Effect of a kanpo medicine, zyuzentaihotô, on the immune reactivity of tumor-bearing mice.
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Biomedical subjects
Publications and source records attributed to N Yamaguchi.
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Two types of pancreatic gamma-glutamyltranspeptidase (GGTP) (EC 2.3.2.2), sialic acid poor and sialic acid rich, were purified by the following: anion-exchange chromatography, wheat germ agglutinin (WGA)-Sepharose chromatography, gel filtration chromatography, phenyl-Superose chromatography, and hydroxylapatite chromatography. Among these, WGA-Sepharose chromatography helped to increase the specific activity of the GGTPs by approximately 20-30-fold in one effort. On dodecyl sulfate polyacrylamide gel electrophoresis, the two pancreatic GGTPs had different molecular weights. Sialic acid-rich GGTP had two subunits of Mr 67,000 and 27,000; however, the sialic acid-poor type had two subunits of Mr 72,000 and 29,000. The pI value of the sialic acid-poor GGTP was 5.9, and that of the sialic acid-rich GGTP 3.6.
A boy suffering from epileptic seizures experienced five episodes of a twilight state. His twilight states continued for at least two weeks, and were characterized by behavioral disorders and severe autonomic symptoms. Sometimes functional ileus was present. The electroencephalographic finding in the first episode was 6-per-second phantom spike and wave complex (PSW). For treatment, a combination of carbamazepine and sodium valproate was useful in preventing the reappearance of the episode of the twilight state and in suppressing PSW. From the clinical and electroencephalographic findings and therapeutic response to antiepileptics, the episodes were considered to have originated in localized epileptic discharges in the hippocampal, amygdaloidal and hypothalamic regions.
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The age at onset of schizophrenia was investigated in 2,417 inpatients (1,433 males and 984 females) meeting the DSM-III criteria for schizophrenia. About 80% of the patients became schizophrenic before the age of 30. The mean age at onset of the male patients was slightly earlier than that of the female patients. There was a higher cumulative percentage of the male patients who became affected at each age quinquennium. More men than women became schizophrenic before the age of 30.
The relationship between clomipramine (CMP) brain concentration and its inhibitory effect on serotonin (5HT) turnover was investigated in rats treated with a single dose and multiple doses of CMP. CMP reduced the 5-hydroxyindole acetic acid (5HIAA) brain levels in two groups of rats. Concerning the 5HT turnover measured by the probenecid (PBC) technique, there were significant correlations between the CMP brain level (x) and 5HIAA brain level (y) after PBC injections in both acute and chronic experiments. The regression lines for the respective groups were y = 764 - 117 log x (r = 0.84, P less than 0.001) and y = 770 - 97.7 log x (r = 0.68, P less than 0.001). The regression coefficient for the acute experiment was greater than that for the chronic one (p less than 0.001), indicating a less dose-response in the latter. From these findings, the acute dosing with CMP seemed to reduce the 5HT turnover without reference to the dose but a prolonged administration seemed to vary in its effect. This may be due to a compensatory mechanism in the 5HT system induced by chronic CMP-treatment.
We report here the clinical features of 3 affected siblings and neuropathological findings of the CNS from an autopsied case among them. Their common clinical features consisted of cerebellar ataxia and tremors through movements and postures. Two of the 3 siblings showed autonomic abnormalities, hard-of-hearing, pyramidal sign and areflexia. Then they always had xanthochromia and an elevated protein without pleocytosis in their CSFs. Neuropathologically, intracytoplasmic eosinophilic inclusion bodies were found in the neurons of some restricted nuclei or nerve cell groups of the brain stem, cerebellum and spinal cord. Similar bodies appeared also in glial, ependymal and choroid plexus epithelial cells. Such eosinophilic bodies are thought to consist of protein-rich substances from histochemical properties, and result from an unknown inherited metabolic error.
