematically investigated, and we achieved significantly improved device performance and stability with Parylene-C passivation. Based on the excitation-power-dependent photoluminescence (PL) data, we confirmed that Parylene-C can reduce the carrier losses in MAPbI3, leading to the enhancement of photocurrent and PL in MAPbI3 photodetectors.

Protoheme (hereafter referred to as heme) is an essential cellular cofactor and signaling molecule that is also potentially cytotoxic. To mitigate heme toxicity, heme synthesis and degradation are tightly coupled to heme utilization in order to limit the intracellular concentration of “free” heme. Such a model, however, would suggest that a readily accessible steady-state, bioavailable labile heme (LH) pool is not required for supporting heme-dependent processes. Using the yeast Saccharomyces cerevisiae as a model and fluorescent heme sensors, site-specific heme chelators, and molecular genetic approaches, we found here that 1) yeast cells preferentially use LH in heme-depleted conditions; 2) sequestration of cytosolic LH suppresses heme signaling; and 3) lead (Pb(2+)) stress contributes to a decrease in total heme, but an increase in LH, which correlates with increased heme signaling. We also observed that the proteasome is involved in the regulation of the LH pool and that loss of proteasomal activity sensitizes cells to Pb(2+) effects on heme homeostasis. Overall, these findings suggest an important role for LH in supporting heme-dependent functions in yeast physiology.

Mechanistic details of intramembrane aspartyl protease (IAP) chemistry, which is central to many biological and pathogenic processes, remain largely obscure. Here, we investigated the in vitro kinetics of a microbial intramembrane aspartyl protease (mIAP) fortuitously acting on the renin substrate angiotensinogen and the C-terminal transmembrane segment of amyloid precursor protein (C100), which is cleaved by the presenilin subunit of γ-secretase, an Alzheimer disease (AD)-associated IAP. mIAP variants with substitutions in active-site and putative substrate-gating residues generally exhibit impaired, but not abolished, activity toward angiotensinogen and retain the predominant cleavage site (His–Thr). The aromatic ring, but not the hydroxyl substituent, within Tyr of the catalytic Tyr–Asp (YD) motif plays a catalytic role, and the hydrolysis reaction incorporates bulk water as in soluble aspartyl proteases. mIAP hydrolyzes the transmembrane region of C100 at two major presenilin cleavage sites, one corresponding to the AD-associated Aβ42 peptide (Ala–Thr) and the other to the non-pathogenic Aβ48 (Thr–Leu). For the former site, we observed more favorable kinetics in lipid bilayer–mimicking bicelles than in detergent solution, indicating that substrate–lipid and substrate–enzyme interactions both contribute to catalytic rates. High-resolution MS analyses across four substrates support a preference for threonine at the scissile bond. However, results from threonine-scanning mutagenesis of angiotensinogen demonstrate a competing positional preference for cleavage. Our results indicate that IAP cleavage is controlled by both positional and chemical factors, opening up new avenues for selective IAP inhibition for therapeutic interventions.

OBJECTIVES: Previous evidence suggests that vitamin B6 deficiency may have a deleterious impact on aging and the metabolism of polyunsaturated fatty acids (PUFA). However, the relationship of aging with vitamin B6 status and PUFA metabolism is poorly understood; population-based studies to assess the relationship between plasma pyridoxal 5′-phosphate (PLP; an active form of vitamin B6) and PUFA status for older adults are lacking. Thus, we examined the associations between plasma PLP concentration and plasma PUFA concentrations and ratios [eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), arachidonic acid (AA), EPA + DHA, EPA/AA, and (EPA + DHA)/AA] among US older adults. We further investigated the association of adequate (PLP ≥ 20 nmol/L) versus deficient (PLP

