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THE REPEATED ENVELOPING SEMIGROUP COMPACTIFICATIONS
FATTAHI, A,MILNES, P 호남수학회 2002 한국수학학술지 Vol.24 No.1
This note consists of some efficient examples to support the notion of enveloping semigroup campactigication and also employ this notion to obtain the universal reductive compactification
THE REPEATED ENVELOPING SEMIGROUP COMPACTIFICATIONS
FATTAHI, A.,MILNES, P. The Honam Mathematical Society 2002 호남수학학술지 Vol.24 No.1
This note consists of some efficient examples to support the notion of enveloping semigroup compactification and also employ this notion to obtain the universal reductive compactification.
Kim, Shang-Jin,Zhang, Haifei,Khaliulin, Igor,Choisy, Sté,phanie C.M.,Bond, Richard,Lin, Hua,El Haou, Said,Milnes, James T.,Hancox, Jules C.,Suleiman, M. Saadeh,James, Andrew F. Ovid Technologies Wolters Kluwer -American Heart A 2012 Circulation. Arrhythmia and electrophysiology Vol.5 No.6
<P>Cardiac ATP-sensitive K(+) channels have been suggested to contribute to the adaptive physiological response to metabolic challenge after β-adrenoceptor stimulation. However, an increased atrial K(+)-conductance might be expected to be proarrhythmic. We investigated the effect of ATP-sensitive K(+) channel blockade on the electrophysiological responses to β-adrenoceptor-induced metabolic challenge in intact atria.</P>
Milne, Roger L.,Bení,tez, Javier,Nevanlinna, Heli,Heikkinen, Tuomas,Aittomä,ki, Kristiina,Blomqvist, Carl,Arias, José,Ignacio,Zamora, M. Pilar,Burwinkel, Barbara,Bartram, Claus R.,Mein Oxford University Press 2009 Journal of the National Cancer Institute Vol.101 No.14
<P>BACKGROUND: A recent genome-wide association study identified single-nucleotide polymorphism (SNP) 2q35-rs13387042 as a marker of susceptibility to estrogen receptor (ER)-positive breast cancer. We attempted to confirm this association using the Breast Cancer Association Consortium. METHODS: 2q35-rs13387042 SNP was genotyped for 31 510 women with invasive breast cancer, 1101 women with ductal carcinoma in situ, and 35 969 female control subjects from 25 studies. Odds ratios (ORs) were estimated by logistic regression, adjusted for study. Heterogeneity in odds ratios by each of age, ethnicity, and study was assessed by fitting interaction terms. Heterogeneity by each of invasiveness, family history, bilaterality, and hormone receptor status was assessed by subclassifying case patients and applying polytomous logistic regression. All statistical tests were two-sided. RESULTS: We found strong evidence of association between rs13387042 and breast cancer in white women of European origin (per-allele OR = 1.12, 95% confidence interval [CI] = 1.09 to 1.15; P(trend) = 1.0 x 10(-19)). The odds ratio was lower than that previously reported (P = .02) and did not vary by age or ethnicity (all P > or = .2). However, it was higher when the analysis was restricted to case patients who were selected for a strong family history (P = .02). An association was observed for both ER-positive (OR = 1.14, 95% CI = 1.10 to 1.17; P = 10(-15)) and ER-negative disease (OR = 1.10, 95% CI = 1.04 to 1.15; P = .0003) and both progesterone receptor (PR)-positive (OR = 1.15, 95% CI = 1.11 to 1.19; P = 5 x 10(-14)) and PR-negative disease (OR = 1.10, 95% CI = 1.06 to 1.15; P = .00002). CONCLUSION: The rs13387042 is associated with both ER-positive and ER-negative breast cancer in European women.</P>
Identification of ten variants associated with risk of estrogen-receptor-negative breast cancer
Milne, Roger L,Kuchenbaecker, Karoline B,Michailidou, Kyriaki,Beesley, Jonathan,Kar, Siddhartha,Lindströ,m, Sara,Hui, Shirley,Lemaç,on, Audrey,Soucy, Penny,Dennis, Joe,Jiang, Xia,Rostamianfa Nature Pub. Co 2017 Nature genetics Vol.49 No.12
<P>Most common breast cancer susceptibility variants have been identified through genome-wide association studies (GWAS) of predominantly estrogen receptor (ER)-positive disease(1). We conducted a GWAS using 21,468 ER-negative cases and 100,594 controls combined with 18,908 BRCA1 mutation carriers (9,414 with breast cancer), all of European origin. We identified independent associations at P < 5 x 10(-8) with ten variants at nine new loci. At P < 0.05, we replicated associations with 10 of 11 variants previously reported in ER-negative disease or BRCA1 mutation carrier GWAS and observed consistent associations with ER-negative disease for 105 susceptibility variants identified by other studies. These 125 variants explain approximately 16% of the familial risk of this breast cancer subtype. There was high genetic correlation (0.72) between risk of ER-negative breast cancer and breast cancer risk for BRCA1 mutation carriers. These findings may lead to improved risk prediction and inform further fine-mapping and functional work to better understand the biological basis of ER-negative breast cancer.</P>
