We produced a monoclonal antibody against epithelioid cell granulomas (ECGs) by immunizing mice with a crude tissue extract of lymph nodes with sarcoidosis. The established antibody (ECM antibody) strongly reacted with epithelioid cells and Langhans' type giant cells of ECGs not only in cases of sarcoidosis, but also in cases of other granulomatous diseases such as tuberculosis and Crohn's disease. In this study, we used the ECM antibody to improve the histopathological diagnosis of Crohn's disease, in which the demonstration of ECGs is critical for diagnosis, but morphological identification of ECGs by hematoxyline and eosin (HE) staining is frequently difficult. When we examined the tissues removed at operation from 11 patients with Crohn's disease, we observed a total of 29 lesions of morphologically recognizable ECGs, all of which were immuonohistologically positive for the ECM anti­body (granuloma pattern). In addition the ECM antibody revealed 43 nests of tiny inflammatory lesions (nested pattern) that could not be morphologically recognized as ECGs by HE staining only. Both the granuloma and nested patterns of ECM immunoreactivity were present in all cases of Crohn's disease we examined, but were absent in all 15 cases of ulcerative colitis that were used as controls.

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Cortical neurons develop into neuronal death four days after transient cerebral ischemia. The aim of this study is to detect early post-ischemic changes in the cortex that will develop into cortical neuronal death later. The detection is important for starting adequate treatment within the therapeutic window. We have examined changes in middle-latency auditory evoked potentials (MAEPs) and cortical blood flow (CBF) in relation to the histological changes in the auditory cortex of Mongolian gerbils subjected to transient cerebral ischemia. At 2 min after bilateral carotid occlusion, the amplitude of MAEPs and CBF were reduced to 22.2 to 23.4% and 24.3 to 27.4% of the pre-ischemic level, respectively. In the 4-min ischemia group, the amplitude of each parameter recovered rapidly to the pre-ischemic level. In the 12-min ischemia group, the recovery of MAEPs and CBF was delayed by, from 20 to 30 min, and about 10 min, respectively. Also, scattered eosinophilic neurons were observed in the auditory cortex, and a mild but significant decrease in the number of surviving neurons was also detectable. The recovery of MAEPs in both groups was characterized by the appearance of a transient high amplitude (2.67 ± 0.6 µV) low frequency (62.2 ± 3.4Hz) wave. The present findings show that cortical neuronal death in the auditory cortex, which results from transient cerebral ischemia in the gerbil, is predictable by detecting the delay in the recovery of MAEPs amplitude and CBF during the very early post-ischemic phase. Clinical data is mandatory for the application of the presented method in clinical cases to save many patients with acute cerebrovascular diseases in the future.

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