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Article ; Online: Long-term effects of atmospheric deposition on British plant species richness.

Tipping, Edward / Davies, Jessica A C / Henrys, Peter A / Jarvis, Susan G / Smart, Simon M

Environmental pollution (Barking, Essex : 1987)

2021 Volume 281, Page(s) 117017

Abstract: The effects of atmospheric pollution on plant species richness ( ... ...

Abstract	The effects of atmospheric pollution on plant species richness (n
MeSH term(s)	Ecosystem ; Forests ; Nitrogen/analysis ; Plants ; Soil
Chemical Substances	Soil ; Nitrogen (N762921K75)
Language	English
Publishing date	2021-03-25
Publishing country	England
Document type	Journal Article
ZDB-ID	280652-6
ISSN	1873-6424 ; 0013-9327 ; 0269-7491
ISSN (online)	1873-6424
ISSN	0013-9327 ; 0269-7491
DOI	10.1016/j.envpol.2021.117017
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Article: Long-term effects of atmospheric deposition on British plant species richness

Tipping, Edward / Davies, Jessica A.C / Henrys, Peter A / Jarvis, Susan G / Smart, Simon M

Environmental pollution. 2021 July 15, v. 281

2021

Abstract: The effects of atmospheric pollution on plant species richness (nₛₚ) are of widespread concern. We carried out a modelling exercise to estimate how nₛₚ in British semi-natural ecosystems responded to atmospheric deposition of nitrogen (Ndₑₚ) and sulphur ( ...

Abstract	The effects of atmospheric pollution on plant species richness (nₛₚ) are of widespread concern. We carried out a modelling exercise to estimate how nₛₚ in British semi-natural ecosystems responded to atmospheric deposition of nitrogen (Ndₑₚ) and sulphur (Sdₑₚ) between 1800 and 2010. We derived a simple four-parameter equation relating nₛₚ to measured soil pH, and to net primary productivity (NPP), calculated with the N14CP ecosystem model. Parameters were estimated from a large data set (n = 1156) of species richness in four vegetation classes, unimproved grassland, dwarf shrub heath, peatland, and broadleaved woodland, obtained in 2007. The equation performed reasonably well in comparisons with independent observations of nₛₚ. We used the equation, in combination with modelled estimates of NPP (from N14CP) and soil pH (from the CHUM-AM hydrochemical model), to calculate changes in average nₛₚ over time at seven sites across Britain, assuming that variations in nₛₚ were due only to variations in atmospheric deposition. At two of the sites, two vegetation classes were present, making a total of nine site/vegetation combinations. In four cases, nₛₚ was affected about equally by pH and NPP, while in another four the effect of pH was dominant. The ninth site, a chalk grassland, was affected only by NPP, since soil pH was assumed constant. Our analysis suggests that the combination of increased NPP, due to fertilization by Ndₑₚ, and decreased soil pH, primarily due to Sdₑₚ, caused an average species loss of 39% (range 23–100%) between 1800 and the late 20th Century. The modelling suggests that in recent years nₛₚ has begun to increase, almost entirely due to reductions in Sdₑₚ and consequent increases in soil pH, but there are also indications of recent slight recovery from the eutrophying effects of Ndₑₚ.
Keywords	air pollution ; atmospheric deposition ; chalk grasslands ; data collection ; ecological models ; equations ; hydrochemistry ; net primary productivity ; nitrogen ; peatlands ; shrubs ; soil pH ; species richness ; sulfur ; woodlands ; United Kingdom
Language	English
Dates of publication	2021-0715
Publishing place	Elsevier Ltd
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	280652-6
ISSN	1873-6424 ; 0013-9327 ; 0269-7491
ISSN (online)	1873-6424
ISSN	0013-9327 ; 0269-7491
DOI	10.1016/j.envpol.2021.117017
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Article ; Online: Are podocytes passive or provocative in proteinuric glomerular pathology?

Tipping, Peter G

Journal of the American Society of Nephrology : JASN

2008 Volume 19, Issue 4, Page(s) 651–653

MeSH term(s)	Humans ; Kidney Glomerulus ; Podocytes/physiology ; Proteinuria/etiology
Language	English
Publishing date	2008-04
Publishing country	United States
Document type	Comment ; Editorial ; Review
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2008020156
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Article ; Online: Crescentic nephritis--is it in your genes?

