[Fatal case of Crow-Fukase syndrome with kidney failure, acute consciousness disorder and thrombocytopenia].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Takano.
Explore the source record for details and available documents.
MEF2D, a member of myocyte-specific enhancer binding factor 2 (MEF2) gene family, was shown by Northern blot hybridization to be strongly expressed in the head portion of mouse embryos at later stages of ontogenesis, in the cerebellum and the cerebrum of adult mice, in cultured cell lines of neuronal origin, and in skeletal and cardiac muscles. During ontogenesis, MEF2D transcripts were detected by in situ hybridization in the olfactory bulb, entorhinal cortex, pyriform cortex, and hippocampus, in Purkinje and granule cells, and in large neurons in both the ventral and dorsal horns of spinal cord. Adult mice continued to express MEF2D in these limited areas of the central nervous system. Thus, MEF2D seems to be involved in either the differentiation process or the function of these neurons.
Explore the source record for details and available documents.
Orthotopic penetrating guinea pig to rat and chicken to rat corneal xenografts were performed to examine the nature of the host response. Guinea pig to rat xenografts failed at a median of day 3 after surgery. A similar but slightly accelerated pattern of failure was seen in guinea pig xenografts performed in prevascularized recipient rat corneas. Chicken to rat xenografts failed at a median of day 2 after grafting. Rat corneal isograft controls survived indefinitely. Corneal endothelial cells were visible by silver staining on the xenografts immediately after operation, which indicates that failure was not due to loss of these cells during surgery. Histopathology and immunoperoxidase staining indicated that xenograft failure in euthymic recipients was characterized by early corneal epithelial and endothelial cell damage, granulocytic infiltration, and hemorrhage from recipient corneal and iris capillaries, followed at 7-14 days by infiltration with T cells, macrophages, and eosinophils. An accelerated pattern of graft failure was also observed in guinea pig grafts into homozygous nude rat recipients, which suggests that preformed anti-donor antibody and complement were responsible for some of the early graft damage. Flow cytometry demonstrated the presence of pre-existing natural antibodies to guinea pig and chicken lymphocytes and erythrocytes, as expected from other studies. Immunohistochemistry showed the presence of rat IgG2a, IgG1, and IgM, but not IgD deposited on grafts in immunocompetent recipients on the first postoperative day. We conclude that orthotopic corneal xenografts undergo substantial accelerated damage mediated by pre-existing antibody, followed at 7-14 days by a cell-mediated response that causes further destruction.
Protein kinase C (PKC) isozyme(s) involved in regulation of platelet-activating factor (PAF)-induced phospholipase D (PLD) activation was investigated in CHO cells stably expressing cloned guinea-pig PAF receptor (WT-H cells). Three PKC isozymes, alpha, epsilon, and zeta, were identified by Western blotting, which displayed different kinetics of translocation from cytosol to membrane upon PAF stimulation. Cytosolic PKC alpha was rapidly translocated to membrane in response to PAF within 30 s and then returned to cytosol by 10 min. This kinetics was well correlated with PAF-induced transient PLD activation. Pretreatment of the cells with 100 nM 4 beta-phorbol 12-myristate 13-acetate (PMA) for 2 h resulted in down-regulation of PKC alpha, leaving PKC epsilon and zeta unchanged. Under the same conditions, PAF and PMA-mediated PLD activation were markedly reduced. These data suggest that PKC alpha is involved in the regulation of PAF-stimulated PLD activation in WT-H cells.
Desensitization of a chemotactic receptor is an adaptive process that terminates inflammation. Although homologous desensitization can be well explained by the action of specific receptor kinases, the mechanisms of heterologous desensitization remain elusive. As an approach to evaluate the roles of Gq pathway in desensitization of calcium signaling, we expressed a constitutively active Gq alpha mutant (Gq alpha Q-L) together with platelet-activating factor (PAF) receptor in Xenopus laevis oocytes. Gq alpha Q-L expression completely attenuated the calcium-sensitive chloride current and the 45Ca release elicited by PAF. The Gq-mediated desensitization could not be ascribed to G protein/receptor uncoupling via receptor phosphorylation, because (i) PAF-induced inositol 1,4,5-trisphosphate (IP3) synthesis was only partially suppressed and (ii) a mutated PAF receptor devoid of all Ser and Thr in the third cytoplasmic loop and in the C-terminal tail was also completely desensitized by Gq alpha Q-L. In Gq alpha Q-L expressing oocytes, microinjection of IP3 failed to elicit the calcium response, and the IP3 receptor, detected by a specific antibody, disappeared. Thus, the Gq-mediated desensitization can be most likely explained by IP3 receptor down-regulation. These novel mechanisms may explain in part heterologous desensitization in chemotactic factor-stimulated inflammatory cells.
