Publications
347 results found
Mille-Baker B, Rezende SM, Simmonds RE, et al., 2003, Deletion or replacement of the second EGF-hke domain of protein S results in loss of APC cofactor activity, BLOOD, Vol: 101, Pages: 1416-1418, ISSN: 0006-4971
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- Citations: 24
Ryan PJ, Harper RJ, Laffan M, et al., 2002, Site assessment for farm forestry in Australia and its relationship to scale, productivity and sustainability, International Symposium on Sustainability of Forest Soils, Publisher: ELSEVIER, Pages: 133-152, ISSN: 0378-1127
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- Citations: 13
Mumford AD, Laffan M, O'Donnell J, et al., 2002, A Tyr346→Cys substitution in the interdomain acidic region <i>a1</i> of factor VIII in an individual with factor VIII:C assay discrepancy, BRITISH JOURNAL OF HAEMATOLOGY, Vol: 118, Pages: 589-594, ISSN: 0007-1048
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- Citations: 40
O'Donnell J, Boulton FE, Laffan MA, 2002, The relationship between plasma concentration of α<sub>2</sub>-macroglobulin and AB0 blood group, THROMBOSIS AND HAEMOSTASIS, Vol: 88, Pages: 167-168, ISSN: 0340-6245
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- Citations: 5
O'Donnell J, Boulton FE, Manning RA, et al., 2002, Amount of <i>H</i> antigen expressed on circulating von Willebrand factor is modified by ABO blood group genotype and is a major determinant of plasma von Willebrand factor antigen levels, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 22, Pages: 335-341, ISSN: 1079-5642
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- Citations: 115
Rezende SM, Lane DA, Zöller B, et al., 2002, Genetic and phenotypic variability between families with hereditary protein S deficiency, THROMBOSIS AND HAEMOSTASIS, Vol: 87, Pages: 258-265, ISSN: 0340-6245
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- Citations: 30
O'Donnell J, Boulton FE, Manning RA, et al., 2002, Genotype at the <i>Secretor</i> blood group locus is a determinant of plasma von Willebrand factor level, BRITISH JOURNAL OF HAEMATOLOGY, Vol: 116, Pages: 350-356, ISSN: 0007-1048
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- Citations: 40
Bowcock SJ, Rassam SMB, Ward SM, et al., 2002, Thromboembolism in patients on thalidomide for myeloma., Hematology, Vol: 7, Pages: 51-53, ISSN: 1024-5332
Seven cases of thromboembolism were found amongst 23 patients treated with thalidomide for myeloma over a total of 141.5 patient treatment months. Five thromboembolic events were venous (two severe) and two arterial. A historical control of 18 similar patients not given thalidomide had one thromboembolism over 289 months. We found no underlying thrombophilic tendency in the affected patients. We suggest that the thalidomide may predispose to thromboembolism at even lower doses than previously reported (mean dose 150 mg). The two most severe thromboses occurred on 100 mg thalidomide alone, not associated with chemotherapy or glucocorticoids. We raise the possibility that arterial thromboembolism may also occur in association with thalidomide. Some patients continued thalidomide after the event, together with warfarin, with no further thromboembolism.
Laffan MA, 2001, Fibrinogen polymorphisms and disease, EUROPEAN HEART JOURNAL, Vol: 22, Pages: 2224-2226, ISSN: 0195-668X
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- Citations: 5
O'Donnell J, Mumford AD, Manning RA, et al., 2001, Marked elevation of thrombin generation in patients with elevated FVIII:C and venous thromboembolism, BRITISH JOURNAL OF HAEMATOLOGY, Vol: 115, Pages: 687-691, ISSN: 0007-1048
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- Citations: 50
O'Donnell J, Laffan MA, 2001, The relationship between ABO histo-blood group, factor VIII and von Willebrand factor, TRANSFUSION MEDICINE, Vol: 11, Pages: 343-351, ISSN: 0958-7578
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- Citations: 217
Mercuri E, Cowan F, Gupte G, et al., 2001, Prothrombotic disorders and abnormal neurodevelopmental outcome in infants with neonatal cerebral infarction, PEDIATRICS, Vol: 107, Pages: 1400-1404, ISSN: 0031-4005
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- Citations: 116
O'Donnell J, Mille-Baker B, Laffan M, 2001, Human umbilical vein endothelial cells differ from other endothelial cells in failing to express ABO blood group antigens, JOURNAL OF VASCULAR RESEARCH, Vol: 37, Pages: 540-547, ISSN: 1018-1172
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- Citations: 43
O'Donnell J, Laffan M, 2001, Elevated plasma factor VIII levels--a novel risk factor for venous thromboembolism., Clin Lab, Vol: 47, Pages: 1-6, ISSN: 1433-6510
An association between elevated plasma levels of FVIII:C and arterial thrombosis was first described 20 years ago. More recently a growing literature has centered on the potential role for elevated FVIII:C in venous thromboembolic disease. 25% of patients have plasma FVIII:C levels greater than 1500 IU/l six months following venous thrombosis. This increased FVIII:C appears unrelated to any ongoing acute phase reaction, and reflects a true increase in circulating FVIII protein. Furthermore the increase in FVIII:C is sustained in the vast majority of subjects for years following the thrombotic episode. Multivariate analysis of the Leiden thrombophilia study has demonstrated that increased FVIII is an independent risk factor for venous thromboembolism. Individuals with FVIII:C exceeding 1500 IU/l had a six-fold increased risk, compared to those with FVIII:C levels less than 1000 IU/l. Also, prospective follow-up has shown that patients with high FVIII:C levels are at increased risk for episodes of recurrent venous thrombosis. These findings support the theory that increased plasma levels of FVIII:C represent a constitutional prothrombotic tendency. However the mechanism underlying the elevation in FVIII remains unknown.
