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Lessard, Christopher J.,Adrianto, Indra,Kelly, Jennifer A.,Kaufman, Kenneth M.,Grundahl, Kiely M.,Adler, Adam,Williams, Adrienne H.,Gallant, Caroline J.,Anaya, Juan-Manuel,Bae, Sang-Cheol,Boackle, Sus Elsevier 2011 American journal of human genetics Vol.88 No.1
<P>Systemic lupus erythematosus (SLE) is considered to be the prototypic autoimmune disease, with a complex genetic architecture influenced by environmental factors. We sought to replicate a putative association at 11p13 not yet exceeding genome-wide significance (p < 5 × 10<SUP>−8</SUP>) identified in a genome-wide association study (GWAS). Our GWA scan identified two intergenic SNPs located between <I>PDHX</I> and <I>CD44</I> showing suggestive evidence of association with SLE in cases of European descent (rs2732552, p = 0.004, odds ratio [OR] = 0.78; rs387619, p = 0.003, OR = 0.78). The replication cohort consisted of >15,000 subjects, including 3562 SLE cases and 3491 controls of European ancestry, 1527 cases and 1811 controls of African American (AA) descent, and 1265 cases and 1260 controls of Asian origin. We observed robust association at both rs2732552 (p = 9.03 × 10<SUP>−8</SUP>, OR = 0.83) and rs387619 (p = 7.7 × 10<SUP>−7</SUP>, OR = 0.83) in the European samples with p<SUB>meta</SUB> = 1.82 × 10<SUP>−9</SUP> for rs2732552. The AA and Asian SLE cases also demonstrated association at rs2732552 (p = 5 × 10<SUP>−3</SUP>, OR = 0.81 and p = 4.3 × 10<SUP>−4</SUP>, OR = 0.80, respectively). A meta-analysis of rs2732552 for all racial and ethnic groups studied produced p<SUB>meta</SUB> = 2.36 × 10<SUP>−13</SUP>. This locus contains multiple regulatory sites that could potentially affect expression and functions of <I>CD44</I>, a cell-surface glycoprotein influencing immunologic, inflammatory, and oncologic phenotypes, or PDHX, a subunit of the pyruvate dehydrogenase complex.</P>
Benoît H. Lessard,Sarah Mackay,Adrien Métafiot,Milan Marić 한국고분자학회 2016 Macromolecular Research Vol.24 No.8
Poly(styrene-alt-maleic anhydride)-block-poly(methacrylate-ran-styrene) block copolymers were synthesized from low dispersity (Mw/Mn=1.24) and perfectly alternating poly(styrene-alt-maleic anhydride) macroinitiators, by nitroxide mediated controlled radical polymerization (NMP), using various methacrylate-rich mixtures: methyl methacrylate/styrene (MMA/S), ethyl methacrylate/styrene (EMMA/S), n-butyl methacrylate/styrene (BMA/S) and benzyl methacrylate/styrene (BzMA/S). Some irreversible termination was present during the chain extension from the macroinitiator, resulting in some bimodality in the molecular weight distribution of the final block copolymer (≈2% to ≈25% dead chains) which is common for methacrylate/styrene copolymerizations by NMP. The resulting final block copolymers were determined to be methacrylate-rich (molar ratio XMA/S ≈3.3 to 5.5) by 1H NMR and the resulting glass transition temperature (Tg) of the chain-extended segments were found to be similar to the coresponding pure poly(methacrylate)s. NMP allows the controlled placement of functional maleic anhydride containing segments within a block copolymer with tunable mechanical properties by simple substitution of methacrylate monomer used in synthesis.
비침습적 뇌내압 측정 시스템의 개발을 위한 청각유발전위와 경막혈종간의 상관관계 분석에 관한 연구
임재중,C.S. Lessard 대한의용생체공학회 1995 의공학회지 Vol.16 No.2
Development of a noninvasive intensive care system calls for the use of evoked potentials (EPs) as a means of diagnosing traumatic head-injured patients. The experiment entails surgically placing two subarachnoid bolts and a subdural balloon through the skull to simulate a subdural hematoma. Using various levels of intracranial pressure (ICP) and/or different sizes of balloons, auditory evoked potentials (AEPs) were recorded from a rabbit. Six positive peak latencies ($P_1 - P_6$) and five negative peak latencies ($N_l- N_5$) were extracted from an averaged AEP waveform. Multiple regression analyses were performed for determining. a relationship between the ICP and AEP peak latencies. The results indicate that a major correlation of ch, mges on AEP peak latencies is due to mechanical forces of a mass (inflated balloon simulating a hematoma) in the distortion of the brain matter rather than increased ICP itself.
