Effects of additional electrical stimulation and pre-rigor conditioning temperature on the ageing potential of hot-boned bovine muscles

Balan Prabhu,Farouk Mustafa M.,Staincliffe Maryann,Stuart Adam D,Kemp Robert,Craigie Cameron 아세아·태평양축산학회 2020 Animal Bioscience Vol.33 No.10

Objective: The aim of this study is to characterize the impact of additional electrical stimulation (AES) and various pre-rigor holding temperatures (for 3 h) on the ageing-potential of hot boned bovine M. longissimus lumborum (LL). Methods: Paired LL loins from 12 bulls were hot-boned within 40 min of slaughter, immediate AES applied and subjected to various holding temperatures (5°C, 15°C, 25°C, and 35°C) for 3 h. Results: AES did not accelerate the rate of rigor attainment, but the 3 h pre-rigor holding temperature did. Shear force values decreased as the pre-rigor holding temperatures increased. AES and holding for 3 h (at 25°C) resulted in higher water-holding capacity. Conclusion: Data confirmed that AES did not influence the various meat quality parameters in the present study, but pre-rigor holding temperature (25°C) alone or in combination with AES resulted in superior meat quality.

Variation in the ICAM1-ICAM4-ICAM5 locus is associated with systemic lupus erythematosus susceptibility in multiple ancestries.

Kim, Kwangwoo,Brown, Elizabeth E,Choi, Chan-Bum,Alarc?n-Riquelme, Marta E,Kelly, Jennifer A,Glenn, Stuart B,Ojwang, Joshua O,Adler, Adam,Lee, Hye-Soon,Boackle, Susan A,Criswell, Lindsey A,Alarc?n, Gra British Medical Association 2012 Annals of the Rheumatic Diseases Vol.71 No.11

<P>Systemic lupus erythematosus (SLE; OMIM 152700) is a chronic autoimmune disease for which the aetiology includes genetic and environmental factors. ITGAM, integrin α(M) (complement component 3 receptor 3 subunit) encoding a ligand for intracellular adhesion molecule (ICAM) proteins, is an established SLE susceptibility locus. This study aimed to evaluate the independent and joint effects of genetic variations in the genes that encode ITGAM and ICAM.</P>

Association of two independent functional risk haplotypes in <i>TNIP1</i> with systemic lupus erythematosus

Adrianto, Indra,Wang, Shaofeng,Wiley, Graham B.,Lessard, Christopher J.,Kelly, Jennifer A.,Adler, Adam J.,Glenn, Stuart B.,Williams, Adrienne H.,Ziegler, Julie T.,Comeau, Mary E.,Marion, Miranda C.,Wa Wiley Subscription Services, Inc., A Wiley Company 2012 Vol.64 No.11

<P><B>Abstract</B></P><P><B>Objective</B></P><P>Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoantibody production and altered type I interferon expression. Genetic surveys and genome‐wide association studies have identified >30 SLE susceptibility genes. One of these genes, <I>TNIP1</I>, encodes the ABIN1 protein. ABIN1 functions in the immune system by restricting NF‐κB signaling. The present study was undertaken to investigate the genetic factors that influence association with SLE in genes that regulate the NF‐κB pathway.</P><P><B>Methods</B></P><P>We analyzed a dense set of genetic markers spanning <I>TNIP1</I> and <I>TAX1BP1</I>, as well as the <I>TNIP1</I> homolog <I>TNIP2</I>, in case–control populations of diverse ethnic origins. <I>TNIP1</I>, <I>TNIP2</I>, and <I>TAX1BP1</I> were fine‐mapped in a total of 8,372 SLE cases and 7,492 healthy controls from European‐ancestry, African American, Hispanic, East Asian, and African American Gullah populations. Levels of <I>TNIP1</I> messenger RNA (mRNA) and ABIN1 protein in Epstein‐Barr virus–transformed human B cell lines were analyzed by quantitative reverse transcription–polymerase chain reaction and Western blotting, respectively.</P><P><B>Results</B></P><P>We found significant associations between SLE and genetic variants within <I>TNIP1</I>, but not in <I>TNIP2</I> or <I>TAX1BP1</I>. After resequencing and imputation, we identified 2 independent risk haplotypes within <I>TNIP1</I> in individuals of European ancestry that were also present in African American and Hispanic populations. Levels of <I>TNIP1</I> mRNA and ABIN1 protein were reduced among subjects with these haplotypes, suggesting that they harbor hypomorphic functional variants that influence susceptibility to SLE by restricting ABIN1 expression.</P><P><B>Conclusion</B></P><P>Our results confirm the association signals between SLE and <I>TNIP1</I> variants in multiple populations and provide new insight into the mechanism by which <I>TNIP1</I> variants may contribute to SLE pathogenesis.</P>

