Transfer-matrix approach to tunneling between Kolmogorov-Arnold-Moser tori.
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Biomedical subjects
Publications and source records attributed to S Takada.
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In order to clarify the difficulties which handicapped people experienced in the Hanshin-Awaji earthquake disaster, 678 families with handicapped children were studied 1.5 months after the earthquake. All the students who were enrolled in this study were going to some type of school or training classes for handicapped children in January 1995. The study was completed between 1 and 10 March. The questionnaires which were designed for this study consisted of three parts: the difficulties which the families were faced with, their requirements for social and medical services and the symptoms and reactions of their children after the earthquake. A total of 466 answers were obtained from their parents. The kinds of difficulties differed between the families of mentally retarded children and those of the physically handicapped. While many parents with physically handicapped children desired better medical information or materials, many parents with mentally retarded children wanted better care services for their children. Physical and psychological effects of the earthquake were only temporary in most cases. However, some of the handicapped children were still suffering from such reactions as of 10 March. From the results of our study it became evident that a systematic relief program for these handicapped people should be established. The relief program should include the distribution of information regarding medical and social services. Psychological reactions such as panic, excitement and suppression of mental activity were still observed in some handicapped children on 10 March. Further observation will therefore be necessary.
We investigated the toxic effect of levofloxacin (LVFX), a quinolone antibacterial agent, on cartilage by examining aspects of its in vivo toxicokinetics and effect on the function of cultured chondrocytes of the femoral articular cartilage from juvenile New Zealand White rabbits. Repeated administration of LVFX (100 mg/kg) orally for 7 days induced focal necrosis and superficial erosion in the articular cartilage of the femoral condyle, but 30 mg/kg did not. Concentrations of LVFX in the cartilage were highest at the first sampling point (30 min) after a single administration, being 4.93 and 12.2 micrograms/g in the 30- and 100-mg/kg groups, respectively. The arthropathic concentration of LVFX in the cartilage was then shown to be 12.2 micrograms/g or more. For an in vitro study, chondrocytes were separated from the articular cartilage of the rabbit femoral condyle and cultured for 7 days until confluence. 35SO4 uptake by cultured chondrocyte sheets was most susceptible to LVFX, decreasing at drug concentrations of 5 micrograms/ml or more in 24- and 48-h cultures but not in a 72-h culture. Furthermore, 3H-thymidine uptake was decreased at concentrations of 10 micrograms/ml or more in a 48-h culture but not in 24- and 72-h cultures. Rhodamine 123 accumulation was susceptible to inhibition in cultured chondrocytes at an LVFX concentration of 10 micrograms/ml or more. These results suggest that LVFX inhibits glycosaminoglycan synthesis initially and DNA synthesis and mitochondrial function secondarily at actual arthropathic concentrations in cultured rabbit chondrocytes but that these changes are reversible and not enough to kill the cells.
Hepatitis B virus X gene codes for a small basic cytoplasmic protein and is able to transactivate viral and cellular genes, although X protein exhibits no DNA-binding activity. The mechanism of transactivation by X protein has been suggested to be via protein-protein interaction(s). X protein had amino acid sequences homologous to the functionally essential domain of Kunitz-type serine protease inhibitors, and these sequences were indispensable for transactivation function. X protein activated X-gene transcription itself and an X-responsive element were localized in their minimal promoter. Furthermore, tumor suppressor gene product p53, but not mutant p53, repressed X-gene transcription from the minimal promoter, indicating that X protein disrupts the function of normal p53, which represses transcription of X gene or cellular gene. Data suggest that inhibition of a hepatic serine protease by X protein leads to eliminate the suppressor effect of p53 on the basic transcription machinery in nucleus.
To determine the effects of maternal administration of dexamethasone (DEX) and thyrotropin-releasing hormone (TRH) on fetal lung maturation, 16 pregnant rats were divided into the following four groups: 20 micrograms/kg TRH twice a day was given intraperitoneally to the TRH group rats, 0.5 mg/kg/day DEX to the DEX group and both DEX and TRH to the DEX + TRH group for 3 consecutive days from gestational day 17. The control rats were given an equivalent volume of saline. The pregnant rats were sacrificed on gestational day 20 and the fetal lungs were removed. The relative amounts of surfactant protein A (SP-A), B (SP-B) and C (SP-C) mRNAs were analyzed by Northern blotting and the total lung disaturated phosphatidylcholine (DSPC) contents were determined using an enzymatic method. The SP-B and -C mRNA and DSPC contents in the DEX and DEX + TRH groups were significantly higher than those in the control group, whereas the SP-A mRNA levels did not differ significantly among the four groups. The SP-B and -C mRNA and DSPC contents in the DEX and DEX + TRH groups did not differ significantly. These findings suggest that TRH has no effects on the regulation of surfactant protein mRNAs or DSPC contents in the fetal rat lung and has no additive effects when combined with DEX.
