Effect of support structure of Pt/silicaite-1 catalyst on non-thermal plasma (NTP) assisted chlorobenzene degradation and PCDD/Fs formation.

Development of efficient catalysts for non-thermal plasma (NTP) assisted catalysis to mitigate the formation of harmful by-products is a significant challenge in the degradation of chlorinated volatile organic compounds (Cl-VOCs). In this study, catalytically active Pt nanoparticles supported on non-porous SiO2 and silicalite-1 zeolites (S1) with different pore structure were comparatively investigated for catalytic chlorobenzene degradation under NTP condition. It was shown that the pore structure could significantly impact the metal size and metal dispersion rate. Pt supported on modified S1 hierarchical meso-micro-porous silicalite-1 (Pt/D-S1) exhibited the smallest particle size (∼6.19 nm) and the highest dispersion rate (∼1.87). Additionally, Pt/D-S1 demonstrated superior catalytic performance compared to the other catalysts, achieving the highest chlorobenzene conversion and COx selectivity at about 80% and 75%, respectively. Furthermore, the pore structure also affected the formation of by-products according to the findings from GC-MS analysis. Pt/SiO2 generated a total of 18 different species of organic compounds, whereas only 12 species of organic by-products were identified in the Pt/D-S1 system (e.g. polychlorinated compounds like 3,4 dichlorophenol were exclusively identified in Pt/SiO2). Moreover, dioxin-like polychlorinated biphenyl and other chlorinated organic compounds, which have potential to form highly toxic dioxins, were detected in the catalysts. HRGC-HRMS confirmed and quantified the 17 different dioxin/furans formed on Pt/SiO2 (25,100 ng TEQ kg-1), Pt/S1 (515 ng TEQ kg-1) and Pt/D-S1 (367 ng TEQ kg-1). The correlation between synthesis-structure-performance in this study provides insights into the design of catalysts for deep oxidation of Cl-VOCs in NTP system.

Improving the Quality of Bio-oil Using the Interaction of Plastics and Biomass through Copyrolysis Coupled with Nonthermal Plasma Processing.

Bio-oil produced from the pyrolysis of biomass is chemically complex, viscous, highly acidic, and highly oxygenated. Copyrolysis of biomass and plastics can enhance oil quality by raising the H/C ratio, leading to improved biofuel properties. In this work, copyrolysis of polystyrene and biomass was passed to a second-stage dielectric barrier discharge nonthermal plasma reactor with the aim to further improve the product bio-oil. Pyrolysis of the polystyrene and biomass produces volatiles that pass to the second stage to undergo cracking and autohydrogenation reactions under nonthermal plasma conditions. There was a synergistic interaction between biomass and polystyrene in terms of overall oil and gas yield and composition even in the absence of the nonthermal plasma. However, the introduction of the nonthermal plasma produced a marked increase in monocyclic aromatic hydrocarbons (e.g., ethylbenzene), whereas polycyclic aromatic compounds decreased in concentration. Most notably, the influence of the plasma markedly reduced the quantity of oxygenated compounds in the product oil. It is suggested that the unique reactive environment produced by the plasma involving high-energy electrons, excited radicals, ions, and intermediates increases the interaction of the polystyrene and biomass pyrolysis volatiles. Increasing input plasma power from 50 to 70 W further enhanced the effects of the nonthermal plasma.

Dechlorination of waste polyvinyl chloride (PVC) through non-thermal plasma.

Dechlorination is essential for the chemical recycling of waste polyvinyl chloride (PVC) plastics. This study investigated the use of non-thermal plasma (NTP) for chlorine removal, with a focus on the effects of treatment time and discharge power on dechlorination efficiency. The results showed that longer treatment times and higher discharge powers led to better dechlorination performance. The maximum efficiency (98.25%) and HCl recovery yield (55.72%) were achieved at 180 W power after 40 min of treatment where 96.44% of Cl existed in the form of HCl gas, 1.44% in the liquid product, and 2.12% in the solid residue product. NTP at a discharge power of 150 W showed better dechlorination performance compared to traditional thermal pyrolysis treatment in temperatures ranging from 200 to 400 °C. The activation energy analysis of the chlorine removal showed that compared to pyrolysis-based dechlorination (137.09 kJ/mol), NTP-based dechlorination (23.62 kJ/mol) was more easily achievable. This work presents a practical method for the dechlorination of waste PVC plastic using a novel technology without requiring additional thermal and pressure input.

Hydrogen Production by Three-Stage (i) Pyrolysis, (ii) Catalytic Steam Reforming, and (iii) Water Gas Shift Processing of Waste Plastic.

