Significant progress has been made in determining the action of sulfide on the primary target organs. It is reasonably clear that sulfide causes both K(+)-channel-mediated hyperpolarization of neurons and potentiation of other inhibitory mechanisms. It is not clear whether these processes are similar to those that occur in anoxia. Changes in perinatal and adult brain neurotransmitter content and release may be related to clinical impairment of cognition. H2S exposures at concentrations below the current occupational limits cause physiological changes in pulmonary function, thus suggesting that asthmatics are at risk. Studies of fetal and neonatal brain tissue have shown an abnormal development, and the long-term consequences of these neuronal changes have not yet been assessed. Finally, new approaches to therapy are required, such as the use of agents that actively remove sulfide from its sites of action. This may prove more useful in preventing some of the long-term adverse sequelae than the use of nitrites and hyperbaric O2, although the latter should be used in cases of pulmonary edema.

The traditional teaching that testicular torsion occurs primarily in the medial direction is misleading since in a third of cases it occurs in the lateral direction. While manual detorsion should be guided by response and return of normal anatomy, surgical exploration remains necessary since residual torsion still poses a risk to testicular viability. Long-term followup is warranted to assess the true incidence of subsequent atrophy after the management of acute testicular torsion.

No abstract

This randomized controlled trial provides Class I evidence that Web-based teaching as an adjunct to clinical experiences can significantly and durably improve medical students' learning.