Poullis M, Manning R, Laffan M, et al., 2000, The antithrombotic effect of aprotinin: Actions mediated via the protease-activated receptor 1, JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, Vol: 120, Pages: 370-378, ISSN: 0022-5223
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- Citations: 84
Mumford AD, O'Donnell J, Gillmore JD, et al., 2000, Bleeding symptoms and coagulation abnormalities in 337 patients with AL-amyloidosis, BRITISH JOURNAL OF HAEMATOLOGY, Vol: 110, Pages: 454-460, ISSN: 0007-1048
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- Citations: 146
O'Donnell J, Mumford AD, Manning RA, et al., 2000, Elevation of FVIII:C in venous thromboembolism is persistent and independent of the acute phase response, THROMBOSIS AND HAEMOSTASIS, Vol: 83, Pages: 10-13, ISSN: 0340-6245
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- Citations: 178
Vakalopoulou S, Mille-Baker B, Mumford A, et al., 1999, Fibrinogen Bβ14 Arg→Cys:: further evidence for a role in thrombosis, BLOOD COAGULATION & FIBRINOLYSIS, Vol: 10, Pages: 403-408, ISSN: 0957-5235
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- Citations: 9
Mansvelt EPG, Laffan M, McVey JH, et al., 1998, Analysis of the <i>F8</i> gene in individuals with high plasma factor VIII:C levels and associated venous thrombosis, THROMBOSIS AND HAEMOSTASIS, Vol: 80, Pages: 561-565, ISSN: 0340-6245
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- Citations: 78
Gorog DA, Rakhit R, Parums D, et al., 1998, Raised factor VIII is associated with coronary thrombotic events, HEART, Vol: 80, Pages: 415-417, ISSN: 1355-6037
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- Citations: 17
Laffan M, Dawson P, Gooding RP, 1997, A comparison between the platelet activating properties of different contrast media used in radiology and MRI, BRITISH JOURNAL OF RADIOLOGY, Vol: 70, Pages: 798-804, ISSN: 0007-1285
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- Citations: 9
Laffan M, Tuddenham E, 1997, Thrombophilia: an expanding group of genetic defects that predispose to thrombosis, MOLECULAR MEDICINE TODAY, Vol: 3, Pages: 303-309, ISSN: 1357-4310
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- Citations: 2
ODonnell J, Tuddenham EGD, Manning R, et al., 1997, High prevalence of elevated factor VIII levels in patients referred for thrombophilia screening: Role of increased synthesis and relationship to the acute phase reaction, THROMBOSIS AND HAEMOSTASIS, Vol: 77, Pages: 825-828, ISSN: 0340-6245
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- Citations: 197
Chen FE, Owen I, Savage D, et al., 1997, Late onset haemolysis and red cell autoimmunisation after allogeneic bone marrow transplant, BONE MARROW TRANSPLANTATION, Vol: 19, Pages: 491-495, ISSN: 0268-3369
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- Citations: 78
ODonnell J, Tuddenham EGD, Manning R, et al., 1997, High Prevalence of Elevated Factor VIII Levels in Patients Referred for Thrombophilia Screening: Role of Increased Synthesis and Relationship to the Acute Phase Reaction, Thrombosis and Haemostasis, Vol: 77, Pages: 0825-0828, ISSN: 0340-6245
<jats:title>Summary</jats:title><jats:p>A recent report from the Leiden Thrombophilia Survey identified high factor VIII activity levels as an independent risk factor for venous thromboembolism in a population survey. As the study measure for factor VIII was a one-stage coagulation assay, and since markers for the acute phase reaction were not assessed, it remained uncertain whether the increase was due to a constitutional increased rate of synthesis, to circulating activated factor VIII, or to an acute phase response.</jats:p><jats:p>We added factor VIII activity assay (FVIII:C), factor VIII antigen (FVIILAg), vWF antigen (vWF:Ag), ABO blood group, fibrinogen and C-reactive protein to our routine thrombophilia screen of patients referred because of unexplained thromboembolism.</jats:p><jats:p>Elevated FVIILC (>1.5 iu/ml) emerged as the single commonest abnormality detected in 25.4% of a group of 260 such patients.</jats:p><jats:p>FVIILC and FVIILAg were highly correlated (p = 0.003), showing that this represented a true increase in FVIII. In 4 of 46 patients this was clearly attributable to an acute phase reaction. Eleven others showed minor elevation of ESR and one of CRP. Neither FVIILC or FVIII:Ag showed significant correlation with fibrinogen, ESR or C-reactive protein by non parametric analysis.</jats:p><jats:p>Although there was an excess of patients with B blood group (known to be associated with FVIILC levels which are -15% higher than those in blood group 0), this could not account for the marked elevation of factor VIII observed in these patients.</jats:p><jats:p>We conclude that factor VIII activity assay should be a routine part of thrombophilia screening. We are investigating the cause of the increased synthesis, initially by means of family studies and linkage analysis with polymorphic markers of the FVIII locus. We postulate that it may be constitutive in some cases
