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Sökning: WFRF:(Hao Ke)

  • Resultat 141-150 av 154
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141.
  • Ni, Ming-jiang, et al. (författare)
  • Naphthalene decomposition in a DC corona radical shower discharge
  • 2011
  • Ingår i: Journal of Zhejiang University: Science A. - 1673-565X. ; 12:1, s. 71-77
  • Tidskriftsartikel (refereegranskat)abstract
    • The naphthalene decomposition in a corona radical shower discharge (CRS) was investigated, with attention paid to the influences of voltage and initial naphthalene density. The OH emission spectra were investigated so as to know the naphthalene decomposing process. The by-products were analyzed and a decomposing theory in discharge was proposed. The results showed that higher voltage and relative humidity were effective on decomposition. The initial concentration affected the decomposing efficiency of naphthalene. When the initial naphthalene density was 17 mg/m(3), the decomposition rate was found to be 70% under 14 kV. The main by-products were carbon dioxide and water. However, a small amount of carbonic oxide, 1,2-ethanediol and acetaldehyde were found due to the incomplete oxidization.
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142.
  • Pan, Lang, et al. (författare)
  • 8-Oxoguanine targeted by 8-oxoguanine DNA glycosylase 1 (OGG1) is central to fibrogenic gene activation upon lung injury
  • 2023
  • Ingår i: Nucleic Acids Research. - : Oxford University Press (OUP). - 0305-1048 .- 1362-4962. ; 51:3, s. 1087-1102
  • Tidskriftsartikel (refereegranskat)abstract
    • Reactive oxygen species (ROS) are implicated in epithelial cell-state transition and deposition of extracellular matrix upon airway injury. Of the many cellular targets of ROS, oxidative DNA modification is a major driving signal. However, the role of oxidative DNA damage in modulation profibrotic processes has not been fully delineated. Herein, we report that oxidative DNA base lesions, 8-oxoG, complexed with 8-oxoguanine DNA glycosylase 1 (OGG1) functions as a pioneer factor, contributing to transcriptional reprogramming within airway epithelial cells. We show that TGFβ1-induced ROS increased 8-oxoG levels in open chromatin, dynamically reconfigure the chromatin state. OGG1 complexed with 8-oxoG recruits transcription factors, including phosphorylated SMAD3, to pro-fibrotic gene promoters thereby facilitating gene activation. Moreover, 8-oxoG levels are elevated in lungs of mice subjected to TGFβ1-induced injury. Pharmacologic targeting of OGG1 with the selective small molecule inhibitor of 8-oxoG binding, TH5487, abrogates fibrotic gene expression and remodeling in this model. Collectively, our study implicates that 8-oxoG substrate-specific binding by OGG1 is a central modulator of transcriptional regulation in response to tissue repair.
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143.
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144.
  • Ren, Long Jun, et al. (författare)
  • Effect of conventional physiotherapy on pain and muscle stiffness in patients with low back pain assessed by a wireless hand-held tissue ultrasound palpation system (TUPS)
  • 2019
  • Ingår i: International Journal of Physical Medicine Rehabilitation. - : Omics Publishing Group. - 2329-9096. ; 7:2, s. 1-5
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Low back pain (LPB) is a common health problem. While physiotherapy can relieve pain and the muscle stiffness of patients with LBP was shown to be different from healthy people, few studies have investigated the effect of physiotherapy on back muscle stiffness in patients with LBP.Objective: To investigate the effect of a 5-day conventional physiotherapy treatment on muscle stiffness of patients with LBP using a newly developed wireless hand-held ultrasound probe.Methods: A total of ten patients with LBP participated in this study. They received customized conventional physiotherapy containing electrical therapy, traditional Chinese medicine, manipulation and wax therapy. The pain level was evaluated by the visual analogue scale, and the muscle stiffness was measured by a wireless hand-held tissue ultrasound palpation system. The muscle stiffness of left and right sides at L1 and L4 levels and pain level were evaluated in two conditions, including baseline and 5-day post treatments.Results and discussion: After receiving the treatment, the muscle stiffness of all tested low back regions increased significantly (p=0.040). The muscle stiffness at L4 level was significantly higher than that of L1 level (p=0.021). No significant difference of muscle stiffness between left and right sides was found. The correlation between the muscle stiffness and VAS score appeared to decrease after receiving the treatment (R2 changed from 0.3598 to 0.0533).Conclusion: A five-day conventional physiotherapy treatment could relieve the pain level and increase the muscle stiffness of patients with LBP as evaluated by a wireless hand-held ultrasound probe. The stiffness of back muscle at L4 level was significantly higher than that of L1 level in patients with LBP. The treatment may change the correlation between the muscle stiffness and VAS score at low back region.
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145.
