Institution
Dalhousie University
Education•Halifax, Nova Scotia, Canada•
About: Dalhousie University is a(n) education organization based out in Halifax, Nova Scotia, Canada. It is known for research contribution in the topic(s): Population & Health care. The organization has 25660 authors who have published 58465 publication(s) receiving 2082403 citation(s). The organization is also known as: Dalhousie College & The Governors of Dalhousie College and University.
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University of Massachusetts Amherst1, University of Michigan2, University of New Mexico3, University of British Columbia4, Texas A&M University5, University of Minnesota6, University of Warwick7, Dalhousie University8, Colorado School of Mines9, University of Ljubljana10, Graz University of Technology11, Louisiana State University12
TL;DR: M mothur is used as a case study to trim, screen, and align sequences; calculate distances; assign sequences to operational taxonomic units; and describe the α and β diversity of eight marine samples previously characterized by pyrosequencing of 16S rRNA gene fragments.
Abstract: mothur aims to be a comprehensive software package that allows users to use a single piece of software to analyze community sequence data. It builds upon previous tools to provide a flexible and powerful software package for analyzing sequencing data. As a case study, we used mothur to trim, screen, and align sequences; calculate distances; assign sequences to operational taxonomic units; and describe the alpha and beta diversity of eight marine samples previously characterized by pyrosequencing of 16S rRNA gene fragments. This analysis of more than 222,000 sequences was completed in less than 2 h with a laptop computer.
14,946 citations
Abstract: Methods We estimated deaths and disability-adjusted life years (DALYs; sum of years lived with disability [YLD] and years of life lost [YLL]) attributable to the independent eff ects of 67 risk factors and clusters of risk factors for 21 regions in 1990 and 2010. W e estimated exposure distributions for each year, region, sex, and age group, and relative risks per unit of exposure by systematically reviewing and synthesising published and unpublished data. We used these estimates, together with estimates of cause-specifi c deaths and DALYs from the Global Burden of Disease Study 2010, to calculate the burden attributable to each risk factor exposure compared with the theoretical-minimum-risk exposure. We incorporated uncertainty in disease burden, relative risks, and exposures into our estimates of attributable burden. Findings In 2010, the three leading risk factors for global disease burden were high blood pressure (7·0% [95% uncertainty interval 6·2–7·7] of global DALYs), tobacco smoking including second-hand smoke (6·3% [5·5–7·0]), and alcohol use (5·5% [5·0–5·9]). In 1990, the leading risks were childhood underweight (7·9% [6·8–9·4]), household air pollution from solid fuels (HAP; 7·0% [5·6–8·3]), and tobacco smoking including second-hand smoke (6·1% [5·4–6·8]). Dietary risk factors and physical inactivity collectively accounted for 10·0% (95% UI 9·2–10·8) of global DALYs in 2010, with the most prominent dietary risks being diets low in fruits and those high in sodium. Several risks that primarily aff ect childhood communicable diseases, including unimproved water and sanitation and childhood micronutrient defi ciencies, fell in rank between 1990 and 2010, with unimproved water
8,301 citations
TL;DR: The results demonstrate that phylogeny and function are sufficiently linked that this 'predictive metagenomic' approach should provide useful insights into the thousands of uncultivated microbial communities for which only marker gene surveys are currently available.
Abstract: Profiling phylogenetic marker genes, such as the 16S rRNA gene, is a key tool for studies of microbial communities but does not provide direct evidence of a community's functional capabilities. Here we describe PICRUSt (phylogenetic investigation of communities by reconstruction of unobserved states), a computational approach to predict the functional composition of a metagenome using marker gene data and a database of reference genomes. PICRUSt uses an extended ancestral-state reconstruction algorithm to predict which gene families are present and then combines gene families to estimate the composite metagenome. Using 16S information, PICRUSt recaptures key findings from the Human Microbiome Project and accurately predicts the abundance of gene families in host-associated and environmental communities, with quantifiable uncertainty. Our results demonstrate that phylogeny and function are sufficiently linked that this 'predictive metagenomic' approach should provide useful insights into the thousands of uncultivated microbial communities for which only marker gene surveys are currently available.
5,291 citations
Abstract: In Study 1, the Pain Catastrophizing Scale (PCS) was administered to 425 undergraduates. Analyses yielded a three component solution comprising (a) rumination, (b) magnification, and (c) helplessness. In Study 2, 30 undergraduate participants were classified as catastrophizers (n = 15) or noncatastrophizers (n = 15) on the basis of their PCS scores and participated in an cold pressor procedure. Catastrophizers reported significantly more negative pain-related thoughts, greater emotional distress, and greater pain intensity than noncatastrophizers. Study 3 examined the relation between PCS scores, negative pain-related thoughts, and distress in 28 individuals undergoing an aversive electrodiagnostic medical procedure. Catastrophizers reported more negative pain-related thoughts, more emotional distress, and more pain than noncatastrophizers. Study 4 examined the relation between the PCS and measures of depression, trait anxiety, negative affectivity, and fear of pain. Analyses revealed moderate correlations among these measures, but only the PCS contributed significant unique variance t o the prediction of pain intensity.
5,200 citations
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.
4,756 citations
Authors
Showing all 25660 results
Name | H-index | Papers | Citations |
---|---|---|---|
Salim Yusuf | 231 | 1439 | 252912 |
Gordon H. Guyatt | 231 | 1620 | 228631 |
Michael Rutter | 188 | 676 | 151592 |
Mark E. Cooper | 158 | 1463 | 124887 |
Roberto Romero | 151 | 1516 | 108321 |
Rui Zhang | 151 | 2625 | 107917 |
Thomas J. Smith | 140 | 1775 | 113919 |
Dafna D. Gladman | 129 | 1036 | 75273 |
Marcello Tonelli | 128 | 701 | 115576 |
Shi Xue Dou | 122 | 2028 | 74031 |
J. R. Dahn | 120 | 832 | 66025 |
Scott Chapman | 118 | 579 | 46199 |
Kerry S. Courneya | 112 | 608 | 49504 |
Robert C. Haddon | 112 | 577 | 52712 |
Rodney J. Bartlett | 109 | 700 | 56154 |