| 1. |
- Berg, L., et al.
(författare)
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LIR-1 expression on lymphocytes, and cytomegalovirus disease in lung-transplant recipients
- 2003
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Ingår i: Lancet. - 0140-6736. ; 361:9363, s. 1099-101
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Tidskriftsartikel (refereegranskat)abstract
- Human cytomegalovirus infection is a major cause of morbidity after lung transplantation. LIR-1 (leucocyte immunoglobulin-like receptor-1) is an inhibitory cell surface receptor that has high affinity for an MHC class I homologue (UL18) encoded by human cytomegalovirus. We aimed to investigate whether reactivation of human cytomegalovirus affects the expression of LIR-1. We measured LIR-1 expression on peripheral blood lymphocytes from 13 lung-transplant recipients and established human cytomegalovirus load using PCR. Eight patients developed cytomegalovirus disease. The percentage of cells expressing LIR-1 increased in the patients who developed cytomegalovirus disease several weeks before viral DNA was detectable by PCR. Measurement of LIR-1 expression might allow early identification of cytomegalovirus disease in lung-transplant patients.
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| 2. |
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| 3. |
- Ventura, M, et al.
(författare)
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Recurrent sites for new centromere seeding
- 2004
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Ingår i: Genome research. - : Cold Spring Harbor Laboratory. - 1088-9051. ; 14:9, s. 1696-1703
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Tidskriftsartikel (refereegranskat)abstract
- Using comparative FISH and genomics, we have studied and compared the evolution of chromosome 3 in primates and two human neocentromere cases on the long arm of this chromosome. Our results show that one of the human neocentromere cases maps to the same 3q26 chromosomal region where a new centromere emerged in a common ancestor of the Old World monkeys ∼25-40 million years ago. Similarly, the locus in which a new centromere was seeded in the great apes' ancestor was orthologous to the site in which a new centromere emerged in the New World monkeys' ancestor. These data suggest the recurrent use of longstanding latent centromeres and that there is an inherent potential of these regions to form centromeres. The second human neocentromere case (3q24) revealed unprecedented features. The neocentromere emergence was not accompanied by any chromosomal rearrangement that usually triggers these events. Instead, it involved the functional inactivation of the normal centromere, and was present in an otherwise phenotypically normal individual who transmitted this unusual chromosome to the next generation. We propose that the formation of neocentromeres in humans and the emergence of new centromeres during the course of evolution share a common mechanism.
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