The three-stage (i) pyrolysis, (ii) catalytic steam reforming, and (iii) water gas shift processing of waste plastic for the production of hydrogen have been investigated. The (i) pyrolysis and (ii) catalytic steam reforming process conditions were maintained throughout, and the experimental program investigated the influence of process conditions in the (iii) water gas shift reactor in terms of catalyst type (metal-alumina), catalyst temperature, steam/carbon ratio, and catalyst support material. The metal-alumina catalysts investigated in the (iii) water gas shift stage showed distinct maximization of hydrogen yield, which was dependent on the catalyst type at either higher temperature (550 °C) (Fe/Al2O3, Zn/Al2O3, Mn/Al2O3) or lower temperature (350 °C) (Cu/Al2O3, Co/Al2O3). The highest hydrogen yield was found with the Fe/Al2O3 catalyst; also, increased catalyst Fe metal loading resulted in improved catalytic performance, with hydrogen yield increasing from 107 mmol gplastic -1 at 5 wt % Fe loading to 122 mmol gplastic -1 at 40 wt % Fe/Al2O3 Fe loading. Increased addition of steam to the (iii) water gas shift reactor in the presence of the Fe/Al2O3 catalyst resulted in higher hydrogen yield; however, as further steam was added, the hydrogen yield decreased due to catalyst saturation. The Fe-based catalyst support materials investigated alumina (Al2O3), dolomite, MCM-41, silica (SiO2), and Y-zeolite; all showed similar hydrogen yields of ∼118 mmol gplastic -1, except for the Fe/MCM-41 catalyst, which produced only 88 mmol gplastic -1 of hydrogen yield.

SARS-CoV-2 Aerosol and Surface Detections in COVID-19 Testing Centers and Implications for Transmission Risk in Public Facing Workers.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and resulting COVID-19 (coronavirus disease 2019) pandemic have required mass diagnostic testing, often taking place in testing sites within hospitals, clinics, or at satellite locations. To establish the potential of SARS-CoV-2 aerosol transmission and to identify junctures during testing that result in increased viral exposure, aerosol and surface samples were examined for the presence of SARS-CoV-2 RNA from locations within Nebraska Medicine COVID-19 testing and vaccine clinics. Aerosols containing SARS-CoV-2 RNA detected within clinics suggest viral shedding from infected individuals. SARS-CoV-2 RNA detection in aerosol samples was shown to correlate with clinic operation and patient infection, as well as with community infection findings. Additionally, SARS-CoV-2 RNA was detected in surface samples collected from clinics. The presence of SARS-CoV-2 RNA in aerosols in these clinics supports the continued use of respiratory protection and sanitization practices for healthcare workers, and other workers with public facing occupations.

Recent advances in the abatement of volatile organic compounds (VOCs) and chlorinated-VOCs by non-thermal plasma technology: A review.

Most of the volatile organic compounds (VOCs) and especially the chlorinated volatile organic compounds (Cl-VOCs), are regarded as major pollutants due to their properties of volatility, diffusivity and toxicity which pose a significant threat to human health and the eco-environment. Catalytic degradation of VOCs and Cl-VOCs to harmless products is a promising approach to mitigate the issues caused by VOCs and Cl-VOCs. Non-thermal plasma (NTP) assisted catalysis is a promising technology for the efficient degradation of VOCs and Cl-VOCs with higher selectivity under relatively mild conditions compared with conventional thermal catalysis. This review summarises state-of-the-art research of the in plasma catalysis (IPC) of VOCs degradation from three major aspects including: (i) the design of catalysts, (ii) the strategies of deep catalytic degradation and by-products inhibition, and (iii) the fundamental research into mechanisms of NTP activated catalytic VOCs degradation. Particular attention is also given to Cl-VOCs due to their characteristic properties of higher stability and toxicity. The catalysts used for the degradation Cl-VOCs, chlorinated by-products formation and the degradation mechanism of Cl-VOCs are systematically reviewed in each chapter. Finally, a perspective on future challenges and opportunities in the development of NTP assisted VOCs catalytic degradation were discussed.

Quantile-Specific Heritability of Mean Platelet Volume, Leukocyte Count, and Other Blood Cell Phenotypes.

