Communication between members of the cardiac arrest team--a postal survey

Aims: Effective communication enhances team building and is perceived to improve the quality of team performance. A recent publication from the Resuscitation Council (UK) has highlighted this fact and recommended that cardiac arrest team members make contact daily. We wished to identify how often members of this team communicate prior to a cardiopulmonary arrest. Method: A questionnaire on cardiac arrest team composition, leadership, communication and debriefing was distributed nationally to Resuscitation Training Officers (RTOs) and their responses analysed. Results: One hundred and thirty (55%) RTOs replied. Physicians and anaesthetists were the most prominent members of the team. The Medical Senior House Officer is usually nominated as the team leader. Eighty-seven centres (67%) have no communication between team members prior to attending a cardiopulmonary arrest. In 33%, communication occurs but is either informal or fortuitous. The RTOs felt that communication is important to enhance team dynamics and optimise task allocation. Only 7% achieve a formal debrief following a cardiac arrest. Conclusion: Communication between members of the cardiac arrest team before and after a cardiac arrest is poor. Training and development of these skills may improve performance and should be prioritised. Team leadership does not necessarily reflect experience or training.     

Locked fracture dislocation of the calcaneus treated with minimal open reduction and percutaneous fixation: a report of two cases and review of the literature

Fractures of the calcaneus with associated locked dislocation of the posterior facet have been previously described. Two patients with a calcaneal fracture with a locked dislocation of a portion of the posterior facet were treated with minimally invasive open reduction and percutaneous screw fixation of the fragment with cannulated screws. Both patients had satisfactory reductions and healed the fractures without any soft-tissue complications. This technique can be a useful addition to the armamentarium of the surgeon treating these injuries, especially in the patient at high risk for wound complications.     

Comparative effects of long-term continuous release of 16 alpha-hydroxyestrone and 17 beta-estradiol on bone,uterus, and serum cholesterol in ovariectomized adult rats

16Alpha-hydroxyestrone (16alpha-OHE(1)), an endogenous estrogen metabolite, is associated with increased bone density in postmenopausal women. This study was designed to evaluate the long-term activity of this metabolite on bone, uterus, and serum cholesterol in an animal model for postmenopausal bone loss. A preliminary dose-response study performed in weanling rats determined 2000 microg/kg/day to be the optimal dose of 16alpha-OHE(1) for studying estrogenic effect on bone. The long-term experiment was performed in 6-month-old animals that were either sham-operated or OVX. The OVX rats were implanted sc with 60-day continuous-release carrier, 17beta-estradiol (E(2)) (33 microg/kg/day) or 16alpha-OHE(1) pellets (2000 microg/kg/day). OVX decreased uterine weight, increased body weight, serum cholesterol, and all dynamic bone histomorphometric measurements in cortical and cancellous bone, and resulted in a 54% bone loss at the tibial metaphysis. E(2) completely prevented OVX-induced bone loss, suppressed bone turnover, and induced uterine hypertrophy and hypercholesterolemia. 16alpha-OHE(1) acted as an E(2) agonist on bone, suppressing bone formation and resorption. However, the estrogen metabolite lowered serum cholesterol and was only a partial E(2) agonist on uterine weight and epithelial cell height. These results suggest that 16alpha-OHE(1) is an estrogen agonist on bone and may be responsible, in part, for the cholesterol-lowering activity attributed to estrogen. As a consequence of its skeletal effects, older women who produce high levels of 16alpha-OHE(1) could have a lower risk for developing postmenopausal osteoporosis than women who produce less-active estrogen metabolites.     

Marijuana alters the human cerebellar clock

The effects of marijuana on brain perfusion and internal timing were assessed using [15O] water PET in occasional and chronic users. Twelve volunteers who smoked marijuana recreationally about once weekly, and 12 volunteers who smoked daily for a number of years performed a self-paced counting task during PET imaging, before and after smoking marijuana and placebo cigarettes. Smoking marijuana increased rCBF in the ventral forebrain and cerebellar cortex in both groups, but resulted in significantly less frontal lobe activation in chronic users. Counting rate increased after smoking marijuana in both groups, as did a behavioral measure of self-paced tapping, and both increases correlated with rCBF in the cerebellum. Smoking marijuana appears to accelerate a cerebellar clock altering self-paced behaviors.     

The effect of housing interventions on neuropsychological functioning among homeless persons with mental illness

The authors tested the hypotheses that neuropsychological functioning would improve after homeless persons with severe and persistent mental illness were provided with housing and that executive functioning would improve more among those placed in group homes than among those placed in independent apartments. A total of 114 persons with serious and persistent mental illness who were stable residents of homeless shelters completed neuropsychological testing and were randomly assigned to group homes or independent apartments; 91 participants (52 assigned to group homes and 39 assigned to independent apartments) were retested after 18 months. Overall neuropsychological functioning improved significantly across the full study sample. Executive performance, measured by the Wisconsin Card Sorting Test, decreased significantly among persons assigned to independent apartments and increased, but not significantly, among those assigned to group homes. The findings suggest that providing housing for persons who have severe and persistent mental illness improves cognitive functioning but that independent living may diminish executive functioning.     

Opposing effects of low and high-dose clozapine on survival of transgenic amyotrophic lateral sclerosis mice

Clozapine is a potent atypical neuroleptic or antipsychotic agent used to relieve symptoms of early-diagnosed schizophrenia. Aside from well-described dopamine and serotonin receptor blockade effects, clozapine may also be neuroprotective through its modulation of the p75 neurotrophin receptor (p75(NTR)) and superoxide dismutase 1 (SOD1) expression. The death-signalling activities of both p75(NTR) and mutant SOD1 are implicated in motor neuron degeneration in humans and transgenic mice with amyotrophic lateral sclerosis (ALS). We therefore investigated the effects of clozapine in cell culture and mouse models of ALS. Clozapine dose-dependently inhibited full-length and cleaved p75(NTR) but not SOD1 protein expression in the motor neuron-like (NSC-34) cell line. Furthermore, low concentrations of clozapine protected NSC-34 cells from paraquat-mediated superoxide toxicity, nerve growth factor (NGF)-induced death signalling, and serum deprivation, whereas high concentrations potentiated death. Systemic thrice-weekly administration of low and high-dose clozapine to mutant superoxide dismutase 1 (SOD1(G93A)) mice produced differential effects on disease onset and survival. Low-dose treatment was associated with delayed locomotor impairment and death, compared to high-dose clozapine, which accelerated paralysis and mortality (P < 0.05). Increased death was not attributable to toxicity, as clozapine-induced agranulocytosis was not detected from blood analysis. High-dose clozapine, however, produced extrapyramidal symptoms in mice manifest by hindlimb rigidity, despite reducing spinal cord p75(NTR) levels overall. These results suggest that although clozapine may exert p75(NTR)-mediated neuroprotective activity in vitro, its profound antagonistic effects on dopaminergic and serotonergic systems in vivo at high doses may exacerbate the phenotype of transgenic ALS mice.