Impact of rotavirus vaccination in Australian children below 5 years of age: a database study.

This study was conducted to assess the impact of administration of two-dose rotavirus (RV) vaccine (RIX4414; GlaxoSmithKline Vaccines) among children aged less than 5 y in three states/territories of Australia. Aggregated and de-identified data on rotavirus gastroenteritis (RVGE) and all-cause gastroenteritis (AGE) from July 1998-June 2009 were obtained from the Australian Institute of Health and Welfare database. The baseline incidence (July 1998-June 2006) of RVGE hospitalizations before RV vaccine introduction in New South Wales (NSW), the Australian Capital Territory (ACT) and the Northern Territory (NT) were 33.75, 42.93 and 288.67 per 10,000 child-years, respectively among children aged 0-11 mo. Following RV vaccine introduction in NSW, the ACT and the NT, incidence of RVGE hospitalizations reduced to 13.06, 17.35 and 47.52 per 10,000 child-years, respectively, during July 2007-June 2008 and 3.87, 8.40 and 122.79 per 10,000 child-years, respectively, during July 2008-June 2009 among children aged 0-11 mo. Reductions in RVGE and AGE were also observed in all children below 5 y of age in NSW and the ACT. Overall reduction in hospitalizations due to RVGE and AGE was observed following RV vaccine introduction into the NIP in Australia.

Latrunculin B or ATP depletion induces cofilin-dependent translocation of actin into nuclei of mast cells.

Increasing cellular G-actin, using latrunculin B, in either intact or permeabilized rat peritoneal mast cells, caused translocation of both actin and an actin regulatory protein, cofilin, into the nuclei. The effect was not associated with an increase in the proportion of apoptotic cells. The major part of the nuclear actin was not stained by rhodamine-phalloidin but could be visualized with an actin antibody, indicating its monomeric or a conformationally distinct state, e.g. cofilin-decorated filaments. Introduction of anti-cofilin into permeabilized cells inhibited nuclear actin accumulation, implying that an active, cofilin-dependent, import exists in this system. Nuclear actin was localized outside the ethidium bromide-stained region, in the extrachromosomal nuclear domain. In permeabilized cells, the appearance of nuclear actin and cofilin was not significantly affected by increasing [Ca(2+)] and/or adding guanosine 5'-O-(3-thiotriphosphate), but was greatly promoted when ATP was withdrawn. Similarly, ATP depletion in intact cells also induced nuclear actin accumulation. In contrast to the effects of latrunculin B, ATP depletion was associated with an increase in cortical F-actin. Our results suggest that the presence of actin in the nucleus may be required for certain stress-induced responses and that cofilin is essential for the nuclear import of actin.