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  • 1
    In: Arthritis & Rheumatology, Wiley, Vol. 74, No. 12 ( 2022-12), p. 1984-1990
    Abstract: Previous observational studies demonstrated that a subset of patients with systemic lupus erythematosus (SLE) have markedly short telomere length in leukocytes. This study was undertaken to test whether leukocyte telomere length is causally associated with risk of SLE. Methods A 2‐sample Mendelian randomization (MR) analysis was conducted to estimate causality of telomere length on SLE in European populations. A replication 2‐sample MR study using Asian genetic data was also conducted. A reverse MR analysis was then performed to test the effects of SLE on telomere length. The autoantibodies targeting telomere‐associated protein (telomeric repeat–binding factor 1 [TERF1] autoantibodies) were detected in patients with SLE, healthy controls, and patients with rheumatoid arthritis. Results The results of the inverse variance–weighted method (odds ratio [OR] 2.96 [95% confidence interval (95% CI) 1.58–5.55] , P   〈  0.001) showed strong evidence for a causal relationship between longer telomere length and risk of SLE in people with European ancestry. The outcomes of MR‐Egger regression analysis (OR 29.46 [95% CI 3.02–287.60], P  = 0.033) and MR pleiotropy residual sum and outlier analysis (OR 3.62 [95% CI 2.03–6.46], P  = 0.002) also showed that longer telomere length was significantly associated with increased risk of SLE in a European population. Sensitivity analyses using different methods and summary data sets showed that the results were still broadly consistent. A replication MR study using Asian genetic data yielded similar findings. However, the reverse MR analysis showed that genetically predicted SLE was not causally associated with telomere length. In addition, we found that TERF1 autoantibodies were present in 2 of 40 SLE patients (5.0%). Conclusion In contrast with previous observational studies, MR analyses show that longer telomere length is significantly associated with increased risk of SLE.
    Type of Medium: Online Resource
    ISSN: 2326-5191 , 2326-5205
    URL: Issue
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    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2754614-7
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  • 2
    In: Journal of Medical Virology, Wiley, Vol. 94, No. 12 ( 2022-12), p. 5640-5652
    Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection can cause coronavirus disease 2019 (COVID‐19), an acute respiratory inflammation that has emerged worldwide since December 2019, and it quickly became a global epidemic. Inflammatory bowel disease (IBD) is a group of chronic nonspecific intestinal inflammatory diseases whose etiology has not been elucidated. The two have many overlapping symptoms in clinical presentation, such as abdominal pain, diarrhea, pneumonia, etc. Imbalance of the autoimmune system in IBD patients and long‐term use of immunosuppressive drugs may increase the risk of infection; and systemic symptoms caused by COVID‐19 may also induce or exacerbate intestinal inflammation. It has been found that the SARS‐CoV‐2 receptor angiotensin converting enzyme 2, which is highly expressed in the lung and intestine, is an inflammatory protective factor, and is downregulated and upregulated in COVID‐19 and IBD, respectively, suggesting that there may be a coregulatory pathway. In addition, the immune activation pattern of COVID‐19 and the cytokine storm in the inflammatory response have similar roles in IBD, indicating that the two diseases may influence each other. Therefore, this review aimed to address the following research questions: whether SARS‐CoV‐2 infection leads to the progression of IBD; whether IBD increases the risk of COVID‐19 infection and poor prognosis; possible common mechanisms and genetic cross‐linking between the two diseases; new treatment and care strategies for IBD patients, and the feasibility and risk of vaccination in the context of the COVID‐19 epidemic.
    Type of Medium: Online Resource
    ISSN: 0146-6615 , 1096-9071
    URL: Issue
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    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 752392-0
    detail.hit.zdb_id: 1475090-9
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  • 3
    Online Resource
    Online Resource
    Wiley ; 2022
    In:  Immunology Vol. 165, No. 4 ( 2022-04), p. 386-401
    In: Immunology, Wiley, Vol. 165, No. 4 ( 2022-04), p. 386-401
    Abstract: Coronavirus disease 2019 (COVID‐19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has led to an unprecedented setback for global economy and health. Vaccination is one of the most effective interventions to substantially reduce severe disease and death due to SARS‐CoV‐2 infection. Vaccination programmes are being rolled out globally, but most of these vaccines have been approved without extensive studies on their side‐effects and efficacy. Recently, new‐onset autoimmune phenomena after COVID‐19 vaccination have been reported increasingly (e.g. immune thrombotic thrombocytopenia, autoimmune liver diseases, Guillain–Barré syndrome, IgA nephropathy, rheumatoid arthritis and systemic lupus erythematosus). Molecular mimicry, the production of particular autoantibodies and the role of certain vaccine adjuvants seem to be substantial contributors to autoimmune phenomena. However, whether the association between COVID‐19 vaccine and autoimmune manifestations is coincidental or causal remains to be elucidated. Here, we summarize the emerging evidence about autoimmune manifestations occurring in response to certain COVID‐19 vaccines. Although information pertaining to the risk of autoimmune disease as a consequence of vaccination is controversial, we merely propose our current understanding of autoimmune manifestations associated with COVID‐19 vaccine. In fact, we do not aim to disavow the overwhelming benefits of mass COVID‐19 vaccination in preventing COVID‐19 morbidity and mortality. These reports could help guide clinical assessment and management of autoimmune manifestations after COVID‐19 vaccination.