Tipping, Peter G

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2008 Volume 23, Issue 10, Page(s) 3065–3066

MeSH term(s)	Animals ; Disease Models, Animal ; Genes, jun ; Genetic Predisposition to Disease ; Glomerulonephritis/etiology ; Glomerulonephritis/genetics ; Glomerulonephritis/immunology ; Humans ; Mice ; Rats ; Rats, Inbred WKY ; Transcription Factor AP-1/genetics
Chemical Substances	Transcription Factor AP-1
Language	English
Publishing date	2008-10
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfn402
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Article: Toll-like receptors: the interface between innate and adaptive immunity.

Tipping, Peter G

Journal of the American Society of Nephrology : JASN

2006 Volume 17, Issue 7, Page(s) 1769–1771

MeSH term(s)	Animals ; Autoimmunity/physiology ; Epithelial Cells/metabolism ; Glomerulonephritis/immunology ; Humans ; Kidney/cytology ; Lipopeptides ; Peptides/immunology ; Toll-Like Receptor 2/agonists ; Toll-Like Receptor 2/immunology
Chemical Substances	Lipopeptides ; Pam(3)CSK(4) peptide ; Peptides ; Toll-Like Receptor 2
Language	English
Publishing date	2006-07
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2006050489
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Article: Quantitative validation of Monte Carlo SPECT simulation: application to a Mediso AnyScan GATE simulation.

Pells, Sophia / Cullen, David M / Deidda, Daniel / Denis-Bacelar, Ana M / Fenwick, Andrew / Ferreira, Kelley M / Hamilton, David / Heetun, Warda / Julyan, Peter / Needham, George / Pietras, Ben / Price, Emlyn / Scuffham, James / Tipping, Jill / Robinson, Andrew P

EJNMMI physics

2023 Volume 10, Issue 1, Page(s) 60

Abstract: Background: Monte Carlo (MC) simulations are used in nuclear medicine imaging as they provide unparalleled insight into processes that are not directly experimentally measurable, such as scatter and attenuation in an acquisition. Whilst MC is often used ...

Abstract	Background: Monte Carlo (MC) simulations are used in nuclear medicine imaging as they provide unparalleled insight into processes that are not directly experimentally measurable, such as scatter and attenuation in an acquisition. Whilst MC is often used to provide a 'ground-truth', this is only the case if the simulation is fully validated against experimental data. This work presents a quantitative validation for a MC simulation of a single-photon emission computed tomography (SPECT) system. Methods: An MC simulation model of the Mediso AnyScan SCP SPECT system installed at the UK National Physical Laboratory was developed in the GATE (Geant4 Application for Tomographic Emission) toolkit. Components of the detector head and two collimator configurations were modelled according to technical specifications and physical measurements. Experimental detection efficiency measurements were collected for a range of energies, permitting an energy-dependent intrinsic camera efficiency correction function to be determined and applied to the simulation on an event-by-event basis. Experimental data were collected in a range of geometries with [Formula: see text]Tc for comparison to simulation. The procedure was then repeated with [Formula: see text]Lu to determine how the validation extended to another isotope and set of collimators. Results: The simulation's spatial resolution, sensitivity, energy spectra and the projection images were compared with experimental measurements. The simulation and experimental uncertainties were determined and propagated to all calculations, permitting the quantitative agreement between simulated and experimental SPECT acquisitions to be determined. Statistical agreement was seen in sinograms and projection images of both [Formula: see text]Tc and [Formula: see text]Lu data. Average simulated and experimental sensitivity ratios of ([Formula: see text]) were seen for emission and scatter windows of [Formula: see text]Tc, and ([Formula: see text]) and ([Formula: see text]) for the 113 and 208 keV emissions of [Formula: see text]Lu, respectively. Conclusions: MC simulations will always be an approximation of a physical system and the level of agreement should be assessed. A validation method is presented to quantify the level of agreement between a simulation model and a physical SPECT system.
Language	English
Publishing date	2023-09-30
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2768912-8
ISSN	2197-7364
ISSN	2197-7364
DOI	10.1186/s40658-023-00581-4
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Article: Leukocytes in glomerular injury.