With regard to "acute kindling" that signifies progressive changes in various epileptiform discharges produced with repeated electrical stimulations in a brief time span in acute experiments, the interstimulation interval effect was examined. Kindling developments produced respectively with 3 and 30-minute interval stimulations to the visual cortex of rabbits were compared with each other. Eventually, in kindling with a longer interstimulation interval, after-discharges induced in every trial of stimulation were often lengthened in duration more prominently than those with the shorter interstimulation interval and, furthermore, occasional slight relapses in the afterdischarge duration occurred more infrequently in the former than in the latter. These results suggest that the interstimulation interval plays an important role in the development of acute kindling, presumably in relation to postictal inhibition. In addition, spontaneous interictal or ictal epileptiform discharges occasionally arising during the 3-minute interstimulation intervals were reported. These spontaneous discharges may suggest a high epileptogenicity in acute kindling.
For studies on acute kindling that signifies the progressive changes in various epileptiform discharges produced with repeated electrical stimulations within a brief time span in acute experiments, changes in field EPSP and IPSP evoked in the unilateral visual cortex of rabbits by single shocks to the adjacent visual region were serially observed during and after kindling produced with a 15-minute interval stimulation repeatedly applied to the same visual cortex. Eventually, both the field EPSP and IPSP in the primary kindled site were progressively potentiated at each postictal or interictal stage during the acute kindling, and these potentiations lasted for hours allowed for acute experiments. However, a clear discrepancy was observed between the increase in the field EPSP and the lengthening of the after-discharge duration reflecting a progressive development of epileptiform discharges in acute kindling. These results suggest that long-term potentiation (LTP) has no parallel correlation to kindling development, although there is no denying the fact that LTP may be at least partly responsible for kindling development.
Visual cortical kindling was studied in chronically prepared rabbits with regard to the electrographic progress of epileptiform discharge trains following the daily stimulation and corresponding ictal behaviors. The spread of epileptiform discharges from the stimulated visual cortex to the parietal and frontal cortices of the stimulated side was observed early with the development of independent discharges in these parietal and frontal regions, accompanied by ictal motor symptoms of the contralateral side. In view of the past studies on rats, cats and monkeys, it was considered that such a spread in the neocortex and corresponding ictal behaviors might be specific to the rabbit.
Epileptic photosensitivity was acquired as a result of kindling in the lateral geniculate body (GL), and a GL-kindled cat pretreated with DL-allylglycine was found to be a useful model of epilepsy for assessing the efficacy of anticonvulsant drugs. In the present study the acute anticonvulsant effects of sodium valproate (VPA) were examined in the GL-kindled cat under DL-allylglycine. An intravenous injection of VPA at 50 mg/kg induced a protective action against photically induced seizures and paroxysmal EEG activities. This protection persisted for up to 4 hours of the observation period and corresponded to plasma concentrations (61 to 123 micrograms/ml) similar to those considered therapeutic in humans. The present findings are consistent with those obtained in other animal models of photosensitive epilepsy, and lend experimental support to the idea that VPA possesses antiepileptic activity in human photosensitive epilepsy.
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The relation between age at onset of schizophrenia diagnosed using DSM-III criteria and the presence or absence of this illness among first-degree relatives was investigated in 2417 patients. The mean age at onset among those with a family history of schizophrenia was slightly and nonsignificantly earlier than that of schizophrenic patients without a positive family history. The former developed their illness before the age of 25 years more frequently than did the latter.
