Online Maximum k-Coverage

We study an online model for the maximum k-vertex-coverage problem, where given a graph G = (V,E) and an integer k, we ask for a subset A ⊆ V, such that |A | = k and the number of edges covered by A is maximized. In our model, at each step i, a new vertex vi is revealed, and we have to decide whether we will keep it or discard it. At any time of the process, only k vertices can be kept in memory; if at some point the current solution already contains k vertices, any inclusion of any new vertex in the solution must entail the irremediable deletion of one vertex of the current solution (a vertex not kept when revealed is irremediably deleted). We propose algorithms for several natural classes of graphs (mainly regular and bipartite), improving on an easy 1/2-competitive ratio. We next settle a set-version of the problem, called maximum k-(set)-coverage problem. For this problem we present an algorithm that improves upon former results for the same model for small and moderate values of k

Novel Loci for Adiponectin Levels and Their Influence on Type 2 Diabetes and Metabolic Traits : A Multi-Ethnic Meta-Analysis of 45,891 Individuals

J. Kaprio, S. Ripatti ja M.-L. Lokki työryhmien jäseniä.Peer reviewe

Molecular events in uterine cervical cancer

OBJECTIVE: To review the literature regarding the molecular events which occur in the development of uterine cervical cancer, with particular reference to human papillomavirus (HPV) infection. METHODOLOGY: Bibliographic searches of Medline and the ISI citation databases using appropriate keywords, including the following: papillomavirus, cervix, pathology, cyclin, chromosome, heterozygosity, telomerase, smoking, hormones, HLA, immune response, HIV, HSV, EBV. CONCLUSIONS: It has become clear that most cervical neoplasia, whether intraepithelial or invasive, is attributable in part to HPV infection. However, HPV infection alone is not sufficient, and, in a small proportion of cases, may not be necessary for malignant transformation. There is increasing evidence that HPV gene products interfere with cell cycle control leading to secondary accumulation of small and large scale genetic abnormalities. This may explain the association of viral persistence with lesion progression but, in many patients, secondary factors, such as smoking and immune response, are clearly important. However, the mechanisms involved in the interaction between HPV and host factors are poorly understood. 



Multiethnic Exome-Wide Association Study of Subclinical Atherosclerosis

Pathophysiology, epidemiology and therapy of agein