On a new iterative method for solving linear systems and comparison results

AbstractIn Ujević [A new iterative method for solving linear systems, Appl. Math. Comput. 179 (2006) 725–730], the author obtained a new iterative method for solving linear systems, which can be considered as a modification of the Gauss–Seidel method. In this paper, we show that this is a special case from a point of view of projection techniques. And a different approach is established, which is both theoretically and numerically proven to be better than (at least the same as) Ujević's. As the presented numerical examples show, in most cases, the convergence rate is more than one and a half that of Ujević

anti-tick vaccines to prevent tick-borne diseases in Europe

Ixodes ricinus transmits bacterial, protozoal and viral pathogens, causing disease and forming an increasing health concern in Europe. ANTIDotE is an European Commission funded consortium of seven institutes, which aims to identify and characterize tick proteins involved in feeding and pathogen transmission. The knowledge gained will be used to develop and evaluate anti- tick vaccines that may prevent multiple human tick-borne diseases. Strategies encompassing anti-tick vaccines to prevent transmission of pathogens to humans, animals or wildlife will be developed with relevant stakeholders with the ultimate aim of reducing the incidence of tick-borne diseases in humans

Mouse Bone Marrow-Derived Endothelial Progenitor Cells Do Not Restore Radiation-Induced Microvascular Damage

Background. Radiotherapy is commonly used to treat breast and thoracic cancers but it also causes delayed microvascular damage and increases the risk of cardiac mortality. Endothelial cell proliferation and revascularization are crucial to restore microvasculature damage and maintain function of the irradiated heart. We have therefore examined the potential of bone marrow-derived endothelial progenitor cells (BM-derived EPCs) for restoration of radiation-induced microvascular damage. Material &amp; Methods. 16 Gy was delivered to the heart of adult C57BL/6 mice. Mice were injected with BM-derived EPCs, obtained from Eng+/+ or Eng+/− mice, 16 weeks and 28 weeks after irradiation. Morphological damage was evaluated at 40 weeks in transplanted mice, relative to radiation only and age-matched controls. Results. Cardiac irradiation decreased microvascular density and increased endothelial damage in surviving capillaries (decrease alkaline phosphatase expression and increased von Willebrand factor). Microvascular damage was not diminished by treatment with BM-derived EPCs. However, BM-derived EPCs from both Eng+/+ and Eng+/− mice diminished radiation-induced collagen deposition. Conclusion. Treatment with BM-derived EPCs did not restore radiation-induced microvascular damage but it did inhibit fibrosis. Endoglin deficiency did not impair this process.</jats:p

Microvascular alterations at 4, 20 or 40 weeks after irradiation or sham treatment.

<p>(A) MVD per unit area expressed as percentage of age matched unirradiated control values. (B) ALP positive tissue areas as % of age-matched unirradiated controls. (C) vWF positive tissue areas as % of age-matched unirradiated controls. Values represents mean ± SEM with 4–5 mice in the 4 and 20 weeks group and 4–7 mice in the 40 weeks group,*p<0.05 compared to age-matched unirradiated controls.</p

Comparison of top 5 functional pathways from Eng^+/+ (dark blue) and Eng^+/− (light blue), generated by IPA analysis.

<p>Bars indicate top networks expressed and y-axis displays the – (log) significance. Taller bars are more significant than shorter bars. P-value display Benjamini-Hochberg multiple testing correction.</p

Endoglin Haplo-Insufficiency Modifies the Inflammatory Response in Irradiated Mouse Hearts without Affecting Structural and Mircovascular Changes

<div><p>Background</p><p>It is now widely recognized that radiotherapy of thoracic and chest wall tumors increases the long-term risk of cardiovascular damage although the underlying mechanisms are not fully elucidated. There is increasing evidence that microvascular damage is involved. Endoglin, an accessory receptor for TGF-β1, is highly expressed in damaged endothelial cells and may play a crucial role in cell proliferation and revascularization of damaged heart tissue. We have therefore specifically examined the role of endoglin in microvascular damage and repair in the irradiated heart.</p><p>Materials & Methods</p><p>A single dose of 16 Gy was delivered to the heart of adult Eng^+/+ or Eng^+/− mice and damage was evaluated at 4, 20 and 40 weeks, relative to age-matched controls. Gated single photon emission computed tomography (gSPECT) was used to measure cardiac geometry and function, and related to histo-morphology, microvascular damage (detected using immuno- and enzyme-histochemistry) and gene expression (detected by microarray and real time PCR).</p><p>Results</p><p>Genes categorized according to known inflammatory and immunological related disease were less prominently regulated in irradiated Eng^+/− mice compared to Eng^+/+ littermates. Fibrosis related genes, TGF-β1, ALK 5 and PDGF, were only upregulated in Eng^+/+ mice during the early phase of radiation-induced cardiac damage (4 weeks). In addition, only the Eng^+/+ mice showed significant upregulation of collagen deposition in the early fibrotic phase (20 weeks) after irradiation. Despite these differences in gene expression, there was no reduction in inflammatory invasion (CD45+cells) of irradiated Eng^+/− hearts. Microvascular damage (microvascular density, alkaline phosphatase and von-Willebrand-Factor expression) was also similar in both strains.</p><p>Conclusion</p><p>Eng^+/− mice displayed impaired early inflammatory and fibrotic responses to high dose irradiation compared to Eng^+/+ littermates. This did not result in significant differences in microvascular damage or cardiac function between the strains.</p></div

Graphical representation of the top networks of differentially regulated genes (4 weeks).

<p>Each network symbolizes the biological functions and/or diseases that were most significantly regulated 4 weeks after cardiac irradiation of Eng ^+/+ mice (n = 5) (A) and Eng ^+/− mice (n = 4) (B). The genes marked in red represent the upregulated genes and in green the downregulated genes. The solid arrows represent direct interactions and the dotted arrows indirect interactions. Genes circled in dark blue represents central molecules and the light blue lines indicate interaction with other genes.</p