Giant cell tumor arising from the spinous process of the sacrum.
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Biomedical subjects
Publications and source records attributed to H Yoshikawa.
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Cathepsins D, K, and L were immunolocalized in tissue undergoing endochondral ossification in the human. Cathepsins D, K, and L were localized in osteoclasts and chondroclasts attached to bone matrix and cartilage matrix, respectively. Cathepsins D and L were immunostained in chondrocytes. Immunolocalization of cathepsin D was limited to hypertrophic chondrocytes adjacent to the osteochondral junction. In contrast, cathepsin L was immunolocalized in both proliferating and hypertrophic chondrocytes. In the bone marrow space, cathepsins D, K, and L were localized in multinucleated cells. Cathepsin D was diffusely detected in mononuclear bone marrow cells which were negative for cathepsins K and L. The present findings indicated that cathepsins K, D, and L were associated with the process of endochondral ossification in the human, and suggested that these cathepsins share roles in bone and cartilage turnover in the human.
Myelin-associated oligodendrocytic basic protein is a member of the proteins constituting the central nervous system myelin. By morphometric analysis, we demonstrated that axons of myelin-associated oligodendrocytic basic protein-deficient mice had larger diameters and more myelin lamellae as compared to those of wild-type mice at the same age. It is known that the number of myelin lamellae increases linearly with axonal diameter, and that the rate of radial axonal growth is the factor controlling the rate of myelin formation. In line with these observations, we found that the regression line for axonal diameter and the number of myelin lamellae in myelin-associated oligodendrocytic basic protein-deficient mice appeared to be identical to that in wild-type mice, indicating that the increase in the number of myelin lamellae was the result of the increase in axonal diameter. Furthermore, we generated myelin basic protein/myelin-associated oligodendrocytic basic protein-double-deficient mice through mating myelin-associated oligodendrocytic basic protein-deficient mice with shiverer mice, an autosomal recessive mutant characterized by a lack of all isoforms of myelin basic protein. With these knock-out mice, we showed that axons of the double-deficient mice had larger diameters and smaller form factor, an index of the deformation of the fiber contour, in ensheathed fibers than those of shiverer mice, although there was no difference in axonal diameter of unmyelinated fibers between them. Taken together, myelin-associated oligodendrocytic basic protein seemed to play a role in controlling axonal diameter and in keeping axons round.
Tone burst evoked otoacoustic emissions (TBEOAEs) were measured for two tone bursts presented separately and as a two-tone burst complex to examine the linearity of TBEOAE generators for different frequency separations of the stimuli. The stimuli were: (a) tone bursts of 5-ms duration and center frequencies of 1, 1.5, 2 and 3 kHz; (b) complex stimuli with the 1-kHz tone burst combined digitally with each of the other specified tone bursts. Signals were delivered at 70 dB SPL using a non-linear processing method and at 60 dB SPL using a linear method to 21 ears of normally hearing adults. Spectra of TBEOAEs obtained with single-tone bursts were superimposed (composite) and compared to those of the two-tone burst complex. A close correspondence between the composite and complex spectra was present in all ears. However, the components on the higher-frequency slope of the 1-kHz spectral peak were reduced in the complex spectra obtained with a frequency separation of 0.5 kHz when compared to the corresponding composite spectra. The reduction was greater at a stimulus level of 70 dB SPL than with 60 dB SPL. The effect was smaller for a frequency separation of 1 kHz, and almost absent for the tone burst separation of 2 kHz. Thus, suppression leads to weak non-linear frequency superposition for higher-level, closely spaced stimuli.
A 6-year-old severely handicapped boy with haloperidol-induced mild rhabdomyolysis without neuroleptic malignant syndrome is reported. He had suffered from frontal lobe epilepsy, severe mental retardation and involuntary movements. To reduce the involuntary movements, oral administration of haloperidol was started. Haloperidol was effective for the involuntary movements, and he became well. However, his urine was sometimes dark brown, and the myoglobin level in his urine was increased. After discontinuation of haloperidol, his urine never became dark brown. It was suspected that haloperidol might cause mild rhabdomyolysis without neuroleptic malignant syndrome. Neuroleptic malignant syndrome is a rare but severe adverse effect of neuroleptics, and is usually accompanied by rhabdomyolysis. Although there have been a few adult cases presenting rhabdomyolysis without neuroleptic malignant syndrome, this patient might be the first child case with such symptoms. We have to pay attention to this syndrome when using haloperidol even in children.
Midazolam is a water-soluble benzodiazepine, and has recently emerged as a safe and effective treatment option after ordinary antiepileptic therapy in the management of status epilepticus. However, midazolam as a first-line agent for status epilepticus in children has not been fully investigated. Intravenous midazolam was used for status epilepticus in 27 children (38 convulsive episodes) from January 1997 to December 1999 in our hospital. Among them, 10 patients (16 convulsive episodes) were treated with intravenous midazolam as a first-line agent. The causes of the seizures varied. Midazolam was administered as an intravenous bolus dose (0.1-0.3 mg/kg), followed by continuous intravenous infusion (1-8 microg/kg per min). In all epileptic episodes but one, the seizures stopped within 1 min without any adverse effects. These results were compatible with the previously reported ones. It is important to terminate status epilepticus which can cause brain damage. Midazolam seems to be effective and safe as a first-line therapy for status epilepticus in children.
