5 results on '"Bichsel C"'
Search Results
2. Conflict transformation in Central Asia : Irrigation disputes in the Ferghana Valley
- Author
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Bichsel, C, University of Zurich, and Bichsel, C
- Subjects
10122 Institute of Geography ,950 History of Asia ,180 Ancient, medieval & eastern philosophy ,910 Geography & travel ,U2 Asia and Europe - Published
- 2009
3. Water, infrastructure and political rule: Introduction to the special issue
- Author
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Obertreis, J., Moss, T., Peter Mollinga, and Bichsel, C.
- Subjects
rule ,lcsh:Hydraulic engineering ,lcsh:TC1-978 ,Oriental despotism ,Water ,infrastructure - Abstract
This introductory article sets the scene for this special issue on water, infrastructure and political rule. It makes the case for revisiting the complex relationships between these three dimensions which have fascinated scholars since Wittfogel’s pioneering – if much criticised – work on causal links between large-scale irrigation systems and autocratic leadership. Scholarship on water, on infrastructure, as well as on political rule has made huge advances since Wittfogel’s days, requiring a wholesome reappraisal of their triangular relationship. In this article, we review the relevant advances in scientific knowledge and epistemological approaches on each dimension. We subsequently summarise the different ways in which each of the following papers takes up and interrogates the relationship between water, infrastructure and political rule prior to the final paper which synthesises the principal findings emerging from the special issue.
4. Targeted delivery of protein arginine deiminase-4 inhibitors to limit arterial intimal NETosis and preserve endothelial integrity
- Author
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Grasiele Sausen, Frederik Kloss, Mi Kyung Yu, Gha Young Lee, Roberto Molinaro, Eduardo J. Folco, Jinjun Shi, Omid C. Farokhzad, Peter Libby, Yevgenia Tesmenitsky, Kevin Croce, Claudia Corbo, Galina K. Sukhova, Colette A. Bichsel, Eugenia Shvartz, Yuan Liu, Molinaro, R, Yu, M, Sausen, G, Bichsel, C, Corbo, C, Folco, E, Lee, G, Liu, Y, Tesmenitsky, Y, Shvartz, E, Sukhova, G, Kloss, F, Croce, K, Farokhzad, O, Shi, J, and Libby, P
- Subjects
0301 basic medicine ,Male ,Physiology ,Mice, Knockout, ApoE ,02 engineering and technology ,Extracellular Traps ,Basement Membrane ,Extracellular matrix ,Protein-Arginine Deiminase Type 4 ,Medicine ,Nanotechnology ,Tissue Distribution ,Enzyme Inhibitors ,Cells, Cultured ,Drug Carriers ,Fibrous cap ,Protein-arginine deiminase ,021001 nanoscience & nanotechnology ,Plaque, Atherosclerotic ,Endothelial stem cell ,medicine.anatomical_structure ,Atherosclerosi ,Systemic administration ,0210 nano-technology ,Cardiology and Cardiovascular Medicine ,Protein Binding ,Collagen Type IV ,Endothelium ,Surface Properties ,Drug Compounding ,Cardiovascular nanomedicine ,03 medical and health sciences ,Physiology (medical) ,Animals ,Humans ,Cell Culture Techniques, Three Dimensional ,Targeted nanoparticle ,Basement membrane ,Experimental superficial erosion ,business.industry ,Endothelial Cells ,Neutrophil extracellular traps ,Original Articles ,Atherosclerosis ,Disease Models, Animal ,Drug Liberation ,030104 developmental biology ,Cancer research ,Nanoparticles ,business ,Neutrophil extracellular trap - Abstract
Aims Recent evidence suggests that ‘vulnerable plaques’, which have received intense attention as underlying mechanism of acute coronary syndromes over the decades, actually rarely rupture and cause clinical events. Superficial plaque erosion has emerged as a growing cause of residual thrombotic complications of atherosclerosis in an era of increased preventive measures including lipid lowering, antihypertensive therapy, and smoking cessation. The mechanisms of plaque erosion remain poorly understood, and we currently lack validated effective diagnostics or therapeutics for superficial erosion. Eroded plaques have a rich extracellular matrix, an intact fibrous cap, sparse lipid, and few mononuclear cells, but do harbour neutrophil extracellular traps (NETs). We recently reported that NETs amplify and propagate the endothelial damage at the site of arterial lesions that recapitulate superficial erosion in mice. We showed that genetic loss of protein arginine deiminase (PAD)-4 function inhibited NETosis and preserved endothelial integrity. The current study used systemic administration of targeted nanoparticles to deliver an agent that limits NETs formation to probe mechanisms of and demonstrate a novel therapeutic approach to plaque erosion that limits endothelial damage. Methods and results We developed Collagen IV-targeted nanoparticles (Col IV NP) to deliver PAD4 inhibitors selectively to regions of endothelial cell sloughing and collagen IV-rich basement membrane exposure. We assessed the binding capability of the targeting ligand in vitro and evaluated Col IV NP targeting to areas of denuded endothelium in vivo in a mouse preparation that recapitulates features of superficial erosion. Delivery of the PAD4 inhibitor GSK484 reduced NET accumulation at sites of intimal injury and preserved endothelial continuity. Conclusions NPs directed to Col IV show selective uptake and delivery of their payload to experimentally eroded regions, illustrating their translational potential. Our results further support the role of PAD4 and NETs in superficial erosion.
