showed that simple reduction of net positive charge does not reduce TIMP-2 affinity. Because the double mutation K566A/K568A also did not alter TIMP-2 binding, these data do not confirm previously reported chimera studies that indicated the importance of the triple lysine cluster at positions 566/567/568 in TIMP-2 binding. Nonetheless, a subtle role in TIMP-2 interaction for the 566/567/568-lysine triad is indicated from the enhanced reduction in TIMP-2 binding that occurs when mutations here were combined with K617A. Thus, these analyses indicate that the TIMP-2 binding surface lies at the junction of hemopexin modules III and IV on the peripheral rim of the gelatinase A C domain. This location implies that considerable molecular movement of the TIMP-2⅐C domain complex would be needed for the bound TIMP-2 to inhibit in cis the gelatinase A active site.

Vancomycin-induced neutropenia is most likely associated with prolonged vancomycin exposure. Patients receiving vancomycin for longer than 7 days should have WBC count, differential, monitored weekly. Vancomycin should be discontinued if there is a high clinical suspicion of it causing neutropenia, and an alternative agent should be initiated. Prospective case-controlled studies are needed to better characterize this adverse event.

The antimicrobial stewardship programme reduced antimicrobial use in leukaemia patients without affecting inpatient mortality and length of stay.