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270 results on '"Gallagher, J.A."'

6. Increased prevalence of Parkinson's disease in alkaptonuria

Author

Ranganath, L., Khedr, M., Milan, A.M., Davison, A.S., Norman, B.P., Janssen, M.C.H., Lock, E., Bou-Gharios, G., Gallagher, J.A., Ranganath, L., Khedr, M., Milan, A.M., Davison, A.S., Norman, B.P., Janssen, M.C.H., Lock, E., Bou-Gharios, G., and Gallagher, J.A.

Abstract

Contains fulltext : 297410.pdf (Publisher’s version ) (Open Access), Amongst a cohort of 88 alkaptonuria (AKU) patients attending the United Kingdom National Alkaptonuria Centre (NAC), four unrelated patients had co-existing Parkinson's disease (PD). Two of the NAC patients developed PD before receiving nitisinone (NIT) while the other two developed overt PD during NIT therapy. NIT lowers redox-active homogentisic acid (HGA) and profoundly increases tyrosine (TYR). A further unpublished case of a Dutch patient with AKU and PD on deep brain stimulation is included in this report. A Pubmed search revealed a further five AKU patients with PD, all without NIT usage. The prevalence of PD in AKU in the NAC appears to be nearly 20-times higher than in the non-AKU population (p < 0.001) even when adjusted for age. We propose that life-long exposure to redox-active HGA may account for the higher prevalence of PD in AKU. Furthermore, the appearance of PD in AKU patients during NIT therapy may be due to unmasking dopamine deficiency in susceptible individuals, as a result of the tyrosinaemia during NIT therapy inhibiting the rate-limiting brain tyrosine hydroxylase.

Published
2023

11. Characterization of changes in the tyrosine pathway by 24-h profiling during nitisinone treatment in alkaptonuria

Author

Ranganath, L.R., primary, Milan, A.M., additional, Hughes, A.T., additional, Davison, A.S., additional, Khedr, M., additional, Norman, B.P., additional, Bou-Gharios, G., additional, Gallagher, J.A., additional, Gornall, M., additional, Jackson, R., additional, Imrich, R., additional, Rovensky, J., additional, Rudebeck, M., additional, and Olsson, B., additional

Published
2022
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12. “Lessons from Rare Forms of Osteoarthritis”

Author

Shepherd, R.F., Kerns, J.G., Ranganath, L.R., Gallagher, J.A., Taylor, A.M., Shepherd, R.F., Kerns, J.G., Ranganath, L.R., Gallagher, J.A., and Taylor, A.M.

Abstract

Osteoarthritis (OA) is one of the most prevalent conditions in the world, particularly in the developed world with a significant increase in cases and their predicted impact as we move through the twenty-first century and this will be exacerbated by the covid pandemic. The degeneration of cartilage and bone as part of this condition is becoming better understood but there are still significant challenges in painting a complete picture to recognise all aspects of the condition and what treatment(s) are most appropriate in individual causes. OA encompasses many different types and this causes some of the challenges in fully understanding the condition. There have been examples through history where much has been learnt about common disease(s) from the study of rare or extreme phenotypes, particularly where Mendelian disorders are involved. The often early onset of symptoms combined with the rapid and aggressive pathogenesis of these diseases and their predictable outcomes give an often-under-explored resource. It is these “rarer forms of disease” that William Harvey referred to that offer novel insights into more common conditions through their more extreme presentations. In the case of OA, GWAS analyses demonstrate the multiple genes that are implicated in OA in the general population. In some of these rarer forms, single defective genes are responsible. The extreme phenotypes seen in conditions such as Camptodactyly Arthropathy-Coxa Vara-pericarditis Syndrome, Chondrodysplasias and Alkaptonuria all present potential opportunities for greater understanding of disease pathogenesis, novel therapeutic interventions and diagnostic imaging. This review examines some of the rarer presenting forms of OA and linked conditions, some of the novel discoveries made whilst studying them, and findings on imaging and treatment strategies. © 2021, The Author(s).

Published
2021

14. Caveolin-1 and caveolin-3 regulate [Ca.sup.2+] homeostasis of single smooth muscle cells from rat cerebral resistance arteries

Author

Kamishima, T., Burdyga, T., Gallagher, J.A., and Quayle, J.M.

Subjects
Muscle cells -- Research, Smooth muscle -- Research, Cellular control mechanisms -- Research, Cerebral circulation -- Research, Cerebral arteries -- Physiological aspects, Cerebral arteries -- Research, Cell research, Biological sciences
Abstract