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>
Alain Joe Azzi,Jordan Gornitsky,Alex Viezel-Mathieu,Lucie Lessard 대한암예방학회 2018 Journal of cancer prevention Vol.23 No.2
Background: There is a paucity of data comparing the oncologic properties of breast cancer among patients previously having undergone breast augmentation in either the subglandular or subpectoral planes. The objective of the present systematic review was to evaluate whether implant location influenced the characteristics of breast tumors in previously augmented women. Methods: A systematic literature search was performed to identify relevant articles reporting tumor characteristics in augmented patients. The search included published articles in three electronic databases; Ovid MEDLINE, EMBASE, and PubMed. Comparative studies (subglandular vs. subpectoral) were included. Results: Analysis of data pooled from the included studies showed that subglandular implants had a higher frequency of tumors between 2 to 5 cm (26.5% vs. 9.9%, P = 0.0130). Subglandular implants also had a higher frequency of stage 2 tumors (42.9% vs. 23.7%, P = 0.0308). There was no significant difference in lymphovascular invasion between the 2 groups. These results of this systematic review suggest that the prognosis of patients undergoing augmentation is unaffected by implant location (subpectoral vs. subglandular). Conclusions: With the absence of large randomized controlled trials, our study provides surgeons with an evidence-based reference to improve informed consent with regards to implant placement.
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.
Association of a functional variant downstream of TNFAIP3 with systemic lupus erythematosus
Adrianto, Indra,Wen, Feng,Templeton, Amanda,Wiley, Graham,King, Jarrod B,Lessard, Christopher J,Bates, Jared S,Hu, Yanqing,Kelly, Jennifer A,Kaufman, Kenneth M,Guthridge, Joel M,Alarc처n-Riquelme, Mart Nature Publishing Group, a division of Macmillan P 2011 Nature genetics Vol.43 No.3
Systemic lupus erythematosus (SLE, MIM152700) is an autoimmune disease characterized by self-reactive antibodies resulting in systemic inflammation and organ failure. TNFAIP3, encoding the ubiquitin-modifying enzyme A20, is an established susceptibility locus for SLE. By fine mapping and genomic re-sequencing in ethnically diverse populations, we fully characterized the TNFAIP3 risk haplotype and identified a TT>A polymorphic dinucleotide (deletion T followed by a T to A transversion) associated with SLE in subjects of European (P = 1.58 ? 10<SUP>??8</SUP>, odds ratio = 1.70) and Korean (P = 8.33 ? 10<SUP>??10</SUP>, odds ratio = 2.54) ancestry. This variant, located in a region of high conservation and regulatory potential, bound a nuclear protein complex composed of NF-觀B subunits with reduced avidity. Further, compared with the non-risk haplotype, the haplotype carrying this variant resulted in reduced TNFAIP3 mRNA and A20 protein expression. These results establish this TT>A variant as the most likely functional polymorphism responsible for the association between TNFAIP3 and SLE.
Guthridge, Joel M.,Lu, R.,Sun, H.,Sun, C.,Wiley, Graham B.,Dominguez, N.,Macwana, Susan R.,Lessard, Christopher J.,Kim-Howard, X.,Cobb, Beth L.,Kaufman, Kenneth M.,Kelly, Jennifer A.,Langefeld, Carl D University of Chicago Press [etc.] 2014 American journal of human genetics Vol.94 No.4
Efforts to identify lupus-associated causal variants in the FAM167A/BLK locus on 8p21 are hampered by highly associated noncausal variants. In this report, we used a trans-population mapping and sequencing strategy to identify a common variant (rs922483) in the proximal BLK promoter and a tri-allelic variant (rs1382568) in the upstream alternative BLK promoter as putative causal variants for association with systemic lupus erythematosus. The risk allele (T) at rs922483 reduced proximal promoter activity and modulated alternative promoter usage. Allelic differences at rs1382568 resulted in altered promoter activity in B progenitor cell lines. Thus, our results demonstrated that both lupus-associated functional variants contribute to the autoimmune disease association by modulating transcription of BLK in B cells and thus potentially altering immune responses.