INTRODUCTION: "Quantile-dependent expressivity" occurs when the effect size of a genetic variant depends upon whether the phenotype (e.g., mean platelet volume, MPV) is high or low relative to its distribution. METHODS: Offspring-parent regression slopes (ßOP) were estimated by quantile regression, from which quantile-specific heritabilities (h2) were calculated (h2 = 2ßOP/[1 + rspouse]) for blood cell phenotypes in 3,929 parent-offspring pairs from the Framingham Heart Study. RESULTS: Quantile-specific h2 (±SE) increased with increasing percentiles of the offspring's age- and sex-adjusted MPV distribution (plinear = 0.0001): 0.48 ± 0.09 at the 10th, 0.53 ± 0.04 at the 25th, 0.70 ± 0.06 at the 50th, 0.74 ± 0.06 at the 75th, and 0.90 ± 0.12 at the 90th percentile. Quantile-specific h2 also increased with increasing percentiles of the offspring's white blood cell (WBC, plinear = 0.002), monocyte (plinear = 0.01), and eosinophil distributions (plinear = 0.0005). In contrast, heritibilities of red blood cell (RBC) count, hematocrit (HCT), and hemoglobin (HGB) showed little evidence of quantile dependence. Quantile-dependent expressivity is consistent with gene-environment interactions reported by others, including (1) greater increases in WBC and PLT concentrations in subjects who are glutathione-S-transferase Mu1 (GSTM1) null homozygotes than GSTM1 sufficient when exposed to endotoxin; (2) significantly higher WBC count in AA homozygotes than carriers of the G-allele of the glutathione S-transferase P1 (GSTP1) rs1695 polymorphism at low but not high benzene exposure in shoe factory workers; (3) higher WBC counts in TT homozygotes than C-allele carriers of the interleukin-1ß (IL1B) c.315C>T polymorphism after undergoing surgery for infective endocarditis but not before surgery. DISCUSSION/CONCLUSION: Quantile-dependent expressivity may explain several purported gene-environment interactions involving blood cell phenotypes.

Quantile-Dependent Expressivity of Serum Interleukin-6 Concentrations as a Possible Explanation of Gene-Disease Interactions, Gene-Environment Interactions, and Pharmacogenetic Effects.

Interleukin 6 (IL-6) is a moderately heritable pleiotropic cytokine whose elevated concentrations in coronary artery disease, peripheral arterial disease, pulmonary arterial hypertension, Eales' disease, Sjògren's syndrome, osteoarthritis, adenocarcinoma, neuroblastoma, polymyalgia rheumatica, pulmonary tuberculosis, and enterovirus 71 infection, and following coronary artery bypass graft show larger genetic effects than in unaffected low IL-6 controls. We hypothesize that genetic effects may depend upon whether average IL-6 concentrations are high or low, i.e., quantile-dependent expressivity. Quantile-specific offspring-parent (ßOP) and full-sib regression slopes (ßFS) were estimated by applying quantile regression to the age- and sex-adjusted serum IL-6 concentrations in families surveyed in the Framingham Heart Study. Quantile-specific heritabilities were calculated as h2 = 2ßOP / (1 + rspouse) and h2 = {(1 + 8rspouseßFS)0.5 -1} / (2rspouse)). Heritability (h2 ± SE) of IL-6 concentrations increased from 0.01 ± 0.01 at the 10th percentile (NS), 0.02 ± 0.01 at the 25th (P = 0.009), 0.03 ± 0.01 at the 50th (P = 0.007), 0.04 ± 0.02 at the 75th (P = 0.004), and 0.13 ± 0.05 at the 90th percentile (P = 0.03), or 0.0005 ± 0.0002 for each 1% increase in the offspring's phenotype distribution (Plinear trend = 0.02) when estimated from ßOP and from 0.02 ± 0.02 at the 10th (NS), 0.02 ± 0.02 at the 25th (NS), 0.06 ± 0.02 at the 50th (P = 0.01), 0.12 ± 0.04 at the 75th (P = 0.001), and 0.30 ± 0.03 at the 90th percentile (P < 10-16), or 0.0015 ± 0.0007 for each 1% increase in the sibling phenotype distribution (Plinear trend = 0.02) when estimated from ßFS. Thus the heritability of serum IL-6 concentrations is quantile dependent, which may contribute in part to the larger genetic effect size reported for diseases and environmental conditions that elevate IL-6 concentrations vis-à-vis unaffected controls.

Quantile-Specific Heritability of Inflammatory and Oxidative Stress Biomarkers Linked to Cardiovascular Disease.

