| 2971. |
- Wang, B., et al.
(författare)
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An Association Study of SNP+45 T > G of the AdipoQ Gene with Type 2 Diabetes in Yi and Han People in China
- 2011
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Ingår i: International Journal for Vitamin and Nutrition Research. - : Hogrefe Publishing Group. - 0300-9831 .- 1664-2821. ; 81:6, s. 392-397
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Tidskriftsartikel (refereegranskat)abstract
- Background: The Yi people are considered the most primitive society in China, and live in the remote mountainous areas of Southwestern China. There have been no previous publications on genetic research concerning type 2 diabetes (T2D) in the Yi people. This is the first report that presents the association between SNP + 45 T > G (rs2241766) of the AdipoQ gene and T2D in Yi people. Our previous study showed that the prevalence of T2D in Yi people was lower than the national level in 2008. Genetic differences between Yi and Han people might be one possible explanation for this observation. Studies on the single nucleotide polymorphism SNP + 45 T > G (rs2241766) of the AdipoQ gene in Chinese Han people showed inconsistent results. This study was designed to identify genetic variants of the AdipoQ gene that contribute to the development of T2D in Yi and Han people. Methods: A case-control study on the association between SNP + 45 T > G (rs2241766) of the AdipoQ gene and T2D was carried out based on a cross-sectional study in the Liangshan area, Sichuan province in Southwestern China. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique was used to test for the presence of SNP + 45 T > G (rs2241766) in the AdipoQ gene. Results: Distributions of genotypes variants (TT/GG/TG) were not significantly different between T2D cases and controls both in Yi and Han people in China (p > 0.05). The allele frequencies (T/G) demonstrated a non-significant association with T2D, displaying OR of 1.1 (95 % CI: 0.8, 1.6) in Yi people and OR of 1.0 (95 % CI: 0.7, 1.4) in Han people. Conclusions: The SNP + 45 (rs2241766) of the AdipoQ gene is not associated with T2D neither in Yi nor in Han people in southwestern China.
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| 2972. |
- Wang, D. Q., et al.
(författare)
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Boost-DiLeu: Enhanced Isobaric N,N-Dimethyl Leucine Tagging Strategy for a Comprehensive Quantitative Glycoproteomic Analysis
- 2022
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Ingår i: Analytical Chemistry. - : American Chemical Society (ACS). - 0003-2700 .- 1520-6882. ; 94:34, s. 11773-11782
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Tidskriftsartikel (refereegranskat)abstract
- Intact glycopeptide analysis has been of great interest because it can elucidate glycosylation site information and glycan structural composition at the same time. However, mass spectrometry (MS)-based glycoproteomic analysis is hindered by the low abundance and poor ionization efficiency of glycopeptides. Relatively large amounts of starting materials are needed for the enrichment, which makes the identification and quantification of intact glycopeptides from samples with limited quantity more challenging. To overcome these limitations, we developed an improved isobaric labeling strategy with an additional boosting channel to enhance N,N-dimethyl leucine (DiLeu) tagging-based quantitative glycoproteomic analysis, termed as Boost-DiLeu. With the integration of a one-tube sample processing workflow and high- pH fractionation, 3514 quantifiable N-glycopeptides were identified from 30 mu g HeLa cell tryptic digests with reliable quantification performance. Furthermore, this strategy was applied to human cerebrospinal fluid (CSF) samples to differentiate N-glycosylation profiles between Alzheimer's disease (AD) patients and non-AD donors. The results revealed processes and pathways affected by dysregulated N-glycosylation in AD, including platelet degranulation, cell adhesion, and extracellular matrix, which highlighted the involvement of N-glycosylation aberrations in AD pathogenesis. Moreover, weighted gene co expression network analysis (WGCNA) showed nine modules of glycopeptides, two of which were associated with the AD phenotype. Our results demonstrated the feasibility of using this strategy for in-depth glycoproteomic analysis of size-limited clinical samples. Taken together, we developed and optimized a strategy for the enhanced comprehensive quantitative intact glycopeptide analysis with DiLeu labeling, showing significant promise for identifying novel therapeutic targets or biomarkers in biological systems with a limited sample quantity.
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| 2973. |
- Wang, F. M., et al.
