An update of the Canadian Organ Replacement Register (1998).

CORR reports that 21,451 transplants have been performed from 1981-1996. Approximately 78% of these have been kidney transplantations. Survival statistics revealed that progress has been made to improve both patient and graft survival, particularly during the period between 1991-1996. Consequently, the number of patients being followed with a functioning transplant increased to 11,645. There has been a rise in the number of kidney transplants, which is largely attributed to an increase in the number of living donors. Data also revealed that there was increasing acceptance of elderly patients, who were not transplant candidates, into dialysis programs. Furthermore, the percentage of the number of patients alive with functioning kidney transplants to the total number of patients with ESRD increased from 41% in 1981 to 46% in 1996. Non-renal transplant activity has increased in the recent past. Overall, 5-year patient and graft survival was about 70%. This improvement in survival was associated with a reduction in 30-, 60- and 90-day mortality. The organ donation rate has increased slightly from 13.9 donors per million population in 1994 to 14.1 in 1996. The majority of Canadian donors were multi-organ donors, while fewer were kidney, liver, heart or lung-specific donors only. The proportion of female donors has increased. The number of patients waiting for transplants continues to increase. Approximately 3,072 patients are on waiting lists; the majority are for kidney transplants. As the increase in the number of donors does not match the increasing numbers of transplants needed, this suggests that greater efforts are necessary to reduce this difference.

Characterization of an angiosarcoma-inducing mutation in the erbB oncogene.

The erbB oncogenes of two transducing viruses that arose in chicken 5005 have been molecularly characterized. One of these viruses, AEV-5005, caused erythroblastosis. The other, AAV-5005, caused angiosarcoma. Both viruses had identical 5' junctions of viral and host sequences, indicating that both arose from the same proviral insertion. The erbB oncogenes of both viruses encoded transmembrane, kinase and C-terminal domains of the chicken epidermal growth factor receptor. The C-terminal domain of the AEV-5005 erbB was complete, whereas that of AAV-5005 contained a 59 amino acid internal deletion (amino acids 993-1051 of the chicken epidermal growth factor receptor). Oncogenicity tests using retroviral constructs containing the erbB sequences from AEV-5005 and AAV-5005 demonstrated that both erbB genes caused erythroblastosis and that the 59 amino acid deletion conferred the ability to induce angiosarcoma. The 59 amino acid deletion also caused increased levels of erbB autophosphorylation in cells grown in the presence of sodium orthovanadate.

Differences in sequences encoding the carboxyl-terminal domain of the epidermal growth factor receptor correlate with differences in the disease potential of viral erbB genes.

Eleven recently isolated erbB-transducing viruses as well as avian erythroblastosis virus (AEV)-R (ES4) and AEV-H have been characterized for the type of disease they cause, their ability to transform fibroblasts in culture, their ability to cause disease in pedigrees of chicken that differ in susceptibility to erbB-induced erythroblastosis, and the structure of their erbB genes. Differences in each of the biological parameters correlated with differences in erbB sequences encoding the C-terminal domain of the epidermal growth factor receptor (EGFR). Seven viruses were strain restricted in their ability to induce erythroblastosis and did not transform fibroblasts. These seven viruses contained v-erbB genes encoding the complete C terminus of the EGFR. AEV-R and AEV-H were not pedigree restricted in their ability to induce erythroblastosis and could transform fibroblasts. These viruses contain v-erbB genes that lack codons for the immediate C terminus of the EGFR. Three viruses caused angiosarcoma and one caused fibrosarcoma. The angiosarcoma and fibrosarcoma-inducing viruses were not strain restricted and did not cause erythroblastosis. The v-erbB genes of each of these viruses contained extensive internal deletions or 3' truncations in sequences encoding the C-terminal domain of the EGFR.

Induction of angiosarcoma by a c-erbB transducing virus.

Recently, 12 new transductions of c-erbB have been identified in a series of Rous-associated virus type 1-induced erythroleukemias. During the passage of these new transducing viruses it has become apparent that the erythroleukemia in chicken 5005 contained two different c-erbB transducing viruses. One induces erythroblastosis, whereas the second induces angiosarcoma. The angiosarcoma- and erythroblastosis-inducing viruses appear to have had a common ancestor, since tumors induced by each contain a novel, 4.3-kilobase c-erbB-related EcoRI fragment. The angiosarcoma-inducing virus has been named avian angiosarcoma virus and is designated for the chicken in which it originated.

Bronchovascular adjustments after pulmonary embolism.

We determined the time course of bronchial blood flow alterations after pulmonary microembolization. Embolization was induced by injecting 100-micrometers-diam glass beads into the right atrium so as to increase pulmonary arterial pressure from 13.8 +/- 1.8 to 35.7 +/- 2.6 Torr in 14 dogs. The increase in pulmonary vascular resistance averaged threefold after embolization (PE). The bronchial blood flow (Qb) was measured using the reference sample method with the 15 +/- 5-micrometers-diam labeled microspheres injected into the left atrium. Simultaneous blood reference samples were collected at constant rates from a femoral artery and the pulmonary artery. The pulmonary arterial reference sample was used to quantify the contribution of peripheral arteriovenous shunts to the total pulmonary activity, and the femoral arterial reference blood was used to quantify Qb. The Qb was decreased to one-third of its base-line value at 60-min PE (P less than 0.05) but not at 5 min PE. Qb was increased 300% at 2 wk PE. The decrease in flow was associated with an increased bronchovascular resistance, whereas the increase in flow was associated with a decreased resistance. The decrease in Qb at 60 min PE may be due to release of peripheral vasoconstrictor substances associated with pulmonary embolism. The finding that bronchial perfusion increased gradually after pulmonary vascular obstruction suggests that increased flow is due to neovascularization.