PURPOSE: Heritability (h2 , the proportion of the phenotypic variance attributable to additive genetic effects) is traditionally assumed to be constant throughout the distribution of the phenotype. However, the heritabilities of circulating C-reactive protein, interleukin-6, plasminogen activator inhibitor type-1 (PAI-1), and monocyte chemoattractant protein-1 (MCP-1) concentrations depend upon whether the phenotype is high or low relative to their distributions (quantile-dependent expressivity), which may account for apparent gene-environment interactions. Whether the heritabilities of other inflammatory biomarkers linked to cardiovascular disease are quantile-dependent remain to be determined. PATIENTS AND METHODS: Quantile-specific offspring-parent (ßOP) and full-sib regression slopes (ßFS) were estimated by applying quantile regression to the age- and sex-adjusted phenotypes of families surveyed as part of the Framingham Heart Study. Quantile-specific heritabilities were calculated as: h2 =2ßOP/(1+rspouse) and h2 ={(1+8rspouseßFS)0.5-1}/(2rspouse). RESULTS: Heritability (h2 ± SE) of lipoprotein-associated phospholipase A2 (Lp-PLA2) mass concentrations increased from 0.11 ± 0.03 at the 10th percentile, 0.08 ± 0.03 at the 25th, 0.12 ± 0.03 at the 50th, 0.20 ± 0.04 at the 75th, and 0.26 ± 0.06 at the 90th percentile, or 0.0023 ± 0.0006 per each one-percent increase in the phenotype distribution (Plinear trend= 0.0004). Similarly, h2 increased 0.0029 ± 0.0011 (Plinear trend= 0.01) for sP-selectin, 0.0032 ± 0.0009 (Plinear trend= 0.0001) for soluble intercellular adhesion molecule 1 (sICAM-1), and 0.0026 ± 0.0006 for tumor necrosis factor receptor 2 (TNFR2) (Plinear trend= 5.0 × 10-6) per each one-percent increase in their distributions when estimated from ßOP. Osteoprotegerin and soluble ST2 heritability also increased significantly with increasing percentiles of their distributions when estimated from ßFS. Lp-PLA2 activity, CD40 ligand, TNFα, interleukin-18, and myeloperoxidase heritability showed no significant quantile-dependence. CONCLUSION: The heritabilities of circulating Lp-PLA2-mass, sP-selectin, sICAM-1, TNFR2, osteoprotegerin and soluble ST2 concentrations are quantile-dependent, which may contribute to purported genetic modulations of: 1) sP-selectin's relationships to venous thrombosis, pulmonary hypertension, type 2 diabetes and atorvastatin treatment; 2) sICAM-I's relationships to brain abscess and atorvastatin treatment; and 3) Lp-PLA2's relationships to myocardial infarction and preeclampsia.

Quantile-specific heritability of plasma fibrinogen concentrations.

BACKGROUND: Fibrinogen is a moderately heritable blood protein showing different genetic effects by sex, race, smoking status, pollution exposure, and disease status. These interactions may be explained in part by "quantile-dependent expressivity", where the effect size of a genetic variant depends upon whether the phenotype (e.g. plasma fibrinogen concentration) is high or low relative to its distribution. PURPOSE: Determine whether fibrinogen heritability (h2) is quantile-specific, and whether quantile-specific h2 could account for fibrinogen gene-environment interactions. METHODS: Plasma fibrinogen concentrations from 5689 offspring-parent pairs and 1932 sibships from the Framingham Heart Study were analyzed. Quantile-specific heritability from offspring-parent (ßOP, h2 = 2ßOP/(1+rspouse)) and full-sib regression slopes (ßFS, h2 = {(1+8rspouseßFS)0.05-1}/(2rspouse)) were robustly estimated by quantile regression with nonparametric significance assigned from 1000 bootstrap samples. RESULTS: Quantile-specific h2 (±SE) increased with increasing percentiles of the offspring's age- and sex-adjusted fibrinogen distribution when estimated from ßOP (Ptrend = 5.5x10-6): 0.30±0.05 at the 10th, 0.37±0.04 at the 25th, 0.48±0.05 at the 50th, 0.61±0.06 at the 75th, and 0.65±0.08 at the 90th percentile, and when estimated from ßFS (Ptrend = 0.008): 0.28±0.04 at the 10th, 0.31±0.04 at the 25th, 0.36±0.03 at the 50th, 0.41±0.05 at the 75th, and 0.50±0.06 at the 90th percentile. The larger genetic effect at higher average fibrinogen concentrations may contribute to fibrinogen's greater heritability in women than men and in Blacks than Whites, and greater increase from smoking and air pollution for the FGB -455G>A A-allele. It may also explain greater fibrinogen differences between: 1) FGB -455G>A genotypes during acute phase reactions than usual conditions, 2) GTSM1 and IL-6 -572C>G genotypes in smokers than nonsmokers, 3) FGB -148C>T genotypes in untreated than treated diabetics, and LPL PvuII genotypes in macroalbuminuric than normoalbuminuric patients. CONCLUSION: Fibrinogen heritability is quantile specific, which may explain or contribute to its gene-environment interactions. The analyses do not disprove the traditional gene-environment interpretations of these examples, rather quantile-dependent expressivity provides an alternative explanation that warrants consideration.

Quantile-Dependent Heritability of Glucose, Insulin, Proinsulin, Insulin Resistance, and Glycated Hemoglobin.

