Multiparticle simulation for morphological transitions in diffusion-limited aggregation.
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Biomedical subjects
Publications and source records attributed to T Nagatani.
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d-AP159 is a d-optical isomer, and in rats it has a high affinity for 5-hydroxytryptamine1A (5-HT1A) receptors and potent anticonflict activity, equal to that of buspirone. The anticonflict effects of d-AP159 and buspirone were investigated in animals in which lesions of the serotonergic neurons were caused by intradorsal raphe (d-RA) injection of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). The anticonflict effect of buspirone, but not that of d-AP159, was attenuated in 5-HT neuron-lesioned rats. The anticonflict effect of d-AP159 injected into various brain sites was also studied. d-AP159 and buspirone microinjected into the d-RA caused significant anticonflict activity in rats. There was a significant anticonflict effect of d-AP159 injected into the amygdala centralis (ACE), but not the dorsal hippocampus (d-HC). The anticonflict effect of d-AP159 injected into the d-RA was antagonized by systemic administration of (-)propranolol but not Ro 15-1788. This effect of d-AP159 injected into the ACE was antagonized by systematic administration of Ro 15-1788 but not (-)propranolol. These results suggest that the d-RA and the ACE play important roles in the anticonflict effects of d-AP159 but that the mechanisms by which this drug acts at these sites are different.
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Two sets of oligonucleotide primers were used to amplify the genomic DNA of Rickettsia tsutsugamushi, the causative agent of scrub typhus (tsutsugamushi disease), by the polymerase chain reaction. Each set of primers amplified 538-bp and 109-bp products, representing part of a gene encoding a possible major 58-kDa immunogenic protein, from whole genomic DNA extracted from R. tsutsugamushi strains Karp, Kato, Gilliam, Kuroki and Kawasaki. No amplification was observed from R. sibirica, R. rickettsii, mouse and human genomic DNA. DNA amplification was observed from crude lysates of peripheral whole blood, tissue homogenates and paraffin-embedded skin biopsy sections obtained from patients with scrub typhus disease. Southern blot analysis demonstrated the specificity of the amplified DNA fragments following hybridisation with a DNA probe generated from R. tsutsugamushi strain Karp. By means of this procedure, a rapid and sensitive diagnosis of scrub typhus disease can be made during the acute stage of this infection.
Bullous pemphigoid (BP) is characterized by the production of autoantibodies against BP antigens. gamma-interferon (gamma-IFN), a T-cell lymphokine, is known to enhance the expression of several cell-surface proteins. In this study, keratinocytes were cultured in the presence of gamma-IFN, the expression of BP antigen protein was examined by flow cytometry and BP antigen messenger RNA (mRNA) (encoding 230-kDa protein) was quantified by slot-blot hybridization. The results indicated that BP antigen gene expression by keratinocytes was upregulated by gamma-IFN. This enhancement of gene expression was detected at both the protein and mRNA level, suggesting pretranslational regulation. These results imply the involvement of not only humoral immunity but also cell-mediated immunity in the development of BP.
Twenty-one patients with ATL were assessed. The predominant physical findings were lymph node and bone marrow involvement, skin involvement, hepatosplenomegaly and leukemic manifestations. The predominant histopathological findings in both skin and lymph node specimens were the diffuse medium-sized cell type and the diffuse mixed cell type. Some phenotypic discrepancy was found between the neoplastic cells in the peripheral blood, lymph nodes and skin of patients with ATL with respect to CD45RA and CD45RO, and CD7, CD29, CD25 and HLA-DR. That is, the predominant neoplastic cell phenotype was the helper T-cell, which was CD3+, CD4+, CD7+, CD25+, CD45RA+ and HLA-DR+, and CD29- and CD45RO- in peripheral blood and lymph nodes, and CD3+, CD4+, CD7+, CD29+, CD45RO+ and HLA-DR+, and CD45RA- in the skin. In other words, we have described the phenotypic heterogeneity of ATL cells and demonstrated the heterogeneity of CD45R isoform expression on ATL cells in different organs--the skin, peripheral blood and lymph nodes--of the same patient.
Lateral, uni-directional aggregates of collagen, segment-long-spacing crystallites (SLS), were made by dialyzing collagen solutions against acetic acid containing ATP, and were examined by transmission electron microscopes without electron staining. There detected were at least 20 dark (electron dense) cross-striations within SLS. The banding pattern was compared with the biochemical and biophysical properties of the amino acid side chains along the collagen molecule. The banding pattern of unstained SLS was mostly correlated with the intramolecular distribution of basic amino acid residues. Since basic amino acids have relatively large side chains, the distribution of mass (molecular weight of amino acids) along the molecule (local density profile) partially explained the cross-striation. Addition of fractions of molecular weight of ATP to basic residues made the local density profile much better correlate to the banding pattern. We conclude that the electron microscopic banding pattern of unstained SLS was generated by the local amount of material or local density profile along the collagen aggregates, which was enhanced by ATP bound to positively charged basic residues. The concept that the electron density correlates with the amount of material is fundamental in electron microscopy, and it has been proven with biological materials in this paper.
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We investigated the effects of propyl-beta-carboline-3-carboxylate (beta-CCP) on learning and memory tasks in a passive avoidance test in mice to clarify whether beta-CCP is an agonist or antagonist at benzodiazepine (BZP) receptors. At doses up to 10 mg/kg i.v., beta-CCP had no effect on mice in the passive avoidance test. Diazepam impaired passive avoidance behavior and methyl-beta-carboline-3-carboxylate(beta-CCM) enhanced it. beta-CCP blocked these effects of diazepam and beta-CCM in a dose-dependent manner similar to the effect of Ro15-1788. These effects of beta-CCP, which are thought to be mediated by BZP receptors, indicate that beta-CCP is an antagonist in the passive avoidance test.
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