Population-based epidemiology of human immunodeficiency virus infection in Western Australia. Western Australian AIDS Advisory Committee

A total of 328 cases of infection with human immunodeficiency virus (HIV) in Western Australia in 1983-1987 was studied with respect to demographic factors, the risk profile, the clinical progression of disease, the utilization of inpatient services and trends in incidence over time. The crude incidence rates were 8.8 cases/100,000 person-years in men and 0.4 cases/100,000 person-years in women. Age-specific rates peaked at 25 to 29 years of age in men. The risk of HIV infection was associated with metropolitan residence, low socioeconomic level, and two specific occupational groups. Homosexual and bisexual men constituted 86% of all cases; the incidence rate of HIV infection in such men was approximately 1000-times higher than was the incidence rate by apparent sexual transmission in heterosexual persons. However, the proportion of cases that occurred in women or that apparently was caused by heterosexual sexual transmission increased from zero in 1983-1984 to 7.5% and 5.4%, respectively, in 1987. After two years of follow-up, 71% of preclinical (category-C) patients had developed signs, symptoms or evidence of immune dysfunction, and 12% of those patients with lymphadenopathy or with other early clinical features of disease (category-B) had progressed to the acquired immunodeficiency syndrome (AIDS). At 21 months of follow-up, the survival rate with AIDS was 9%. Patients with AIDS utilized an average of 68.9 short-stay hospital bed-days per person-year, while category-B patients used 11.5 hospital bed-days per person-year. Notifications of HIV infection increased each year from 1983 to 1986, but fell by 22% in 1987. The latter may have been as a result of chance, a screening artefact or a real reduction in the incidence rate.     

Effects of autologous mesothelial cell seeding on prostacyclin production within Dacron arterial prostheses

Canine abdominal aortas have been replaced with Dacron arterial prostheses to assess the effects of mesothelial cell seeding on graft prostacyclin and thromboxane A2 release. At both 2 weeks and 6 weeks after surgery, three seeded and two unseeded control grafts were examined for prostacyclin release. In addition, thromboxane release was assessed in one seeded and one unseeded graft. Sections of aorta and graft were removed and incubated in PBS containing either 10 microM calcium ionophore A23187 or 20 microM arachidonic acid. The incubation mixture was sub-sampled at 5 min intervals over a 20 min period to assess the progressive release of prostacyclin and thromboxane A2 using a radioimmunoassay for 6-keto-prostaglandin F1 alpha and thromboxane B2 respectively. In seeded grafts, 6-keto-prostaglandin F1 alpha release averaged 15 per cent compared with aorta at 2 weeks and 45 per cent compared with aorta at 6 weeks. By contrast, release from unseeded grafts was undetectable at 2 weeks; however, by 6 weeks there was some release amounting to 15 per cent compared with aorta. There was a statistically significant increase in the release of 6-keto-prostaglandin F1 alpha from mesothelial cell seeded grafts at 6 weeks compared with unseeded grafts (P less than 0.01). Thromboxane release from the graft sections was variable and unrelated to whether the grafts had been seeded or not. These preliminary results, showing that grafts seeded with autologous peritoneal mesothelial cells release more prostacyclin than unseeded grafts, further highlight the role of the mesothelial cell as an alternative to the endothelial cell for improving the patency of arterial Dacron prostheses in the early postoperative days.