University of Aberdeen
Education•Aberdeen, United Kingdom•
About: University of Aberdeen is a(n) education organization based out in Aberdeen, United Kingdom. It is known for research contribution in the topic(s): Population & Randomized controlled trial. The organization has 21174 authors who have published 49962 publication(s) receiving 2105479 citation(s). The organization is also known as: Aberdeen University.
Papers published on a yearly basis
•01 May 1986
TL;DR: In this article, the authors present a graphical representation of data using Principal Component Analysis (PCA) for time series and other non-independent data, as well as a generalization and adaptation of principal component analysis.
Abstract: Introduction * Properties of Population Principal Components * Properties of Sample Principal Components * Interpreting Principal Components: Examples * Graphical Representation of Data Using Principal Components * Choosing a Subset of Principal Components or Variables * Principal Component Analysis and Factor Analysis * Principal Components in Regression Analysis * Principal Components Used with Other Multivariate Techniques * Outlier Detection, Influential Observations and Robust Estimation * Rotation and Interpretation of Principal Components * Principal Component Analysis for Time Series and Other Non-Independent Data * Principal Component Analysis for Special Types of Data * Generalizations and Adaptations of Principal Component Analysis
••15 Oct 2005
TL;DR: Principal component analysis (PCA) as discussed by the authors replaces the p original variables by a smaller number, q, of derived variables, the principal components, which are linear combinations of the original variables.
Abstract: When large multivariate datasets are analyzed, it is often desirable to reduce their dimensionality. Principal component analysis is one technique for doing this. It replaces the p original variables by a smaller number, q, of derived variables, the principal components, which are linear combinations of the original variables. Often, it is possible to retain most of the variability in the original variables with q very much smaller than p. Despite its apparent simplicity, principal component analysis has a number of subtleties, and it has many uses and extensions. A number of choices associated with the technique are briefly discussed, namely, covariance or correlation, how many components, and different normalization constraints, as well as confusion with factor analysis. Various uses and extensions are outlined. Keywords: dimension reduction; factor analysis; multivariate analysis; variance maximization
Stephan Ripke1, Stephan Ripke2, Benjamin M. Neale2, Benjamin M. Neale1 +351 more•Institutions (102)
TL;DR: Associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses.
Abstract: Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain, providing biological plausibility for the findings. Many findings have the potential to provide entirely new insights into aetiology, but associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that have important roles in immunity, providing support for the speculated link between the immune system and schizophrenia.
TL;DR: In this article, an arachidonylethanthanolamide (anandamide) was identified in a screen for endogenous ligands for the cannabinoid receptor and its structure was determined by mass spectrometry and nuclear magnetic resonance spectroscopy and confirmed by synthesis.
Abstract: Arachidonylethanolamide, an arachidonic acid derivative in porcine brain, was identified in a screen for endogenous ligands for the cannabinoid receptor. The structure of this compound, which has been named "anandamide," was determined by mass spectrometry and nuclear magnetic resonance spectroscopy and was confirmed by synthesis. Anandamide inhibited the specific binding of a radiolabeled cannabinoid probe to synaptosomal membranes in a manner typical of competitive ligands and produced a concentration-dependent inhibition of the electrically evoked twitch response to the mouse vas deferens, a characteristic effect of psychotropic cannabinoids. These properties suggest that anandamide may function as a natural ligand for the cannabinoid receptor.
Daniel J. Klionsky1, Kotb Abdelmohsen2, Akihisa Abe3, Joynal Abedin4 +2519 more•Institutions (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.
Showing all 21174 results
|Paul M. Thompson||183||2271||146736|
|Ian J. Deary||166||1795||114161|
|Peter A. R. Ade||162||1387||138051|
|David W. Johnson||160||2714||140778|
|John R. Hodges||149||812||82709|
|Ruth J. F. Loos||142||647||92485|
|Alan J. Silman||141||708||92864|
|Michael J. Keating||140||1169||76353|
|John D. Scott||135||625||83878|
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