Preferential association of a functional variant in complement receptor 2 with antibodies to double-stranded DNA

Zhao, Jian,Giles, Brendan M,Taylor, Rhonda L,Yette, Gabriel A,Lough, Kara M,Ng, Han Leng,Abraham, Lawrence J,Wu, Hui,Kelly, Jennifer A,Glenn, Stuart B,Adler, Adam J,Williams, Adrienne H,Comeau, Mary E H. K. Lewis 2016 Annals of the rheumatic diseases Vol.75 No.1

<P><B>Objectives</B></P><P>Systemic lupus erythematosus (SLE; OMIM 152700) is characterised by the production of antibodies to nuclear antigens. We previously identified variants in complement receptor 2 (<I>CR2/CD21</I>) that were associated with decreased risk of SLE. This study aimed to identify the causal variant for this association.</P><P><B>Methods</B></P><P>Genotyped and imputed genetic variants spanning <I>CR2</I> were assessed for association with SLE in 15 750 case-control subjects from four ancestral groups. Allele-specific functional effects of associated variants were determined using quantitative real-time PCR, quantitative flow cytometry, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP)-PCR.</P><P><B>Results</B></P><P>The strongest association signal was detected at rs1876453 in intron 1 of <I>CR2</I> (p<SUB>meta</SUB>=4.2×10<SUP>−4</SUP>, OR 0.85), specifically when subjects were stratified based on the presence of dsDNA autoantibodies (case-control p<SUB>meta</SUB>=7.6×10<SUP>−7</SUP>, OR 0.71; case-only p<SUB>meta</SUB>=1.9×10<SUP>−4</SUP>, OR 0.75). Although allele-specific effects on B cell <I>CR2</I> mRNA or protein levels were not identified, levels of complement receptor 1 (<I>CR1/CD35)</I> mRNA and protein were significantly higher on B cells of subjects harbouring the minor allele (p=0.0248 and p=0.0006, respectively). The minor allele altered the formation of several DNA protein complexes by EMSA, including one containing CCCTC-binding factor (CTCF), an effect that was confirmed by ChIP-PCR.</P><P><B>Conclusions</B></P><P>These data suggest that rs1876453 in <I>CR2</I> has long-range effects on gene regulation that decrease susceptibility to lupus. Since the minor allele at rs1876453 is preferentially associated with reduced risk of the highly specific dsDNA autoantibodies that are present in preclinical, active and severe lupus, understanding its mechanisms will have important therapeutic implications.</P>

Evaluation of <i>TRAF6</i> in a large multiancestral lupus cohort

Namjou, Bahram,Choi, Chan‐,Bum,Harley, Isaac T. W.,Alarcó,n‐,Riquelme, Marta E.,Kelly, Jennifer A.,Glenn, Stuart B.,Ojwang, Joshua O.,Adler, Adam,Kim, Kwangwoo,Gallant, Caroline J.,B Wiley Subscription Services, Inc., A Wiley Company 2012 Vol.64 No.6

