科研成果

Gasoline vehicle exhaust is an important contributor to secondary organic aerosol (SOA) formation in urban atmosphere. Fuel composition has a potentially considerable impact on gasoline SOA production, but the link between fuel components and SOA production is still poorly understood. Here, we present chamber experiments to investigate the impacts of gasoline aromatic content on SOA production through chamber oxidation approach. A significant amplification factor of 3-6 for SOA productions from gasoline exhausts is observed as gasoline aromatic content rose from 29 to 37 %. Considerably higher emission of aromatic volatile organic compounds (VOCs) using high-aromatic fuel plays an essential role in the enhancement of SOA production, while semi-volatile organic compounds (e.g., gas-phase PAHs) may also contribute to the higher SOA production. Our findings indicate that gasoline aromatics significantly influence ambient PM2.5 concentration in urban areas and emphasize that more stringent regulation of gasoline aromatic content will lead to considerable benefits for urban air quality.

Gasoline vehicle exhaust is an important contributor to secondary organic aerosol (SOA) formation in urban atmosphere. Fuel composition has a potentially considerable impact on gasoline SOA production, but the link between fuel components and SOA production is still poorly understood. Here, we present chamber experiments to investigate the impacts of gasoline aromatic content on SOA production through chamber oxidation approach. A significant amplification factor of 3-6 for SOA productions from gasoline exhausts is observed as gasoline aromatic content rose from 29 to 37 %. Considerably higher emission of aromatic volatile organic compounds (VOCs) using high-aromatic fuel plays an essential role in the enhancement of SOA production, while semi-volatile organic compounds (e.g., gas-phase PAHs) may also contribute to the higher SOA production. Our findings indicate that gasoline aromatics significantly influence ambient PM2.5 concentration in urban areas and emphasize that more stringent regulation of gasoline aromatic content will lead to considerable benefits for urban air quality.

Gasoline vehicle exhaust is an important contributor to secondary organic aerosol (SOA) formation in urban atmosphere. Fuel composition has a potentially considerable impact on gasoline SOA production, but the link between fuel components and SOA production is still poorly understood. Here, we present chamber experiments to investigate the impacts of gasoline aromatic content on SOA production through chamber oxidation approach. A significant amplification factor of 3-6 for SOA productions from gasoline exhausts is observed as gasoline aromatic content rose from 29 to 37 %. Considerably higher emission of aromatic volatile organic compounds (VOCs) using high-aromatic fuel plays an essential role in the enhancement of SOA production, while semi-volatile organic compounds (e.g., gas-phase PAHs) may also contribute to the higher SOA production. Our findings indicate that gasoline aromatics significantly influence ambient PM2.5 concentration in urban areas and emphasize that more stringent regulation of gasoline aromatic content will lead to considerable benefits for urban air quality.

In this letter, a gate recessed normally-off GaN metal-oxide-semiconductor high-electron-mobility transistor on silicon substrate is fabricated using AlN/Si3N4 as the passivation layer. The thin AlN layer serves the dual role of protecting the gate channel region from direct plasma bombardment during the RIE Si3N4 removal and passivating the surface states in the access region. As a result, the effective carrier mobility in the normally-off channel is found to improve from the 568 cm(2)/V . s in conventional Si3N4 passivation process to a high value of 1154 cm(2)/V . s. A saturated output current density of 603 mA/mm and an ON-resistance of 5.3 Omega . mm was obtained for devices with L-G/L-GS/L-GD/W-G = 1.5/1.5/3/20 mu m. Meanwhile, the degradation of dynamic ON-resistance is significantly suppressed due to the effective passivation of surface states by the AlN layer grown by plasma-enhanced atomic layer deposition.