BACKGROUND: "Quantile-dependent expressivity" is a dependence of genetic effects on whether the phenotype (e.g., insulin resistance) is high or low relative to its distribution. METHODS: Quantile-specific offspring-parent regression slopes (ßOP) were estimated by quantile regression for fasting glucose concentrations in 6,453 offspring-parent pairs from the Framingham Heart Study. RESULTS: Quantile-specific heritability (h2), estimated by 2ßOP/(1 + rspouse), increased 0.0045 ± 0.0007 (p = 8.8 × 10-14) for each 1% increment in the fasting glucose distribution, that is, h2 ± SE were 0.057 ± 0.021, 0.095 ± 0.024, 0.146 ± 0.019, 0.293 ± 0.038, and 0.456 ± 0.061 at the 10th, 25th, 50th, 75th, and 90th percentiles of the fasting glucose distribution, respectively. Significant increases in quantile-specific heritability were also suggested for fasting insulin (p = 1.2 × 10-6), homeostatic model assessment of insulin resistance (HOMA-IR, p = 5.3 × 10-5), insulin/glucose ratio (p = 3.9 × 10-5), proinsulin (p = 1.4 × 10-6), proinsulin/insulin ratio (p = 2.7 × 10-5), and glucose concentrations during a glucose tolerance test (p = 0.001), and their logarithmically transformed values. DISCUSSION/CONCLUSION: These findings suggest alternative interpretations to precision medicine and gene-environment interactions, including alternative interpretation of reported synergisms between ACE, ADRB3, PPAR-γ2, and TNF-α polymorphisms and being born small for gestational age on adult insulin resistance (fetal origin theory), and gene-adiposity (APOE, ENPP1, GCKR, IGF2BP2, IL-6, IRS-1, KIAA0280, LEPR, MFHAS1, RETN, TCF7L2), gene-exercise (INS), gene-diet (ACSL1, ELOVL6, IRS-1, PLIN, S100A9), and gene-socioeconomic interactions.

Quantile-specific heritability of monocyte chemoattractant protein-1, and relevance to rs1024611-disease interactions.

BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) concentrations are 34% to 47% heritable. Larger -2518 G/A (rs1024611) genotypes differences are reported for: 1) MCP-1 production in stimulated vs. basal cells; and 2) MCP-1 concentrations in diseased (sepsis, brain abscess, hepatitis B virus, Alzheimer's disease, Behcet's disease, and systemic lupus erythematosus) vs. healthy patients. Those results suggest that the -2518 G/A effect size may depend on whether the phenotype is high or low relative to its distribution (quantile-dependent expressivity). METHOD: To test whether quantile-dependent expressivity applies more broadly to genetic influences on MCP-1 concentrations, quantile-specific offspring-parent (ßOP) and full-sib regression slopes (ßFS) were estimated by applying quantile regression to the age- and sex-adjusted serum MCP-1 concentrations of Framingham Heart Study families. Quantile-specific heritabilities were calculated as h2 = 2ßOP/(1 + rspouse) and h2={(1 + 8rspouseßFS)0.5-1}/(2rspouse)). RESULTS: Heritability (h2 ± SE) of MCP-1 concentrations increased from 0.15 ± 0.05 at the 10th percentile of the MCP-1 distribution, 0.23 ± 0.04 at the 25th, 0.32 ± 0.05 at the 50th, 0.43 ± 0.07 at the 75th, and 0.44 ± 0.07 at the 90th percentile, or an 0.0041 ± 0.0009 increase for each one-percent increment in the MCP-1 distribution (Plinear trend = 2.4 × 10-5) when estimated from ßOP, and (Plinear trend = 7.7 × 10-9) when estimated from ßFS. Compared to the 10th percentile, ßOP-estimated h2 was 3-fold greater at the 90th percentile (Pdifference = 0.0003), and 6.9-fold greater when estimated from ßFS (Pdifference = 3.3 × 10-6). Re-analysis of in vivo comparison of MCP-1 concentrations in controls vs. patients with MCP-1-elevating conditions, and in vitro studies of MCP-1 production in basal vs. stimulated cells, show rs1024611 genotypes differences that were consistent with quantile-dependent expressivity. CONCLUSION: The heritability of circulating MCP-1 concentrations is quantile-dependent.

Quantile-specific heritability of 8-isoprostane and the modulating effects of smoking, alcohol, cardiovascular disease and diabetes on 8-isoprostane-gene interactions.