In order to define the acute effects of a moderate quantity of alcohol on balance, related to the vestibular function, vestibulo-ocular reflex (VOR) test, caloric test and dynamic posturography (EquiTest) were performed. Ten healthy male volunteers aged 19-27 average 22.8) years old imbibed 1.5 ml whisky (alcohol content 43%) per kilogram of body weight within 5 min. Blood alcohol level (BAL) was measured before administration and then after 30, 90, and 150 min. Equilibrium examinations were performed immediately after each blood sample was taken. At the highest alcohol level, significant reductions were found in VOR gain, in the maximum slow-phase velocity of the caloric test and in the equilibrium score of the sensory organization test in condition 5, when compared with those before drinking. In some typical cases, the subjects' response in all tests were most disturbed at the time when the highest alcohol level was measured. From our results, we conclude that a moderate quantity of alcohol affects not only the oculomotor system but also the vestibular system. Furthermore, it was suggested that one of the reasons for postural instability after drinking alcohol may be reduced vestibular function.
The purpose of this retrospective study was to elucidate 1) which subgroups are prone to have ischemic cerebrovascular disease (CVD) among patients with atrial fibrillation (Af), 2) vulnerable period of CVD after the diagnosis of chronic Af and 3) the clinical efficacy of antiplatelet therapy in chronic nonvalvular Af patients. During 9 years, a total of 479 patients included 124 cases with paroxysmal Af, 30 cases with paroxysmal Af initially which later changed to chronic Af and 325 cases with chronic Af were enrolled. Among these 355 cases with chronic Af, 57 cases had valvular heart disease (VHD). The results were as follows: 1) The high risk subgroups (incidence rate/100 person-years is more than 6) were chronic Af with VHD or hypertension. The low risk subgroups (less than 2) were paroxysmal Af under 60 years of age, chronic Af with mitral valve prolapse syndrome or with hyperthyroidism. 2) There was no vulnerable period for occurrence of CVD during 9 years' follow-up from the onset of Af. 3) No significant difference in the incidence of CVD was seen in the groups with antiplatelet therapy and without.
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To examine the involvement of lymphocytes in the development of MDP-Lys(L18)-induced arthritis (MIA) in rats and the exacerbation of MIA by cyclosporin A (CsA), we analysed the spleen lymphocyte subset using monoclonal antibodies and flow cytometry during the development of arthritis and compared the results with those found in adjuvant-induced arthritis (AIA). Subcutaneous injection of MDP-Lys(L18) 4 mg/kg to male Lewis rats for 14 days caused very slight and quite clear increases in tarsal joint thickness on days 8 and 15, respectively. This increase was significantly enhanced by co-administration of CsA 10 mg/kg on both of these days. Adjuvant intracutaneously injected once increased the thickness only on day 15, and this was completely inhibited by CsA. The populations of CD4+ and CD8+ cells were increased and decreased, respectively, increasing the CD4+/CD8+ ratio, from day 8 in MIA. CsA enhanced the MDP-Lys(L18)-induced changes in these populations and caused additional decreases in the number of CD5+ cells. Only the CD4+ cell population was increased on day 15 in AIA, and this increase was inhibited by CsA. These results suggest that the spleen lymphocyte subsets in MIA have a different role from those in AIA, and that the contribution of enhancement of the subset changes to the exacerbating effect of CsA on MIA.
Muramyl dipeptide-Lys(L18) given by daily subcutaneous injection for 14 days induced arthritis in male Lewis, Fischer and nude rats, to a lesser degree in the last two than in the first strain. On the other hand, a single intradermal administration of Freund's complete adjuvant induced arthritis in Lewis and Fischer but not nude rats. Cyclosporin A (CsA) co-administered for 14 days markedly exacerbated the muramyl dipeptide-Lys(L18) induced arthritis (MIA) in rats of all three strains, but completely blocked the development of the adjuvant induced arthritis (AIA) in Lewis rats. Furthermore, AIA was transferred to recipient Lewis rats through spleen cells obtained from the donors with AIA, whereas MIA was not. Antibodies against type II collagen and DNA were not detected in sera from MIA or AIA rats. These data show a clear difference between MIA and AIA in the pattern of development of arthritis and suggest that delayed hypersensitivity reactions may be involved in the pathogenetic mechanisms of AIA, but not in MIA.