Holdsworth, Stephen R / Tipping, Peter G

Seminars in immunopathology

2007 Volume 29, Issue 4, Page(s) 355–374

Abstract: Leukocytes of the innate immune system play a central protective role in immune defense to pathogens but may also mediate injurious inflammatory responses resulting in tissue injury. These leukocytes provide the first rapid cellular defense mechanisms ... ...

Abstract	Leukocytes of the innate immune system play a central protective role in immune defense to pathogens but may also mediate injurious inflammatory responses resulting in tissue injury. These leukocytes provide the first rapid cellular defense mechanisms through a limited repertoire of rapid pre-programmed responses, but they are also involved in chronic inflammation and tissue repair. They are directed to sites of pathogen challenge and inflammation by a variety of mechanisms and are activated in response to both exogenous and endogenous stimuli. They do not show the capacity of self-non-self discrimination and memory, which are defining characteristics of the adaptive immune system, although macrophages in particular may show some capacity for differentiation of their effector responses. However, they do play an integral role in adaptive immune responses by their capacity to present antigen, modify T-cell development, and function as effectors of adaptive cell-mediated immunity.
MeSH term(s)	Animals ; Cell Differentiation/immunology ; Chronic Disease ; Humans ; Immunity, Cellular ; Immunity, Innate ; Immunologic Memory ; Inflammation/immunology ; Inflammation/pathology ; Kidney Glomerulus/immunology ; Kidney Glomerulus/injuries ; Kidney Glomerulus/pathology ; Macrophages/immunology ; Macrophages/pathology ; Regeneration/immunology ; Self Tolerance ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology
Language	English
Publishing date	2007-10-16
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-007-0097-9
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Article: Cytokines in glomerulonephritis.

Tipping, Peter G / Holdsworth, Stephen R

Seminars in nephrology

2007 Volume 27, Issue 3, Page(s) 275–285

Abstract: Cytokines play central roles in both innate and adaptive immune responses that lead to renal inflammation. They are involved systemically in cross-talk between antigen-presenting cells, leukocytes, and regulatory cells to initiate and modulate ... ...

Abstract	Cytokines play central roles in both innate and adaptive immune responses that lead to renal inflammation. They are involved systemically in cross-talk between antigen-presenting cells, leukocytes, and regulatory cells to initiate and modulate nephritogenic immunity. Within the kidney, cytokines play a central role in signaling between infiltrating leukocytes and intrinsic renal cells and orchestrate the effector responses that lead to renal damage. Glomerulonephritis (GN) is an important cause of renal inflammation leading to renal failure that results from adaptive responses targeted at the kidney. Animal models of GN have shown that cytokines play critical roles in initiation and modulation of renal inflammatory responses through their ability to modulate the T helper 1/T helper 2 balance of nephritogenic immune responses. Evidence from clinical studies is now confirming the importance of this paradigm in directing the inflammatory mechanisms, histologic patterns, and clinical consequences of human GN. Cytokines also have critical intrarenal effector roles in the development, perpetuation, and resolution of GN. The proinflammatory role of intrarenal cytokine production by leukocytes in GN is well recognized, but, more recently, the role of intrinsic renal cell cytokine production in amplifying renal inflammation has been shown in animal models of GN. Studies showing benefits of specific anticytokine therapies directed at tumor necrosis factor in human GN are now appearing.
MeSH term(s)	Animals ; Cytokines/genetics ; Cytokines/immunology ; Cytokines/metabolism ; Cytokines/physiology ; Glomerulonephritis/immunology ; Glomerulonephritis/pathology ; Humans
Chemical Substances	Cytokines
Language	English
Publishing date	2007-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2007.02.002
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Article: T cells in crescentic glomerulonephritis.

Tipping, Peter G / Holdsworth, Stephen R

Journal of the American Society of Nephrology : JASN

2006 Volume 17, Issue 5, Page(s) 1253–1263

Abstract: Crescent formation in glomerulonephritis (GN) is a manifestation of severe glomerular injury that usually results in a poor clinical outcome. In humans, crescentic GN is frequently associated with evidence of either systemic or organ-specific ... ...

