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In JoVE (1)
- Time-lapse imagens de fluorescência de crescimento de raiz Arabidopsis com Manipulação acelerada do meio root usando o RootChip
Other Publications (2)
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Articles by Matthias Meier in JoVE
Time-lapse imagens de fluorescência de crescimento de raiz Arabidopsis com Manipulação acelerada do meio root usando o RootChip
Guido Grossmann1, Matthias Meier2,3,4, Heather N. Cartwright1, Davide Sosso1, Stephen R. Quake2,3, David W. Ehrhardt1, Wolf B. Frommer1
1Department of Plant Biology, Carnegie Institution for Science, 2Howard Hughes Medical Institute, 3Departments of Applied Physics and Bioengineering, Stanford University, 4Department of Microsystems Engineering (IMTEK) and Center for Biological Signaling Studies (BIOSS), University of Freiburg
Este artigo fornece um protocolo para o cultivo de mudas de Arabidopsis no RootChip, uma plataforma microfluídica imagem que combina controle automatizado das condições de crescimento com acompanhamento raiz microscópica e FRET baseado em medição de níveis de metabólitos intracelulares.
Other articles by Matthias Meier on PubMed
Journal of Nephrology. Dec, 2011 | Pubmed ID: 22180224
Background: C57BL/6 and 129/Sv are the 2 most commonly used strains of mice in renal ischemia-reperfusion injury (IRI) studies, yet there are currently no studies that contrast differences in the degree of renal injury after ischemia-reperfusion. Methods: To evaluate renal IRI in male C57BL/6 and 129/Sv mice, we performed unilateral clamping of the left renal pedicle for 45 minutes and compared the degree of renal tissue damage and function. To measure function and tissue damage we examined: glomerular filtration rate (GFR; by inulin clearance), renal blood flow (RBF; by p-aminohippurate [PAH] clearance), renal morphology, immunohistochemistry for infiltrating leukocytes, and fibrogenic markers by Sirius red staining. Results: After unilateral IRI, 129/sv mice had significantly less GFR and RBF disfunction at both day 14 (d14) and d28. 129/sv mice also had significantly less acute tubular necrosis on d1 and fewer infiltrating leukocytes on d28, as well as less collagen deposition on d28 than C57BL/6 mice. Conclusions: C57BL/6 mice were much more sensitive to damage caused by renal IRI than are 129/Sv mice.
The Journal of Pathology. May, 2012 | Pubmed ID: 22570261
The incidence of chronic kidney diseases (CKD) is constantly rising, reaching epidemic proportions in the western world and leading to an enormous threat, even to modern health-care systems, in industrialized countries. Therapies of CKD have greatly improved following the introduction of drugs targeting the renin-angiotensin system (RAAS) but even this refined pharmacological approach has failed to stop progression to end-stage renal disease (ESRD) in many individuals. In vitro historical data and recent new findings have suggested that progression of renal fibrosis might occur as a result of an altered tubulo-interstitial microenvironment and, more specifically, as a result of an altered epithelial-mesenchymal crosstalk. Here we the review biological findings that support the hypothesis of an altered cellular crosstalk in an injured local tubulo-interstitial microenvironment leading to renal disease progression. Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.