Biomedical subjects
Publications and source records attributed to H Aoki.
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The effect of direct electric current (5 muamp) on mesenchymal cell differentiation into cartilage was investigated in explants of fetal rat muscle and bone matrix gelatin. In this system, chondrogenesis in vitro corresponds in developmental potential to osteogenesis in vivo. Application of electric current inhibited differentiation of muscle derived mesenchymal cells, but enhanced proliferation of differentiated chondrocytes and formation of cartilage at the cathode region, and had no effect on mature hypertrophic chondrocytes. Application of electric current may be contraindicated in fracture at the very early stage of fracture treatment and effective at the cathode region only for preexisting and proliferating cells. Electric current also may not be effective for mature cells having no potential for proliferation.
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A 61-year-old and right handed man was admitted to our department on August 11, 1980. The patient had three month history of focal fits, progressive hemiplegia, and motor dominant aphasia. The neuroradiological examination revealed a space taking lesion at the left frontoparietal area, which showed a small tumor stain with early filled draining vein on the left carotid angiogram, and iso-high dense mass with marked contrast enhancement on the CT scan. The EEG findings showed polymorphous delta rhythm in the left frontal and parietal areas. On August 28, total removal of the tumor was performed. The tumor was a intracerebral, fibrous cystic mass without involvement of the pia and dura mater. The removed tumor was measured approximately 6 X 5 X 4 cm in size, and consistence of the tumor was mostly elastic hard and partially soft and hemorrhagic. Histologically, the tumor composed of an admixture of bizarre histiocytes and fibroblasts, multinucleated giant cells, xanthoma cells and siderophages, with fibrous stroma. After surgery, no distinct lesion was demonstrated on the whole body CT scan and garium and technetium scintigram in the abdomen and the lung. The right hemiplegia and aphasia were improved gradually, and the patient discharged on December 20, 1980. We discussed the origin of this tumor, and angiographic and CT scan findings on the literature.
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When 1-5C-4 cells were infected with von Magnus virus derived from influenza A/RI/5+ virus by successive undiluted passages in chick embryos, virus-specific proteins were synthesized but production of infectious virus was inhibited. In these cells the synthesis of viral RNA was suppressed and the nucleoprotein (NP) antigen was found predominantly in the nucleus in contrast to standard virus-infected cells in which the antigen was distributed throughout the whole cell. The intracellular location and migration of NP were determined by isotope labeling and sucrose gradient centrifugation of subcellular fractions. In standard virus-infected cell NP polypeptide was present predominantly in the cytoplasm in the form of viral ribonucleoprotein (RNP) and intranuclear RNP was detected in reduced amounts. In contrast, in von Magnus virus-infected cells NP polypeptide was present predominantly in the nucleus in a nonassembled, soluble from and the amount of cytoplasmic RNP was considerably reduced. After short-pulse labeling NP was detected exclusively in the cytoplasm in a soluble form and after a chase a large proportion of such soluble NP was seen in the nucleus. It is suggested that a large proportion of the NP synthesized in von Magnus virus-infected cells in not assembled into cytoplasmic RNP because of the lack of available RNA and the NP migrated into the nucleus and remained there.
When influenza A/RI/5+ virus-infected cells were incubated in medium to which 2 micrograms of canavanine (arginine analog) per ml had been added 4 hr after infection, all viral polypeptides were synthesized but the budding-like process with the appearance of extracellular virus was completely inhibited. The plasma membrane isolated from these cells contained exclusively hemagglutinin (HA), and membrane (M) protein and nucleoprotein (NP) appeared to be associated with the nucleus, in contrast to untreated cells whose plasma membrane contained abundant HA, M protein, and NP. Disruption of canavanine-treated cells by freeze-thawing generated a number of hemagglutinating membranous vesicles or fragments containing exclusively HA. By isotope labeling it was found that the M protein synthesized in the presence of canavanine, together with HA and NP, is a canavanine-substituted polypeptide. It is suggested that canavanine inhibits the formation of the mature envelope of influenza RI/5+, because of the inability of M protein to associate with the plasma membrane.
