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Institution

University of Zurich

EducationZurich, Switzerland
About: University of Zurich is a education organization based out in Zurich, Switzerland. It is known for research contribution in the topics: Population & Medicine. The organization has 50842 authors who have published 124042 publications receiving 5304521 citations. The organization is also known as: UZH & Uni Zurich.


Papers
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Journal ArticleDOI
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
Abstract: In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.

1,129 citations

Journal ArticleDOI
TL;DR: In this article, a field experiment at the University of Zurich showed that people behave pro-socially, conditional on others, and that the more others cooperate, the more one is inclined to do so as well.
Abstract: People behave pro-socially in a wide variety of situations that standard economic theory is unable to explain. Social comparison is one explanation for such pro-social behavior: people contribute if others contribute or cooperate as well. This paper tests social comparison in a field experiment at the University of Zurich. Each semester every single student has to decide whether he or she wants to contribute to two Social Funds. We provided 2500 randomly selected students with information about the average behavior of the student population. Some received the information that a high percentage of the student population contributed, while others received the information that a relatively low percentage contributed. The results show that people behave pro-socially, conditional on others. The more others cooperate, the more one is inclined to do so as well. The type of person is important. We are able to fix the i?½typesi?½ by looking at revealed past behavior. Some persons seem to care more about the pro-social behavior of others, while other i?½typesi?½ are not affected by the average behavior of the reference group.

1,126 citations

Journal ArticleDOI
21 Oct 1999-Nature
TL;DR: In this article, a histidine-to-arginine point mutation at position 101 of the murine α1-subunit gene was found to render α-type GABAA receptors insensitive to allosteric modulation by benzodiazepine-site ligands, whilst regulation by the physiological neurotransmitter γ-aminobutyric acid is preserved.
Abstract: GABAA (γ-aminobutyric acidA) receptors are molecular substrates for the regulation of vigilance, anxiety, muscle tension, epileptogenic activity and memory functions, which is evident from the spectrum of actions elicited by clinically effective drugs acting at their modulatory benzodiazepine-binding site. Here we show, by introducing a histidine-to-arginine point mutation at position 101 of the murine α1-subunit gene, that α1-type GABAA receptors, which are mainly expressed in cortical areas and thalamus1, are rendered insensitive to allosteric modulation by benzodiazepine-site ligands, whilst regulation by the physiological neurotransmitter γ-aminobutyric acid is preserved. α1(H101R) mice failed to show the sedative, amnesic and partly the anticonvulsant action of diazepam. In contrast, the anxiolytic-like, myorelaxant, motor-impairing and ethanol-potentiating effects were fully retained, and are attributed to the nonmutated GABAA receptors found in the limbic system (α2, α5), in monoaminergic neurons (α3) and in motoneurons (α2, α5)1. Thus, benzodiazepine-induced behavioural responses are mediated by specific GABAA receptor subtypes in distinct neuronal circuits, which is of interest for drug design.

1,126 citations

Journal ArticleDOI
TL;DR: Activated microglia rather than astrocytes or endothelial cells are the candidates as intrinsic antigen presenting cel of the brain due to their pronounced antigen presenting function in vitro.

1,122 citations


Authors

Showing all 51384 results

NameH-indexPapersCitations
Richard A. Flavell2311328205119
Peer Bork206697245427
Thomas C. Südhof191653118007
Stuart H. Orkin186715112182
Ruedi Aebersold182879141881
Tadamitsu Kishimoto1811067130860
Stanley B. Prusiner16874597528
Yang Yang1642704144071
Tomas Hökfelt158103395979
Dan R. Littman157426107164
Hans Lassmann15572479933
Matthias Egger152901184176
Lorenzo Bianchini1521516106970
Robert M. Strieter15161273040
Ashok Kumar1515654164086
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023265
20221,039
20218,997
20208,398
20197,336
20186,832