Client acceptability of the use of computers in a sexual health clinic

Computers in sexual health medicine largely remain provider-centred for use in client care, data collection, administration and education. As a formative study for further work we undertook a cross-sectional survey of 679 consecutive new clients attending Melbourne Sexual Health clinic (MSHC) between 9 September 2002 and 15 October 2002 to establish client familiarity and experience with computers and acceptance of computer use in the clinic. A response rate of 616/679 (91%) was achieved. Important findings were: 1. 491/612 (80%) participants reported experience with a personal computer. 2. The majority 488/609 (80%) of clients expected computer technologies to be used in the clinic. 3. The proportion of clients not willing to supply their registration, general health or sexual behaviour details using a computer was 9%, 7% and 21%, respectively. 4. Clients assessed as being at higher risk of acquiring a sexually transmitted infection were no more reluctant than others to provide their details using a computer-assisted self-interview.     

Subepidermal blistering induced by human autoantibodies to BP180 requires innate immune players in a humanized bullous pemphigoid mouse model

Bullous pemphigoid (BP) is a cutaneous autoimmune inflammatory disease associated with subepidermal blistering and autoantibodies against BP180, a transmembrane collagen and major component of the hemidesmosome. Numerous inflammatory cells infiltrate the upper dermis in BP. IgG autoantibodies in BP fix complement and target multiple BP180 epitopes that are highly clustered within a non-collagen linker domain, termed NC16A. Anti-BP180 antibodies induce BP in mice. In this study, we generated a humanized mouse strain, in which the murine BP180NC14A is replaced with the homologous human BP180NC16A epitope cluster region. We show that the humanized NC16A (NC16A+/+) mice injected with anti-BP180NC16A autoantibodies develop BP-like subepidermal blisters. The F(ab')(2) fragments of pathogenic IgG fail to activate the complement cascade and are no longer pathogenic. The NC16A+/+ mice pretreated with mast cell activation blocker or depleted of complement or neutrophils become resistant to BP. These findings suggest that the humoral response in BP critically depends on innate immune system players.