Triculamin, a new antituberculosis substance.
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Biomedical subjects
Publications and source records attributed to I Suzuki.
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Continuous ingestion of a thymus-dependent (TD) antigen differentially affects two compartments of the immune system. A secretory IgA antibody response is induced in mucosal tissues, concurrent with a state of antigen-specific systemic unresponsiveness to parenteral challenge, termed oral tolerance. The precise mechanisms whereby gut antigenic exposure induces oral tolerance are unknown, although T-suppressor cells, anti-idiotypic networks and immune complex formation have all been proposed. Here we show that the systemic unresponsiveness of mice made orally tolerant to the TD antigen sheep red blood cells (SRBC) is reversed by the adoptive transfer of Lyt-1+,2-, Vicia villosa lectin-adherent and I-J+ T cells derived from mice which are genetically resistant to the induction of oral tolerance to SRBC. This T-cell subpopulation has the characteristics of contrasuppressor effector T cells (Tcs). Small numbers of these Tcs cells reverse SRBC-specific tolerance both in vivo and in vitro. This finding offers new insight into the mechanisms of oral tolerance induction and maintenance, and suggests that a network of T cells are involved in the regulation of host responses to ingested antigens.
BACKGROUND: Hypopharyngeal cancer is closely associated with smoking, drinking, and malnutrition. Recent findings reveal that carcinogenesis depends on genetic aberrations. MATERIALS AND METHODS: Eighty-one patients with hypopharyngeal cancer were analyzed for p53, CCND1, and p27, and 72 patients were analyzed for p21, immunohistochemically. RESULTS: p53 overexpression was found in 70%, CCND1 in 17%, p21 in 29%, and p27 in 32%. The low intensity of p27 expression correlated with poor prognosis, but the level of expression of p53, CCND1, and p21 did not. CONCLUSION: The immunohistochemical analysis of p27 provides a possible tool in determining the prognosis of patients with hypopharyngeal cancer.
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The alpha 2-adrenoceptor antagonistic potency of midaglizole was evaluated and compared with that of the selective alpha 2-adrenoceptor antagonists yohimbine and idazoxan. Intravenously administered midaglizole, like yohimbine and idazoxan, reversed the clonidine-induced inhibition of the tachycardic response to cardiac nerve stimulation in pithed rats. Midaglizole, yohimbine and idazoxan inhibited the pressor responses to B-HT 920 (alpha 2-adrenoceptor agonist), in a dose-related manner, to a greater extent than the response to methoxamine (alpha 1-adrenoceptor agonist). Conversely, prazosin produced a highly selective antagonism of the methoxamine-evoked response in this preparation. Midaglizole failed to antagonize centrally mediated hypotension and bradycardia induced by intravenous clonidine, whereas the other alpha 2-antagonists attenuated the clonidine-induced cardiovascular responses in intact rats. These results suggest that midaglizole is a selective alpha 2-adrenoceptor antagonist and, unlike yohimbine and idazoxan, is characterized by its ability to block peripheral but not central alpha 2-adrenoreceptors when administered systemically.