Simmonds RE, Ireland H, Kunz G, et al., 1996, Identification of 19 protein S gene mutations in patients with phenotypic protein S deficiency and thrombosis, BLOOD, Vol: 88, Pages: 4195-4204, ISSN: 0006-4971
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- Citations: 32
Simmonds RE, Ireland H, Kunz G, et al., 1996, Identification of 19 protein S gene mutations in patients with phenotypic protein S deficiency and thrombosis. Protein S Study Group., Blood, Vol: 88, Pages: 4195-4204, ISSN: 0006-4971
Protein S is a protein C-dependent and independent inhibitor of the coagulation cascade. Deficiency of protein S is an established risk factor for venous thromboembolism. We have used a strategy of specific amplification of the coding regions and intron/exon boundaries of the active protein S gene (PROS1) and direct single-strand solid phase sequencing, to seek mutations in 35 individuals with phenotypic protein S deficiency. Nineteen point mutations (16 novel) in 19 probands (or relatives of probands) with venous thromboembolism are reported here. Fifteen of the 19 mutations were expected to be causal and included 10 missense mutations (Lys9Glu, Glu26Ala, Gly54Glu, Cys145Tyr, Cys200Ser, Ser283Pro, Gly340Asp, Cys408Ser, Ser460Pro, and Cys625Arg). Three of the 15 mutations resulted in premature stop codons (delete T 635 producing a stop codon at position 126, Lys368stop and Tyr595stop) and two were at intron/exon boundaries (+1 G to A in intron d and +3 A to C in intron j). Of the remaining four mutations, three were within intronic sequence and one was a silent mutation within the coding region and did not alter amino acid composition. In two of the 10 missense mutations, reduced plasma protein S activity compared with antigen level suggested the presence of variant (type II) protein S.
Ireland H, Thompson E, Lane DA, et al., 1996, Gene mutations in 21 unrelated cases of phenotypic heterozygous protein C deficiency and thrombosis, THROMBOSIS AND HAEMOSTASIS, Vol: 76, Pages: 867-873, ISSN: 0340-6245
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- Citations: 12
Ireland H, Thompson E, Lane DA, 1996, Gene mutations in 21 unrelated cases of phenotypic heterozygous protein C deficiency and thrombosis. Protein C Study Group., Thromb Haemost, Vol: 76, Pages: 867-873, ISSN: 0340-6245
Mutations have been identified in the protein C gene in 21 patients with venous thromboembolism and phenotypic heterozygous protein C deficiency. In 20 probands, single mutations were the only abnormalities identified by sequencing all coding regions, intron exon boundaries and the promoter region back to -1540. In one proband 2 mutations were identified and in another family 2 mutations were identified (but not both in the proband). Of the 23 mutations, 18 resulted in predicted amino acid substitutions, 3 were mutations resulting in stop codons, one was a mutation within a consensus splice sequence and another a 9 base pair insertion within exon 5 (this region within exon 5 is proposed as a deletion/insertion hot spot). A novel polymorphism was also, uniquely, identified in the propeptide region of the molecule (Pro-21Pro; CCT to CCC) in a kindred from Hong Kong. Cosegregation of the protein C gene mutation with protein C deficiency could be determined in 13 families. In a further family, phenotypic protein C deficiency and the genetic mutation cosegregated in only 4/5 members. The first thrombotic incident occurred in the probands between the ages of 11 and 59 years and 12 individuals suffered recurrent thrombosis. Thrombosis occurred in at least one other family member in 9/21 families, but in 2 of these it was inconsistently associated with protein C deficiency. An independent genetic risk factor, factor V Arg506Gln (FV Leiden) was identified in 2 probands (and 3 family members) and in 4 protein C deficient members of a third family but not in the proband. The results suggest that in the majority of probands with thrombosis and phenotypic protein C deficiency, a single protein C gene mutation is associated with thrombosis. However, it is also possible that additional unknown genetic risk factors contribute to the thrombotic risk. An added, acquired, risk factor leads to thrombosis at an early age (< 25 years).
Laffan MA, Manning R, 1996, The influence of factor VIII on measurement of activated protein C resistance, BLOOD COAGULATION & FIBRINOLYSIS, Vol: 7, Pages: 761-765, ISSN: 0957-5235
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- Citations: 68
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