BACKGROUND: Urinary 8-isoprostane provides a significantly heritable measure of oxidative stress. Prior reports suggest that genetic variants may modulate oxidative stress due to smoking, other environmental factors, and disease. Alternatively, these apparent modulations may reflect a dependence of genetic effects on 8-isoprostane concentrations. METHOD: To test whether genetic effects on 8-isoprostane concentrations are quantile-dependent, quantile-specific offspring-parent (ßOP) and full-sib regression slopes (ßFS) were estimated by applying quantile regression to the age- and sex-adjusted creatinine-standardized urinary 8-isoprostane concentrations of Framingham Heart Study families. Quantile-specific heritabilities were calculated as h2 = 2ßOP/(1+rspouse) and h2 = {(1+8rspouseßFS)0.5-1}/(2rspouse)). RESULTS: Spouse 8-isoprostane concentrations were weakly concordant (rspouse = 0.06). 8-isoprostane heritability (h2±SE) increased significantly with increasing percentiles of its distribution (Plinear trend = 0.0009, Pquadratic trend = 0.0007, Pcubic trend = 0.003) when estimated from ßOP, and when estimated from ßFS (Plinear trend = 0.005, Pquadratic trend = 0.09, Pcubic trend = 0.06). Compared to the 10th percentile, ßOP-estimated h2 was over 22-fold greater at the 90th percentile (Pdifference = 9.2 × 10-5), and 5.3-fold greater when estimated from ßFS (Pdifference = 0.004). Significantly higher 8-isoprostane heritability in smokers than nonsmokers (0.352 ± 0.147 vs. 0.061 ± 0.036, Pdifference = 0.01), and heavier than lighter drinkers (0.449 ± 0.216 vs. 0.078 ± 0.037, Pdifference = 0.01) were eliminated when corrected for the higher 8-isoprostane concentrations of the smokers and heavier drinkers. CONCLUSION: Heritability of oxidative stress as measured by 8-isoprostane is quantile-dependent, which may contribute to the larger reported effects on oxidative stress by UCP2 -866G > A, IL6 -572C > G and LTA 252A > G polymorphisms in smokers than nonsmokers, by the UCP2 -866G > A polymorphism in coronary heart disease patients, by the ESRRG rs1890552 A > G polymorphism in type 2 diabetics, by the CYBA 242C > T polymorphism after exercise training, by the PLIN 11482G > A/14995A > T haplotype before weight loss, and by the CYBA -930A > G and GSTP1 I105V haplotypes in patients with pulmonary edema.

High-value products from ex-situ catalytic pyrolysis of polypropylene waste using iron-based catalysts: the influence of support materials.

Catalytic pyrolysis is considered a promising strategy for the utilisation of plastic waste from the economic and environmental perspectives. As such, the supporting materials play a critical role in the properties of the catalyst. This study clarified this influence on the dispersion of the iron (Fe) within an experimental context. Four different types of typical supports with different physical structures were introduced and explored in a two-stage fixed-bed reactor; these included metallic oxides (Al2O3, TiO2), a non-metallic oxide (SiO2), and molecular sieves (ZSM-5). The results show that the liquid products were converted into carbon deposits and lighter gaseous products, such as hydrogen. The Al2O3-supported catalyst with a relatively moderate specific surface areas and average pore diameter exhibited improved metal distribution with higher catalytic activity. In comparison, the relatively low specific surface areas of TiO2 and small average pore diameters of ZSM-5 had a negative impact on metal distribution and the subsequent catalytic reformation process; this was because of the inadequate reaction during the catalytic process. The Fe/Al2O3 catalyst produced a higher yield of carbon deposits (30.2 wt%), including over 65% high-value carbon nanotubes (CNTs) and hydrogen content (58.7 vol%). Additionally, more dispersive and uniform CNTs were obtained from the Fe/SiO2 catalyst. The Fe/TiO2 catalyst promoted the formation of carbon fibre twisted like fried dough twist. Notably, there was interesting correspondence between the size of the reduced Fe nanoparticles and the product distribution. Within certain limits, the smaller Fe particle size facilitates the catalytic activity. The smaller and better dispersed Fe particles over the support materials were observed to be essential for hydrocarbon cracking and the subsequent formation of carbon deposits. The findings from this study may provide specific guidance for the preparation of different forms of carbon materials.

Quantile-Dependent Expressivity of Serum Uric Acid Concentrations.