Abstract	Crescent formation in glomerulonephritis (GN) is a manifestation of severe glomerular injury that usually results in a poor clinical outcome. In humans, crescentic GN is frequently associated with evidence of either systemic or organ-specific autoimmunity. T cells play a major role in initiation of adaptive immune responses that lead to crescentic injury. In experimental models of crescentic GN, Th1 predominant immune responses have been shown to promote crescent formation. Perturbation of regulatory T cell function may contribute to development of autoimmune crescentic GN. The presence of T cells and macrophages in crescentic glomeruli, frequently in the absence of humoral mediators of immunity, suggest a dominant effector role for T cells in crescentic GN. The association of cellular immune mediators with local fibrin deposition implicates cell-mediated "delayed-type hypersensitivity-like" mechanisms in crescent formation. Intrinsic renal cells also contribute to T cell-driven effector mechanisms in crescentic GN, via expression of MHC II and co-stimulatory molecules and by production of chemokines and cytokines that amplify leukocyte recruitment and injury.
MeSH term(s)	Animals ; Computer Simulation ; Glomerulonephritis/immunology ; Glomerulonephritis/pathology ; Humans ; Immunologic Factors/immunology ; Lymphocyte Activation/immunology ; Models, Immunological ; T-Lymphocytes/immunology
Chemical Substances	Immunologic Factors
Language	English
Publishing date	2006-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2005091013
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Article ; Online: The cytoplasmic domain of tissue factor restricts physiological albuminuria and pathological proteinuria associated with glomerulonephritis in mice.

Apostolopoulos, Jim / Moussa, Leon / Tipping, Peter G

Nephron. Experimental nephrology

2010 Volume 116, Issue 4, Page(s) e72–83

Abstract: Background/aims: Tissue factor (TF) is a transmembrane protein that is essential for coagulation. TF is expressed on podocytes and its cytoplasmic domain has cell signalling functions in epithelial cells.: Methods: Mice lacking the cytoplasmic domain ...

Abstract	Background/aims: Tissue factor (TF) is a transmembrane protein that is essential for coagulation. TF is expressed on podocytes and its cytoplasmic domain has cell signalling functions in epithelial cells. Methods: Mice lacking the cytoplasmic domain of TF (TF(CT-/-) mice) were used to study its role in physiological albuminuria and pathological proteinuria following induction of glomerulonephritis (GN). Results: Absence of the cytoplasmic domain of TF was associated with increased albuminuria, podocyte effacement, reduced podocyte numbers and increased spontaneous glomerular tumour necrosis factor α(TNFα) production under physiological conditions. In mice developing GN, absence of the cytoplasmic domain of TF resulted in increased proteinuria and enhanced renal TNFα production without altering other parameters of renal inflammation and injury. Studies in TF(CT-/-) chimeric mice (created by bone marrow transplantation) showed increased proteinuria and renal TNFα mRNA in GN was associated with absence of the cytoplasmic domain of TF in the kidney and was independent of the leucocyte phenotype. Conclusion: These studies demonstrate that the cytoplasmic domain of TF contributes to renal albumin retention and its renal expression protects against proteinuria in leucocyte-mediated renal inflammation. Increased glomerular production of TNFα in the absence of cytoplasmic domain of TF may contribute to podocyte injury resulting in albuminuria and proteinuria.
MeSH term(s)	Albuminuria/pathology ; Albuminuria/physiopathology ; Animals ; Cytoplasm/metabolism ; Glomerulonephritis/metabolism ; Glomerulonephritis/physiopathology ; Intracellular Signaling Peptides and Proteins ; Kidney Glomerulus/metabolism ; Membrane Proteins/biosynthesis ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Podocytes/metabolism ; Podocytes/pathology ; Protein Structure, Tertiary/physiology ; Proteinuria/metabolism ; Proteinuria/physiopathology ; Thromboplastin/deficiency ; Thromboplastin/physiology ; Tumor Necrosis Factor-alpha/biosynthesis
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; NPHS2 protein ; Tumor Necrosis Factor-alpha ; nephrin ; Thromboplastin (9035-58-9)
Language	English
Publishing date	2010
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	207121-6
ISSN	1660-2129 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
ISSN (online)	1660-2129 ; 1423-0186 ; 2235-3186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000319320
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