Alkene-alkyl interconversion: an experimental and computational study of the olefin insertion and ß-hydride elimination processes.

The preparation and characterization of various alkyl, allyl or alkene Rh(iii) and Ir(iii) complexes as well as studies on the intramolecular reactions leading to transformation of one into another are reported. The silyl-hydrido-Rh(iii) complex {Rh(H)[SiMe(o-C6H4SMe)2](PPh3)}[BArF4], with a vacant coordination site, reacts with 1,5-cyclooctadiene (cod) leading to olefin insertion into the Rh-H bond and rearrangement to yield the 16e cyclooctenyl-Rh(iii) complex {Rh(η3-cyclooctenyl)[SiMe(o-C6H4SMe)2]}[BArF4] (1). This compound can be also synthesized by reaction of the 18e chloride precursor {Rh(η3-cyclooctenyl)[SiMe(o-C6H4SMe)2]Cl} with NaBArF4. The reaction of the thioether-silane SiMeH(o-C6H4SMe)2 with [Rh(nbd)Cl]2 (nbd = norbornadiene) leads to {Rh(σ-ntyl)[SiMe(o-C6H4SMe)2]Cl} (ntyl = nortricyclyl) (2). The abstraction of chloride from this neutral 16e ntyl-Rh(iii) complex with NaBArF4 results in the unusual isomerization of σ-nortricyclyl into σ,π-norbornenyl forming the 16e and cationic {Rh(σ,π-nbyl)[SiMe(o-C6H4SMe)2][BArF4] (nbyl = norbornenyl)} compound 3. Coordinatively saturated {Ir(η3-cyclooctenyl)[SiMe(o-C6H4SMe)2]Cl} (4) has been synthesized by the reaction of [Ir(cod)Cl]2 with SiMeH(o-C6H4SMe)2. The reaction of 4 with NaBArF4 led to the formation of the unsaturated and cationic Ir(iii) compound {Ir(η3-cyclooctenyl)[SiMe(o-C6H4SMe)2]}[BArF4] (5). Compound 5 shows low stability in solution and undergoes successive ß-hydride elimination and olefin insertion steps, which were elucidated by DFT calculations, to form 18e {Ir(H)[SiMe(o-C6H4SMe)2](η4-cod)}[BArF4] (6).

Eosinophilic ascites secondary to toxocariasis.

Eosinophilic ascites is a very rare disorder. It can be a manifestation of the eosinophilic gastroenteritis in its serosal form or it can be secondary to infections, malignancies, vasculitis or hypereosinophilic syndrome. Among all infections, the ones produced by invasive helminth parasites should be initially suspected and ruled out. We report the case of a patient with eosinophilic ascites associated with diarrhea, abdominal pain and eosinophilia in peripheral blood. Eosinophilic colitis was also demonstrated in a colonic biopsy and empirical steroid treatment was started for suspected eosinophilic gastroenteritis. Later on, the patient improved; the ascites disappeared and the eosinophil blood count returned to normal. Subsequently, serologic testing for toxocariasis was received positive and therefore, the diagnosis of eosinophilic gastroenteritis was discarded; albendazole was also added to treatment. The patient remained asymptomatic on follow-up. We emphasize the need to rule out parasitic infections in all patients with gastrointestinal symptoms, eosinophilia and eosinophilic infiltration of gastrointestinal tissues.

Positron emission tomograghy with [¹³N]ammonia evidences long-term cerebral hyperperfusion after 2h-transient focal ischemia.

BACKGROUND AND PURPOSE: It is well known that after cerebral ischemia, brain suffers blood flow changes over time that have been correlated with inflammation, angiogenesis and functional recovery processes. Nevertheless, post-ischemic spatiotemporal changes of brain perfusion have not been fully investigated to date. Here we tested whether PET with [¹³N]ammonia would evidence the perfusion changes presented by different brain regions in an experimental model of brain ischemia. EXPERIMENTAL PROCEDURES: Seven rats were subjected to a 2-h transient middle cerebral artery occlusion with reperfusion. PET studies were performed longitudinally using [¹³N]ammonia at 1, 3, 7, 14, 21 and 28 days after cerebral ischemia. RESULTS: In vivo PET imaging showed a significant increase in [¹³N]ammonia uptake at 7 days after cerebral ischemia with respect to one day after the occlusion in the cerebral territory irrigated by the MCA in both the ischemic and contralateral hemispheres. This increase was followed by a return to control values at day 28 after ischemia onset. Brain regions located both inside and outside the primary infarct areas showed similar perfusion changes after cerebral ischemia. CONCLUSIONS: [¹³N]ammonia shows hemodynamic changes after stroke involving hyperperfusion that might be related to angiogenesis and functional recovery. Long-term blood hyperperfusion is found both in ischemic and remote areas to infarction. These results may contribute to a better understanding of the evolution of cerebral ischemic lesion in animal models.