Publications
562 results found
David AL, Themis M, Cook T, et al., 2001, Fetal gene therapy, Ultrasound Rev Obstet Gynecol, Vol: 1, Pages: 14-27, ISSN: 1472-2240
Cook HT, 2001, Complement deficiencies, lupus and apoptosis., Adv Nephrol Necker Hosp, Vol: 31, Pages: 29-41, ISSN: 0084-5957
Salama AD, Delikouras A, Pusey CD, et al., 2001, Transplant accommodation in highly sensitized patients: a potential role for Bcl-xL and alloantibody, Am J Transplant, Vol: 1, Pages: 260-269, ISSN: 1600-6135
Coutelle C, Themis M, Schneider H, et al., 2001, Fetal somatic gene therapy - A preventive approach to the treatment of genetic disease: The case for, STEM CELLS FORM CORD BLOOD, IN UTERO STEM CELL DEVELOPMENT, AND TRANSPLANTATION-INCLUSIVE GENE THERAPY, Vol: 33, Pages: 99-114, ISSN: 0947-6075
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- Citations: 3
Cook HT, Pusey CD, 2001, Pathology of vascular disease, Pages: 3-21, ISBN: 9780849313356
Coutelle C, Themis M, Schneider H, et al., 2001, Fetal somatic gene therapy - a preventive approach to the treatment of genetic disease: the case for, Pages: 99-114, ISBN: 9783540677017
Dupont PJ, Lightstone L, Clutterbuck EJ, et al., 2000, Lesson of the week - Cholesterol emboli syndrome, BMJ-BRITISH MEDICAL JOURNAL, Vol: 321, Pages: 1065-1067, ISSN: 1756-1833
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- Citations: 20
Taylor PR, Carugati A, Fadok VA, et al., 2000, A hierarchical role for classical pathway complement proteins in the clearance of apoptotic cells in vivo, Journal of Experimental Medicine, Vol: 192, Pages: 359-366, ISSN: 1540-9538
The strongest susceptibility genes for the development of systemic lupus erythematosus (SLE) in humans are null mutants of classical pathway complement proteins. There is a hierarchy of disease susceptibility and severity according to the position of the missing protein in the activation pathway, with the severest disease associated with C1q deficiency. Here we demonstrate, using novel in vivo models of apoptotic cell clearance during sterile peritonitis, a similar hierarchical role for classical pathway complement proteins in vivo in the clearance of apoptotic cells by macrophages. Our results constitute the first demonstration of an impairment in the phagocytosis of apoptotic cells by macrophages in vivo in a mammalian system. Apoptotic cells are thought to be a major source of the autoantigens of SLE, and impairment of their removal by complement may explain the link between hereditary complement deficiency and the development of SLE.
Ehrenstein MR, Cook HT, Neuberger MS, 2000, Deficiency in serum immunoglobulin (Ig)M predisposes to development of IgG autoantibodies, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 191, Pages: 1253-1257, ISSN: 0022-1007
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- Citations: 199
Wangoo A, Brown IN, Marshall BG, et al., 2000, Bacille Calmette-Guerin (BCG)-associated inflammation and fibrosis:: modulation by recombinant BCG expressing interferon-gamma (IFN-γ), CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 119, Pages: 92-98, ISSN: 0009-9104
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- Citations: 39
Lord GM, Tagore R, Cook T, et al., 1999, Nephropathy caused by Chinese herbs in the Uh, LANCET, Vol: 354, Pages: 481-482, ISSN: 0140-6736
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- Citations: 192
Tam FWK, Smith J, Morel D, et al., 1999, Development of scarring and renal failure in a rat model of crescentic glomerulonephritis, NEPHROLOGY DIALYSIS TRANSPLANTATION, Vol: 14, Pages: 1658-1666, ISSN: 0931-0509
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- Citations: 61
Clarke HC, Cook HT, Hendry BM, 1999, Gene therapy for renal fibroblasts, NEPHROLOGY DIALYSIS TRANSPLANTATION, Vol: 14, Pages: 1615-1617, ISSN: 0931-0509
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- Citations: 7
Themis M, Schneider H, Kiserud T, et al., 1999, Successful expression of β-galactosidase and factor IX transgenes in fetal and neonatal sheep after ultrasound-guided percutaneous adenovirus vector administration into the umbilical vein, GENE THERAPY, Vol: 6, Pages: 1239-1248, ISSN: 0969-7128