  • Shrine, Nick, et al. (författare)
  • New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries
  • 2019
  • Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 51:3, s. 481-493
  • Tidskriftsartikel (refereegranskat)abstract
    • Reduced lung function predicts mortality and is key to the diagnosis of chronic obstructive pulmonary disease (COPD). In a genome-wide association study in 400,102 individuals of European ancestry, we define 279 lung function signals, 139 of which are new. In combination, these variants strongly predict COPD in independent populations. Furthermore, the combined effect of these variants showed generalizability across smokers and never smokers, and across ancestral groups. We highlight biological pathways, known and potential drug targets for COPD and, in phenome-wide association studies, autoimmune-related and other pleiotropic effects of lung function-associated variants. This new genetic evidence has potential to improve future preventive and therapeutic strategies for COPD.
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146.
  • Tan, Liangxiao, et al. (författare)
  • Electrostatically cooperative host-in-host of metal cluster ⊂ ionic organic cages in nanopores for enhanced catalysis
  • 2022
  • Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 13
  • Tidskriftsartikel (refereegranskat)abstract
    • The construction of hierarchically nanoporous composite for high-performance catalytic application is still challenging. In this work, a series of host-in-host ionic porous materials are crafted by encapsulating ionic organic cages into a hyper-crosslinked, oppositely charged porous poly(ionic liquid) (PoPIL) through an ion pair-directed assembly strategy. Specifically, the cationic cage (C-Cage) as the inner host can spatially accommodate a functional Au cluster, forming a [Au⊂C-Cage+]⊂PoPIL− supramolecular composite. This dual-host molecular hierarchy enables a charge-selective substrate sorting effect to the Au clusters, which amplifies their catalytic activity by at least one order of magnitude as compared to Au confined only by C-Cage as the mono-host (Au⊂C-Cage+). Moreover, we demonstrate that such dual-host porous system can advantageously immobilize electrostatically repulsive Au⊂C-Cage+ and cationic ferrocene co-catalyst (Fer+) together into the same microcompartments, and synergistically speed up the enzyme-like tandem reactions by channelling the substrate to the catalytic centers via nanoconfinement. 
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147.
  • Tang, Qingquan, et al. (författare)
  • Topological Effects on Cyclic Co-Poly(ionic liquid)s Self-Assembly
  • 2023
  • Ingår i: Macromolecular Chemistry and Physics. - : Wiley. - 1022-1352 .- 1521-3935. ; 224:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Topological geometry of poly(ionic liquid)s (PILs), such as brush-like, knot-like, hyperbranched and randomly coiled, often exerts a strong influence on their self-assembly behaviors. As a primary topological form, the cyclic topology-derived effects have not been investigated on PILs, which concerns synergy of charges and zero chain end. Herein, linear and cyclic poly(ionic liquid) copolymers (co-PILs) with randomly distributed counter anions of B(Ph)4− and Br− by a template method in combination with a follow-up partial anion exchange is prepared. The self-assembly phenomena of linear and cyclic co-PILs are studied in selective solvents, where the hydrophobic counter anions B(Ph)4− and hydrophilic counter anions Br− aggregated to form cores and corona in the assembled nanospheres, showing the average size of cyclic co-PILs nanospheres is 46.2% smaller (≈120 nm) than linear co-PILs nano-assemblies (≈176 nm). Based on the CGMD simulations, the authors speculate that the spherical aggregates are formed by transitioning from micelles with gradient block-like structures, which formed by enriched hydrophobic counter anions in the core and enriched hydrophilic counter anions in the corona. These results indicate a novel synergy of topology effects and dynamic anion movements, as revealed by cyclic co-PIL self-assembly in this work. 
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148.
