Posterior fossa chondroma arising from the tentorium: a case report.
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Biomedical subjects
Publications and source records attributed to S Nagata.
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A peptide with paralytic activity in larvae of the silkworm, Bombyx mori, was isolated from its hemolymph. Purification procedures consisted of extraction with 50% acetone, Vydac C4 reversed-phase cartridge elution and 4 steps of reversed-phase HPLC. Injection of the purified peptide into 4th instar B. mori larvae caused rapid and rigid paralysis for 2 min at a dose of 3.4 ng/larva. This paralytic peptide consists of 23 amino acid residues containing 2 cysteines with an intra-disulfide bond. The complete amino acid sequence is: H-Glu-AsnPhe-Val-Gly-Gly-Cys-Ala-Thr-Gly-Phe-Lys-Arg-Thr-Ala-Asp-G ly-Arg-Cys-Lys-Pro-Thr-Phe-OH. The relationship between structure and the biologic activity of synthetic analogs indicated that the entire amino acid sequence and the intra-disulfide bond were necessary for biological activity.
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Caspase-activated DNase (CAD) degrades chromosomal DNA during apoptosis, whereas ICAD (inhibitor of CAD) inhibits the CAD's DNase by binding to it. Here, we describe the assignment of murine CAD and ICAD genes to the distal part of murine chromosome 4. Molecular cloning and structural analysis indicated that CAD and ICAD genes are comprised of 7 and 6 exons, respectively. Two different ICAD mRNAs coding for two forms of ICAD proteins (ICAD-S and ICAD-L) were found to be produced by alternative splicing of intron 5. The CAD and ICAD mRNAs were detected ubiquitously in various murine tissues. Analyses of the promoter activity with a series of deletion mutants of their 5' flanking regions indicated that a 190-bp 5' flanking region of the CAD gene was sufficient to promote the transcription. Whereas, a 120-bp flanking region of ICAD gene was required to promote its transcription. These regions do not show similarity between CAD and ICAD genes, suggesting that expression of CAD and ICAD genes is regulated by different mechanisms.
Autoimmune diseases, especially autoimmune thyroid disease, frequently develop after delivery due to the immune rebound mechanism. Most cases have transient dysfunction of affected organs. Cardiac dysfunction developed after delivery is called postpartum or peripartum cardiomyopathy. However, the aetiology of the disease is not clarified yet. Here we report three cases that developed acute heart failure in the postpartum period. One was complicated with an atrioventricular block and postpartum autoimmune thyroiditis. All patients recovered to normal cardiac function or pre-attack condition after 1 month of therapy with conventional drugs and bed rest. All three had positive antiheart antibody detected by indirect immunofluorescence assay, and one had antibody to heart myosin detected by enzyme-linked immunosorbent assay. Moreover, one of two patients examined revealed lymphocytic infiltration by endomyocardial biopsy. Antibodies to 26 viruses were not elevated significantly during the first 2 weeks after admission in any case. It is strongly suggested that heart failure is induced by postpartum autoimmune myocarditis, and thus clinicians should be aware of this disease.
Several anti-Fas ligand (FasL) inhibitory mAb (FLIM) were raised and characterized in this study. One, FLIM58, showed more potent neutralizing activity than Fas-Fc, the previously established artificial neutralizing agent for FasL. Several murine models of acute graft-versus-host disease (GVHD) after allogeneic bone marrow transplantation have been used to show that both FasL and perforin, the major effector molecules of cytotoxic T lymphocytes, are involved in this disease. In our GVHD model, FasL rather than perforin was associated with lethality. Administration of FLIM58 or Fas-Fc reduced the weight loss and mortality caused by GVHD, although other signs of GVHD, such as skin lesions, lymphoid hypoplasia and mononuclear cell infiltration in the liver, did not improve significantly. FLIM58 was more effective than Fas-Fc in reducing mortality. Our results demonstrated that neutralizing agents for FasL are therapeutic for lethal GVHD.