<P><B>Abstract</B></P><P><B>Objective</B></P><P>Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease with significant immune system aberrations resulting from complex heritable genetics as well as environmental factors. We undertook to study the role of <I>TRAF6</I> as a candidate gene for SLE, since it plays a major role in several signaling pathways that are important for immunity and organ development.</P><P><B>Methods</B></P><P>Fifteen single‐nucleotide polymorphisms (SNPs) across <I>TRAF6</I> were evaluated in 7,490 SLE patients and 6,780 control subjects from different ancestries. Population‐based case–control association analyses and meta‐analyses were performed. <I>P</I> values, false discovery rate q values, and odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated.</P><P><B>Results</B></P><P>Evidence of associations was detected in multiple SNPs. The best overall <I>P</I> values were obtained for SNPs rs5030437 and rs4755453 (<I>P</I> = 7.85 × 10<SUP>−5</SUP> and <I>P</I> = 4.73 × 10<SUP>−5</SUP>, respectively) without significant heterogeneity among populations (<I>P</I> = 0.67 and <I>P</I> = 0.50, respectively, in Q statistic). In addition, SNP rs540386, which was previously reported to be associated with rheumatoid arthritis (RA), was found to be in linkage disequilibrium with these 2 SNPs (r<SUP>2</SUP> = 0.95) and demonstrated evidence of association with SLE in the same direction (meta‐analysis <I>P</I> = 9.15 × 10<SUP>−4</SUP>, OR 0.89 [95% CI 0.83–0.95]). The presence of thrombocytopenia improved the overall results in different populations (meta‐analysis <I>P</I> = 1.99 × 10<SUP>−6</SUP>, OR 0.57 [95% CI 0.45–0.72], for rs5030470). Finally, evidence of family‐based association in 34 African American pedigrees with the presence of thrombocytopenia was detected in 1 available SNP (rs5030437) with a Z score magnitude of 2.28 (<I>P</I> = 0.02) under a dominant model.</P><P><B>Conclusion</B></P><P>Our data indicate the presence of association of <I>TRAF6</I> with SLE, consistent with the previous report of association with RA. These data provide further support for the involvement of <I>TRAF6</I> in the pathogenesis of autoimmunity.</P>

Identification of IRF8, TMEM39A, and IKZF3-ZPBP2 as Susceptibility Loci for Systemic Lupus Erythematosus in a Large-Scale Multiracial Replication Study

Marta E. Alarcon-Riquelme for the BIOLUPUS and GENLES Networks,Lessard, Christopher J.,Adrianto, I.,Ice, John A.,Wiley, Graham B.,Kelly, Jennifer A.,Glenn, Stuart B.,Adler, Adam J.,Li, H.,Rasmussen, A University of Chicago Press [etc.] 2012 American journal of human genetics Vol.90 No.4

Systemic lupus erythematosus (SLE) is a chronic heterogeneous autoimmune disorder characterized by the loss of tolerance to self-antigens and dysregulated interferon responses. The etiology of SLE is complex, involving both heritable and environmental factors. Candidate-gene studies and genome-wide association (GWA) scans have been successful in identifying new loci that contribute to disease susceptibility; however, much of the heritable risk has yet to be identified. In this study, we sought to replicate 1,580 variants showing suggestive association with SLE in a previously published GWA scan of European Americans; we tested a multiethnic population consisting of 7,998 SLE cases and 7,492 controls of European, African American, Asian, Hispanic, Gullah, and Amerindian ancestry to find association with the disease. Several genes relevant to immunological pathways showed association with SLE. Three loci exceeded the genome-wide significance threshold: interferon regulatory factor 8 (IRF8; rs11644034; p<SUB>meta-Euro</SUB> = 2.08 x 10<SUP>-10</SUP>), transmembrane protein 39A (TMEM39A; rs1132200; p<SUB>meta-all</SUB> = 8.62 x 10<SUP>-9</SUP>), and 17q21 (rs1453560; p<SUB>meta-all</SUB> = 3.48 x 10<SUP>-10</SUP>) between IKAROS family of zinc finger 3 (AIOLOS; IKZF3) and zona pellucida binding protein 2 (ZPBP2). Fine mapping, resequencing, imputation, and haplotype analysis of IRF8 indicated that three independent effects tagged by rs8046526, rs450443, and rs4843869, respectively, were required for risk in individuals of European ancestry. Eleven additional replicated effects (5 x 10<SUP>-8</SUP> < p<SUB>meta-Euro</SUB> < 9.99 x 10<SUP>-5</SUP>) were observed with CFHR1, CADM2, LOC730109/IL12A, LPP, LOC63920, SLU7, ADAMTSL1, C10orf64, OR8D4, FAM19A2, and STXBP6. The results of this study increase the number of confirmed SLE risk loci and identify others warranting further investigation.