TRF has originally been defined as a T-cell-derived lymphokine that triggers activated B cells for a terminal differentiation into Ig-secreting cells. HPLC-purified TRF from Sup of a murine TRF-producing B151 cell is an acidic glycoprotein, exerts BCGF II activity and induces expression of IL-2 receptors. It does not show IL-1, IL-2, IL-3, BSF-1/IL-4, or IFN gamma activity. We prepared monoclonal TB13 and NC17 antibodies against HPLC-purified B151-TRF which are specific for and can inhibit TRF as well as BCFG II activity of B151-TRF. Moreover, TB13 as well as NC17 antibody can immunoprecipitate the 46 Kd molecule from B151 Sup which exerts TRF as well as BCGF II activity. Complementary DNA (pSP6K-mTRF23) encoding for murine TRF/IL-5 was cloned and its entire nucleotide sequences were determined. The murine TRF/IL-5 cDNA encodes 133 amino acids including N-terminal strongly hydrophobic regions. Secreted recombinant TRF/IL-5 (apparent m.w. of 46 Kd) has 113 amino acid residues and also comprises homodimers of a molecule with an apparent m.w. of 25 to 30 Kd. TRF/IL-5 mRNA is constitutively expressed in constitutively TRF-producing B151 and is inducible in some T cell lines upon stimulation with PMA or Con A. TRF/IL-5 mRNA is also expressed in Tbc-primed T cells upon the stimulation with PPD, whereas its expression is not effectively induced in non-primed spleen cells by stimulation with Con A or PMA plus calcium ionophore. The translation product of murine TRF/IL-5 cDNA triggers resting as well as activated (DNP-primed or LPS-stimulated) murine B cells for terminal differentiation into Ig-secreting cells (IgM, IgG1, or IgA) accompanied by increased mRNA expression for secreted forms of relevant Ig heavy chain (mu, gamma, or alpha). Among these, increases in the level of mu, and alpha-specific mRNA for the secreted form of IgM and IgA, respectively, are prominent. Moreover, TRF/IL-5 induces maturation of resting B cells into IgM-secreting cells. TRF/IL-5 promotes growth of activated B cells as well as BCL1 cells. TRF/IL-5 is, therefore, a growth as well as a differentiation inducing factor for B cells. Moreover, it induces functional IL-2 receptors on resting as well as activated B cells, besides TRF and BCGF II activities.(ABSTRACT TRUNCATED AT 400 WORDS)
Plasma epinephrine (E) and norepinephrine (NE) concentrations were measured (radioenzymatic assay) in blood samples simultaneously withdrawn from the aorta (Ao) and coronary sinus (CS) on 10 anesthetized dogs immediately before and during a 1-min period of electrical stimulation of the left stellate ganglion (4 V, 4 ms, 10 Hz). Heart rate and systolic blood pressure significantly increased in response to electrical stimulation (152 +/- 8 to 180 +/- 15 beats/min and 128 +/- 12 to 149 +/- 12 mmHg, mean +/- SE; P less than 0.05). Plasma NE concentrations were not significantly different in the Ao and the CS (432 +/- 110 and 319 +/- 67 pg/ml) before the stimulation, whereas a net removal of E was present across the myocardium (Ao, 172 +/- 61; CS, 71 +/- 22 pg/ml). A large NE spillover in the CS was observed during the stimulation (Ao, 1,555 +/- 513; CS, 10,583 +/- 3,753 pg/ml). A significant output of E from the myocardium was also present (Ao, 165 +/- 42; CS, 291 +/- 74 pg/ml) during the stimulation. Determination of NE and E concentrations by high-performance liquid chromatography in five of the dogs confirmed the observation made with the radioenzymatic assay, i.e., a significant uptake (66%) of blood-borne E was present across the myocardium in the control situation (Ao, 320 +/- 97; CS, 110 +/- 23 pg/ml), whereas plasma E concentrations in the CS (280 +/- 61 pg/ml) were 1.5 times the values found in Ao (184 +/- 56 pg/ml) under electrical stimulation. These observations give further support to the hypothesis that endogenous tissue E can act as a cotransmitter of sympathetic fibers.
The authors evaluated the distensibility of the coronary arterial wall by pharmacoangiography with intravenous administration of dipyridamole in 38 patients with Kawasaki disease. In the acute stage of the illness, the coronary arteries were evaluated for aneurysms by two-dimensional echocardiography. After the acute stage of the illness, selective coronary cineangiographies were performed by Seldinger's method under general anesthesia before and after intravenous administration of 0.6 mg/kg of dipyridamole for four minutes. The calibers of aneurysms and normal appearing segments of coronary arteries, at most 7 segments in 1 patient, were measured before and after dipyridamole administration on the high-quality cineangioanalyzer and percentages of coronary arterial dilatation were calculated. In 14 cases without evidence of coronary arterial lesions, the distensibility was 10.2 +/- 4.7% (mean +/- SD). The distensibility of 32 aneurysms in 16 cases was 0.6 +/- 1.1% and was significantly decreased (p less than 0.001). In 24 cases with coronary arterial lesions, aneurysms, stenosis, or obstruction, the distensibility of normal appearing segments of coronary arteries was 4.5 +/- 4.9% and was significantly decreased (p less than 0.001). This method is useful in evaluating distensibility and appears to be effective in detecting pathologic changes of the coronary arterial wall, even if it appears normal in shape. The patient with previously diseased coronary arteries should be kept under careful longterm surveillance.
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