Electrons can be accelerated to a GeV level in centimeters by plasma wakefield driven by laser. With the development of chirped pulse amplification technique, the accelerating field can reach 100 GV/m. The laser driven wakefield acceleration experiments with ionization injection are carried out using 68 TW (1.7 J, 25 fs) laser and a mixture gas of 99% He and 1% N-2. In experiment, the output electron beam has broadband spectrum with a maximum cut-off energy of about 290 MeV and a maximum output energy is quite stable in a certain range of laser focal positions. Two-dimensional particle-in-cell simulation is carried out. It is found that the longitudinal phase space is occupied by the continuously injected electrons and the phase space distribution is quite stable after the laser has propagated several millimeters inside plasma. This acceleration process can lead to quite stable maximum output energy of electron beam. These experiments reveal the physical nature of continuous ionization injection, which is very important for improving the performance of ionization injection.

Modulation of n-3 fatty acids on genetic susceptibility to type 2 diabetes (T2D) is still not clear. In a case-control study of 622 Chinese T2D patients and 293 healthy controls, a genetic risk score (GRS) was created based on nine T2D genetic variants. Logistic regression was used to examine the interaction of the GRS with erythrocyte phospholipid n-3 fatty acids for T2D risk. Every 1-unit (corresponding to 1 risk allele) increase in GRS was associated with 12% (Odds ratio (OR): 1.12; 95% confidence intervals (CI): 1.04-1.20) higher risk of T2D. Compared with the lowest quartile, participants had lower T2D risk in the 2nd (OR: 0.55; 95% CI: 0.36-0.84), 3rd (OR: 0.58; 95% CI: 0.38-0.88) and 4th (OR: 0.67; 95% CI: 0.44-1.03) quartile of alpha-linolenic acid (ALA) levels. Significant interaction (p-interaction = 0.029) of GRS with ALA for T2D risk was observed. Higher ALA levels were associated with lower T2D risk only among participants within the lowest GRS tertile, with ORs 0.51 (95% CI: 0.26-1.03), 0.44 (95% CI: 0.22-0.89) and 0.49 (95% CI: 0.25-0.96) for the 2nd, 3rd and 4th ALA quartile, compared with the 1st. This study suggests that higher erythrocyte ALA levels are inversely associated with T2D risk only among participants with low T2D genetic risk, with high genetic risk abolishing the ALA-T2D association.

Whether change in physical activity over time modifies the genetic susceptibility to long-term weight gain is unknown. We calculated a BMI-genetic risk score (GRS) based on 77 BMI-associated single nucleotide polymorphisms (SNPs) and a body fat percentage (BF%)-GRS based on 12 BF%-associated SNPs in 9,390 women from the Nurses' Health Study (NHS) and 5,291 men from the Health Professionals Follow-Up Study (HPFS). We analyzed the interactions between each GRS and change in physical activity on BMI/body weight change within five 4-year intervals from 1986 to 2006 using multivariable generalized linear models with repeated-measures analyses. Both the BMI-GRS and the BF%-GRS were associated with long-term increases in BMI/weight, and change in physical activity consistently interacted with the BF%-GRS on BMI change in the NHS (P for interaction = 0.025) and HPFS (P for interaction = 0.001). In the combined cohorts, 4-year BMI change per 10-risk allele increment was -0.02 kg/m(2) among participants with greatest increase in physical activity and 0.24 kg/m(2) among those with greatest decrease in physical activity (P for interaction < 0.001), corresponding to 0.01 kg versus 0.63 kg weight changes every 4 years (P for interaction = 0.001). Similar but marginal interactions were observed for the BMI-GRS (P for interaction = 0.045). Our data indicate that the genetic susceptibility to weight gain may be diminished by increasing physical activity.

Background: Coffee consumption has been associated with glucose metabolism and risk of type 2 diabetes.Objective: We examined whether the genetic variation determining habitual coffee consumption affected glycemic changes in response to weight-loss dietary intervention.Design: A genetic risk score (GRS) was calculated based on 8 habitual coffee consumption-associated single nucleotide polymorphisms. We used general linear models to test changes in glycemic traits in groups randomly assigned to high- and low-fat diets according to tertiles of the GRS.Results: We observed significant interactions between the GRS and low compared with high dietary fat intake on 6-mo changes in fasting insulin and homeostasis model assessment of insulin resistance (HOMA-IR) (P-interaction = 0.023 and 0.022, respectively), adjusting for age, sex, race, physical activity, smoking, alcohol, seasonal variation, and baseline values of the respective outcomes. Participants with a higher GRS of habitual coffee consumption showed a greater reduction in fasting insulin and a marginally greater decrease in HOMA-IR in the low-fat diet intervention group.Conclusions: Our data suggest that participants with genetically determined high coffee consumption may benefit more by eating a low-fat diet in improving fasting insulin and HOMA-IR in a short term. This trial was registered at clinicaltrials.gov as NCT00072995 and NCT03258203.

