Separable Image Warping with Spatial Lookup Tables

Image warping refers to the 2-D resampling of a source image onto a target image. In the general case, this requires costly 2-D filtering operations. Simplifications are possible when the warp can be expressed as a cascade of orthogonall-D transformations. In these cases, separable transformations have been introduced to realize large performance gains. The central ideas in this area were formulated in the 2-pass algorithm by Catmull and Smith. Although that method applies over an important class of transformations, there are intrinsic problems which limit its usefulness. The goal of this work is to extend the 2-pass approach to handle arbitrary spatial mapping functions. We address the difficulties intrinsic to 2-pass scanline algorithms: bottlenecking, foldovers, and the lack of closed-form inverse solutions. These problems are shown to be resolved in a general, efficient, separable technique, with graceful degradation for transformations of increasing complexity

Ueber Dibromo-tetramminkobaltsalze

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Venous Thromboembolism: Risk Factors, Biomarkers, and Treatment

Articles in this series: •Zhu T, Martinez I, Emmerich J. Venous thromboembolism: risk factors for recurrence. Arterioscler Thromb Vasc Biol. 2009;29:298–310. •Jang MJ, Choi W, Bang SM, Lee T, Yeo-Kyeoung K, Ageno W, Doyeun Oh. Metabolic syndrome is associated with venous thromboembolism in the Korean population. Arterioscler Thromb Vasc Biol. 2009;29:311–315. •Sousou T, Khorana AA. New insights into cancer-associated thrombosis. Arterioscler Thromb Vasc Biol. 2009;29:316–320. •Farmer-Boatwright MK, Roubey RAS. Venous thrombosis in the antiphospholipid syndrome. Arterioscler Thromb Vasc Biol. 2009;29:321–325. •James AH. Venous thromboembolism in pregnancy. Arterioscler Thromb Vasc Biol. 2009;29:326–331. •Pabinger I, Ay C. Biomarkers and venous thromboembolism. Arterioscler Thromb Vasc Biol. 2009;29:332–336. In 2005, the U.S. Senate declared March as deep vein thrombosis (DVT) awareness month. This is the second year in which we have highlighted this event with a collection of 6 articles in Arteriosclerosis, Thrombosis, and Vascular Biology focused on DVT. It is estimated that 2 million Americans per year develop DVT, which is associated with life-threatening pulmonary embolism (PE). DVT and PE are collectively termed venous thromboembolism (VTE). Despite the large number of cases, a survey conducted by the American Public Health Association in 2002 found that 74% of Americans were unaware of venous thrombosis.1 The risk of VTE increases with thrombophilias, age, pregnancy, and comorbidities, including cancer and antiphospholipid syndrome (APS). It has not yet been determined whether similar mechanisms lead to VTE in each of these disorders. The articles in this issue describe current research into disorders associated with increased VTE risk, including potential pathophysiologic mechanisms, treatment of these clinical situations, and a review on biomarkers for the detection and prevention of VTE.

Thrombin generation, fibrin clot formation and hemostasis

Hemostatic clot formation entails thrombin-mediated cleavage of fibrinogen to fibrin. Previous in vitro studies have shown that the thrombin concentration present during clot formation dictates the ultimate fibrin structure. In most prior studies of fibrin structure, clotting was initiated by adding thrombin to a solution of fibrinogen; however, clot formation in vivo occurs in an environment in which the concentration of free thrombin changes over the reaction course. These changes depend on local cellular properties and available concentrations of pro- and anti-coagulants. Recent studies suggest that abnormal thrombin generation patterns produce abnormally structured clots associated with an increased risk of bleeding or thrombosis. Further studies of fibrin formation during in situ thrombin generation are needed to understand fibrin clot formation in vivo

Book Reviews

Book 1Book Title: Getting into Residency: A Guide for Medical StudentsBook Author: Kenneth V. IsersonPp. xviii + 431. $28,95. Tucson: Galen Press. 1993. ISBN 1-883620-10-4.Book 2Book Title: Molecular Biology of Digestive DiseaseBook Author: Ed. by Philip QuirkePp. vii + 116. £15. London: BMJ. 1994. ISBN 0-7279-0827-8.Book 3Book Title: Parkinson's DiseaseBook Author:  Ed. by Merton Sandler.Pp. ix + 65. £12/US$24. London: John Libbey, 1993. ISBN 0-86196-404-7.Book 4Book Title: Brain Work and Mental Activity: Quantitative Studies With Radioactive TracersBook Author: Ed. by N. A. Lassen, D. A. Ingvar, M. A. Raichle & L. FribergPP. 446. Illustrated. Copenhagen: Munksgaard. 1991. ISBN 87-16-10698-9.Book 5Book Title: Guidelines for Quality Assurance Programmes for Blood Transfusion ServicesBook Author: WHOPp. IV + 50. (Available in English; French and Spanish in preparation). SFr.12/US$10,80 (in developing countries SFr.8,40). Geneva: WHO. 1993. ISBN 92-4-154448-1. Order No. 1150392.Book 6Book Title: ABC of AlcoholBook Author: Ed. by Alex PatonPp. ix + 32. illustrated. £10. London: BMJ. 1994. ISBN 0-7279-D812-X.Book 7Book Title: Atlas of Surgical Exposures ofthe Lower ExtremityBook Author: A. Masquelet, C. McCullough, R Tubiana, I. Fyfe, L. Klenerman, E. LetoumelPp. 414. Illustrated. London: Manin Dunitz. 1993. ISBN 1-85317-D03-8

Rich interaction and feedback supported mammographic training: A trial of an augmented reality approach

The conventional ‘keyboard and workstation’ approach allows complex medical image presentation and manipulation during mammographic interpretation. Nevertheless, providing rich interaction and feedback in real time for navigational training or computer assisted detection of disease remains a challenge. Through computer vision and state of the art AR (Augmented Reality) technique, this study proposes an ‘AR mammographic workstation’ approach which could support workstation-independent rich interaction and real-time feedback. This flexible AR approach explores the feasibility of facilitating various mammographic training scenes via AR as well as its limitations

Human Factor IX Binds to Specific Sites on the Collagenous Domain of Collagen IV

The primary region of factor IX that mediates binding to bovine aortic endothelial cells resides in residues 3-11 of the N-terminal region known as the Gla domain. Recently, it was proposed that the observed binding to endothelial cells is actually a measure of the interaction between factor IX and collagen IV (Cheung, W. F., van den Born, J., Kuhn, K., Kjellen, L., Hudson, B. G., and Stafford, D. W. (1996) Proc. Natl. Acad. Sci. U. S. A. 93, 11068-11073). To confirm that factor IX binds to collagen IV and to examine the specificity of this interaction, we used scanning force microscopy to examine factor IX binding to collagen IV. We imaged collagen IV in the presence and the absence of factor IX and observed specific interactions between factor IX and collagen IV. Our results demonstrate that factor IX binds to collagen IV at specific sites in the collagenous domain approximately 98 and approximately 50 nm from the C-terminal pepsin-cleaved end

Differential contributions of monocyte- and platelet-derived microparticles towards thrombin generation and fibrin formation and stability: Differential MP procoagulant activity

Microparticles (MPs) are submicron vesicles shed by activated or apoptotic cells, including platelets and monocytes. Increased circulating MPs are associated with thrombosis; however, their role in thrombogenesis is poorly understood

Cellular Procoagulant Activity Dictates Clot Structure and Stability as a Function of Distance From the Cell Surface

Thrombin concentration modulates fibrin structure and fibrin structure modulates clot stability; however, the impact of localized, cell surface-driven in situ thrombin generation on fibrin structure and stability has not previously been evaluated