The role of caveolins, signature proteins of caveolae, in arterial [Ca.sup.2+] regulation is unknown. We investigated modulation of [Ca.sup.2+] homeostasis by caveolin-1 and caveolin-3 using smooth muscle cells from rat cerebral resistance arteries. Membrane current and [Ca.sup.2+] transients were simultaneously measured with voltage-clamped single cells. Membrane depolarization triggered [Ca.sup.2+] current and increased intracellular [Ca.sup.2+] concentration ([[Ca.sup.2+]].sub.i]). After repolarization, elevated [[Ca.sup.2+]].sub.i] returned to the resting level. [Ca.sup.2+] removal rate was determined from the declining phase of the [Ca.sup.2+] transient. Application of caveolin-1 antibody or caveolin-1 scaffolding domain peptide, corresponding to amino acid residues 82-101 of caveolin-1, significantly slowed [Ca.sup.2+] removal rate at a measured [[Ca.sup.2+]].sub.i] of 250 nM, with little effect at a measured [[Ca.sup.2+]].sub.i] of 600 nM. Application of caveolin-3 antibody or caveolin-3 scaffolding domain peptide, corresponding to amino acid residues 55-74 of caveolin-3, also significantly slowed [Ca.sup.2+] removal rate at a measured [[Ca.sup.2+]].sub.i] of 250 nM, with little effect at a measured [[[Ca.sup.2+]].sub.i] of 600 nM. Likewise, application of calmodulin inhibitory peptide, autocamtide-2-related inhibitory peptide, and cyclosporine A, inhibitors for calmodulin, [Ca.sup.2+]/calmodulin-dependent protein kinase II, and calcineurin, also significantly inhibited [Ca.sup.2+] removal rate at a measured [[Ca.sup.2+]].sub.i] of 250 nM but not at 600 nM. Application of cyclopiazonic acid, a sarcoplasmic reticulum [Ca.sup.2+] ATPase inhibitor, also significantly inhibited [Ca.sup.2+] removal rate at a measured [[Ca.sup.2+]].sub.i] of 250 nM but not at 600 nM. Our results suggest that caveolin-1 and caveolin-3 are important in [Ca.sup.2+] removal of resistance artery smooth muscle cells. caveolin-1 scaffolding domain peptide; caveolin-3 scaffolding domain peptide; calmodulin; calcium/calmodulin-dependent protein kinase II; calcineurin doi:10.1152/ajpheart.00669.2006

Published
2007

15. Alkaptonuria

Author

Gallagher, J.A., primary, Ranganath, L.R., additional, and Zatkova, A., additional

Published
2013
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21. Starch hydrolytic enzyme activities following defoliation of white clover

Author

Gallagher, J.A., Volenec, J.J., Turner, L.B., and Pollock, C.J.

Subjects
Starch -- Research, Enzyme activation -- Research, Defoliation -- Research, Clover -- Research, Agricultural industry, Business, Research
Abstract

White clover (Trifolium repens L.) is an important legume in grassland ecosystems. Its persistence in mixed grass-clover swards, however, is dependent on utilization of stored carbohydrates during overwintering and subsequent spring regrowth. Reserve carbohydrate is stored as starch in stolons. Our objective was to determine how activities of starch hydrolytic enzymes change during defoliation-induced starch mobilization in clover stolons. Starch degradation was induced by defoliating clonally propagated plants maintained in a controlled environment. Defoliation resulted in rapid, extensive starch remobilization from older stolon tissues, and prevented starch accumulation in young, developing stolon tissues. Amylase activities of stolon tissue were determined immediately, 1, 2, 4, 8, and 12 d post-defoliation. Total amylolytic activity decreased following defoliation. Of the starch hydrolytic enzyme activities determined, only the activity of [Alpha]-amylase increased as a consequence of defoliation (two-fold, with respect to the control). Β-amylase, which constituted the greatest proportion of total amylolytic activity, decreased two- to three-fold in stolons of defoliated plants, but increased six-fold in young stolon tissue, and almost two-fold in old stolon tissue. The increase in enzyme activity correlated with starch deposition in control plants. Starch phosphorylase activity also decreased as a result of defoliation, while activity of [Alpha]-glucosidase changed little following the defoliation treatment. Our results suggest starch degradation in Stolons (If white clover is regulated by [Alpha]-amylase activity., White clover is a perennial forage legume that grows under a wide range of climatic conditions. It plays an increasingly important role in managed grasslands due to its high nutritional [...]

Published
1997

29. Data on items of AKUSSI in Alkaptonuria collected over three years from the United Kingdom National Alkaptonuria Centre and the impact of nitisinone

Author

Griffin, R., primary, Psarelli, E.E., additional, Cox, T.F., additional, Khedr, M., additional, Milan, A.M., additional, Davison, A.S., additional, Hughes, A.T., additional, Usher, J.L., additional, Taylor, S., additional, Loftus, N., additional, Daroszewska, A., additional, West, E., additional, Jones, A., additional, Briggs, M., additional, Fisher, M., additional, McCormick, M., additional, Judd, S., additional, Vinjamuri, S., additional, Sireau, N., additional, Dillon, J.P., additional, Devine, J.M., additional, Hughes, G., additional, Harrold, J., additional, Barton, G.J., additional, Jarvis, J.C., additional, Gallagher, J.A., additional, and Ranganath, L.R., additional

Published
2018
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30. Nitisinone arrests ochronosis and decreases rate of progression of Alkaptonuria: Evaluation of the effect of nitisinone in the United Kingdom National Alkaptonuria Centre

Author

Ranganath, L.R., primary, Khedr, M., additional, Milan, A.M., additional, Davison, A.S., additional, Hughes, A.T., additional, Usher, J.L., additional, Taylor, S., additional, Loftus, N., additional, Daroszewska, A., additional, West, E., additional, Jones, A., additional, Briggs, M., additional, Fisher, M., additional, McCormick, M., additional, Judd, S., additional, Vinjamuri, S., additional, Griffin, R., additional, Psarelli, E.E., additional, Cox, T.F., additional, Sireau, N., additional, Dillon, J.P., additional, Devine, J.M., additional, Hughes, G., additional, Harrold, J., additional, Barton, G.J., additional, Jarvis, J.C., additional, and Gallagher, J.A., additional

Published
2018
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31. Clinical and biochemical assessment of depressive symptoms in patients with Alkaptonuria before and after two years of treatment with nitisinone

Author

Davison, A.S., primary, Harrold, J.A., additional, Hughes, G., additional, Norman, B.P., additional, Devine, J., additional, Usher, J., additional, Hughes, A.T., additional, Khedr, M., additional, Gallagher, J.A., additional, Milan, A.M., additional, J.C.G., Halford, additional, and Ranganath, L.R., additional

Published
2018
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