A Williams

Publications (6)13.1 Total impact

• Article: Antimicrobial resistance changes in enteric Escherichia coli of horses during hospitalisation: Resistance profiling of isolates.

  A Williams, R M Christley, S A McKane, V L H Roberts, P D Clegg, N J Williams
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  ABSTRACT: The aim of this study was to determine whether hospitalisation of horses leads to increased antimicrobial resistance in equine faecal Escherichia coli isolates. E. coli were cultured from faecal samples of horses on admission and after 7days of hospitalisation; antimicrobial susceptibility was determined for eight antimicrobial agents. Resistance profiles of E. coli isolates were grouped into clusters, which were analysed to determine resistance patterns. Resistance to 7/8 antimicrobial agents and multi-drug resistance (MDR; resistance to ⩾3 antimicrobial classes) were significantly higher after 7days of hospitalisation. Forty-eight resistance profiles were identified; 15/48 were present on day 0 only, 16/48 on day 7 only and 17/48 at both times of sampling. There was a significant association between day 7 profiles and resistance detected to an increased number of antimicrobial agents. Hospitalisation of horses for 7days resulted in alterations in equine faecal E. coli antimicrobial resistance profiles.
  The Veterinary Journal 09/2012; · 2.24 Impact Factor
• Article: Suspected primary lactose intolerance in neonatal foals

  V. L. H. Roberts, D. C. Knottenbelt, A. Williams, S. A. McKane
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  ABSTRACT: The intestine of neonatal mammals must be able to secrete lactase enzyme to hydrolyse lactose in its mother's milk. Failure to secrete lactase results in failure to digest lactose. This results in osmotic diarrhoea, weight loss, failure to thrive, lethargy, colic and abdominal distension. Lactose intolerance may occur secondarily to intestinal bacterial infection. Primary lactose intolerance is recognised in human infants. Here we report 2 cases of suspected primary lactose intolerance in foals. The foals responded well to oral administration of exogenous lactase enzyme.
  Equine Veterinary Education. 04/2008; 20(5):249 - 251.
• Article: Systemic lupus erythematosus with C1q deficiency

  N.M. Stone, A. Williams, J.D. Wilkinson, G. Bird
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  ABSTRACT: We report a case of systemic lupus erythematosus associated with C1q deficiency. Our patient presented at the age of 6 years with cutaneous lupus. She later developed Raynaud’s phenomenon, non-scarring alopecia, oral ulceration and grand mal seizures due to cerebral vasculitis. Complement C3 and C4 levels were consistently normal during flares of her lupus and haemolytic activity of her complement was absent, suggesting a deficiency of an early component of the complement cascade. No C1q could be detected.
  British Journal of Dermatology 02/2000; 142(3):521 - 524. · 3.67 Impact Factor
• Article: An essential role for platelet-derived growth factor in neointima formation in human saphenous vein in vitro.

  S J George, A Williams, A C Newby
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  ABSTRACT: The role of platelet-derived growth factor (PDGF), a potent vascular smooth muscle cells (SMC) mitogen and chemoattractant, was investigated during neointima formation in human saphenous vein organ culture. PDGFA and B messenger ribonucleic acid (mRNA) expression was detected by RNase protection assay and in situ hybridisation and PDGF protein by immunocytochemistry. The expression of PDGFA and B mRNA was low in veins before culture while PDGF protein was detected in all cell types. A neointima consisting of densely packed SMC developed after 14 days of culture. The dense packing and high expression of PDGFA and B mRNA in neointimal SMC led to higher PDGF protein concentrations in the neointima, the role of which was examined by culturing with neutralising anti-(human PDGF) antibodies. The anti-PDGF antibodies significantly reduced neointimal thickness by approximately 66% and the number of neointimal cells by approximately 50%, without affecting neointimal or medial proliferation indices or cell viability. These results suggest that PDGF played an essential role in SMC migration into the neointima in human saphenous vein.
  Atherosclerosis 03/1996; 120(1-2):227-40. · 3.79 Impact Factor
• Article: Time-course of medial and intimal thickening in pig venous arterial grafts: relationship to endothelial injury and cholesterol accumulation.

  G D Angelini, A J Bryan, H M Williams, A A Soyombo, A Williams, J Tovey, A C Newby
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  ABSTRACT: With use of an established model of pig saphenous vein grafts in the carotid artery, the time-course of the following changes was related: (1) medial and intimal size by morphometry of transverse sections, (2) cell number by deoxyribonucleic acid concentration, (3) cell density by deoxyribonucleic acid concentration per milligram wet weight and by counting nuclei in transverse sections, (4) endothelial morphology by scanning electron microscopy, and (5) cholesterol concentration. In the first week after grafting, medial and intimal thickening occurred associated with an increase in cell number. Between 1 and 4 weeks after grafting, further rapid medial and intimal thickening occurred with no further increase in cell number but with a reduction in cell density, which suggested that cell migration, hypertrophy, and the laying down of extracellular matrix were responsible. Between 4 and 39 weeks after grafting, a slower increase in medial and intimal size occurred, associated with a parallel increase in cell number and no further change in cell density. The endothelium of grafts showed only localized abnormalities, including loss of cells and leukocyte adhesion, either 1 or 4 weeks after grafting. Cholesterol concentration was slightly elevated 1 week after grafting but returned to values similar to those in vein by 4 weeks after grafting. Distention to 600 mm Hg during surgical preparation of vein for grafting resulted in lower graft patency after either 1 or 4 weeks and caused significant medial and endothelial injury. Distention did not, however, affect changes in medial or intimal size, deoxyribonucleic acid, or cholesterol concentration caused by grafting. We conclude that three processes contribute to medial and intimal thickening, namely: (1) an initial phase of rapid smooth muscle cell proliferation, (2) smooth muscle cell migration, hypertrophy, and synthesis of extracellular matrix, and (3) a late phase of slower smooth muscle cell proliferation. The incomplete late suppression of smooth muscle cell proliferation occurs despite regeneration of a morphologically intact endothelium and in the absence of progressive cholesterol accumulation.
  Journal of Thoracic and Cardiovascular Surgery 07/1992; 103(6):1093-103. · 3.41 Impact Factor
• Article: Neointimal fibrosis in vascular pathologies: role of growth factors and metalloproteinases in vascular smooth muscle proliferation.

  A C Newby, R P Fabunmi, S J George, K M Southgate, A P Banning, V J Thurston, A Williams
  Experimental nephrology 3(2):108-13.