Context: Adiponectin plays key roles in regulating appetite and food intake. Objective: To investigate interactions between the genetic risk score (GRS) for adiponectin levels and weight-loss diets varying in macronutrient intake on long-term changes in appetite and adiponectin levels. Design, Setting, and Participants: A GRS was calculated based on 5 adiponectin-associated variants in 692 overweight adults from the 2-year Preventing Overweight Using Novel Dietary Strategies trial. Main Outcome Measures: Repeated measurements of plasma adiponectin levels and appetite-related traits, including cravings, fullness, prospective consumption, and hunger. Results: Dietary fat showed nominally significant interactions with the adiponectin GRS on changes in appetite score and prospective consumption from baseline to 6 months (P for interaction = 0.014 and 0.017, respectively) after adjusting for age, sex, ethnicity, baseline body mass index, and baseline respective outcome values. The GRS for lower adiponectin levels was associated with a greater decrease in appetite (P < 0.001) and prospective consumption (P = 0.008) among participants consuming a high-fat diet, whereas no significant associations were observed in the low-fat group. Additionally, a significant interaction was observed between the GRS and dietary fat on 6-month changes in adiponectin levels (P for interaction = 0.021). The lower GRS was associated with a greater increase in adiponectin in the low-fat group (P = 0.02), but it was not associated with adiponectin changes in the high-fat group (P = 0.31). Conclusions: Our findings suggest that individuals with varying genetic architecture of circulating adiponectin may respond divergently in appetite and adiponectin levels to weight-loss diets varying in fat intake.

Few genome-wide association studies (GWAS) account for environmental exposures, like smoking, potentially impacting the overall trait variance when investigating the genetic contribution to obesity-related traits. Here, we use GWAS data from 51,080 current smokers and 190,178 nonsmokers (87% European descent) to identify loci influencing BMI and central adiposity, measured as waist circumference and waist-to-hip ratio both adjusted for BMI. We identify 23 novel genetic loci, and 9 loci with convincing evidence of gene-smoking interaction (GxSMK) on obesity-related traits. We show consistent direction of effect for all identified loci and significance for 18 novel and for 5 interaction loci in an independent study sample. These loci highlight novel biological functions, including response to oxidative stress, addictive behaviour, and regulatory functions emphasizing the importance of accounting for environment in genetic analyses. Our results suggest that tobacco smoking may alter the genetic susceptibility to overall adiposity and body fat distribution.

Physical activity (PA) may modify the genetic effects that give rise to increased risk of obesity. To identify adiposity loci whose effects are modified by PA, we performed genome-wide interaction meta-analyses of BMI and BMI-adjusted waist circumference and waist-hip ratio from up to 200,452 adults of European (n = 180,423) or other ancestry (n = 20,029). We standardized PA by categorizing it into a dichotomous variable where, on average, 23% of participants were categorized as inactive and 77% as physically active. While we replicate the interaction with PA for the strongest known obesity-risk locus in the FTO gene, of which the effect is attenuated by ~30% in physically active individuals compared to inactive individuals, we do not identify additional loci that are sensitive to PA. In additional genome-wide meta-analyses adjusting for PA and interaction with PA, we identify 11 novel adiposity loci, suggesting that accounting for PA or other environmental factors that contribute to variation in adiposity may facilitate gene discovery.

