Institution
University of Zurich
Education•Zurich, Switzerland•
About: University of Zurich is a education organization based out in Zurich, Switzerland. It is known for research contribution in the topics: Population & Transplantation. The organization has 50842 authors who have published 124042 publications receiving 5304521 citations. The organization is also known as: UZH & Uni Zurich.
Papers published on a yearly basis
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TL;DR: While the prevalence of overweight and obesity appears to be stabilizing at different levels in different countries, it remains high, and a significant public health issue.
Abstract: Until quite recently, there has been a widespread belief in the popular media and scientific literature that the prevalence of childhood obesity is rapidly increasing However, high quality evidence has emerged from several countries suggesting that the rise in the prevalence has slowed appreciably, or even plateaued This review brings together such data from nine countries (Australia, China, England, France, Netherlands, New Zealand, Sweden, Switzerland and USA), with data from 467,294 children aged 2-19 years The mean unweighted rate of change in prevalence of overweight and obesity was +000 (049)% per year across all age ×sex groups and all countries between 1995 and 2008 For overweight alone, the figure was +001 (056)%, and for obesity alone -001 (024)% Rates of change differed by sex, age, socioeconomic status and ethnicity While the prevalence of overweight and obesity appears to be stabilizing at different levels in different countries, it remains high, and a significant public health issue Possible reasons for the apparent flattening are hypothesised
600 citations
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TL;DR: Failure of cranial closure between 9 and 9.5 days postcoitum coincided with increased apoptosis in the midbrain, anterior hindbrain and proximal mesenchyme of the first branchial arch, but did not involve loss of expression of twist or Pax-3, two other regulatory genes known to be required for Cranial closure.
Abstract: DURING closure of the neural tube in the mouse, transcription factor AP-2 (refs 1–4) is expressed in ectoderm and in neural-crest cells migrating from the cranial neural folds5. Cranial neural crest cells provide patterning information for craniofacial morphogenesis, generate most of the skull bones, and, together with placodal ectoderm, form the cranial ganglia6–8. To study the role of AP-2 during embryogenesis, we undertook a targeted mutagenesis of the AP-2 gene in the mouse. Here we report that AP-2–/– mice died perinatally with cranio-abdominoschisis and severe dismorphogenesis of the face, skull, sensory organs and cranial ganglia. Failure of cranial closure between 9 and 9.5 days postcoitum coincided with increased apoptosis in the midbrain, anterior hindbrain and proximal mesenchyme of the first branchial arch, but did not involve loss of expression of twist or Pax-3, two other regulatory genes known to be required for cranial closure.
600 citations
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TL;DR: The findings show that the female control of pollen tube reception is based on a FER-dependent signaling pathway, which may play a role in reproductive isolation barriers, and the FER protein accumulates asymmetrically in the synergid membrane at the filiform apparatus.
Abstract: In flowering plants, signaling between the male pollen tube and the synergid cells of the female gametophyte is required for fertilization. In the Arabidopsis thaliana mutant feronia (fer), fertilization is impaired; the pollen tube fails to arrest and thus continues to grow inside the female gametophyte. FER encodes a synergid-expressed, plasma membrane-localized receptor-like kinase. We found that the FER protein accumulates asymmetrically in the synergid membrane at the filiform apparatus. Interspecific crosses using pollen from Arabidopsis lyrata and Cardamine flexuosa on A. thaliana stigmas resulted in a fer-like phenotype that correlates with sequence divergence in the extracellular domain of FER. Our findings show that the female control of pollen tube reception is based on a FER-dependent signaling pathway, which may play a role in reproductive isolation barriers.
599 citations
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598 citations
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TL;DR: It is postulate that constitutive and induced autophagy is a major protective mechanism against podocyte aging and glomerular injury, representing a putative target to ameliorate human glomersular disease and aging-related loss of renal function.
Abstract: Injury and loss of podocytes are leading factors of glomerular disease and renal failure. The postmitotic podocyte is the primary glomerular target for toxic, immune, metabolic, and oxidant stress, but little is known about how this cell type copes with stress. Recently, autophagy has been identified as a major pathway that delivers damaged proteins and organelles to lysosomes in order to maintain cellular homeostasis. Here we report that podocytes exhibit an unusually high level of constitutive autophagy. Podocyte-specific deletion of autophagy-related 5 (Atg5) led to a glomerulopathy in aging mice that was accompanied by an accumulation of oxidized and ubiquitinated proteins, ER stress, and proteinuria. These changes resulted ultimately in podocyte loss and late-onset glomerulosclerosis. Analysis of pathophysiological conditions indicated that autophagy was substantially increased in glomeruli from mice with induced proteinuria and in glomeruli from patients with acquired proteinuric diseases. Further, mice lacking Atg5 in podocytes exhibited strongly increased susceptibility to models of glomerular disease. These findings highlight the importance of induced autophagy as a key homeostatic mechanism to maintain podocyte integrity. We postulate that constitutive and induced autophagy is a major protective mechanism against podocyte aging and glomerular injury, representing a putative target to ameliorate human glomerular disease and aging-related loss of renal function.
597 citations
Authors
Showing all 51384 results
Name | H-index | Papers | Citations |
---|---|---|---|
Richard A. Flavell | 231 | 1328 | 205119 |
Peer Bork | 206 | 697 | 245427 |
Thomas C. Südhof | 191 | 653 | 118007 |
Stuart H. Orkin | 186 | 715 | 112182 |
Ruedi Aebersold | 182 | 879 | 141881 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Stanley B. Prusiner | 168 | 745 | 97528 |
Yang Yang | 164 | 2704 | 144071 |
Tomas Hökfelt | 158 | 1033 | 95979 |
Dan R. Littman | 157 | 426 | 107164 |
Hans Lassmann | 155 | 724 | 79933 |
Matthias Egger | 152 | 901 | 184176 |
Lorenzo Bianchini | 152 | 1516 | 106970 |
Robert M. Strieter | 151 | 612 | 73040 |
Ashok Kumar | 151 | 5654 | 164086 |