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Institution

University of Buenos Aires

EducationBuenos Aires, Argentina
About: University of Buenos Aires is a education organization based out in Buenos Aires, Argentina. It is known for research contribution in the topics: Population & Large Hadron Collider. The organization has 29353 authors who have published 50947 publications receiving 1086007 citations. The organization is also known as: Universidad de Buenos Aires.


Papers
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Journal ArticleDOI
Daniel J. Klionsky1, Kotb Abdelmohsen2, Akihisa Abe3, Joynal Abedin4  +2519 moreInstitutions (695)
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Abstract: In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure flux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation, it is imperative to target by gene knockout or RNA interference more than one autophagy-related protein. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways implying that not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular assays, we hope to encourage technical innovation in the field.

5,187 citations

Journal ArticleDOI
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Abstract: In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.

4,316 citations

Journal ArticleDOI
11 May 2000-Nature
TL;DR: The large ecological and societal consequences of changing biodiversity should be minimized to preserve options for future solutions to global environmental problems.
Abstract: Human alteration of the global environment has triggered the sixth major extinction event in the history of life and caused widespread changes in the global distribution of organisms. These changes in biodiversity alter ecosystem processes and change the resilience of ecosystems to environmental change. This has profound consequences for services that humans derive from ecosystems. The large ecological and societal consequences of changing biodiversity should be minimized to preserve options for future solutions to global environmental problems.

3,977 citations

Journal ArticleDOI
Lorenzo Galluzzi1, Lorenzo Galluzzi2, Ilio Vitale3, Stuart A. Aaronson4  +183 moreInstitutions (111)
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
Abstract: Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

3,301 citations

Journal Article
TL;DR: The second revision of the ILAR Taskforce on Classification of Childhood Arthritis (ILAR-JIA) was presented at the 2001 ILAR Workshop on Rheumatology as discussed by the authors.
Abstract: The primary aim of the International League of Associations for Rheumatology (ILAR) proposals for classification of juvenile idiopathic arthritis (JIA) is to delineate, for research purposes, relatively homogeneous, mutually exclusive categories of idiopathic childhood arthritis based on predominant clinical and laboratory features. As part of a continuing review process, the ILAR Taskforce on Classification of Childhood Arthritis met in Edmonton in 2001 to discuss modifications to the proposed JIA classification. Since the publication of the first revision of the original classification 1 , a number of descriptive studies using the new classification have been reported 2-11. The aims of this communication are 2-fold: to outline modifications to the revised classification proposed as a result of the Edmonton meeting, and to correct misconceptions highlighted by the published studies concerning the clinical use of the classification. The Edmonton Revision The changes embodied in the second revision of the classification are as follows: 1. Clarification of the definitions of each category. 2. Improvement in the congruity between inclusion and exclusion criteria. 3. Removal of the requirement that a dermatologist make the diagnosis of psoriasis. 4. Removal of the requirement that there be medical confirmation of HLA-B27 associated disease in a relative. 5. Reduction in the age for criterion " 3 " of enthesitis related arthritis, and exclusion " b " from 8 years to 6 years of age. 6. Improvement in the consistency of the structure. The impracticality of the requirement that a diagnosis of psoriasis be made by a dermatologist was recognized, and this requirement was modified so that the diagnosis of psori-asis could be made by a physician (not necessarily a dermatologist). Similarly, it is no longer required that there be medical confirmation of an HLA-B27 associated disease in a relative as contained in exclusion " c. " It is evident that it is very difficult to obtain a reliable history of psoriasis or an HLA-B27 associated disease in a second-degree relative. Therefore, a history of importance to the application of the criteria is restricted to the patient or a first-degree relative (parents or siblings) only. The study of Murray, et al 8 indicated that the HLA-B27 association is important in boys over the age of 6 years at onset of arthritis, and this age was substituted for 8 years in exclusion " b. " Discrepancies between inclusion and exclusion criteria were resolved, and the exclusions were identified by the letters …

3,201 citations


Authors

Showing all 29643 results

NameH-indexPapersCitations
Alexander Belyaev1421895100796
Mitchell Wayne1391810108776
Floyd E. Bloom13961672641
Cecilia Elena Gerber1381727106984
Philip Baringer1381927105322
Randy Ruchti1371832107846
Diego F. Torres13794872180
Harrison Prosper1341587100607
Wladyslaw Dabrowski12999079728
Ariel Schwartzman129106882555
Danuta Kisielewska12895078603
A. Baden128135284403
Stefan Koperny12886775257
Tadeusz Kowalski12881674939
Iwona Grabowska-Bold12893176796
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20251
202391
2022426
20212,753
20203,006
20192,656