Vitamin B6-restricted diets and low plasma pyridoxal 5′-phosphate (PLP) status altered plasma polyunsaturated fatty acids (PUFA) compositions. Evidence suggests the role of gender in the metabolism of vitamin B6 and PUFA. However, no epidemiologic study examined the impact of gender on the relationship between vitamin B6 and PUFA status in adults. Thus, we investigated whether there were gender differences in the association of vitamin B6 intake and plasma PLP concentration with plasma PUFA concentrations and ratios (eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), arachidonic acid (AA), EPA + DHA, EPA/AA, (EPA + DHA)/AA) in US young/middle-aged adults. In total, 864 participants (20–59 years, 484 men, 380 women) from the National Health and Nutrition Examination Survey (NHANES) 2003–2004 were used for this cross-sectional study. Nutrient intakes were estimated from two 24 h recalls and supplement questionnaires, plasma PLP and PUFA were measured. Multivariate linear regression was utilized to obtain unstandardized (b) and standardized (β) coefficients. Covariates included demographic, socioeconomic, dietary variables, physical activity level, cigarette smoking status, alcohol consumption, prescription medication use, and BMI. There were significant interactions between gender and PLP on EPA (P-interaction = 0.004), DHA (P-interaction = 0.020), EPA + DHA (P-interaction = 0.010), EPA/AA (P-interaction = 0.002), (EPA + DHA)/AA (P-interaction = 0.004), whereas no interaction between gender and B6 intake existed. In gender-stratified analyses, in men, PLP was positively associated with EPA (β = 0.138, b = 0.104, p = 0.0004), DHA (β = 0.101, b = 0.058, p = 0.036), EPA + DHA (β = 0.125, b = 0.073, p = 0.005), EPA/AA (β = 0.144, b = 0.099, p = 0.0002), (EPA + DHA)/AA (β = 0.123, b = 0.068, p = 0.005). However, no associations between PLP and PUFA existed in women. In conclusion, gender differences were found in the relationships between plasma PLP and plasma EPA, DHA, EPA + DHA, EPA/AA, and (EPA + DHA)/AA, with significant direct associations in men only among US young/middle-aged adults.

The increasing lifespan in developed countries results in age-associated chronic diseases. Biological aging is a complex process associated with accumulated cellular damage by environmental or genetic factors with increasing age. Aging results in marked changes in brain structure and function. Age-related neurodegenerative diseases and disorders (NDDs) represent an ever-growing socioeconomic challenge and lead to an overall reduction in quality of life around the world. Alzheimer’s disease (AD) and Parkinson’s disease (PD) are most common degenerative neurological disorders of the central nervous system (CNS) in aging process. The low levels of acetylcholine and dopamine are major neuropathological feature of NDDs in addition to oxidative stress, intracellular calcium ion imbalance, mitochondrial dysfunction, ubiquitin-proteasome system impairment and endoplasmic reticulum stress. Current treatments minimally influence these diseases and are ineffective in curing the multifunctional pathological mechanisms. Synthetic neuroprotective agents sometimes have negative reactions as an adverse effect in humans. Recently, numerous ethnobotanical studies have reported that herbal medicines for the treatment or prevention of NDDs are significantly better than synthetic drug treatment. Medicinal herbs have traditionally been used around the world for centuries. Radix Glycyrrhizae (RG) is the dried roots and rhizomes of Glycyrrhiza uralensis or G. glabra or G. inflata from the Leguminosae/Fabaceae family. It has been used for centuries in traditional medicine as a life enhancer, for the treatment of coughs and influenza, and for detoxification. Diverse chemical constituents from RG have reported including flavanones, chalcones, triterpenoid saponins, coumarines, and other glycosides. Among them, flavanone liquiritigenin (LG) and its precursor and isomer chalcone isoliquiritigenin (ILG) are the main bioactive constituents of RG. In the present review, we summarize evidence in the literature on the structure and phytochemical properties and pharmacological applications of LG and ILG in age-related diseases to establish new therapeutics to improve human health and lifespan.