Platelet-activating factor (PAF) is a potent lipid mediator of allergic inflammation through its interaction with eosinophils. Expression of the PAF receptor is modulated by many agents, including those responsible for cell differentiation. We report here that differentiation of a human eosinophilic leukaemia cell line, EoL-1, by sodium n-butyrate is associated with induction of PAF receptor gene expression, as indicated by: PAF receptor mRNA accumulation; increases in the binding of [3H]WEB 2086, a PAF antagonist; analysis of cell-surface expression of PAF receptor protein using a monoclonal anti-(PAF receptor) antibody; and augmentation of PAF-induced increase in the intracellular concentration of calcium. Using cDNA cloning, the receptor expressed in EoL-1 cells was identified as 'Transcript 1', one of two transcripts which was previously reported from human genomic analysis (Mutoh, Bito, Minami, Nakamura, Honda, Izumi, Nakata, Kurachi, Terano and Shimizu (1993) FEBS Lett. 322, 129-134). The PAF-induced calcium response and phosphoinositide turnover were decreased by pertussis toxin (PTX) treatment, suggesting that these signals are coupled largely with PTX-sensitive G-protein(s) in EoL-1 cells. These systems may provide a useful experimental model with which to investigate the relationship between eosinophilic differentiation and PAF receptor induction, and the role of eosinophils in allergic responses.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We found a 81-year-old man with Hashimoto's disease and bullous pemphigoid whose activated partial thromboplastin time (APTT) and prothrombin time (PT) were prolonged. Mixing studies with normal plasma failed to correct APTT and PT, suggesting the presence of circulating inhibitor. The patient's factor V activity was 11% of normal control and was not corrected by mixing with normal plasma, indicating the presence of an inhibitor against factor V. This inhibitory activity was observed up to 32 times dilution of the patient's plasma. The inhibitor activity against factor V was not detected in the fraction of the patient's plasma that passed through Protein A Sepharose, but detected in the elution with glycine-HCl buffer. Furthermore, using SDS-PAGE and immunoblotting method, purified IgG from the patient's plasma reacted with a protein with molecular weight (74KD) equivalent to F1F2 of factor Va which was activated by thrombin. The inhibitory activity was associated with IgG4 subclass. These data indicate that the inhibitor was IgG antibody which inhibit F1F2 of factor V. Autoimmune mechanism was strongly suggested for the development of the antibody.
Neuropathological findings in two siblings with familial erythrophagocytic lymphohistiocytosis (FEL) are reported. Case 1 showed the typical neuropathological findings of FEL with lymphohistiocytic infiltration of the leptomeninges and perivascular spaces. A characteristic erythrophagocytosis was detected in inguinal lymph nodes, lung and bone marrow. Case 2 revealed calcification and necrotic lesions in the brain. In the necrotic areas, parenchymal calcification, vascular medial calcification, and occlusion of many vessels due to subendothelial fibrosis were detected. The areas of necrosis correlated with the distribution of occluded vessels. These changes were most prominent in putamen, internal capsule, thalamus and dentate nucleus. Hypercytokinemia is suspected to be the underlying mechanism for the clinical and laboratory findings in patients with FEL, although the relationship to the vascular pathology is unclear.
A 4-year-old girl was diagnosed as having acute renal failure due to tubulointerstitial nephritis. The girl presented with remittent fever, vomiting and non-oliguric acute renal failure with sterile pyuria and tubular reabsorptive dysfunction. Ultrasound examination revealed that the kidneys were markedly enlarged with diffuse hyperechogenicity in the cortex when the abnormal renal function was present and were restored in size and echogenicity when the renal function normalised. A diagnosis of Yersinia pseudotuberculosis infection was based on a rise in haemagglutination titres against the organism.
This study was designed to (i) analyze community health in post-industrial, densely populated Tokyo, and (ii) find a statistical-based prediction model for the health level of the communities from the environment. For this purpose, we compiled health-level indicators for each city-ward, and indicators for demography, infrastructure, land-use, amenities, education, working conditions, economics, and medical and welfare services. The health factors and the environmental factors were obtained by using weighted principal factor analysis; their relation was examined by weighted correlation analysis and weighted linear regression analysis. One to six environmental factors correlating significantly to health were found for each health-level indicator or factor. The prediction model explained up to 0.98 of the variance of the health-level factors and indicators. This analysis elicited health-determinant factors in various fields. The community health level was well reproduced by the present method; the model will be conducive to decision making pertaining to health policies.