A case of remission of recurrent carcinosarcoma of the uterus with massive ascites by chemotherapy using carboplatin (CBDCA) is reported. A 75-year-old female was diagnosed with cancer of the uterine body. She underwent abdominal total hysterectomy with bilateral salpingo-oophorectomy, which revealed carcinosarcoma of the uterus penetrating the myometrium and reaching the serosa of the uterus. Eight weeks after, she developed abdominal distension, obstruction of bilateral ureters and bleeding tumor measuring 5 cm in diameter at the vaginal cuff ending. Acute retention of bloody ascites of more than 2500 ml was demonstrated. Abdominal centesis, aspiration of ascites and intraperitoneal administration of 600 mg of CBDCA were performed. Two weeks after single use of CBDCA, the ascites completely disappeared and there was recovery from anuria. The remission has lasted more than 4 months, which has suggested the efficacy of CBDCA for uterine carcinosarcoma.
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To evaluate 123I labeled beta-methyl-branched fatty acid (BMIPP) myocardial uptake at rest in the segment with and without stress induced ischemia in patients with coronary artery disease, 123I-beta-methyl-branched fatty acid myocardial scintigraphy was performed at rest and was compared with the findings of stress-reinjection 201Tl myocardial scintigraphy in 31 patients with coronary artery disease. In 159 ischemic myocardial segments, equally decreased uptake on both reinjection 201Tl and fatty acid images was observed in 64 segments, more severely decreased uptake of fatty acid in 76 segments, and more severely decreased uptake of reinjection thallium in 19 segments. On the other hand, in 53 non-reversible defects, each patterns was observed in 41, 3, and 9 segments respectively. When comparing the ischemic segments with more reduced uptake of fatty acid than reinjection thallium (Group 1) and the ischemic segments with equally or less reduced fatty acid uptake than reinjection thallium (Group 2), wall motion was more severely impaired in Group 1 than in Group 2 (severe hypo- to dyskinesis was present in 32 of 54 segments in group 1 and in 21 of 75 segments in group 2, p < 0.005). In conclusion, in patients with coronary artery disease, resting fatty acid uptake was frequently more reduced than reinjection 201Tl in the segments with stress induced ischemia and wall motion was more impaired in these segments. BMIPP myocardial imaging may provide information on metabolic alterations at rest independent of perfusion abnormalities in patients with coronary artery disease.
The transcription factor E2F is known to play an important role in cell cycle progression through interaction with retinoblastoma protein. HL60 cells are able to differentiate into a granulocytic lineage by prolonged exposure to retinoids and into a macrophage-like lineage by exposure to tumor promoter 12-O-tetradecanoylphorbol 13-acetate, with a rapid decrease of c-myc gene expression. In this study, we assessed the changes of the E2F-binding pattern to the P2 promoter region of the c-myc gene during differentiation into both lineages. The observed changes of the E2F-binding pattern were a decrease of free E2F and an appearance of retinoblastoma protein-containing E2F complexes in both lineages. The effects of the anti-c-myc antibody and the recombinant c-Myc protein on the E2F-binding patterns suggest that the c-Myc protein is not involved directly in these changes. These changes also led the suppression of transcriptional initiation from the P2 promoter. The results indicate that, in the course of HL60 cell differentiation, E2F plays a direct role in the transcriptional control of the c-myc gene through interaction with the retinoblastoma protein. A potential role for the c-Myc protein is discussed in relation to an existing state of E2F and E2F-RB complexes in the HL60 cells.
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Asialofetuin-labeled liposomes (AF-liposomes) were developed as a nonviral vector having high transfection activity for receptor-mediated gene transfer to hepatocytes by systemic administration. Initially, the majority of pSV2CAT, a chloramphenicol acetyltransferase (CAT) gene expression plasmid, was associated with AF-liposomes (AF-liposome-pSV2CAT), and they were injected into the portal vein of an adult mouse. Significantly high CAT activity was observed in the liver. The CAT activity in the liver was further increased two-fold by using AF-liposomes completely encapsulating pSV2CAT. Nonlabeled control liposomes, on the other hand, showed lower CAT activity in the liver than in the spleen or lung. The level of CAT mRNA reflected the CAT activity obtained by each liposome preparation in each tissue. Immunohistochemical staining showed that CAT was produced in a large number of parenchymal cells localizing in the periportal area. The plasmid encapsulated in the internal aqueous layer of the liposomes was effectively protected from environmental degradation. Thus, by administration into the blood circulation, AF-liposomes would be successfully incorporated into hepatocytes through receptor-mediated endocytosis, and the encapsulated plasmid would be transferred to the intracellular pathway.
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