When mouse lymphoid cells derived from untreated C57BL/6 mice were cocultivated in liquid cultures with L-cell monolayers for 3 h, overlaid with soft agar, and then further incubated for 12 h, protected foci of L cells against vesicular stomatitis virus infection were formed. Many strains of mice have been found to have the protected focus-forming cells on the L-cell monolayers. The formation of the protected foci was completely suppressed by addition of cycloheximide into soft agar. When anti-interferon (type I) antiserum was added to soft agar, there was a decrease in focus counts of about 80%. These experimental results indicated that the formation of protected foci by untreated mouse lymphoid cells was mediated for the most part by type I interferon that was produced without addition of special inducer. We have designated these focus-forming cells as natural interferon-producing cells (NIPC). NIPC belong to the glass-adherent fraction, and Thy-1 antigen, immunoglobulin, and Ia antigen could not be detected on the surface of the NIPC. NIPC were detected in congenitally athymic nude mice. These findings suggest that NIPC belong to the Ia-negative macrophages. Mouse lymphoid cells obtained from germfree mice could form the protected foci on L-cell monolayers and could produce interferon without the addition of a special inducer. NIPC are considered to be a cellular background for spontaneous interferon production.
Various processes of in vitro immune interferon production by sensitized spleen cells stimulated with allogeneic cells were investigated. When L cells, an interferon-inducing antigen, were fixed with methyl alcohol or paraformaldehyde, the ability to induce immune interferon disappeared. In this immune interferon production system, the majority of sensitized spleen cells adhered to target cells within 1 h of cocultivation. Adherence of immune interferon-producing cells to target cells was observed only when L cell-sensitized spleen cells were cocultured with L cells or with mouse embryo cells derived from C3H mice. Fixation of antigenic cells with methyl alcohol or paraformaldehyde significantly reduced cell adherence. When L cells alone or sensitized spleen cells alone were pretreated separately with cytochalasin D, neither cell type could bind to partner cells. Specific adherence did not take place at 4 degrees C, nor in the presence of dinitrophenol or sodium azide. Continuous protein synthesis in both cells was not required for immune cell adherence. Divalent cations, Ca2+ or Mg2+, were required for this immune specific adherence to take place. However, once stable adherence was established, treatment with cytochalasin D, ethylenediaminetetraacetic acid, or sodium azide, or simple reduction of temperature, did not disrupt the binding. Interaction between immune interferon-producing cells and antigenic cells can be subdivided into two phases according to the requirement for divalent cations: (i) lymphocytes and antigenic cells interact transiently, and divalent cations are required to maintain the binding; (ii) lymphocytes and antigenic cells form a stable interaction, and deprivation of divalent cations does not disrupt the binding. Colchicine showed an inhibitory effect in the period after cell-to-cell adherence. Colchicine did not inhibit the release of interferon. On the other hand, vinblastine, another antimicrotubule agent inhibited the secretion of immune interferon. Since interferon synthesis was not stopped immediately after addition of cycloheximide, continued protein synthesis of sensitized spleen cells was not required for interferon secretion. The present study showed that adherence of immune interferon-producing cells to antigenic cells was a complex phenomenon involving a series of successive events.
The electrical stimulation of the caudate nucleus could induce a caudate spindle in the rat as in case of the cat and monkey. The spindle was enhanced by atropine (3-10 mg/kg, i.v.) or morphine (3-10 mg/kg, i.v.) and the effect of these drugs were completely abolished by eserine (0.3 mg/kg, i.v.), but not by methysergide (1 mg/kg, i.v.), PCPA (400 mg/kg, i.p. for 3 days) or reserpine (3 mg/kg, i.p. for 2 days). An intraventricular injection of atropine (5-10 microgram/rat) or morphine (10 microgram/rat) exerted a facilitatory action on the spindle, while an intrathalamic and intracaudate injection of atropine (5-50 microgram/rat) showed a suppressive action. The spindle was also markedly enhanced by the microinjection of atropine (15-30 microgram/rat) or morphine (30 microgram/rat) into the reticular formation, and these actions were completely antagonized by eserine (0.3 mg/kg i.v.), but only partially by methysergide (4 microgram/rat, intraventricular administration.) These results suggest that the cholinergic system may play an important role in the regulation of the caudate spindle.
A 22-year-old man with myotonic dystrophy associated with sick sinus syndrome is described. The patient showed marked weakness of grasping power, grip myotonia, percussion myotonia, bilateral cataracts, fixed facial expression and elevation of serum CPK level, and was diagnosed as having myotonic dystrophy. The Holter ECG showed marked sinus bradyarrhythmia at the rate of 25 beats per minute and the sinus node recovery time using overdrive suppression test was significantly prolonged. These findings indicated the patient also suffered from the sick sinus syndrome. Although various kinds of ECG abnormalities have been noted in the cases with myotonic dystrophy, there have been very few descriptions concerning the involvement of sinus node dysfunction in this disorder.