OBJECTIVE: "Quantile-dependent expressivity" occurs when the effect size of a genetic variant depends upon whether the phenotype (e.g., serum uric acid) is high or low relative to its distribution. Analyses were performed to test whether serum uric acid heritability is quantile-specific and whether this could explain some reported gene-environment interactions. METHODS: Serum uric acid concentrations were analyzed from 2151 sibships and 12,068 offspring-parent pairs from the Framingham Heart Study. Quantile-specific heritability from offspring-parent regression slopes (ß OP, h 2 = 2ß OP/(1 + r spouse)) and full-sib regression slopes (ß FS, h 2 = {(1 + 8r spouse ß FS)0.5 - 1}/(2r spouse)) was robustly estimated by quantile regression with nonparametric significance assigned from 1000 bootstrap samples. RESULTS: Quantile-specific h 2 (±SE) increased with increasing percentiles of the offspring's sex- and age-adjusted uric acid distribution when estimated from ß OP (P trend = 0.001): 0.34 ± 0.03 at the 10th, 0.36 ± 0.03 at the 25th, 0.41 ± 0.03 at the 50th, 0.46 ± 0.04 at the 75th, and 0.49 ± 0.05 at the 90th percentile and when estimated from ß FS (P trend = 0.006). This is consistent with the larger genetic effect size of (1) the SLC2A9 rs11722228 polymorphism in gout patients vs. controls, (2) the ABCG2 rs2231142 polymorphism in men vs. women, (3) the SLC2A9 rs13113918 polymorphism in obese patients prior to bariatric surgery vs. two-year postsurgery following 29 kg weight loss, (4) the ABCG2 rs6855911 polymorphism in obese vs. nonobese women, and (5) the LRP2 rs2544390 polymorphism in heavier drinkers vs. abstainers. Quantile-dependent expressivity may also explain the larger genetic effect size of an SLC2A9/PKD2/ABCG2 haplotype for high vs. low intakes of alcohol, chicken, or processed meats. CONCLUSIONS: Heritability of serum uric acid concentrations is quantile-specific.

Quantile-specific heritability of plasminogen activator inhibitor type-1 (PAI-1, aka SERPINE1) and other hemostatic factors.

BACKGROUND: Plasminogen activator inhibitor type-1 (PAI-1, aka SERPINE1) is a moderately heritable glycoprotein that regulates fibrin clot dissolution (fibrinolysis). OBJECTIVES: Test whether the heritabilities (h2 ) of PAI-1 and other hemostatic factors are constant throughout their distribution or whether they are quantile-specific (i.e., a larger or smaller h2 depending on whether their concentrations are high or low). METHODS: Quantile regression was applied to 5606 parent-offspring pairs and 5310 full siblings of the Framingham Heart Study. Quantile-specific heritability was estimated from the parent-offspring regression slope (ßPO , h2  = 2ßPO /(1+rspouse )) and the full-sib regression slope (ßFS , h2  = {(1+8rspouse ßFS )0.5 -1}/(2rspouse )). RESULTS: Heritability (h2  ± SE) increased significantly with increasing percentiles of the offspring's age- and sex-adjusted PAI-1 distribution when estimated from ßPO (plinear trend  = 0.0001): 0.09 ± 0.02 at the 10th, 0.09 ± 0.02 at the 25th, 0.16 ± 0.02 at the 50th, 0.29 ± 0.04 at the 75th, and 0.26 ± 0.08 at the 90th percentile of the PAI-1 distribution, and when estimated from ßFS (plinear trend  = 6.5x10-7 ). There was no significant evidence for quantile-specific heritability for factor VII (plinear trend  = 0.35), D-dimer (plinear trend  = 0.08), tPA (plinear trend  = 0.74), or von Willebrand factor (plinear trend  = 0.79). CONCLUSION: Higher mean plasma PAI-1 antigen concentrations tend to accentuate genetic effects (quantile-dependent expressivity), which is consistent with the greater reported differences in PAI-1 concentrations between rs1799889 SERPINE1 (4G/5G) genotypes in patients with osteonecrosis, meningococcal sepsis, obesity, prior myocardial infarction, deep vein thrombosis, and polycystic ovarian syndrome than in healthy controls. It is also consistent with the greater increases in PAI-1 concentrations in 4G-allele carriers than 5G/5G homozygotes following fibrinolytic treatment, low-salt intake, and high saturated fat intake.

Quantile-dependent expressivity of serum C-reactive protein concentrations in family sets.

