Trauma team utilization of universal precautions: if you see something, say something.

PURPOSE: The risks deriving from the lack of compliance with universal safety precautions (USPs) are unequivocal. However, the adoption of these prophylactic precautions by healthcare providers remains unacceptably low. We hypothesized that trauma teams are not routinely adhering to USPs and that a brief educational intervention, followed by real-time peer feedback, would substantially improve compliance rates. METHODS: This before-and-after interventional study took place in the resuscitation bay of a Level I Trauma Center during trauma team activations. Six USPs were examined: hand washing (before and after patient contact), use of gloves, gowns, eye protection, and masks. Surgery and Emergency Medicine attending physicians, residents, and nurses, who had direct patient contact, were included. Following 162 baseline observations, an educational intervention in the form of brief lectures was conducted, emphasizing the danger to self from dereliction of USPs. Subsequently, 167 post-intervention observations were made after a one-month period of knowledge decay. Finally, real-time feedback was provided by trauma team leaders and study staff. Adherence to prophylactic measures was recorded again. RESULTS: Baseline compliance rates were dismal. Only hand washing prior to patient interaction, the use of eye protection, and the use of masks improved significantly (p < 0.05) after the educational initiative. However, compliance rates remained suboptimal. No difference was noted regarding the three other USPs. Impressively, following real-time behavioral corrections, compliance improved to nearly 90 % for all USPs (p < 0.05). CONCLUSIONS: Compliance with OSHA-required USPs during trauma team activations is unacceptably low, but can be dramatically improved through simple educational interventions, combined with real-time peer feedback.

Dysregulation of follicle development in a mouse model of premature ovarian insufficiency.

Premature ovarian insufficiency (POI) occurs in 1% of reproductive-age women. The ovarian manifestation ranges from the presence of a variable population of follicles (follicular) to the absence of follicles (afollicular), and in the majority of cases the cause is unknown. A transgenic mouse model of follicular POI, the Double Mutant (DM), arises from oocyte-specific deletion of Mgat1 and C1galt1 required for the generation of O- and N-glycans. DM females are subfertile at 6 weeks, infertile by 9 weeks and exhibit POI by 12 weeks of age. In this study we investigate the cause of the reduced fertility at 6 weeks and infertility at 9 weeks of DM females. Ovary sections were used to analyse follicle and corpora lutea (CL) numbers, apoptosis, and levels of laminin and 3ß-hydroxysteroid dehydrogenase using immunohistochemistry. After POI, DM females unexpectedly remained sexually receptive. At both 6 and 9 weeks, DM ovaries contained more primary follicles, however, at 9 weeks DM follicles were proportionally healthier, revealed by TUNEL analysis compared with Controls. In 9 week DM ovaries (collected post-mating), secondary follicles had theca and basal lamina structure abnormalities, whilst preovulatory follicles failed to ovulate resulting in the presence of numerous luteinised unruptured follicles, indicative of ovulation failure. Finally, DM ovaries contained more regressing CL with decreased luteal cell apoptosis indicative of a defect in CL regression. Identifying these follicular modifications have provided insight into the aetiology of a model of POI and highlight targets to investigate with the hope of developing new fertility treatments.

The C-terminal activation domain of the STAT-1 transcription factor is necessary and sufficient for stress-induced apoptosis.

It has previously been demonstrated that the STAT-1 transcription factor plays a key role in apoptosis induced by the cellular regulatory factors interferon gamma and TNF-alpha. Here we demonstrate that cells lacking STAT-1 show reduced cell death/apoptosis in response to stressful stimuli such as heat or ischaemia. Expression of STAT-1 in these cells does not enhance basal cell death but restores sensitivity to stress-induced death whereas this effect is not observed upon over-expression of STAT-3. Enhanced sensitivity to stress-induced cell death requires the C-terminal activation domain of STAT-1 and the phosphorylation sites at tyrosine 701 and serine 727. Moreover, we show for the first time in any system that the isolated C-terminal domain of STAT-1 is able to enhance stress-induced cell death in the absence of the DNA binding domain or any other region of STAT-1. Hence, STAT-1 plays a key role in stress-induced cell death, potentially acting via a novel co-activator-type mechanism and represents a possible therapeutic target for strategies aimed at minimising cell death, for example, following ischaemic injury.