| 1. |
- Zhang, Huai, et al.
(author)
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A global survey on the use of the international classification of diseases codes for metabolic dysfunction-associated fatty liver disease.
- 2024
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In: Hepatology international. - 1936-0541.
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Journal article (peer-reviewed)abstract
- With the implementation of the 11th edition of the International Classification of Diseases (ICD-11) and the publication of the metabolic dysfunction-associated fatty liver disease (MAFLD) nomenclature in 2020, it is important to establish consensus for the coding of MAFLD in ICD-11. This will inform subsequent revisions of ICD-11.Using the Qualtrics XM and WJX platforms, questionnaires were sent online to MAFLD-ICD-11 coding collaborators, authors of papers, and relevant association members.A total of 890 international experts in various fields from 61 countries responded to the survey. We also achieved full coverage of provincial-level administrative regions in China. 77.1% of respondents agreed that MAFLD should be represented in ICD-11 by updating NAFLD, with no significant regional differences (77.3% in Asia and 76.6% in non-Asia, p=0.819). Over 80% of respondents agreed or somewhat agreed with the need to assign specific codes for progressive stages of MAFLD (i.e. steatohepatitis) (92.2%), MAFLD combined with comorbidities (84.1%), or MAFLD subtypes (i.e., lean, overweight/obese, and diabetic) (86.1%).This global survey by a collaborative panel of clinical, coding, health management and policy experts, indicates agreement that MAFLD should be coded in ICD-11. The data serves as a foundation for corresponding adjustments in the ICD-11 revision.
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| 2. |
- Long, Feiwu, et al.
(author)
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The impact of immunoglobulin G N-glycosylation level on COVID-19 outcome: evidence from a Mendelian randomization study
- 2023
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In: Frontiers in Immunology. - : FRONTIERS MEDIA SA. - 1664-3224. ; 14
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Journal article (peer-reviewed)abstract
- BackgroundThe coronavirus disease 2019 (COVID-19) pandemic has exerted a profound influence on humans. Increasing evidence shows that immune response is crucial in influencing the risk of infection and disease severity. Observational studies suggest an association between COVID-19 and immunoglobulin G (IgG) N-glycosylation traits, but the causal relevance of these traits in COVID-19 susceptibility and severity remains controversial.MethodsWe conducted a two-sample Mendelian randomization (MR) analysis to explore the causal association between 77 IgG N-glycosylation traits and COVID-19 susceptibility, hospitalization, and severity using summary-level data from genome-wide association studies (GWAS) and applying multiple methods including inverse-variance weighting (IVW), MR Egger, and weighted median. We also used Cochrans Q statistic and leave-one-out analysis to detect heterogeneity across each single nucleotide polymorphism (SNP). Additionally, we used the MR-Egger intercept test, MR-PRESSO global test, and PhenoScanner tool to detect and remove SNPs with horizontal pleiotropy and to ensure the reliability of our results.ResultsWe found significant causal associations between genetically predicted IgG N-glycosylation traits and COVID-19 susceptibility, hospitalization, and severity. Specifically, we observed reduced risk of COVID-19 with the genetically predicted increased IgG N-glycan trait IGP45 (OR = 0.95, 95% CI = 0.92-0.98; FDR = 0.019). IGP22 and IGP30 were associated with a higher risk of COVID-19 hospitalization and severity. Two (IGP2 and IGP77) and five (IGP10, IGP14, IGP34, IGP36, and IGP50) IgG N-glycosylation traits were causally associated with a decreased risk of COVID-19 hospitalization and severity, respectively. Sensitivity analyses did not identify any horizontal pleiotropy.ConclusionsOur study provides evidence that genetically elevated IgG N-glycosylation traits may have a causal effect on diverse COVID-19 outcomes. Our findings have potential implications for developing targeted interventions to improve COVID-19 outcomes by modulating IgG N-glycosylation levels.
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| 3. |
- Guo, Huijie, et al.
(author)
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Regulation of photoinduced charge transfer in all-small-molecule organic solar cells through the synergistic effect of external electric field and solvent
- 2024
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In: Journal of Luminescence. - 0022-2313. ; 268
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Journal article (peer-reviewed)abstract
- The donor (BTR-Cl) and acceptor (BTP-FCl-FCl) have well-defined small molecule properties and excellent repeatability, and they can form charge transfer complexes with a wide spectral absorption range. Using density functional theory (DFT), we simulate the photoinduced charge transfer of bulk-heterojunction (BHJ) organic solar cell (OSC) materials modulated by the external electric field (Fext) at the microscopic level. The excited-state properties, reorganization energy (λ), Gibbs free energy (ΔG), electron coupling matrix elements (VDA) and intermolecular charge transfer (ICT) rate dependent on Fext are systematically analyzed. The results manifest that Fext has apparent positive regulation on the charge separation rate (KCS), and VDA is the main factor affecting KCS. The synergistic effect of solvent and Fext on charge transfer process is further investigated. It is found that the charge transfer rate in solvent is lower than that in solvent-free conditions, and the charge transfer rate in chlorobenzene (CB) solvent does not change significantly under the control of Fext. At the same time, Fext has a positive effect on the charge transfer rate in tetrahydrofuran (THF) solvent. Considering the charge transfer rate under different solvents and Fext intensities, it is found that the solvent and Fext play an essential role in determining the KCS and charge recombination rate (KCR).
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| 4. |
- Zhuang, Ting, et al.
(author)
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SHARPIN stabilizes estrogen receptor a and promotes breast cancer cell proliferation
- 2017
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In: Oncotarget. - : Impact Journals, LLC. - 1949-2553. ; 8:44, s. 77137-77151
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Journal article (peer-reviewed)abstract
- Estrogen receptor a is expressed in the majority of breast cancers and promotes estrogen-dependent cancer progression. In our study, we identified the novel E3 ubiquitin ligase SHARPIN function to facilitate ERα signaling. SHARPIN is highly expressed in human breast cancer and correlates with ERα protein level by immunohistochemistry. SHARPIN expression level correlates with poor prognosis in ERα positive breast cancer patients. SHARPIN depletion based RNA-sequence data shows that ERα signaling is a potential SHARPIN target. SHARPIN depletion significantly decreases ERα protein level, ERα target genes expression and estrogen response element activity in breast cancer cells, while SHARPIN overexpression could reverse these effects. SHARPIN depletion significantly decreases estrogen stimulated cell proliferation in breast cancer cells, which effect could be further rescued by ERα overexpression. Further mechanistic study reveals that SHARPIN mainly localizes in the cytosol and interacts with ERα both in the cytosol and the nuclear. SHARPIN regulates ERα signaling through protein stability, not through gene expression. SHARPIN stabilizes ERα protein via prohibiting ERα protein poly-ubiquitination. Further study shows that SHARPIN could facilitate the mono-ubiquitinaiton of ERα at K302/303 sites and facilitate ERE luciferase activity. Together, our findings propose a novel ERα modulation mechanism in supporting breast cancer cell growth, in which SHARPIN could be one suitable target for development of novel therapy for ERα positive breast cancer.
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