BACKGROUND: "Quantile-dependent expressivity" occurs when the effect size of a genetic variant depends upon whether the phenotype (e.g., C-reactive protein, CRP) is high or low relative to its distribution. We have previously shown that the heritabilities (h 2) of coffee and alcohol consumption, postprandial lipemia, lipoproteins, leptin, adiponectin, adiposity, and pulmonary function are quantile-specific. Whether CRP heritability is quantile-specific is currently unknown. METHODS: Serum CRP concentrations from 2,036 sibships and 6,144 offspring-parent pairs were analyzed from the Framingham Heart Study. Quantile-specific heritability from full-sib (ßFS, h 2 ={(1 + 8rspouseßFS)0.5 - 1}/(2rspouse)) and offspring-parent regression slopes (ßOP, h 2 = 2ßOP/(1 + rspouse)) were estimated robustly by quantile regression with nonparametric significance determined from 1,000 bootstrap samples. RESULTS: Quantile-specific h 2 (±SE) increased with increasing percentiles of the offspring's age- and sex-adjusted CRP distribution when estimated from ßOP (P trend = 0.0004): 0.02 ± 0.01 at the 10th, 0.04 ± 0.01 at the 25th, 0.10 ± 0.02 at the 50th, 0.20 ± 0.05 at the 75th, and 0.33 ± 0.10 at the 90th percentile, and when estimated from ßFS (P trend = 0.0008): 0.03±0.01 at the 10th, 0.06 ± 0.02 at the 25th, 0.14 ± 0.03 at the 50th, 0.24 ± 0.05 at the 75th, and 0.53 ± 0.21 at the 90th percentile. CONCLUSION: Heritability of serum CRP concentration is quantile-specific, which may explain or contribute to the inflated CRP differences between CRP (rs1130864, rs1205, rs1800947, rs2794521, rs3091244), FGB (rs1800787), IL-6 (rs1800795, rs1800796), IL6R (rs8192284), TNF-α (rs1800629) and APOE genotypes following CABG surgery, stroke, TIA, curative esophagectomy, intensive periodontal therapy, or acute exercise; during acute coronary syndrome or Staphylococcus aureus bacteremia; or in patients with chronic rheumatoid arthritis, diabetes, peripheral arterial disease, ankylosing spondylitis, obesity or inflammatory bowel disease or who smoke.

Quantile-specific heritability of serum growth factor concentrations.

BACKGROUND: "Quantile-dependent expressivity" occurs when the effect size of a genetic variant depends upon whether the phenotype (e.g. growth factor concentration) is high or low relative to its distribution. METHODS: Quantile-regression analysis was applied to family sets from the Framingham Heart Study to determine whether the heritability (h2) of vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), angiopoietin-2, and angiopoietin-2 (sTie-2) and VEGFR1 (sFlt-1) receptor concentrations were quantile-specific. RESULTS: Quantile-specific h2 (±SE) increased with increasing percentiles of the age- and sex-adjusted VEGF (Ptrend<10-16), HGF (Ptrend=0.0004), angiopoietin-2 (Ptrend=0.0002), sTie-2 (Ptrend=1.2 × 10-5), and sFlt-1 distributions (Ptrend=0.04). CONCLUSION: Heritabilities of VEGF, HGF, angiopoitein-2, sTie-2 and sFlt-1 concentrations are quantile dependent. This may explain reported interactions of genetic loci (rs10738760, rs9472159, rs833061, rs3025039, rs2280789, rs1570360, rs2010963) with metabolic syndrome, diet, recurrent miscarriage, hepatocellular carcinoma, erysipelas, diabetic retinopathy, and bevacizumab treatment in their effect on VEGF concentrations.

Quantile-specific heritability of total cholesterol and its pharmacogenetic and nutrigenetic implications.

BACKGROUND: "Quantile-dependent expressivity" occurs when the effect size of a genetic variant depends upon whether the phenotype (e.g. cholesterol) is high or low relative to its distribution. We have previously shown that the effect of a 52-SNP genetic-risk score was 3-fold larger at the 90th percentile of the total cholesterol distribution than at its 10th percentile. The objective of this study is to assess quantile-dependent expressivity for total cholesterol in 7006 offspring with parents and 2112 sibships from Framingham Heart Study. METHODS: Quantile-specific heritability (h2) was estimated as twice the offspring-parent regression slope as robustly estimated by quantile regression with nonparametric significance assigned from 1000 bootstrap samples. RESULTS: Quantile-specific h2 increased linearly with increasing percentiles of the offspring's cholesterol distribution (P = 3.0 × 10-9), i.e. h2 = 0.38 at the 10th percentile, h2 = 0.45 at the 25th percentile, h2 = 0.52 at the 50th, h2 = 0.61 at the 75th percentile, and h2 = 0.65 at the 90th percentile of the total cholesterol distribution. Average h2 decreased from 0.55 to 0.34 in 3564 offspring who started cholesterol-lowering medications, but this was attributable to quantile-dependent expressivity and the offspring's 0.94 mmol/L average drop in total cholesterol. Quantile-dependent expressivity likely explains the reported effect of the CELSR2/PSRC1/SORT1 rs646776 and APOE rs7412 gene loci on statin efficacy. Specifically, a smaller genetic effect size at the lower (post-treatment) than higher (pre-treatment) cholesterol concentrations mandates that the trajectories of the genotypes cannot move in parallel when cholesterol is decreased pharmacologically. CONCLUSION: Cholesterol concentrations exhibit quantile-dependent expressivity, which may provide an alternative interpretation to pharmacogenetic and nutrigenetic interactions.