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- Citations: 59
Bickerstaff MCM, Botto M, Hutchinson WL, et al., 1999, Serum amyloid P component controls chromatin degradation and prevents antinuclear autoimmunity, NATURE MEDICINE, Vol: 5, Pages: 694-697, ISSN: 1078-8956
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- Citations: 401
Mitchell DA, Taylor PR, Cook HT, et al., 1999, Cutting edge: C1q protects against the development of glomerulonephritis independently of C3 activation, JOURNAL OF IMMUNOLOGY, Vol: 162, Pages: 5676-5679, ISSN: 0022-1767
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- Citations: 75
Allen AR, McHale J, Smith J, et al., 1999, Endothelial expression of VCAM-1 in experimental crescentic nephritis and effect of antibodies to very late antigen-4 or VCAM-1 on glomerular injury, JOURNAL OF IMMUNOLOGY, Vol: 162, Pages: 5519-5527, ISSN: 0022-1767
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- Citations: 39
Cook HT, Singh SJ, Wembridge DE, et al., 1999, Interleukin-4 ameliorates crescentic glomerulonephritis in Wistar Kyoto rats, KIDNEY INTERNATIONAL, Vol: 55, Pages: 1319-1326, ISSN: 0085-2538
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- Citations: 41
Mosley K, Waddington SN, Ebrahim H, et al., 1999, Inducible nitric oxide synthase induction in Thy 1 glomerulonephritis is complement and reactive oxygen species dependent, EXPERIMENTAL NEPHROLOGY, Vol: 7, Pages: 26-34, ISSN: 1018-7782
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- Citations: 28
Schneider H, Adebakin S, Themis M, et al., 1999, Therapeutic plasma concentrations of human factor IX in mice after gene delivery into the amniotic cavity: A model for the prenatal treatment of haemophilia B, JOURNAL OF GENE MEDICINE, Vol: 1, Pages: 424-432, ISSN: 1099-498X
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- Citations: 34
Waddington SN, Mosley K, Cook HT, et al., 1998, Arginase AI Is upregulated in acute immune complex-induced inflammation, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol: 247, Pages: 84-87, ISSN: 0006-291X
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- Citations: 35
Botto M, Dell'Agnola C, Bygrave AE, et al., 1998, Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies, NATURE GENETICS, Vol: 19, Pages: 56-59, ISSN: 1061-4036
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- Citations: 1165
Robson MG, Cook HT, Botto M, et al., 1998, Delayed resolution of inflammation in heterologous nephrotoxic nephritis in Clq deficient mice, MOLECULAR IMMUNOLOGY, Vol: 35, Pages: 343-343, ISSN: 0161-5890
Cattell V, Cook HT, Ebrahim HB, et al., 1998, Anti-GBM glomerulonephritis in mice lacking nitric oxide synthase type 2, KIDNEY INTERNATIONAL, Vol: 53, Pages: 932-936, ISSN: 0085-2538
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- Citations: 32
Cattell V, Cook HT, Ebrahim H, et al., 1998, Anti-GBM glomerulonephritis in mice lacking nitric oxide synthase type 2 Rapid Communication, Kidney International, Vol: 53, Pages: 932-936, ISSN: 0085-2538
Waddington SN, Tam FWK, Cook HT, et al., 1998, Arginase activity is modulated by IL-4 and HOArg in nephritic glomeruli and mesangial cells, AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, Vol: 274, Pages: F473-F480, ISSN: 1931-857X
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- Citations: 40
Mosley K, Wembridge DE, Cattell V, et al., 1998, Heme oxygenase is induced in nephrotoxic nephritis and hemin, a stimulator of heme oxygenase synthesis, ameliorates disease, KIDNEY INTERNATIONAL, Vol: 53, Pages: 672-678, ISSN: 0085-2538
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- Citations: 84
Powles AV, Hardman CM, Porter WM, et al., 1998, Renal function after 10 years' treatment with cyclosporin for psoriasis., Br J Dermatol, Vol: 138, Pages: 443-449, ISSN: 0007-0963