    Type of Medium: Online Resource
    ISSN: 0019-2805 , 1365-2567
    URL: Issue
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    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2006481-0
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  • 4
    In: Journal of Orthopaedic Research, Wiley, Vol. 37, No. 11 ( 2019-11), p. 2348-2357
    Abstract: Early diagnosis and prevention of glucocorticoid (GC)‐induced osteonecrosis of the femoral head (ONFH) continues to be a challenging problem for clinicians and researchers. However, the role of circulating biomarkers for GC‐induced ONFH, which may reveal individual susceptibility and facilitate earlier diagnosis, remains to be determined. The aim of this study was to identify potential biomarkers that may predict early GC‐induced ONFH. A total of 123 patients scheduled for initial systemic GC therapy were enrolled in this prospective nested case–control study. The serum concentrations of 13 potential biomarkers were measured in seven patients with GC‐induced ONFH, diagnosed instantly after short‐term use of GCs and in 20 controls who did not develop osteonecrosis despite similar GC therapy. Biomarkers were measured both before and after taking GCs to identify any differences in marker levels and the changes during GC therapy between two groups. Type I collagen cross‐linked C‐telopeptide (β‐CTX; p  = 0.000) was significantly lower, high‐density lipoprotein cholesterol ( p  = 0.092) and apolipoprotein (apo)‐B/apo‐A1 ( p  = 0.085) tended to be lower and higher, respectively, before GC treatment in osteonecrosis group. After GC therapy, β‐CTX ( p  = 0.014) was significantly lower and amino terminal telopeptide of procollagen type I (PINP; p  = 0.068) tended to be lower in the osteonecrosis group. As secondary outcomes, we observed remarkable changes in nine potential biomarkers following short‐term GC therapy in both groups. In conclusion, we found that β‐CTX, could potentially be used to predict GC‐induced ONFH before GC therapy. Lower β‐CTX and PINP are promising biomarkers for the early diagnosis of GC‐induced ONFH. These findings need to be confirmed in large‐scale prospective studies. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:2348–2357, 2019
    Type of Medium: Online Resource
    ISSN: 0736-0266 , 1554-527X
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2050452-4
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  • 5
    In: Clinical and Translational Medicine, Wiley, Vol. 11, No. 2 ( 2021-02)
    Type of Medium: Online Resource
    ISSN: 2001-1326 , 2001-1326
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2697013-2
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  • 6
    In: Journal of Separation Science, Wiley, Vol. 39, No. 16 ( 2016-08), p. 3239-3245
    Abstract: A simple and highly efficient interface to couple capillary electrophoresis with inductively coupled plasma mass spectrometry by a microflow polyfluoroalkoxy nebulizer and a quadruple ion deflector was developed in this study. By using this interface, six arsenic species, including arsenite, arsenate, monomethylarsonic acid, dimethylarsinic acid, arsenobetaine, and arsenocholine, were baseline‐separated and determined in a single run within 11 min under the optimized separation conditions. The instrumental detection limit was in the range of 0.02–0.06 ng/mL for the six arsenic compounds. Repeatability expressed as the relative standard deviation ( n = 5) of both migration time and peak area were better than 2.5 and 4.3% for six arsenic compounds. The proposed method, combined with a closed‐vessel microwave‐assisted extraction procedure, was successfully applied for the determination of arsenic species in the Solanum Lyratum Thunb samples from Anhui province in China with the relative standard deviations ( n = 5) ≤4%, method detection limits of 0.2–0.6 ng As/g and a recovery of 98–104%. The experimental results showed that arsenobetaine was the main speciation of arsenic in the Solanum Lyratum Thunb samples from different provinces in China, with a concentration of 0.42–1.30 μg/g.
    Type of Medium: Online Resource
    ISSN: 1615-9306 , 1615-9314
    URL: Issue
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    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2047990-6
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