The responses of plasma adrenocorticotropin (ACTH), cortisol, noradrenaline and adrenaline in 5 Thoroughbred horses to an incremental exercise and 2 relative workload exercises, at 105 and 80% maximal oxygen consumption (VO2max), on a treadmill were examined. These hormone concentrations increased (P < 0.05) with each exercise and the maximal plasma concentrations of ACTH, cortisol were observed between 5 and 30 min after the end of the exercise, while maximal catecholamine concentrations occurred just at exhaustion time. The plasma ACTH, noradrenaline and adrenaline responses during exercise were more sensitive to the intensity of exercise than that of cortisol and showed a significant correlation with blood lactate concentrations (r = 0.605, P < 0.001 for ACTH; r = 0.718, P < 0.001 for noradrenaline; r = 0.738, P < 0.001 for adrenaline). The plasma cortisol response appeared to be connected with the duration of exercise (r = 0.71, P < 0.05). The recovery of these hormones was related to the exercise styles. These results suggest that the autonomic nervous system and the pituitary-adrenal axis of the horse are efficiently stimulated by various treadmill exercises, and these hormones may be used in the evaluation of exercise-induced stress.
Our aim was to investigate plasma catecholamine responses to so-called 'doping' drugs and exercise in Thoroughbreds. Plasma adrenaline (Ad) and noradrenaline (NA) were determined after the administration of caffeine and promazine hydrochloride (PRZ) using a high performance liquid chromatographic method. Caffeine or PRZ was administered i.m. to Thoroughbreds and its effects on plasma catecholamines at rest and during exercise were compared with the saline control. The treadmill exercise was performed 1 h after administration. A dose of 5.0 mg/kg bwt caffeine was found to significantly increase both plasma Ad and NA levels but this was not the case for the 2.5 mg/kg bwt dose and their peak levels at 1.5 h were about 3 and 2.5 times as compared with the control values at 1.5 h (Ad: mean +/- s.e. 21.2 +/- 2.8 pg/ml, NA: 55.5 +/- 4.1 pg/ml), respectively. Both 1.0 and 1.5 mg/kg bwt PRZ doses reduced the plasma Ad to below the detection limit (10 pg/ml) and significantly reduced the plasma NA. The 2.5 mg/kg bwt caffeine dose significantly increased plasma Ad and NA during exercise and approximately doubled their maximal values as compared with the saline control (Ad: mean +/- s.e. 12.328 +/- 4.733 ng/ml, NA: 9.997 +/- 4.146 ng/ml). The 1.5 mg/kg bwt PRZ dose decreased the plasma Ad during exercise but the effect was not significant. On the other hand, PRZ significantly increased the plasma NA as compared with the saline control. In conclusion, the present study demonstrates that the plasma catecholamine responses to caffeine and PRZ were modified by exercise. It is probable that the modification may be related to exercise-induced activation of the sympathetico-adrenal axis.
The immune response is regulated not only by cell proliferation and differentiation, but also by programmed cell death, or apoptosis. In response to various stimuli, death factors bind to their respective receptors and activate the apoptotic death program in target cells. A cascade of specific proteases termed caspases mediates the apoptotic process. The activated caspases cleave various cellular components, a process that leads to morphological changes of the cells and nuclei, as well as to degradation of the chromosomal DNA. Loss-of-function mutations in the signaling molecules involved in apoptosis cause hyper-proliferation of cells in mouse and human. In contrast, exaggeration of this death cascade causes the destruction of various tissues.