Renal function was assessed by measuring serum creatinine and glomerular filtration rate (GFR) in two groups of patients with chronic plaque psoriasis who had been treated with cyclosporin A (CyA), average dose 2.8 mg/kg per day (range 1-5 mg/kg per day). Group I was our original cohort of nine patients, seven of whom had received CyA for an average period of 10 years (range 9.5-11 years). These seven patients showed a persistent increase in serum creatinine > 30% from baseline measurement and four of the seven had persistent increases > 50%. The GFR, which was first measured after 2.5 years of treatment, showed at 10 years a decrease of > 30% in two patients and of > 50% in one patient. Three of the seven showed stable renal function while two had repeat renal biopsy because of deteriorating renal function and histology showed further evidence of CyA nephrotoxicity compared with that after 5 years' treatment. Two of the nine patients in group I had discontinued CyA 5 years previously after 5 years of treatment because of CyA nephrotoxicity on renal biopsy and impaired renal function. This impairment of renal function showed improvement during the 5 years of follow-up, implying reversibility of CyA nephrotoxicity. The second group of 20 patients had received CyA for an average duration of 6 years (range 5-8 years). Nine of the 20 patients showed persistent increases in serum creatinine of > 30% from baseline and five showed persistent increases of > 50%. The GFR showed a persistent decrease of > 30% in seven patients and of > 50% in two patients. This study has shown that nephrotoxicity is associated with long-term treatment with CyA. However, there is patient variation as to when nephrotoxicity commences and its speed of progression. On discontinuing CyA the impairment of renal function improves with time. Providing renal function is monitored with GFR and renal biopsy in addition to serum creatinine then long-term (5-10 years) CyA treatment
Waddington SN, Tam FWK, Cook HT, et al., 1998, Arginase activity is modulated by IL-4 and HOArg in nephritic glomeruli and mesangial cells, American Journal of Physiology - Renal Physiology, Vol: 274, ISSN: 1931-857X
Arginase shares a common substrate, L-arginine, with nitric oxide synthase (NOS). Both enzymes are active at inflammatory sites. To understand regulation of arginase and its relationship to nitric oxide (NO) production, we studied effects of N(G)-hydroxy-L-arginine (HOArg) and interleukin-4 (IL- 4) on urea and NO2/- synthesis by glomeruli during rat immune glomerulonephritis and compared these with macrophages and glomerular mesangial cells (MC). In nephritic glomeruli, elicited macrophages, and MC stimulated with IL-1 and adenosine 3',5'-cyclic monophosphate agonists, increased arginase and induced NOS activity was found. Urea production was inhibited by HOArg and increased by IL-4. NO inhibition [N(G)-monomethyl-L- arginine (L-NMMA)] increased arginase activity in nephritic glomeruli and macrophages but not MC. NO2/- synthesis was inhibited by L-NMMA and IL-4. It was increased with HOArg under conditions of NO inhibition. In contrast, in normal glomeruli and basal MC, where there was no induced NO synthesis, IL-4 had no effect on arginase activity, whereas HOArg consistently reduced it in glomeruli only. Type II arginase (Arg II) mRNA was detected in normal glomeruli; nephritic glomeruli expressed both Arg I and Arg II mRNAs. This is the first demonstration of arginase modulation in glomeruli and MC and of the expression of arginase isoforms in glomeruli. The differential responses to two endogenous compounds generated by inflammation suggest this may be part of coordinated regulation of arginase and inducible NOS in immune injury, whereby arginase is inhibited during high-output NO production and stimulated with NO suppression. This, together with control of arginase and NOS isoforms, may be important in controlling the balance of inflammatory and repair mechanisms.
Taylor GM, Cook HT, 1998, A practical protocol for the demonstration of NOS using in-situ hybridization., Methods Mol Biol, Vol: 100, Pages: 191-204, ISSN: 1064-3745
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