Maastricht University

About: Maastricht University is a education organization based out in Maastricht, Limburg, Netherlands. It is known for research contribution in the topics: Population & Health care. The organization has 19263 authors who have published 53291 publications receiving 2266866 citations. The organization is also known as: Universiteit Maastricht & UM.

A systematic review of faculty development initiatives designed to improve teaching effectiveness in medical education: BEME Guide No. 8

Abstract: Background: Preparing healthcare professionals for teaching is regarded as essential to enhancing teaching effectiveness. Although many reports describe various faculty development interventions, there is a paucity of research demonstrating their effectiveness.Objective: To synthesize the existing evidence that addresses the question: “What are the effects of faculty development interventions on the knowledge, attitudes and skills of teachers in medical education, and on the institutions in which they work?”Methods: The search, covering the period 1980–2002, included three databases (Medline, ERIC and EMBASE) and used the keywords: staff development; in-service training; medical faculty; faculty training/development; continuing medical education. Manual searches were also conducted.Articles with a focus on faculty development to improve teaching effectiveness, targeting basic and clinical scientists, were reviewed. All study designs that included outcome data beyond participant satisfaction were accepted....

Epigenetic inactivation of SFRP genes allows constitutive WNT signaling in colorectal cancer

Abstract: Aberrant WNT pathway signaling is an early progression event in 90% of colorectal cancers1. It occurs through mutations mainly of APC and less often of CTNNB1 (encoding β-catenin)1,2,3 or AXIN2 (encoding axin-2, also known as conductin)4. These mutations allow ligand-independent WNT signaling that culminates in abnormal accumulation of free β-catenin in the nucleus1,2,3. We previously identified frequent promoter hypermethylation and gene silencing of the genes encoding secreted frizzled-related proteins (SFRPs) in colorectal cancer5. SFRPs possess a domain similar to one in the WNT-receptor frizzled proteins and can inhibit WNT receptor binding to downregulate pathway signaling during development6,7,8,9,10. Here we show that restoration of SFRP function in colorectal cancer cells attenuates WNT signaling even in the presence of downstream mutations. We also show that the epigenetic loss of SFRP function occurs early in colorectal cancer progression and may thus provide constitutive WNT signaling that is required to complement downstream mutations in the evolution of colorectal cancer.

Antineutrophil cytoplasmic autoantibodies specific for myeloperoxidase cause glomerulonephritis and vasculitis in mice

Abstract: Antineutrophil cytoplasmic autoantibodies (ANCAs) are identified in the circulation of approximately 80% of patients with pauci-immune necrotizing and crescentic glomerulonephritis and systemic small vessel vasculitis, such as microscopic polyangiitis and Wegener granulomatosis. The most common antigen target for ANCAs is myeloperoxidase (MPO), which is found in neutrophils and monocytes. We report definitive experimental animal evidence that ANCAs are pathogenic. MPO knockout (Mpo(-/-)) mice were immunized with mouse MPO. Splenocytes from these mice or from control mice were injected intravenously into recombinase-activating gene-2-deficient (Rag2(-/-)) mice, which lack functioning B lymphocytes and T lymphocytes. All mice that received splenocytes developed mild to moderate glomerular immune deposits, but only mice that received 1 x 10(8) or 5 x 10(7) anti-MPO splenocytes developed severe necrotizing and crescentic glomerulonephritis, granulomatous inflammation, and systemic necrotizing vasculitis, including necrotizing arteritis and hemorrhagic pulmonary capillaritis. To test the pathogenic potential of antibodies alone, purified anti-MPO IgG or control IgG was injected intravenously into Rag2(-/-) mice and wild-type mice. Mice that received anti-MPO IgG but not mice that received control IgG developed focal necrotizing and crescentic glomerulonephritis with a paucity of glomerular Ig deposition. Thus, anti-MPO IgG alone was able to cause pauci-immune glomerular necrosis and crescent formation in the absence of functional T or B lymphocytes in Rag2(-/-) mice and in the presence of an intact immune system in wild-type C57BL/6J mice. This animal model offers strong support for a direct pathogenic role for ANCA IgG in human glomerulonephritis and vasculitis.