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Institution

University of Aberdeen

EducationAberdeen, United Kingdom
About: University of Aberdeen is a education organization based out in Aberdeen, United Kingdom. It is known for research contribution in the topics: Population & Randomized controlled trial. The organization has 21174 authors who have published 49962 publications receiving 2105479 citations. The organization is also known as: Aberdeen University.


Papers
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Journal ArticleDOI
TL;DR: The theoretical foundation of the relationship between perceptions of safety climate and workers’ behaviour is not well specified in this literature and a model derived from industry research is proposed.

306 citations

Journal ArticleDOI
TL;DR: This in vitro process is validated as a model of in vivo angiogenesis that can be quantified to assay stimulatory and inhibitory agents, signals and drugs.
Abstract: This report describes a model of angiogenesis which develops in admixtures (co-cultures) of human umbilical vein endothelial cells (HUVEC) and human diploid fibroblasts of dermal origin from adult patients. The system does not require the addition of further growth factors other than those normally present in endothelial growth medium (EGM), nor matrix proteins, and cell growth and proliferation are allowed to occur in a standard low (2%) concentration of fetal calf serum. Angiogenesis was specifically stimulated in response to vascular endothelial growth factor (VEGF), resulting in an increased development of structures resembling a microvasculature bed. Alternatively, angiogenesis was inhibited by addition of an excess of neutralising anti-VEGF antibodies, and the anti-angiogenic drugs such as suramin. We briefly show that stimulatory and inhibitory activities can be easily and quickly quantified by image analysis. Tubule formation was confirmed by confocal and electron microscopy, and the development and disposition of these structures within the co-cultures has been analysed immunochemically to show expression of specific endothelial cell determinants, such as PECAM-1. On this and a number of other criteria, the findings validate this in vitro process as a model of in vivo angiogenesis that can be quantified to assay stimulatory and inhibitory agents, signals and drugs.

306 citations

Journal ArticleDOI
TL;DR: The results demonstrate the low sensitivity of the resistance and resilience of both microbial groups to diversity decline provided that cell abundance is similar between treatments.
Abstract: Analysing the consequences of the decrease in biodiversity for ecosystem functioning and stability has been a major concern in ecology. However, the impact of decline in soil microbial diversity on ecosystem sustainability remains largely unknown. This has been assessed for decomposition, which is insured by a large proportion of the soil microbial community, but not for more specialized and less diverse microbial groups. We determined the impact of a decrease in soil microbial diversity on the stability (i.e. resistance and resilience following disturbance) of two more specialized bacterial functional groups: denitrifiers and nitrite oxidizers. Soil microbial diversity was reduced using serial dilutions of a suspension obtained from a non-sterile soil that led to loss of species with low cell abundance, inoculation of microcosms of the same sterile soil with these serial dilutions, and subsequent incubation to enable establishment of similar cell abundances between treatments. The structure, cell abundance and activity of denitrifying and nitrite-oxidizing communities were characterized after incubation. Increasing dilution led to a progressive decrease in community diversity as assessed by the number of denaturating gradient gel electrophoresis (DGGE) bands, while community functioning was not impaired when cell abundance recovered after incubation. The microcosms were then subjected to a model disturbance: heating to 42°C for 24 h. Abundance, structure and activity of each community were measured 3 h after completion of the disturbance to assess resistance, and after incubation of microcosms for 1 month to assess resilience. Resistance and resilience to the disturbance differed between the two communities, nitrite oxidizers being more affected. However, reducing the diversity of the two microbial functional groups did not impair either their resistance or their resilience following the disturbance. These results demonstrate the low sensitivity of the resistance and resilience of both microbial groups to diversity decline provided that cell abundance is similar between treatments.

306 citations

Journal ArticleDOI
TL;DR: This paper will examine metal microbe interactions, both in naturally occurring microbial ecosystems and in two particular cases of biocorrosion, with the objective of putting forward a unifying hypothesis relevant to the understanding of each of these apparently disparate processes.
Abstract: The general term biomineralisation refers to biologically induced mineralisation in which an organism modifies its local microenvironment creating conditions such that there is chemical precipitation of mineral phases extracellularly. Most usually this results from an oxidation or reduction carried out by some microbial species, with the formation of a recognised biomineralised product. These reactions play a major role in microbial physiology and ecology, and are of central importance to such engineering consequences as microbial mining and microbially influenced corrosion. This paper will examine metal microbe interactions, both in naturally occurring microbial ecosystems and in two particular cases of biocorrosion, with the objective of putting forward a unifying hypothesis relevant to the understanding of each of these apparently disparate processes.

306 citations

Journal ArticleDOI
01 Sep 1997-Diabetes
TL;DR: Metabolic abnormalities combine to produce deleterious changes in nerve perfusion that make a major contribution to the etiology of diabetic neuropathy.
Abstract: Reduced nerve perfusion is an important factor in the etiology of diabetic neuropathy. Studies in streptozotocin-induced diabetic rats show that nerve conduction velocity (NCV) and blood flow deficits are corrected by treatment with vasodilator drugs, with angiotensin II and endothelin-1 antagonists being particularly important. The AT 1 antagonist ZD7155 also prevents diabetic deficits in regeneration following nerve damage, indicating that hypoperfusion is an important limitation for nerve repair. Metabolic changes include high polyol pathway flux, increased advanced glycosylation, elevated oxidative stress, and impaired ω-6 essential fatty acid metabolism. Aldose reductase inhibitors (ARIs) restore NCV via their effects on perfusion. ARI action probably depends on blocking the conversion of glucose to sorbitol, thus preventing depletion of vasa nervorum glutathione, an important endogenous free radical scavenger. Free radicals cause vascular endothelium damage and reduced nitric oxide vasodilation. Inhibition of advanced glycosylation and autoxidation (autoxidative glycosylation), major sources of free radicals, by aminoguanidine or transition metal chelators, corrects neurovascular dysfunction. Evening primrose oil supplies γ-linolenic acid (GLA) to improve vasodilator eicosanoid synthesis in diabetes, correcting nerve blood flow and NCV deficits. Interactions between some of these mechanisms have therapeutic implications. Thus, combined ARI and evening primrose oil treatment produced a 10-fold amplification of NCV and blood flow responses. Similarly, GLA effects are markedly enhanced when given in combination with ascorbate as ascorbyl-GLA. Thus, metabolic abnormalities combine to produce deleterious changes in nerve perfusion that make a major contribution to the etiology of diabetic neuropathy. The potential importance of multi-action therapy is stressed.

306 citations


Authors

Showing all 21424 results

NameH-indexPapersCitations
Paul M. Thompson1832271146736
Feng Zhang1721278181865
Ian J. Deary1661795114161
Peter A. R. Ade1621387138051
David W. Johnson1602714140778
Pete Smith1562464138819
Naveed Sattar1551326116368
John R. Hodges14981282709
Ruth J. F. Loos14264792485
Alan J. Silman14170892864
Michael J. Keating140116976353
David Price138168793535
John D. Scott13562583878
Aarno Palotie12971189975
Rajat Gupta126124072881
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023141
2022362
20212,195
20202,118
20191,846
20181,894