Biomedical subjects
Publications and source records attributed to N Yasuda.
The synthesis and antiviral activity of various aminoglycoside derivatives having a palmitoyl group are described. All of these aminoglycoside derivatives exhibited almost the same excellent antiviral activity against herpes simplex virus type I and influenza virus.
X-linked lymphoproliferative disease (XLP) is a rare genetic syndrome that continues to serve as a useful model to understand more broadly the role of immunodeficiency and the pathogenetic mechanisms for the spectrum of Epstein-Barr virus (EBV)-induced diseases to which XLP is predisposed. Apart from XLP, EBV infection is related to the high frequency of non-Hodgkin's lymphoma in children with various primary immune deficiency diseases and in allograft recipients. More recently, EBV has been implicated in several lymphoproliferative diseases in individuals with acquired immune deficiency syndrome. Studies thus far on patients with XLP suggest that immune deficiency is a major determinant of these diseases. Additional molecular aberrations must be necessary in the pathogenesis of lymphoma to convert polyclonal to monoclonal disease.
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In relation to the synthesis of antipseudomonal drugs, namely, gentamicin C2 and 3-de-O-methylsporaricin A, a protected purpurosamine B (15) and 6-epipurpurosamine B (13) were synthesized. The key intermediate, methyl 2,3,4,7- tetradeoxy-6-O-(methylsulfonyl)-2-phthalimido-beta-L-lyxo-++ +heptopyranoside (8), was obtained in 48% yield by Grignard addition to methyl 2,3,4-trideoxy-2-phthalimido-alpha-D-erythro-hexodialdo-1,5-pyrano side (7) proceeding in accordance with Cram's chelate rule, followed by methylsulfonylation. From 8, compound 15 was readily obtained by introduction of the azide group with inversion of configuration at C-6. Compound 13 was obtained by introduction of the azide group with retention of configuration.
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Temporal characteristics of ACTH and beta-endorphin secretion induced by bovine hypothalamic CRF-A (void volume) and CRF-B (Kav = 0.583) separated by Sephadex G-100 were compared to those of synthetic ovine or rat CRF, sauvagine and vasopressin. Dispersed cells or minced fragments of rat adenohypophyses perifused in a column were exposed to various secretagogues, and ACTH and/or beta-endorphin concentrations of the effluent were measured by radioimmunoassays. CRF-A or CRF-B induced an immediate brisk rise of ACTH and beta-endorphin within 1 min after initiation of CRF perifusion. The maximum rate of ACTH or beta-endorphin secretion was reached 1-2 min later. Hormone secretion persisted throughout a 10-min exposure to these secretagogues. More than 80% of the total ACTH or beta-endorphin secretion induced by 10-min perifusion with bovine CRF occurred during exposure to CRF. With 10-min perifusion with 300 ng/ml ovine or rat CRF, the onset of the major CRF-stimulated ACTH or beta-endorphin secretion was markedly delayed compared to that following bovine CRF. During perifusion with ovine or rat CRF, a modest slow increase in ACTH or beta-endorphin secretion was observed. More than 60-70% of the total ACTH or beta-endorphin secretion induced by 10-min perifusion with rat or ovine CRF occurred after CRF withdrawal. The ACTH secretory patterns for sauvagine were very similar to those for synthetic rat or ovine CRF. These results suggest some qualitative differences between partially purified bovine CRF and synthetic ovine or rat CRF.
The incidence of selective IgA deficiency (SIgAD) was determined in a healthy adult population of 222,597 Japanese volunteer blood donors. Of the blood donors screened, only 0.007% (1:14,840) were found to be IgA-deficient (less than 10 mg/dl) by means of the double diffusion method, while 0.005% (1:18,500) were less than 5 mg/dl, and 0.003% (1:31,800) were less than 1 mg/dl by means of the single radial immunodiffusion method. Statistical analysis of the results clearly showed that the incidence of SIgAD in Japanese blood donors is very much lower than that in blood donors of European ancestry. The Japanese population may occupy a unique position in the ethnical peculiarities. Anti-IgA antibodies were found in 3 (25.0%) of 12 IgA-deficient blood donors whose IgA levels were less than 5 mg/dl, a prevalence rate comparable to that in donors of European ancestry. Although it is difficult to develop a suitable file of IgA-deficient donors in Japan, the establishment of a Rare Donor Registry System on IgA deficiency is a matter of urgency.
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Practically all myeloma cells had prominent vacuoles, around and within which the end product of acid phosphatase (AP) reaction was demonstrated. These vacuoles were considered to be autophagic. In remission, only a few myeloma cells were vacuolated. Serial determinations showed transition from an initial high AP score (3.86) to a low score (1.32) in remission. Moreover, there was a trend towards a lower average percentage of positive cells in remission (72%) as compared to the preinduction phase (100%). Intracellular Bence Jones proteins of the present case may be toxic and capable of causing vacuolation with activation of lysosomal enzymes.
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Pathways relaying olfactory information to the deep amygdaloid nuclei (AMYGd) were analyzed with electrophysiological techniques in anesthetized cats. Stimulation of the piriform cortex (PC) produced orthodromic spikes in some AMYGd neurons with a mean latency of 12.2 ms and antidromic responses in other neurons with a mean latency of 9.3 ms. Stimulation of the AMYGd produced antidromic spikes in some PC neurons with a mean latency of 11.5 ms. Some neurons in the entorhinal area (EA) were activated orthodromically from the PC with a mean latency of 22 ms, and a proportion of these cells was also activated antidromically from the AMYGd. Some neurons in the agranular insular cortex were activated orthodromically from the PC, but none of them responded antidromically to AMYGd stimulation. From these observations, it is suggested that olfactory information reaches the AMYGd directly from the PC or indirectly via the EA, and that the direct path conveys the major olfactory input from the PC to the AMYGd.