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  • S. Karger AG  (3)
  • 1
    In: Transfusion Medicine and Hemotherapy, S. Karger AG, Vol. 47, No. 2 ( 2020), p. 160-166
    Abstract: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 The characteristic of ABO blood subgroup is crucial for elucidating the mechanisms of such variant phenotypes and offering useful information in blood transfusion. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 In total, 211 ABO variants including part of available family members were investigated in this study. The phenotypes of these individuals were typed with serologic methods. The full coding regions of 〈 i 〉 ABO 〈 /i 〉 gene and the erythroid cell-specific regulatory elements in intron 1 of them were amplified with polymerase chain reaction and then directly sequenced. The novel alleles were confirmed by cloning and sequencing. Phylogenetic tree was made using CLUSTAL W software. 3D structural analyses of the glycosyltransferases (GTs) with some typical mutations were performed by PyMOL software. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Forty-eight distinctly rare 〈 i 〉 ABO 〈 /i 〉 alleles were identified in 211 Chinese variant individuals, including 16 novel 〈 i 〉 ABO 〈 /i 〉 alleles. All of the alleles were categorized as 5 groups: 16 〈 i 〉 ABO 〈 /i 〉 * 〈 i 〉 A 〈 /i 〉 alleles, 23 〈 i 〉 ABO 〈 /i 〉 * 〈 i 〉 B 〈 /i 〉 alleles, 4 〈 i 〉 ABO 〈 /i 〉 * 〈 i 〉 BA 〈 /i 〉 alleles, 4 〈 i 〉 ABO 〈 /i 〉 * 〈 i 〉 cisAB 〈 /i 〉 alleles, and 1 〈 i 〉 ABO 〈 /i 〉 * 〈 i 〉 O 〈 /i 〉 alleles. 〈 i 〉 ABO 〈 /i 〉 * 〈 i 〉 A2.08 〈 /i 〉 and 〈 i 〉 ABO 〈 /i 〉 * 〈 i 〉 BA.02 〈 /i 〉 were the relatively predominant 〈 i 〉 A 〈 /i 〉 and 〈 i 〉 B 〈 /i 〉 subgroup alleles, respectively. According to the phylogenetic tree, 28 alleles (5 common alleles and 23 alleles identified in our laboratory) were classified into 3 major allelic lineages. The structural analysis of 3D homology modeling predicted reduced protein stability of the mutant GTs and may explain the reduced ABO antigen expression. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 The molecular basis of ABO variants was analyzed, and 16 novel 〈 i 〉 ABO 〈 /i 〉 alleles were identified. The results extended the information of ABO variants and provided a basis for better transfusion strategies and helped to improve blood transfusion safety.
    Type of Medium: Online Resource
    ISSN: 1660-3796 , 1660-3818
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2020
    detail.hit.zdb_id: 2100533-3
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  • 2
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 32, No. 4 ( 2013), p. 972-985
    Type of Medium: Online Resource
    ISSN: 1421-9778 , 1015-8987
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2013
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 3
    In: American Journal of Nephrology, S. Karger AG, Vol. 48, No. 2 ( 2018), p. 127-136
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 The role of serum uric acid (SUA) level in the progression of Immunoglobulin A nephropathy (IgAN) remains controversial. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 In a cohort of 1,965 cases with biopsy-proven IgAN, we examined the associations of SUA concentration with the primary outcome of a composite of all-cause mortality or kidney failure (defined as a reduction of estimated glomerular filtration rate [eGFR] by 40% from baseline, requirements for dialysis and transplantation), or the outcome of kidney failure alone, assessed using Cox and logistic regression models, respectively, with adjustment for confounders. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 At baseline, the mean age was 33.37 ± 11.07 years, eGFR was 101.30 ± 30.49 mL/min/1.73 m 〈 sup 〉 2 〈 /sup 〉 , and mean uric acid level was 5.32 ± 1.76 mg/dL. During a median of 7-year follow-up, 317 cases reached the composite outcome of all-cause mortality (5 deaths) or kidney failure (36 cases of dialysis, 5 cases of renal transplantation, and 271 cases with reduction of eGFR by 40% from baseline). After adjustment for demographic and IgAN specific covariates and treatments, a higher quartile of uric acid was linearly associated with an increased risk of the primary outcome (highest versus lowest quartile, hazard ratio [HR] 2.39; 95% CI 1.52–3.75) and kidney failure (highest versus lowest quartile, HR 2.55; 95% CI 1.62–4.01) in the Cox proportional hazards regression models. In the continuous analysis, a 1 mg/dL greater uric acid level was associated with 16% increased risk of primary outcome (HR 1.16, 95% CI 1.07–1.25) and 17% increased risk of kidney failure (HR 1.17, 95% CI 1.08–1.27), respectively, in the fully adjusted model. The multivariate ­logistic regression analyses for the sensitive analyses drew consistent results. In the subgroup analyses, significant interactions were detected that patients with mean arterial pressure (MAP) & #x3c; 90 mm Hg or mesangial hypercellularity had a higher association of SUA with the incidence of the primary outcome than those with MAP ≥90 mm Hg or those without mesangial hypercellularity respectively. Hyperuricemia was not significantly associated with the risk of developing the primary outcome in elder patients (≥32 years old), patients with eGFR & #x3c; 90 mL/min or with tubular atrophy/interstitial fibrosis. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 SUA level may be positively associated with the progression of IgAN. It was noticeable that the association of hyperuricemia with IgAN progression was less significant in patients with elder age, lower eGFR, or tubular atrophy/interstitial fibrosis, which may be due to some more confounders in association with the IgA progression in these patients. Future prospective studies are warranted to confirm these findings and to investigate the underlying mechanisms.
    Type of Medium: Online Resource
    ISSN: 0250-8095 , 1421-9670
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1468523-1
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