- Published
- 2021
5. The 7q11.23 Protein DNAJC30 Interacts with ATP Synthase and Links Mitochondria to Brain Development
- Author
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Fuchen Liu, Luis Varela, Alice M. Giani, André M. M. Sousa, Tamas L. Horvath, Giuseppe Merla, Paolo Prontera, Amy F.T. Arnsten, Matija Sestan-Pesa, Jae Eun Song, Andrew T.N. Tebbenkamp, Jinmyung Choi, Candace Bichsel, Marina R. Picciotto, Zhuo Li, Constantinos D. Paspalas, Nenad Sestan, Daniel Franjic, Marco Koch, Miguel I. Paredes, Klara Szigeti-Buck, Yann S. Mineur, Yuka Imamura Kawasawa, Mingfeng Li, Zhong-Wu Liu, Tebbenkamp, Atn, Varela, L, Choi, J, Paredes, Mi, Giani, Am, Song, Je, Sestan-Pesa, M, Franjic, D, Sousa, Amm, Liu, Zw, Li, Mf, Bichsel, C, Koch, M, Szigeti-Buck, K, Liu, Fc, Li, Z, Kawasawa, Yi, Paspalas, Cd, Mineur, Y, Prontera, P, Merla, G, Picciotto, Mr, Arnsten, Aft, Horvath, Tl, and Sestan, N
- Subjects
0301 basic medicine ,Male ,Williams Syndrome ,Oxidative phosphorylation ,Mitochondrion ,General Biochemistry, Genetics and Molecular Biology ,Oxidative Phosphorylation ,Article ,03 medical and health sciences ,Mice ,medicine ,Animals ,Humans ,Gene ,Cells, Cultured ,ATP synthase ,biology ,HEK 293 cells ,Brain ,HSP40 Heat-Shock Proteins ,medicine.disease ,Phenotype ,Macaca mulatta ,Cell biology ,Mitochondria ,ATP Synthetase Complexes ,Mice, Inbred C57BL ,030104 developmental biology ,HEK293 Cells ,biology.protein ,Female ,Williams syndrome ,Function (biology) - Abstract
Summary Despite the known causality of copy-number variations (CNVs) to human neurodevelopmental disorders, the mechanisms behind each gene’s contribution to the constellation of neural phenotypes remain elusive. Here, we investigated the 7q11.23 CNV, whose hemideletion causes Williams syndrome (WS), and uncovered that mitochondrial dysfunction participates in WS pathogenesis. Dysfunction is facilitated in part by the 7q11.23 protein DNAJC30, which interacts with mitochondrial ATP-synthase machinery. Removal of Dnajc30 in mice resulted in hypofunctional mitochondria, diminished morphological features of neocortical pyramidal neurons, and altered behaviors reminiscent of WS. The mitochondrial features are consistent with our observations of decreased integrity of oxidative phosphorylation supercomplexes and ATP-synthase dimers in WS. Thus, we identify DNAJC30 as an auxiliary component of ATP-synthase machinery and reveal mitochondrial maladies as underlying certain defects in brain development and function associated with WS.
- Published
- 2018
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