Three non-allelic rat calmodulin (CaM) genes CaMI, CaMII and CaMIII, which share no homology in their 5'-upstream regions, are coordinately expressed in neurons of the central nervous system (CNS). Deletion analysis of the CaMIII promoter showed that the upstream segments longer than 700 bases functioned as efficient promoters, and that the sequence from -133 to -65 was required for the activity of house-keeping type promoter in transient expression assays on a mouse glioma cell line C6. However, the transient expression seemed not to be cell type specific. To determine the temporal and spatial specificity of the promoter function, we produced transgenic mice carrying a fusion gene of the CaMIII segment from -877 to +103 and the lacZ reporter gene. In CNS of the adult transgenic mice, the localization of transgene expression was similar to that of endogenous CaMIII transcripts analyzed by in situ hybridization. The transgene was expressed prominently in pyramidal cells of the cerebral neocortex and the hippocampal regions CA1 to CA3, in Purkinje cells of the cerebellar cortex, and in neurons of the spinal cord, and moderately in granule cells of the dentate gyrus and the cerebellar cortex. In the developing CNS, the overall profiles of neuron-specific expression were also similar for both transgene and endogenous CaMIII that were expressed in the mantle layer and the dorsal root ganglia of the embryonal spinal cord. These results indicated that the neuron-specific expression of rat CaMIII was directed by this 877-base promoter sequence. The CaMIII segment used for the promoter of transgene contained a 29-bp sequence at -410, namely H3, which was conserved in the upstream regions of vertebrate CaMII and CaMIII. H3 seemed to play a pivotal role in the temporal and spatial expression of transgene in CNS, although the deletion of H3 did not decrease CAT activity in the transient expression. The transgene expression was not observed in the external granular cells of the developing cerebellum and in some neurons of the embryonic sensory ganglia in which the endogenous CaMIII was obviously expressed. Therefore, the other cis-acting element(s) located outside of this 877-bp segment seemed to be required for the temporal regulation of CaMIII in certain rudimentary neurons.
The effect of ethanol on nitrite oxidation was investigated in the perfused rat liver. Real-time spectral changes in catalase were obtained using a reflectance scanning spectrophotometer in rat liver perfused with Krebs-Henseleit bicarbonate buffer in a non-recirculating system. The nitrite oxidation rate and nitrate production rate were calculated from the differences in concentrations between the influx and efflux perfusates and from the flow rate/g liver weight. Nitrite infusion caused an increase in absorbance difference delta A (640-660 nm), indicating decomposition of catalase compound I to the free form. Administration of ethanol during the nitrite infusion caused a further increase in delta A (640-660 nm) and significant decreases in both the nitrite oxidation rate and the nitrate production rate. Both the nitrite oxidation rate and nitrate production rate decreased, depending on the concentration of ethanol administered. At 10 mM ethanol, they reached about half the rates before the ethanol infusion. In conclusion, ethanol inhibits nitrite oxidation by catalase in the perfused rat liver at relatively low concentrations that can be realized in blood by daily alcohol consumption.
By immunoblotting using monoclonal antibodies against phosphotyrosine, thyroid stimulating hormone (TSH)-induced changes in tyrosine phosphorylation of intracellular proteins in earlier passages of rat thyroid cells (FRTL-5) were studied. TSH and N6-2'-O-dibutyryladenosine 3'-5'-cyclic monophosphate (Bt2cAMP) decreased the phosphotyrosine content of 110,000-130,000 M(r) substrate (p120) in parallel with a morphological change in FRTL-5 cells. Insulin-like growth factor-I (IGF-I) or phorbol 12-myristate 13-acetate (PMA) only showed an attenuated reaction compared with that of TSH or Bt2cAMP. Further, sodium orthovanadate (a protein tyrosine phosphatase inhibitor) could not inhibit this reaction. These data suggest possible inhibitory effects of TSH and adenosine 3'-5'-cyclic monophosphate (cAMP) on tyrosine kinases that act on this substrate.
Explore the source record for details and available documents.
The relationship between sleep habits and psychosomatic health complaints was investigated by a questionnaire study in 148 bank workers in Tokyo. Daily bedtime was more flexible than daily rising time, and both mean bedtime and rising time tended to be earlier with increasing age. Multiple logistic regression analysis showed that psychosomatic health complaints of sleep disturbances, fatigue, digestive troubles, and depressive mood were significantly associated with sleep habits and perceived mental stress.