BACKGROUND: The present study aimed to determine the psychophysiological changes induced in subjects by standard autogenic training (AT). Physiological measurements were taken under strict experimental conditions. METHODS: Thirty-one healthy students were divided randomly into two groups: the AT group and the control group. In the first session, the physiological variables were measured for all students before and after all were asked to relax in their own way. The AT group were then taught AT for 3 months, after which time the measurements were repeated. In the second session, the AT group practised the standard AT exercise, while the control group repeated their own form of simple relaxation. Electrocardiogram, plethysmogram (PTG) and blood pressure (BP) were measured while the students carried out a breathing rate of 15 cycles/min. The R-R intervals and BP were analysed by an autoregressive model for spectral analysis, and the data were compared by repeated-measures ANOVA. RESULTS: The AT group had a significant increase in the mean R-R interval and a significant decrease in the baseline deflection of the PTG in the second session. There were no significant changes in sympathetic activity except for the change in the PTG, although low frequency amplitude of systolic BP decreased slightly. CONCLUSIONS: AT was found to induce significant changes that were independent of respiration in healthy students, although paced breathing might have operated as a mental stress. The increase in mean R-R interval and the decrease in baseline deflection of the PTG were the most robust correlates of AT.
The Fas ligand is predominantly expressed in activated T lymphocytes and is one of the major effector molecules of cytotoxic T lymphocytes and natural killer cells. Previously, we found excessive apoptosis of epithelial cells and infiltrating lymphocytes expressing Fas ligand mRNA in the lung tissue of bleomycin-induced pulmonary fibrosis in mice. Here we demonstrated that the administration of a soluble form of Fas antigen or anti-Fas ligand antibody prevented the development of this model and that lpr and gld mice were resistant against the induction of pneumopathy. These results suggest that the Fas-Fas ligand pathway plays an essential role in the development of pulmonary fibrosis and that preventing this pathway could have therapeutic value in lung injury and fibrosis.
We have searched for phosphatidylinositol (PI)-3,4,5-trisphosphate (PIP3) binding proteins in Dictyostelium discoideum using beads bearing a PIP3 analogue, PIP3-APB. One of the binding proteins with a molecular mass of 55 kDa was purified and its amino acid sequence was partially analyzed. Database searches showed that the analyzed sequence was identical to that of protein kinase B (PKB) of D. discoideum. The specific activity of D. discoideum PKB, when expressed together with constitutively active PI-3 kinase in mammalian cells, was elevated by about three-fold, suggesting that PKB could also act downstream of PI-3 kinase in Dictyostelium cells.
The aim of this study was to clarify the effect of anabolic steroids on the testicular endocrine function of mature stallions. Mature thoroughbred stallions were treated with 800 mg nandrolone decanoate every 3 weeks for 3 months. After the first treatment, plasma concentrations of LH, immunoreactive inhibin and testosterone decreased rapidly to the nadir. These hormones were maintained at significantly lower concentrations compared with concentrations in intact stallions. Histology of the testicular tissue indicated the arrest of advanced spermatogenesis in the seminiferous tubules and a severe depletion of the number of Leydig cells in the interstitial compartment as a result of treatment. Most of the immunopositive cells for the inhibin alpha-subunit and steroidogenesis enzymes in the interstitial compartment decreased below detectable amounts, whereas immunopositive reactions of inhibin alpha-subunit in the seminiferous tubules were clearly observed. In conclusion, the treatment of mature stallions with nandrolone decanoate caused a decrease in the secretion of ir-inhibin and testosterone from the testis, the depletion of the number of Leydig cells and a decrease below detectable amounts of inhibin alpha-subunit and steroidogenesis enzymes. The concentration of ir-inhibin in the peripheral blood may be a useful marker for the examination of testicular activity in stallions being treated with anabolic steroids.
