In the past Edwin Wong has collaborated on articles with Steve Kwon and Marc B. Schure. One of their most recent publications is Poster AbstractsCharacterisation of a novel hybrid CFH/CFHR3 protein with impaired cell surface complement regulation in atypical haemolytic uraemic syndrome. Which was published in journal The Lancet.

More information about Edwin Wong research including statistics on their citations can be found on their Copernicus Academic profile page.

Edwin Wong's Articles: (4)

Poster AbstractsCharacterisation of a novel hybrid CFH/CFHR3 protein with impaired cell surface complement regulation in atypical haemolytic uraemic syndrome

AbstractBackground60% of patients with atypical haemolytic uraemic syndrome have a rare genetic variant in C3, complement factor B (CFB), complement factor H (CFH), complement factor I (CFI), or CD46. Many of these variants are in the 3' cell recognition domain of CFH. The genes encoding CFH and five CFH-related proteins are found adjacently in the regulators of complement activation (RCA) cluster on chromosome 1q32. This cluster is a region of genomic instability that can lead to genomic disorders causing atypical haemolytic uraemic syndrome.MethodsUsing multiplex-ligation dependent probe amplification, we screened patients with atypical haemolytic uraemic syndrome who did not have a disease-causing genetic variant in C3, CFB, CFH, CFI, or CD46 for a genomic disorder. We used Sanger sequencing to define the breakpoint and identify a transcript for a hybrid CFH/CFHR3 gene. We purified the hybrid CFH/CFHR3 protein using allele specific monoclonal antibodies to the Y402H polymorphism of CFH. We tested its regulatory function using cell surface sheep erythrocyte lytic assays.FindingsWe found one patient who had evidence of a de-novo deletion in CFH. We identified a 6·3 kb deletion extending from exon 20 of CFH to the CFH 3' intergenetic region incorporating exons 21, 22, and 23. Directly flanking the breakpoint was a 7 base-pair region of microhomology. A putative hybrid gene was predicted to include exons 1 to 20 of CFH and exons 2 to 6 of CFHR3. We confirmed mRNA for a CFH/CFHR3 hybrid gene. Western blot analysis showed a hybrid CFH/CFHR3 protein at ∼160 kDa that lacked the cell recognition domain of CFH compared with 150 kDa for CFH. Peptide fragments from the larger band confirmed the CFH/CFHR3 hybrid protein. The purified CFH/CFHR3 hybrid protein showed less cell surface decay acceleration and cofactor activity compared with control.InterpretationScreening for genomic disorders in this patient identified a hybrid CFH/CFHR3 protein that lacked cell surface regulation of complement. This valuable method has led to insight into the disease mechanism of atypical haemolytic uraemic syndrome, thus aiding in patient stratification for future management and prognosis. That the deletion was a de-novo event suggests that it is a dynamic region of the genome and that we can expect to discover further genomic disorders in atypical haemolytic uraemic syndrome.FundingMedical Research Council, Wellcome Trust, EURenOmics.

Patient stratification and therapy in atypical haemolytic uraemic syndrome (aHUS)

AbstractApproximately 50% of aHUS patients have an underlying inherited and/or acquired abnormality of complement which predisposes to excessive activation of the alternative pathway. Use of complement inhibitors such as eculizumab to treat aHUS is therefore logical. Anecdotal reports and subsequent open-label trials demonstrated the efficacy of eculizumab in aHUS leading to approval by both the FDA and EMA. NHS England established in 2013 an interim national service for aHUS including funding for eculizumab for both new patients and those undergoing transplantation. NICE guidance now also recommends eculizumab for funding within the NHS in England under the coordination of an expert centre. The investigation and response to treatment in this cohort provides a unique resource for patient stratification.

Original articleThe impact of accreditation on safety and cost of bariatric surgery

AbstractBackgroundThe objective of this study was to examine how much of the impact of the Centers for Medicare and Medicaid Services’ national coverage decision (NCD) on bariatric surgery was driven by the restriction of reimbursements to Centers of Excellence (COE). We used inpatient care data of those with employer-sponsored insurance plans across United States using the MarketScan Commercial Claims and Encounter Database (2003–2009).MethodsWe performed a retrospective cohort study evaluating the impact of the accreditation on subjects with a difference-in-difference approach (removing the temporal changes occurring in non-COEs) on rates of inpatient mortality, 90-day reoperations, complications, readmissions, and total payments.ResultsA total of 30,755 patients (43.9±11.0 years; 79.9% women) had bariatric surgery. A total of 17,896 patients underwent procedures at sites that became COEs (8455 pre-NCD and 9441 post-NCD, [+10.4%]) compared with 12,859 at non-COEs (6534 pre-NCD and 6325 post-NCD, [−3.3%]). Of the total number of bariatric procedures, laparoscopic Roux-en-Y gastric bypass and laparoscopic adjustable band procedures increased from 42.9% and 3.1% pre-NCD to 64.5% and 19.7% post-NCD, respectively. In the COEs, there were reductions in inpatient mortality (.3% to .1%; P = .02), 90-day reoperations (.8% to .5%; P = .006), complications (36.4% to 27.6%; P<.001), and readmissions (10.8% to 8.8%; P<.001) while payments remained similar ($24,543±$40,145 to $24,510±$37,769; P = .9). After distinguishing from temporal trends and differences occurring at non-COEs, 90-day reoperation (−.8%; P = .02) and complication rates (−2.7%; P = .01) were lower at the COEs after the NCD.ConclusionsThe accreditation-based NCD in bariatric surgery was associated with lower rates of reoperations and complications. Such policies may become a powerful tool to improve surgical safety and quality.

ArticleFood and housing insecurity and health status among U.S. adults with and without prior military service

AbstractFood and housing insecurity may contribute to poorer mental and physical health. It is unclear as to whether those with prior military service, compared to those without, are more vulnerable to these current stressors. The objective of this study was to use U.S. population-based data to determine whether prior military service moderates the association of food and housing insecurity with poor mental and physical health.We analyzed data from nine states administering the Social Context module from the 2011 and 2012 Behavioral Risk Factor Surveillance System. Multivariable logistic regression was used to examine the associations of housing and food insecurity with poor mental and physical health and potential modification by military service. Compared with those with a history of military service, those without had higher prevalence of food insecurity (23.1% versus 13.7%) and housing insecurity (36.0% versus 22.5%). Food insecurity was associated with poor mental and physical health (mental health: odds ratio (OR)=3.47, 95% confidence interval (CI)=[3.18–3.77]; physical health: OR=3.21, 95% CI=[2.92–3.53]). Similar associations were observed between housing insecurity and poor mental and physical health. Prior military service was significantly associated with poor physical health. Interaction terms of prior military service with food and housing were not statistically significant. Food and housing insecurity does not appear to differentially impact mental and physical health among those with and without military service.

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