Genomic mosaicism in parental gametes and peripheral tissues is an important consideration for genetic counseling. We studied a Chinese cohort affected by a severe epileptic disorder, Dravet syndrome (DS). There were 56 fathers who donated semen and 15 parents who donated multiple peripheral tissue samples. We used an ultra-sensitive quantification method, micro-droplet digital PCR (mDDPCR), to detect parental mosaicism of the proband’s pathogenic mutation in SCN1A, the causal gene of DS in 112 families. Ten of the 56 paternal sperm samples were found to exhibit mosaicism of the proband’s mutations, with mutant allelic fractions (MAFs) ranging from 0.03% to 39.04%. MAFs in the mosaic fathers’ sperm were significantly higher than those in their blood (p = 0.00098), even after conditional probability correction (p’ = 0.033). In three mosaic fathers, ultra-low fractions of mosaicism (MAF < 1%) were detected in the sperm samples. In 44 of 45 cases, mosaicism was also observed in other parental peripheral tissues. Hierarchical clustering showed that MAFs measured in the paternal sperm, hair follicles and urine samples were clustered closest together. Milder epileptic phenotypes were more likely to be observed in mosaic parents (p = 3.006e-06). Our study provides new insights for genetic counseling.

Spatial patterns and temporal trends of nitrogen (N) and phosphorus (P) deposition are important for quantifying their impact on forest carbon (C) uptake. In a first step, we modeled historical and future change in the global distributions of the atmospheric deposition of N and P from the dry and wet deposition of aerosols and gases containing N and P. Future projections were compared between two scenarios with contrasting aerosol emissions. Modeled fields of N and P deposition and P concentration were evaluated using globally distributed in situ measurements. N deposition peaked around 1990 in European forests and around 2010 in East Asian forests, and both increased sevenfold relative to 1850. P deposition peaked around 2010 in South Asian forests and increased 3.5-fold relative to 1850. In a second step, we estimated the change in C storage in forests due to the fertilization by deposited N and P (Delta C-v (dep)), based on the retention of deposited nutrients, their allocation within plants, and C:N and C:P stoichiometry. Delta C-v (dep) for 1997-2013 was estimated to be 0.27 +/- 0.13 Pg C year(-1) from N and 0.054 +/- 0.10 Pg C year(-1) from P, contributing 9% and 2% of the terrestrial C sink, respectively. Sensitivity tests show that uncertainty of Delta C-v (dep) was larger from P than from N, mainly due to uncertainty in the fraction of deposited P that is fixed by soil. Delta C-P (dep) was exceeded by Delta C-N (dep) over 1960-2007 in a large area of East Asian and West European forests due to a faster growth in N deposition than P. Our results suggest a significant contribution of anthropogenic P deposition to C storage, and additional sources of N are needed to support C storage by P in some Asian tropical forests where the deposition rate increased even faster for P than for N.

The increasing demand of livestock products and production efficiency of livestock husbandry, and restoration of grassland ecosystem have been inducing the rapid transition of livestock husbandry systems from pastoralism into intensive systems. Such transition has been resulted in changes in the greenhouse gas (GHG) emissions, though it is rarely studied, especially in the pastoral area of China. Aimed to address this question, on the Qinghai-Tibet Plateau we selected Chanaihai village as the pastoralism system, and Guinan Grassland Development Limited Company as the combination of extensive and intensive livestock husbandry system, to compare the GHG emission between the two systems using life cycle assessment method. Our results showed that the GHG emission intensity both in per unit of area and per unit of carcass weight in the combined extensive/intensive livestock husbandry were higher than the pastoralism, indicating that the shift into the combined extensive/intensive livestock husbandry system increased the GHG emission. Such results could be attributed to the lower soil carbon uptake and higher GHG emission derived from the external inputs such as seed, diesel, and electricity in the combined extensive/intensive system. These findings demonstrated that the ongoing transition in the pastoral area of Qinghai-Tibet Plateau may be inappropriate Under the background of global GHG mitigation. As suggestions, we argued that reduction in the manure combustion and increase in soil carbon uptake could be effective measures to reduce the GHG emission intensity of livestock husbandry. (C) 2017 Elsevier Ltd. All rights reserved.