These data show sustained neuroprotection with propofol. This relates to reduced eosinophilic and apoptotic injury. Activated caspase-3-dependent apoptotic pathways were not affected by propofol. This suggests the presence of activated caspase-3-independent apoptotic pathways.

We investigated the long-term effects of sevoflurane on histopathologic injury and key proteins of apoptosis in a rat hemispheric ischemia/reperfusion model. Sixty-four male Sprague-Dawley rats were randomly assigned to Group 1 (fentanyl and N2O/O2; control) and Group 2 (2.0 vol% sevoflurane and O2/air). Ischemia (45 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension (mean arterial blood pressure 40 mm Hg). Animals were killed after 1, 3, 7, and 28 days. In hematoxylin and eosin-stained brain sections eosinophilic hippocampal neurons were counted. Activated caspase-3 and the apoptosis-regulating proteins Bax, Bcl-2, Mdm-2, and p53 were analyzed by immunostaining. No eosinophilic neurons were detected in sevoflurane-anesthetized rats over time, whereas 9%-38% of the hippocampal neurons were eosinophilic (days 1-28) in control animals. On days 1 and 3, the concentration of Bax was 140%-200% larger in fentanyl/N2O-anesthetized animals compared with sevoflurane. Bcl-2 was 100% less in control animals during the first 3 days. Activated caspase-3 was detected in neurons of both groups (0.75%-2.2%). These data support a sustained neuroprotective potency of sevoflurane related to reduced eosinophilic injury after cerebral ischemia/reperfusion.

We present a six years follow up of a 6 1/2 year-old boy with recurrent aphasia, sporadic emotional regression and a convulsive disorder. The electroencephalogram reading during sleep showed continuous, generalized, hypersynchronous activity without clinical evidence of seizure ("subclinical bioelectric status epilepticus"). Clinical, laboratory and instrumental data revealed no evidence of a morphological lesion of the brain, either space-occupying, inflammatory, degenerative, or autoimmune. Remissions occured with and without anticonvulsant and steroid therapy. The hypothetical location, type, and etiology of the process are discussed. The syndrome appears to represent a functional disorganisation of speech-controlling areas of the brain.

This study describes the successful incorporation of CAE in a rodent CPB model and allows identifying suitable CAE volumes for subsequent studies. CAE exhibit a differential effect on outcome in rats undergoing CPB versus those not exposed to CPB. Perioperative administration of xenon remained without any effect on outcome.

A survey on the prevalence of Echinococcus multilocularis in foxes was conducted in the administrative district of Starnberg (federal state of Bavaria, Germany) and some adjacent municipalities from October 2002 to March 2003. The background to the study was the scarcity of recent data for Bavaria, where, in contrast to neighbouring regions, a general increase in the prevalence of the parasite has not yet been demonstrated. To estimate the current infection rate, a total of 268 shot foxes were examined using the intestinal scraping technique, resulting in an overall prevalence of 51%. This was compared with retrospective data collected during the period from 1989 to 2001. For the corresponding area and season, the retrospective prevalence was estimated at 32%, based on 222 shot foxes. The prevalence and its temporal development differ considerably on small spatial scales. The most conspicuous change has taken place in the western part of the study area, where a previous prevalence of 35% has increased to 80% in 2002/2003.