Dopamine (DA), an organic chemical neurotransmitter in the human brain, plays important roles in neuronal reward, motor control, and decision making. Thus, accurate quantification of DA concentration is essential for the investigation of various dopaminergic neural circuits and diagnosis of neurological diseases. Herein, we report an overoxidized polypyrrole/sodium dodecyl sulfate (SDS)-modified multi-walled carbon nanotube (OPPy/SDS-CNT) electrode which allows detection of DA with high resolution and selectivity. By using SDS as a dopant and sodium hydroxide (NaOH) as an oxidizing agent, highly sensitive detection of DA down to 5 nM with a detection limit of 136 pM is achieved. Moreover, due to the strong electrostatic interaction between the negatively-charged electrode and the positively-charged DA molecules, selective electrochemical detection of DA is successfully demonstrated in the presence of ascorbic acid (AA) and glucose (Glc). Lastly, by demonstrating in vitro detection of DA secreted from dopaminergic cells (PC12 cells) and examining biocompatibility of the electrode, we show the potential of our OPPy/SDS-CNT electrode as a promising candidate for a functional neural interface for in vitro and in vivo monitoring of DA concentrations.

Angiotensin II (Ang II)-mediated modification of the redox milieu of vascular smooth muscle cells (VSMCs) has been implicated in several pathophysiological processes, including cell proliferation, migration and differentiation. In this study, we demonstrate that the peroxisome proliferator-activated receptor (PPAR) δ counteracts Ang II-induced production of reactive oxygen species (ROS) in VSMCs. Activation of PPARδ by GW501516, a specific ligand for PPARδ, significantly reduced Ang II-induced ROS generation in VSMCs. This effect was, however, reversed in the presence of small interfering (si)RNA against PPARδ. The marked increase in ROS levels induced by Ang II was also eliminated by the inhibition of phosphatidylinositol 3-kinase (PI3K) but not of protein kinase C, suggesting the involvement of the PI3K/Akt signalling pathway in this process. Accordingly, ablation of Akt with siRNA further enhanced the inhibitory effects of GW501516 in Ang II-induced superoxide production. Ligand-activated PPARδ also blocked Ang II-induced translocation of Rac1 to the cell membrane, inhibiting the activation of NADPH oxidases and consequently ROS generation. These results indicate that ligand-activated PPARδ plays an important role in the cellular response to oxidative stress by decreasing ROS generated by Ang II in vascular cells.

This paper describes a useful means of noninvasively enhancing transdermal delivery efficiency. For this, chitosan nanocapsules with positive surface charges were fabricated by using the in situ precipitation method. These nanocapsules cannot only have an ability to encapsulate the drug molecule (this study used riboflavin 5′-monophosphate), but also electrotatically interact with the stratum corneum layer. To demonstrate this, fluorescence-labeled polymer nanoparticles with different particle sizes as well as surface charges were topically applied onto the skin and their distribution was directly imaged. This demonstration experiment allowed us to figure out that once the nanocapsules were provided with positive surface charges, they readily deposited into the stratum corneum layer due to the electrostatic interaction. Further quantitative characterization of the penetrating amount of riboflavin 5′-monophosphate by using the Frantz diffusion cell method showed that our chitosan nanocapsule system effectively improved transdermal delivery efficiency.

Tea catechin is one of the compounds that are closely related to obesity and insulin sensitivity. In order to determine the effect of catechin on adipocyte differentiation, we treated 3T3-L1 preadipocytes with different kinds of catechins. Our results showed that catechins, especially epigallocatechin gallate (EGCG), significantly reduced intracellular lipid accumulation and repressed the activity of glycerol-3-phosphate dehydrogenase, an enzyme involved in lipid synthesis. Furthermore, glucose and fatty acid transport were also suppressed by catechin. We then analyzed the activity of transcription factors—forkhead transcription factor class O1 (FoxO1) and sterol regulatory element-binding protein-1c (SREBP1c)—which are involved in adipocyte differentiation and lipid synthesis, respectively. The transcriptional activities of both these factors significantly decreased by EGCG. Western blot analysis revealed that EGCG induced the insulin signal-mediated phosphorylation of FoxO1 (Thr24, Ser256). These results suggest that EGCG suppresses the differentiation of adipocytes through the inactivation of FoxO1 and SREBP1c.