To develop an ultrasensitive immunoassay for microcystins (MCs), a group of heptapeptide hepatotoxins produced by cyanobacteria, we produced monoclonal antibodies (MAbs) which specifically recognize the immune complex (IC) formed by an anti-MC MAb (MC MAb) and MCs. The use of the anti-IC MAb (IC MAb) as the secondary antibody made it possible to develop a sandwich type immunoassay, which is theoretically superior to the widely used competitive immunoassay in sensitivity as well as accuracy. A MC MAb mixed with microcystin-LR (MCLR) to form the IC was immunized to mice. Three IC MAbs were obtained, all of which specifically reacted with the IC, but almost never reacted to MC MAb or MCLR in enzyme-linked immunosorbent assays (ELISAs). Binding kinetics study of one of the IC MAbs, 3F7, by a BIAcore biosensor technique revealed that 3F7 IC MAb could associate with free MC MAb as well as the IC, but the binding to free MC MAb was much more easily dissociated than that to the IC, thus resulting in about 300-fold higher affinity of 3F7 for the IC than for MC MAb alone (1.8 x 10(9) M(-1) and 4.6 x 10(6) M(-1) for the IC and MC MAb, respectively). Finally, 3F7 IC MAb was shown to react with the IC formed by the addition of MCLR to MC MAb-coated plates in a dose-dependent manner. Therefore, a new type sandwich immunoassay, anti-immune complex ELISA (IC ELISA) for MCs, was indeed established. The detection limit of the IC ELISA was 2 pg of MCLR ml(-1) (50 fg per assay), making it the most sensitive of all the methods for detecting MCs reported to date.
PURPOSE: To develop a systematic method and model for community health nursing diagnosis to be used in teaching and in community practices. METHOD: From searching the databases of Medline (from Jan. 1966 to May 1997) and the Japana Centra Revuo Medicina (from Jan. 1987 to Jan. 1997), literature on community diagnosis, community health nursing, diagnosis, assessment and analysis were classified into keywords, purposes, subjects, health problems and methods. RESULTS: 1. As an explanation of the process of nursing diagnosis the community-as-partner model (Anderson and McFarlane; 1995) is useful for understanding the target community and the use of the community health nursing diagnosis process. 2. The methodology of the community health nursing diagnosis is based on three strategies of public health diagnosis. The method of interview surveys was strengthened by incorporating the ethnographic method. 3. Several case studies in the partnership between communities and universities in USA were introduced. CONCLUSION: Changes in community health policy require that public health nurses develop specialized and comprehensive practices in their communities. The authors presented the model of the community health nursing diagnosis process and proposed a partnership between communities and universities. The construction of community health nursing diagnosis process in this paper is based on the public health diagnosis framework consisting of three strategies, to which analysis of existing data, a social survey utilized in epidemiological community diagnosis, and free interviewing from ethnographic methods are incorporated. Developing this systematic diagnosis process of facilitates the search for potential or actual community health problems or concerns, the practice of applying data from surveys and the discussion of concrete strategies toward problem solving. It is useful for educational and research processes and in practice in the community.
The binding of Fas ligand to Fas recruits caspase 8 to Fas via an adaptor, FADD/MORT1, and activates a caspase cascade leading to apoptosis. Here, we describe a human Jurkat-derived cell line (JB-6) that is deficient in caspase 8. This cell line was resistant to the apoptosis triggered by Fas engagement. However, the multimerization of Fas-associated protein with death domain, through the use of a dimerizing system, killed the JB-6 cells. This killing process was not accompanied by the activation of caspases or DNA fragmentation. The dying cells showed neither condensation nor fragmentation of cells and nuclei, but the cells and nuclei swelled in a manner similar to that seen in necrosis. These results suggested that Fas-associated protein with death domain can kill the cells via two pathways, one mediated by caspases and another that does not involve them.
Jurkat cells express Fas, and rapidly undergo apoptosis in response to Fas ligand or an agonistic anti-Fas antibody. This apoptotic pathway is mediated by a cascade of caspases. In this report, we show that Fas activation induced the processing of caspase 8 in Jurkat cells with a time frame similar to the activation of caspase 3 and the proteolysis of nuclear proteins. Jurkat cell transformants that overexpress Bcl-2 were partially but not completely resistant to the Fas-induced apoptosis. Little processing of caspase 8 was observed upon Fas activation in these transformants. Furthermore, although caspase 8 was recruited to Fas upon Fas activation in the parental Jurkat cells, the recruitment of caspase 8 to Fas was inhibited in the transformants overexpressing Bcl-2. These results suggest that Bcl-2 inhibits Fas-induced apoptosis by preventing the formation of the death-inducing signaling complex that is composed of Fas, FADD/MORT1, and caspase 8.