| 1. |
- Ingelsson, Erik, et al.
(författare)
-
Detailed Physiologic Characterization Reveals Diverse Mechanisms for Novel Genetic Loci Regulating Glucose and Insulin Metabolism in Humans
- 2010
-
Ingår i: Diabetes. - 0012-1797 .- 1939-327X. ; 59:5, s. 1266-1275
-
Konferensbidrag (refereegranskat)abstract
- OBJECTIVE-Recent genome-wide association studies have revealed loci associated with glucose and insulin-related traits. We aimed to characterize 19 such loci using detailed measures of insulin processing, secretion, and sensitivity to help elucidate their role in regulation of glucose control, insulin secretion and/or action. RESEARCH DESIGN AND METHODS-We investigated associations of loci identified by the Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC) with circulating proinsulin, measures of insulin secretion and sensitivity from oral glucose tolerance tests (OGTTs), euglycemic clamps, insulin suppression tests, or frequently sampled intravenous glucose tolerance tests in nondiabetic humans (n = 29,084). RESULTS-The glucose-raising allele in MADD was associated with abnormal insulin processing (a dramatic effect on higher proinsulin levels, but no association with insulinogenic index) at extremely persuasive levels of statistical significance (P = 2.1 x 10(-71)). Defects in insulin processing and insulin secretion were seen in glucose-raising allele carriers at TCF7L2, SCL30A8, GIPR, and C2CD4B. Abnormalities in early insulin secretion were suggested in glucose-raising allele carriers at MTNR1B, GCK, FADS1, DGKB, and PROX1 (lower insulinogenic index; no association with proinsulin or insulin sensitivity). Two loci previously associated with fasting insulin (GCKR and IGF1) were associated with OGTT-derived insulin sensitivity indices in a consistent direction. CONCLUSIONS-Genetic loci identified through their effect on hyperglycemia and/or hyperinsulinemia demonstrate considerable heterogeneity in associations with measures of insulin processing, secretion, and sensitivity. Our findings emphasize the importance of detailed physiological characterization of such loci for improved understanding of pathways associated with alterations in glucose homeostasis and eventually type 2 diabetes. Diabetes 59:1266-1275, 2010
|
|
| 2. |
|
|
| 3. |
- Collins, Andrew, et al.
(författare)
-
Optimal patrolling of fragmented boundaries
- 2013
-
Ingår i: Annual ACM Symposium on Parallelism in Algorithms and Architectures. - New York, NY, USA : ACM. - 9781450315722 ; , s. 241-250
-
Konferensbidrag (refereegranskat)abstract
- A set of mobile robots is deployed on a simple curve of finite length, composed of a finite set of vital segments separated by neutral segments. The robots have to patrol the vital segments by perpetually moving on the curve, without exceeding their uniform maximum speeds. The quality of patrolling is measured by the idleness, i.e., the longest time period during which any vital point on the curve is not visited by any robot. Given a configuration of vital segments, our goal is to provide algorithms describing the movement of the robots along the curve so as to minimize the idleness. Our main contribution is a proof that the optimal solution to the patrolling problem is attained either by the cyclic strategy, in which all the robots move in one direction around the curve, or by the partition strategy, in which the curve is partitioned into sections which are patrolled separately by individual robots. These two fundamental types of strategies were studied in the past in the robotics community in different theoretical and experimental settings. However, to our knowledge, this is the first theoretical analysis proving optimality in such a general scenario. Throughout the paper we assume that all robots have the same maximum speed. In fact, the claim is known to be invalid when this assumption does not hold, cf. [Czyzowicz et al., Proc. ESA 2011].
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
- Riegman, P, et al.
(författare)
-
Biobanking
- 2012
-
Ingår i: EUROPEAN JOURNAL OF CANCER. - 0959-8049. ; 48, s. S21-S21
-
Konferensbidrag (övrigt vetenskapligt/konstnärligt)
|
|
| 8. |
|
|