  • Thun, Gian Andri, et al. (författare)
  • Causal and Synthetic Associations of Variants in the SERPINA Gene Cluster with Alpha1-antitrypsin Serum Levels
  • 2013
  • Ingår i: PLOS Genetics. - : Public Library of Science (PLoS). - 1553-7390 .- 1553-7404. ; 9:8, s. e1003585-
  • Tidskriftsartikel (refereegranskat)abstract
    • Several infrequent genetic polymorphisms in the SERPINA1 gene are known to substantially reduce concentration of alpha1-antitrypsin (AAT) in the blood. Since low AAT serum levels fail to protect pulmonary tissue from enzymatic degradation these polymorphisms also increase the risk for early onset chronic obstructive pulmonary disease (COPD). The role of more common SERPINA1 single nucleotide polymorphisms (SNPs) in respiratory health remains poorly understood. We present here an agnostic investigation of genetic determinants of circulating AAT levels in a general population sample by performing a genome-wide association study (GWAS) in 1392 individuals of the SAPALDIA cohort. Five common SNPs defined by showing minor allele frequencies (MAFs) >5% reached genome-wide significance all located in the SERPINA gene cluster at 14q32.13. The top-ranking genotyped SNP rs4905179 was associated with an estimated effect of beta = 20.068 g/L per minor allele (P = 1.20*10(-12)). But denser SERPINA1 locus genotyping in 5569 participants with subsequent stepwise conditional analysis as well as exon-sequencing in a subsample (N = 410) suggested that AAT serum level is causally determined at this locus by rare (MAF<1%) and low-frequent (MAF 1-5%) variants only in particular by the well-documented protein inhibitor S and Z (PI S PI Z) variants. Replication of the association of rs4905179 with AAT serum levels in the Copenhagen City Heart Study (N = 8273) was successful (P<0.0001) as was the replication of its synthetic nature (the effect disappeared after adjusting for PI S and Z P = 0.57). Extending the analysis to lung function revealed a more complex situation. Only in individuals with severely compromised pulmonary health (N = 397) associations of common SNPs at this locus with lung function were driven by rarer PI S or Z variants. Overall our meta-analysis of lung function in ever-smokers does not support a functional role of common SNPs in the SERPINA gene cluster in the general population.
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149.
  • Wain, Louise V, et al. (författare)
  • Genome-wide association analyses for lung function and chronic obstructive pulmonary disease identify new loci and potential druggable targets.
  • 2017
  • Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 49:3, s. 416-425
  • Tidskriftsartikel (refereegranskat)abstract
    • Chronic obstructive pulmonary disease (COPD) is characterized by reduced lung function and is the third leading cause of death globally. Through genome-wide association discovery in 48,943 individuals, selected from extremes of the lung function distribution in UK Biobank, and follow-up in 95,375 individuals, we increased the yield of independent signals for lung function from 54 to 97. A genetic risk score was associated with COPD susceptibility (odds ratio per 1 s.d. of the risk score (∼6 alleles) (95% confidence interval) = 1.24 (1.20-1.27), P = 5.05 × 10(-49)), and we observed a 3.7-fold difference in COPD risk between individuals in the highest and lowest genetic risk score deciles in UK Biobank. The 97 signals show enrichment in genes for development, elastic fibers and epigenetic regulation pathways. We highlight targets for drugs and compounds in development for COPD and asthma (genes in the inositol phosphate metabolism pathway and CHRM3) and describe targets for potential drug repositioning from other clinical indications.
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150.
  • Yaghootkar, Hanieh, et al. (författare)
  • Mendelian randomization studies do not support a causal role for reduced circulating adiponectin levels in insulin resistance and type 2 diabetes.
  • 2013
  • Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 62:10, s. 3589-3598
  • Tidskriftsartikel (refereegranskat)abstract
    • Adiponectin is strongly inversely associated with insulin resistance and type 2 diabetes, but its causal role remains controversial. We used a Mendelian randomization approach to test the hypothesis that adiponectin causally influences insulin resistance and type 2 diabetes. We used genetic variants at the ADIPOQ gene as instruments to calculate a regression slope between adiponectin levels and metabolic traits (up to 31,000 individuals) and a combination of instrumental variables and summary statistics-based genetic risk scores to test the associations with gold-standard measures of insulin sensitivity (2,969 individuals) and type 2 diabetes (15,960 case subjects and 64,731 control subjects). In conventional regression analyses, a 1-SD decrease in adiponectin levels was correlated with a 0.31-SD (95% CI 0.26-0.35) increase in fasting insulin, a 0.34-SD (0.30-0.38) decrease in insulin sensitivity, and a type 2 diabetes odds ratio (OR) of 1.75 (1.47-2.13). The instrumental variable analysis revealed no evidence of a causal association between genetically lower circulating adiponectin and higher fasting insulin (0.02 SD; 95% CI -0.07 to 0.11; N = 29,771), nominal evidence of a causal relationship with lower insulin sensitivity (-0.20 SD; 95% CI -0.38 to -0.02; N = 1,860), and no evidence of a relationship with type 2 diabetes (OR 0.94; 95% CI 0.75-1.19; N = 2,777 case subjects and 13,011 control subjects). Using the ADIPOQ summary statistics genetic risk scores, we found no evidence of an association between adiponectin-lowering alleles and insulin sensitivity (effect per weighted adiponectin-lowering allele: -0.03 SD; 95% CI -0.07 to 0.01; N = 2,969) or type 2 diabetes (OR per weighted adiponectin-lowering allele: 0.99; 95% CI 0.95-1.04; 15,960 case subjects vs. 64,731 control subjects). These results do not provide any consistent evidence that interventions aimed at increasing adiponectin levels will improve insulin sensitivity or risk of type 2 diabetes.
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