| 1. |
- Scherer, SW, et al.
(author)
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Human chromosome 7: DNA sequence and biology
- 2003
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In: Science (New York, N.Y.). - : American Association for the Advancement of Science (AAAS). - 1095-9203 .- 0036-8075. ; 300:5620, s. 767-772
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Journal article (peer-reviewed)abstract
- DNA sequence and annotation of the entire human chromosome 7, encompassing nearly 158 million nucleotides of DNA and 1917 gene structures, are presented. To generate a higher order description, additional structural features such as imprinted genes, fragile sites, and segmental duplications were integrated at the level of the DNA sequence with medical genetic data, including 440 chromosome rearrangement breakpoints associated with disease. This approach enabled the discovery of candidate genes for developmental diseases including autism.
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| 2. |
- Berg, LK, et al.
(author)
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GP-zones in Al-Zn-Mg alloys and their role in artificial aging
- 2001
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In: Acta Materialia. - 1359-6454. ; 49:17, s. 3443-3451
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Journal article (peer-reviewed)abstract
- The structure of GP-zones in an industrial, 7xxx-series Al–Zn–Mg alloy has been investigated by transmission electron microscopy methods: selected area diffraction, conventional and high-resolution imaging. Two types of GP-zones, GP(I) and (II) are characterized by their electron diffraction patterns. GP(I)-zones are formed over a wide temperature range, from room temperature to 140–150°C, independently of quenching temperature. The GP(I)-zones are coherent with the aluminum matrix, with internal ordering of Zn and Al/Mg on the matrix lattice, suggested to be based on AuCu(I)-type sub-unit, and anti-phase boundaries. GP(II) are formed after quenching from temperatures above 450°C, by aging at temperatures above 70°C. The GP(II)-zones are described as zinc-rich layers on {111}-planes, with internal order in the form of elongated domains. The structural relation to the η′-precipitate is discussed.
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| 3. |
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| 4. |
- Goldin, LR, et al.
(author)
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Familial risk of lymphoproliferative tumors in families of patients with chronic lymphocytic leukemia: results from the Swedish Family-Cancer Database
- 2004
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In: Blood. - : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 104:6, s. 1850-1854
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Journal article (peer-reviewed)abstract
- The importance of genetic factors in etiology of chronic lymphocytic leukemia (CLL) is suggested by family and population studies. However, the spectrum of malignancies sharing common genetic factors with CLL and the effects of sex and age on familial risk are unknown. We used the Swedish Family-Cancer Database to test for increased familial risks of CLL and other lymphoproliferative tumors. Cancer diagnoses from 1958 to 1998 were assessed in 14 336 first-degree relatives of 5918 CLL cases and in 28 876 first-degree relatives of 11 778 controls. Cancer risks in relatives of cases were compared with those in relatives of controls using marginal survival models. Relatives of cases were at significantly increased risk for CLL (relative risk [RR] = 7.52; 95% confidence interval [CI], 3.63-15.56), for non-Hodgkin lymphoma (RR = 1.45; 95% CI, 0.98-2.16), and for Hodgkin lymphoma (RR = 2.35; 95% CI, 1.08-5.08). CLL risks were similar in parents, siblings, and offspring of cases, in male and female relatives, and were not affected by the case's age at diagnosis. Anticipation was not significant when analyzed using life table methods. We conclude that the familial component of CLL is shared with other lymphoproliferative malignances, suggesting common genetic pathways. However, because clinically diagnosed CLL is uncommon, absolute excess risk to relatives is small.
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