(författare)
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Global blue carbon accumulation in tidal wetlands increases with climate change
- 2021
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Ingår i: National Science Review. - : Oxford University Press (OUP). - 2095-5138 .- 2053-714X. ; 8:9
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Tidskriftsartikel (refereegranskat)abstract
- Coastal tidal wetlands produce and accumulate significant amounts of organic carbon (C) that help to mitigate climate change. However, previous data limitations have prevented a robust evaluation of the global rates and mechanisms driving C accumulation. Here, we go beyond recent soil C stock estimates to reveal global tidal wetland C accumulation and predict changes under relative sea level rise, temperature and precipitation. We use data from literature study sites and our new observations spanning wide latitudinal gradients and 20 countries. Globally, tidal wetlands accumulate 53.65 (95%CI: 48.52-59.01) Tg C yr(-1), which is similar to 30% of the organic C buried on the ocean floor. Modeling based on current climatic drivers and under projected emissions scenarios revealed a net increase in the global C accumulation by 2100. This rapid increase is driven by sea level rise in tidal marshes, and higher temperature and precipitation in mangroves. Countries with large areas of coastal wetlands, like Indonesia and Mexico, are more susceptible to tidal wetland C losses under climate change, while regions such as Australia, Brazil, the USA and China will experience a significant C accumulation increase under all projected scenarios.
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| 2974. |
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| 2975. |
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| 2976. |
- Wang, Gang, et al.
(författare)
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Tumour extracellular vesicles and particles induce liver metabolic dysfunction
- 2023
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Ingår i: Nature. - : NATURE PORTFOLIO. - 0028-0836 .- 1476-4687. ; 618:7964, s. 374-382
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Tidskriftsartikel (refereegranskat)abstract
- Cancer alters the function of multiple organs beyond those targeted by metastasis(1,2). Here we show that inflammation, fatty liver and dysregulated metabolism are hallmarks of systemically affected livers in mouse models and in patients with extrahepatic metastasis. We identified tumour-derived extracellular vesicles and particles (EVPs) as crucial mediators of cancer-induced hepatic reprogramming, which could be reversed by reducing tumour EVP secretion via depletion of Rab27a. All EVP subpopulations, exosomes and principally exomeres, could dysregulate hepatic function. The fatty acid cargo of tumour EVPs-particularly palmitic acid-induced secretion of tumour necrosis factor (TNF) by Kupffer cells, generating a pro-inflammatory microenvironment, suppressing fatty acid metabolism and oxidative phosphorylation, and promoting fatty liver formation. Notably, Kupffer cell ablation or TNF blockade markedly decreased tumour-induced fatty liver generation. Tumour implantation or pre-treatment with tumour EVPs diminished cytochrome P450 gene expression and attenuated drug metabolism in a TNF-dependent manner. We also observed fatty liver and decreased cytochrome P450 expression at diagnosis in tumour-free livers of patients with pancreatic cancer who later developed extrahepatic metastasis, highlighting the clinical relevance of our findings. Notably, tumour EVP education enhanced side effects of chemotherapy, including bone marrow suppression and cardiotoxicity, suggesting that metabolic reprogramming of the liver by tumour-derived EVPs may limit chemotherapy tolerance in patients with cancer. Our results reveal how tumour-derived EVPs dysregulate hepatic function and their targetable potential, alongside TNF inhibition, for preventing fatty liver formation and enhancing the efficacy of chemotherapy.
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| 2977. |
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| 2978. |
- Wang, H. L., et al.
(författare)
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Genetic association study of adaptor protein complex 4 with cerebral palsy in a Han Chinese population
- 2013
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Ingår i: Molecular Biology Reports. - : Springer Science and Business Media LLC. - 0301-4851 .- 1573-4978. ; 40:11, s. 6459-6467
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Tidskriftsartikel (refereegranskat)abstract
- Adaptor protein complex 4 (AP-4) plays a key role in vesicle formation, trafficking, and sorting processes that are critical for brain development and function. AP-4 consists of four subunits encoded by the AP4E1, AP4B1, AP4M1, and AP4S1 genes. A number of studies have pointed to the involvement of AP-4-mediated vesicular trafficking pathways in the etiology of cerebral palsy (CP), the most notable of which are the causative mutations that have recently been identified in each of the AP-4 genes in different CP families. We postulated, therefore, that variations in AP-4 genes might influence an indivual's susceptibility to CP. In the present study, 16 SNPs were genotyped among 517 CP patients and 502 healthy controls from the Han Chinese population. We systematically analyzed the association of the AP4E1, AP4B1, AP4M1, and AP4S1 genes with CP on the basis of clinical characteristics. No significant associations were found between these variants and the overall risk of CP. Subgroup analysis showed that rs1217401 of AP4B1 was significantly associated with CP as a sequela of hypoxic-ischemic encephalopathy (HIE) (CP + HIE) (allele: p = 0.042151; genotype: p = 4.46 x 10(-6)). Our results indicate that the 16 variants studied in the genes of the four subunits of AP-4 have no detectable effects on the overall susceptibility to CP, but AP4B1 appears to be a susceptibility gene for CP + HIE in the Han Chinese population.
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| 2979. |
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| 2980. |
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