| 21. |
- Deijfen, Maria, et al.
(author)
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Percolation in invariant Poisson graphs with i.i.d. degrees
- 2012
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In: Arkiv for Matematik. - : International Press of Boston. - 0004-2080 .- 1871-2487. ; 50:1, s. 41-58
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Journal article (peer-reviewed)abstract
- Let each point of a homogeneous Poisson process in R-d independently be equipped with a random number of stubs (half-edges) according to a given probability distribution mu on the positive integers. We consider translation-invariant schemes for perfectly matching the stubs to obtain a simple graph with degree distribution mu. Leaving aside degenerate cases, we prove that for any mu there exist schemes that give only finite components as well as schemes that give infinite components. For a particular matching scheme which is a natural extension of Gale-Shapley stable marriage, we give sufficient conditions on mu for the absence and presence of infinite components.
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| 22. |
- Holroyd, A. E., et al.
(author)
-
Wald for non-stopping times: The rewards of impatient prophets
- 2014
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In: Electronic Communications in Probability. - 1083-589X. ; 19, s. 1-9
-
Journal article (peer-reviewed)abstract
- Let X-1 , X-2 , ... be independent identically distributed nonnegative random variables. Wald's identity states that the random sum S-T := X-1 + ... + X-T has expectation ET . EX1 provided T is a stopping time. We prove here that for any 1 < alpha <= 2, if T is an arbitrary nonnegative random variable, then S-T has finite expectation provided that X-1 has finite alpha-moment and T has finite 1/(alpha - 1)-moment. We also prove a variant in which T is assumed to have a finite exponential moment. These moment conditions are sharp in the sense that for any i.i.d. sequence X-i violating them, there is a T satisfying the given condition for which S-T (and, in fact, X-T) has infinite expectation. An interpretation is given in terms of a prophet being more rewarded than a gambler when a certain impatience restriction is imposed.
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| 23. |
- Vijayakrishnan, Jayaram, et al.
(author)
-
The 9p21.3 risk of childhood acute lymphoblastic leukaemia is explained by a rare high-impact variant in CDKN2A.
- 2015
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In: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 5
-
Journal article (peer-reviewed)abstract
- Genome-wide association studies (GWAS) have provided strong evidence for inherited predisposition to childhood acute lymphoblastic leukaemia (ALL) identifying a number of risk loci. We have previously shown common SNPs at 9p21.3 influence ALL risk. These SNP associations are generally not themselves candidates for causality, but simply act as markers for functional variants. By means of imputation of GWAS data and subsequent validation SNP genotyping totalling 2,177 ALL cases and 8,240 controls, we have shown that the 9p21.3 association can be ascribed to the rare high-impact CDKN2A p.Ala148Thr variant (rs3731249; Odds ratio = 2.42, P = 3.45 × 10(-19)). The association between rs3731249 genotype and risk was not specific to particular subtype of B-cell ALL. The rs3731249 variant is associated with predominant nuclear localisation of the CDKN2A transcript suggesting the functional effect of p.Ala148Thr on ALL risk may be through compromised ability to inhibit cyclin D within the cytoplasm.
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| 24. |
- Went, Molly, et al.
(author)
-
Genetic correlation between multiple myeloma and chronic lymphocytic leukaemia provides evidence for shared aetiology
- 2018
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In: Blood Cancer Journal. - : Springer Science and Business Media LLC. - 2044-5385. ; 9:1
-
Journal article (peer-reviewed)abstract
- The clustering of different types of B-cell malignancies in families raises the possibility of shared aetiology. To examine this, we performed cross-trait linkage disequilibrium (LD)-score regression of multiple myeloma (MM) and chronic lymphocytic leukaemia (CLL) genome-wide association study (GWAS) data sets, totalling 11,734 cases and 29,468 controls. A significant genetic correlation between these two B-cell malignancies was shown (Rg = 0.4, P = 0.0046). Furthermore, four of the 45 known CLL risk loci were shown to associate with MM risk and five of the 23 known MM risk loci associate with CLL risk. By integrating eQTL, Hi-C and ChIP-seq data, we show that these pleiotropic risk loci are enriched for B-cell regulatory elements and implicate B-cell developmental genes. These data identify shared biological pathways influencing the development of CLL and, MM and further our understanding of the aetiological basis of these B-cell malignancies.
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