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In this paper, we present the critical experiment performed in March 2008 in the high-flux reactor (HFR) to reproduce physical conditions similar to the core light water introduction accident. We present the HFR, the context of the study and two Monte Carlo models: TRIPOLI4 – JEFF3.1 and MCNP – ENDF/BVII. All comparisons between calculations and experimental results show, within both models, that the safety rods efficiencies, in AIC alloy, are always underestimated in normal as well as in accidental configuration of the reactor.

Fat that is well demarcated from underlying muscle is found on the right ventricular free wall and around epicardial coronary vessels. Fat is not present in the left ventricle in normal subjects. In right ventricular dysplasia, fat and fibrosis may massively displace right ventricular myocardial tissue. It is frequently associated with some clusters of fat and fibrosis in the left ventricle. Adipocytes may be also found within fibrous tissue. In this situation it may be associated with inflammatory cellular infiltrates in both ventricles and this is called metaplastic fat. All these findings may be seen and sometimes are associated to a variable degree in the same myocardial specimen. However, fat may be interspersed with right ventricular myocardial fibres but without fibrosis or signs of inflammation. This situation is observed in more than half of the normal hearts and represents an over-looked pathologic condition only observed in the human species. The term "fat dissociation syndrome" is proposed to identify this condition. This new understanding of right ventricular myocardial structure which may be investigated by MRI may have important clinical consequences.

The effects of various peptidase inhibitors were examined upon the K+-evoked overflow of substance-like immunoreactive material (SPLI) from slices of rat substantia nigra in order to assess the possible involvement of "enkephalinase," angiotensin-converting enzyme (ACE) and calpain in the enzymatic inactivation of endogenous substance P in brain tissues. The calpain inhibitor leupeptin and the enkephalinase inhibitors thiorphan and phosphoramidon increased markedly SPLI overflow, whereas the two ACE inhibitors, captopril and enalaprilat (up to 10 microM in the superfusing medium), were inactive. Surprisingly kelatorphan, which inhibits not only enkephalinase but also aminopeptidase and dipeptidylaminopeptidase activities, was less potent than thiorphan or phosphoramidon to enhance SPLI overflow. However, in the presence of ICI-154129 or naloxone to block opiate receptors, kelatorphan was as potent as thiorphan, therefore suggesting some negative influence of endogenous opioids on SPLI release with kelatorphan but not thiorphan. In agreement with this interpretation, the direct stimulation of delta opiate receptors by deltakephalin was found to significantly reduce SPLI overflow. Furthermore, an increased outflow of [Met]enkephalin-like material was observed from substantia nigra slices superfused with kelatorphan but not thiorphan. These results indicate that endogenous substance P released within the substantia nigra is very probably inactivated by enkephalinase and calpain, but not ACE. They also demonstrate that endogenous opioids can exert a negative control upon substance P release in this brain region.