Ruptured Spleen

On the morning of Dec. 23, 1940, the author was summoned to see a four year old Holstein cow. The owner said she had become ill the previous day

UHGromos at the National Center for Supercomputing Applications

We describe our experiences with UHGromos, a molecular dynamics application that has been extended for use with SPMD (single program, multiple data) systems. The application and supporting software have been retargeted to a number of current-generation workstation- and supercomputerclass systems; we describe the software structure and present performance results on a variety of machines available at the National Center for Supercomputing Applications (NCSA). Our future directions are described. 1 Overview Many problems of interest to the computational biology community are characterized by extremely high computational resource requirements. One indication of these requirements is the 1994 total of supercomputing resources grants awarded by the NSF MetaCenter Allocations Committee to research in the areas of chemistry and molecular biosciences (over 425,000 "Service Units" awarded, each SU roughly equal to an hour of CPU time). A great deal of effort has been made in recent years to i..

Quebec platelet disorder is linked to the urokinase plasminogen activator gene (PLAU) and increases expression of the linked allele in megakaryocytes

Quebec platelet disorder (QPD) is an autosomal dominant disorder with high penetrance that is associated with increased risks for bleeding. The hallmark of QPD is a gain-of-function defect in fibrinolysis due to increased platelet content of urokinase plasminogen activator (uPA) without systemic fibrinolysis. We hypothesized that increased expression of uPA by differentiating QPD megakaryocytes is linked to PLAU. Genetic marker analyses indicated that QPD was significantly linked to a 2-Mb region on chromosome 10q containing PLAU with a maximum multipoint logarithm of the odds (LOD) score of +11 between markers D10S1432 and D10S1136. Analysis of PLAU by sequencing and Southern blotting excluded mutations within PLAU and its known regulatory elements as the cause of QPD. Analyses of uPA mRNA indicated that QPD distinctly increased transcript levels of the linked PLAU allele with megakaryocyte differentiation. These findings implicate a mutation in an uncharacterized cis element near PLAU as the cause of QPD