A cluster of oligonucleotide repeat sequences was identified that is linked to the melon (Cucumis melo L.) andromonoecious (a) locus, which controls andromonoecy. Six different repeat units, ranging from 11 to 49 base pairs, were clustered within a 0.6-kb intergenic region. The number of repeat units varied from two to six. After sequence analysis of diverse melon germplasms, four haplotypes of this cluster were identified. Length variations among the four haplotypes resulted from insertion or deletion of repeat sequences. Particularly, a tandem array of six repeats of 21 nucleotides was a hotspot for insertion/deletion mutations. A simple PCR-based marker was developed to identify haplotypes of this cluster based on the length polymorphism. In practice, this marker was successfully used in genetic purity tests of melon F1 hybrid cultivars. Four self-pollinated contaminants, which were confirmed by phenotypic examination in grow-out tests, were easily discriminated from 99 F1 hybrid individuals. In addition, the genetic distance between this marker and the andromonoecious (a) locus was calculated as 7.9 cM, after analyzing melon F2 populations originating from a cross between monoecious and andromonoecious parental lines. Therefore, this marker will be useful as a recombinant selection marker in marker-assisted backcrossing of monoecy in melon breeding programs.

EGCG [(−)-epigallocatechin gallate], tea catechin, is one of the compounds that has been reported to act against obesity and diabetes. To determine the effect of EGCG on adipocyte differentiation, we treated 3T3-L1 preadipocytes with different catechins. Oil Red O staining showed significantly reduced intracellular lipid accumulation, especially with EGCG. Cell cycle analysis showed that EGCG inhibited cell proliferation by disturbing the cell cycle during the clonal expansion of 3T3-L1. RT-PCR (real-time PCR) demonstrated that EGCG noticeably reduced mRNA expression of PPARγ (peroxisome proliferator-activated receptor γ), C/EBPα (CCAAT/enhancer-binding protein α) and FoxO1 (forkhead box class O1). EGCG also caused a significant decrease in the transcription of FoxO1 – the forkhead transcription factor class O1 involved in adipocyte differentiation – via the PI3K (phosphoinositide 3-kinase)/Akt and MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase] pathways. These results suggest that EGCG suppresses the clonal expansion of adipocytes by inactivating FoxO1 via insulin signalling and stress-dependent MAPK pathways.

Increased adipose tissue positively correlates with circulating inflammatory cytokines such as IL-6. We previously reported that adipose stem cells from genetically obese ob/ob mice produce significantly higher levels of IL-6 compared with other cell types such as adipocytes and macrophages within adipose tissue. We also demonstrated that (n-3) PUFA have antiinflammatory effects on adipocyte IL-6 secretion. Based on these findings, we hypothesized that EPA [20:5 (n-3)] and stearidonic acid [SDA, 18:4 (n-3)] would decrease LPS (200 μg/L)-induced IL-6 secretion and IL-6 mRNA content in the adipose stem cells. SDA (100 μmol/L) and EPA (100 μmol/L) significantly reduced LPS-induced IL-6 secretion and decreased IL-6 mRNA expression. To determine the underlying intracellular mechanisms, we tested whether LPS-induced Toll-like-receptor (TLR) 4 and TLR2 expression were modulated by these fatty acids using Western-blot analysis. EPA and SDA suppressed LPS-induced TLR2 but not TLR4 protein expression in the adipose stem cells. Furthermore, SDA and EPA significantly lowered the activation and translocation of NF-κB, a TLR2 downstream signaling target, while protein expression of extracellular signal-regulated kinases-1/2 were unaffected. Collectively, our results suggest that EPA and SDA inhibit LPS-induced IL-6 secretion and IL-6 mRNA expression in the adipose stem cells by decreasing TRL2-mediated signaling pathways.