A Cosmopolitical Philosophy to Come : Derrida and the Ends of Humanity
Milne, Peter 이화여자대학교 이화인문과학원 2012 탈경계 인문학 Vol.5 No.1
Although Derrida is often taken to be “anti-humanist,” this paper argues that his engagement with the legacy of humanism is not only much more complex, but that it retains and alters this legacy in such a way as to provide a new way of thinking about the human in a trans-national or “global” context. This argument is at the same time an occasion to briefly explore some of the implications of this for Derrida’s relation to philosophy as a humanistic discipline. It first tracks some of Derrida’s most explicit discussions of humanism over the course of several works and lines of inquiry, showing what I take to be a shift in his work from the critical stance of “The Ends of Man” to the more nuanced discussions in some of the later “political” writings. My main goal is to link Derrida’s discussions of humanism to his work on cosmopolitanism and particularly to his argument that political thinking must negotiate the troubling but important legacy of a philosophical universalism that is nonetheless tied to a very particular cultural and historical past. I take this problem to be analogous to the ambiguity of a humanist legacy that is potentially violent and limiting in its conception of universal humanity while being at the same time what underwrites important political concepts such as human rights. Derrida argues that philosophy is the “other way” and is thus always open to redirection and reap- propriation by traditions other than its own. Taking the “human” as an Idea in the Kantian sense, I argue that it too can wander from its end, liberate itself from the strictures of universal humanity while nonetheless retaining the promise and the political consideration due that humanity. Derrida thus offers an innovative way to rethink the humanist legacy in the context of a plurality of cultures. I end by suggesting that philosophy and the humanities more generally, far from being irrelevant, may thus be more relevant than ever.
Milne, Roger L.,Burwinkel, Barbara,Michailidou, Kyriaki,Arias-Perez, Jose-Ignacio,Zamora, M. Pilar,Mené,ndez-Rodrí,guez, Primitiva,Hardisson, David,Mendiola, Marta,Gonzá,lez-Neira, A IRL Press 2014 Human molecular genetics Vol.23 No.22
<P>Candidate variant association studies have been largely unsuccessful in identifying common breast cancer susceptibility variants, although most studies have been underpowered to detect associations of a realistic magnitude. We assessed 41 common non-synonymous single-nucleotide polymorphisms (nsSNPs) for which evidence of association with breast cancer risk had been previously reported. Case-control data were combined from 38 studies of white European women (46 450 cases and 42 600 controls) and analyzed using unconditional logistic regression. Strong evidence of association was observed for three nsSNPs: <I>ATXN7-</I>K264R at 3p21 [rs1053338, per allele OR = 1.07, 95% confidence interval (CI) = 1.04–1.10, <I>P</I> = 2.9 × 10<SUP>−6</SUP>], <I>AKAP9-</I>M463I at 7q21 (rs6964587, OR = 1.05, 95% CI = 1.03–1.07, <I>P</I> = 1.7 × 10<SUP>−6</SUP>) and <I>NEK10-</I>L513S at 3p24 (rs10510592, OR = 1.10, 95% CI = 1.07–1.12, <I>P</I> = 5.1 × 10<SUP>−17</SUP>). The first two associations reached genome-wide statistical significance in a combined analysis of available data, including independent data from nine genome-wide association studies (GWASs): for <I>ATXN7-</I>K264R, OR = 1.07 (95% CI = 1.05–1.10, <I>P</I> = 1.0 × 10<SUP>−8</SUP>); for <I>AKAP9-</I>M463I, OR = 1.05 (95% CI = 1.04–1.07, <I>P</I> = 2.0 × 10<SUP>−10</SUP>). Further analysis of other common variants in these two regions suggested that intronic SNPs nearby are more strongly associated with disease risk. We have thus identified a novel susceptibility locus at 3p21, and confirmed previous suggestive evidence that rs6964587 at 7q21 is associated with risk. The third locus, rs10510592, is located in an established breast cancer susceptibility region; the association was substantially attenuated after adjustment for the known GWAS hit. Thus, each of the associated nsSNPs is likely to be a marker for another, non-coding, variant causally related to breast cancer risk. Further fine-mapping and functional studies are required to identify the underlying risk-modifying variants and the genes through which they act.</P>