Hepatitis HGV/GBV-C in New Zealand blood donors.
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Biomedical subjects
Publications and source records attributed to G Woodfield.
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We identified the mutations causing factor XIII A subunit deficiency in two families. Two distinct mutations were identified in the S family: the nonsense mutation Tyr 441-->stop in exon 11, inherited through the paternal line, and the missense mutation Asn 60-->Lys in exon 3, inherited through the maternal line. Two members of the J family were heterozygous for the previously described type 3 A subunit. The substitution giving rise to the type 3 variant was found to be Gly 501-->Arg in exon 12. The Asn 60-->Lys and Gly 501-->Arg mutations were constructed in cDNA clones and expressed in yeast (Saccharomyces cerevisiae AH22). Although mRNA could be detected, protein containing the Asn 60-->Lys substitution could not be detected, suggesting extreme instability or susceptibility to proteolysis. A subunits containing the Gly 501-->Arg substitution were expressed and found to be enzymatically active in fresh yeast lysates. This variant has thermal instability and lost activity during storage or purification. Gel filtration studies suggested that the type 3 variant assembled as a dimer, as do normal A subunits. The data suggest that the Gly 501-->Arg (Type 3 variant) would cause severe factor XIII deficiency if inherited in the homozygous form or as a compound heterozygote with another deleterious mutation.
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AIM: To determine class I HLA gene, antigen and haplotype frequencies for New Zealand Maori and Europeans. METHODS: Statistical analysis was performed using accumulated data from Maori (n = 576) and European (n = 1747) parentage studies. RESULTS: HLA class I gene, antigen and haplotype frequencies are as tabulated. Significant statistical differences were shown to exist between New Zealand Maori, New Zealand Europeans and Europeans. Gene frequencies of HLA A1, 3, 9, 11, 19 and HLA B7, 8, 12, 16, 22, and 40 differed significantly between New Zealand Maori and New Zealand European data. Gene frequencies of HLA A1 and B12 differed significantly between New Zealand European and European data. CONCLUSIONS: This HLA frequency data can be used for calculating more reliable indices of paternity or for determining the potential availability of matched organs for transplantation, as well as for anthropological studies. The data may also be useful in forensic investigations.
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Quality assurance has an important contribution to make in the judicious use of scarce resources. Auckland Hospital has established a transfusion committee because there was an escalating usage of blood and blood products which are expensive prescription medicines. A pilot audit of red cell transfusions indicated that 29% of red cell transfusions may have been unnecessary. A wide range of initiatives at Auckland Hospital has reduced blood product usage. Inappropriate use of blood carries an opportunity cost and may subject patients to unnecessary risk of reactions, including potential disease transmission. Strategies which need to be employed by transfusion committees include the introduction of clinical audit, physician education, restrictions on availability, and clinical budgeting. It is recommended that transfusion committees be set up in all major hospitals.
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Six patients on regular haemodialysis in the Auckland renal dialysis unit developed the antibody anti-N. All utilised formaldehyde resterilisation dialyser procedures. Four patients with anti-N underwent renal transplantation unsuccessfully. Histological changes were difficult to interpret and could not be closely correlated with serological findings, although vessel thrombi and renal tissue infarcts were seen in some kidneys. It is recommended that renal patients should be screened at 4 degrees C and room temperature for anti-N and that resterilisation of dialysers be carefully controlled. Where transplantation is to be performed in a patient with anti-N, the organ should be warmed and perfused with warm saline prior to grafting.
The sera from 89 patients from the Eastern Higlands of Papua New Guinea, all with histologically diagnosed liver disease, were tested for Hepatitis B Antigen (HB Ag) and Hepatitis B antibody (HB Ab) and alpha1 fetoprotein (AFP) by a variety of techniques which included radioimmunoassay. In the three main forms of liver disease, viral hepatitis, cirrhosis and hepatoma, HB Ag was found with a higher frequency than in patients with non specific liver disease. The frequency of HB Ab was decreased in cirrhosis and hepatoma. AFP was detected in all hepatoma patients by radioimmunoassay, levels being very high in most subjects. In hepatitis, cirrhosis and non specific liver disease, elevated levels of AFP were again frequently present, but at generally lower levels. It is conlcuded that HB Ag and AFP frequency and levels in liver disease are similar to those reported from other tropical countries. Further study is required to elicit the cellular immunological changes in liver disease.