We investigated the time-dependent natural course of experimental osteonecrosis (ON), including initial changes in ON and the reparative process, using in vivo serial repetitive magnetic resonance imaging (MRI) in a non-traumatic rabbit serum sickness ON model. Some necrotic lesions were detected at 1 week (3 of 16 femora with necrotic lesions) and some in the metaphysis were detected by 12 weeks (2 of 6 femora with lesions) on T(1)-weighted, T(2)-weighted, and fat suppression T(1)-weighted images. On contrast-enhanced MRI, extravasation of the erythrocytes was detected at 72 h (7 of 26 femora with lesions) as a small, focal enhanced area. Necrotic lesions were detected in all abnormal femora by 6 weeks (16 of 16 femora with lesions) as focal, homogeneously or inhomogeneously enhanced areas. Reparative tissue replaced with new vascular and trabecular formation in necrotic areas was detected as an extended marginal enhanced area at 12 weeks. These results suggest that the enhancement patterns on contrast-enhanced MRI may provide helpful information about the developmental and reparative process of clinical ON.
We report a 12-month-old Japanese female with incontinentia pigmenti, in whom magnetic resonance imaging (MRI) disclosed a small transient lesion in the white matter. After birth, she developed some vesicular skin eruptions that mainly involved the lower extremities. These skin lesions increased in size and number and became hyperpigmented within 2 weeks. At 1 month of age, MRI revealed a small hypointense lesion on T(1)-weighted imaging, with water density on T(2)-weighted imaging, in the right centrum semiovale. At 4 months of age, her hyperpigmented lesions had faded, and at 7 months of age, MRI disclosed the disappearance of the previously observed abnormality. She exhibited no neurologic abnormalities. No cases have been reported concerning a transient lesion in the white matter revealed by MRI in incontinentia pigmenti. Although the pathogenesis is unknown, transient central nervous system involvement might have occurred in early infancy as did the fading skin lesions.
In the course of studying carboxypeptidase Y (CPY) production, we found that the expression level of the gene, which is under the control of the GAL10 promoter, increased in a Saccharomyces cerevisiae gal80 mutant grown in a medium containing ethanol as the sole carbon source. In the cultivation of the gal80 mutant KS58-2D/pCY303 carrying a multicopy plasmid, which contains the PRC1 gene fused to the GAL10 promoter, CPY production continued after the consumption of galactose. In this phase, the cells utilized ethanol as the carbon source. To increase the CPY production level, we examined the effect of carbon source feeding in a fed-batch culture. The production level in the fed-batch culture using ethanol was 1.3-fold higher than that in a batch culture and 1.6-fold higher than that in a fed-batch culture using galactose. By 5'-deletion analysis of the GAL10 promoter, the region between -256 and -232 was found to be important for the promoter activity in the gal80 mutant growing in the presence of ethanol.
A method for industrial-scale preparation of carboxypeptidase Y (CPY), which was secreted by Saccharomyces cerevisiae KS58-2D/pCY303 into the culture broth, was developed. Because the purification process consists of a few simple unit operations including only one chromatography step, a higher CPY recovery was achieved than that in the process using disrupted baker's yeast. Approximately 100 g of purified CPY powder was constantly obtained using the final culture broth from a 500-l fermentor.
This article explores the implications of recent welfare-related policy change for the well-being of children in low-income families, and for research investigating child development processes and outcomes. It provides an overview of current welfare-related policies and explores the implications for developmental researchers. The article also synthesizes early findings from research, highlighting both overall impacts and the more nuanced evidence that while families are transitioning off welfare, only a small number are transitioning out of poverty, and a subgroup of families at risk are not faring well. It then examines, from a theoretical and methodological framework, what developmental psychopathology might bring to the study of welfare-related impacts on children in the context of this complex and changing policy landscape, and what welfare researchers might bring to the field of developmental psychopathology. The article concludes with broad recommendations for both research and policy.
PURPOSE: For determination of the transit time through various parts of the gastrointestinal (GI) tract, we developed a method that provides the location of disintegration and drug release. This method involves GI magnetomarkergraphy (GIMG) using a 129-channel Shimadzu vector biomagnetic measurement system (BMS). METHODS: To magnetically label the pressure-controlled colon delivery capsule (PCDC) containing 75.0 +/- 0.5 mg of caffeine as a tracer drug, small capsule caps containing 90 mg of ferric oxide powdered magnetite (Fe2O3) were attached to PCDCs. After orally administration to fasted human volunteers, saliva samples were collected hourly and salivary caffeine concentration was measured. At the same time, locations of the magnetic PCDC were detected by BMS just after the PCDCs were magnetized with the coils of a magnetic resonance imaging (MRI) system. The magnetic field distributions were analyzed and the estimated positions were shown on the MRI picture of the same subject's abdominal structure. RESULTS: We magnetized PCDC with permanent magnets or an electromagnet before ingestion and the estimated locations of PCDC in the GI tract exhibited high estimation error. In order to increase the precision of estimated localization of PCDCs, PCDCs were magnetized within the coils of the MRI. As a result, these PCDCs had strong magnetic dipoles that were parallel to the sensor unit of BMS in every measurement, and therefore the spatial resolution of the PCDC's two-dimensional positions in the organs of the GI tract was within a range of several millimeters. CONCLUSIONS: GIMG is a powerful tool for the study of colon delivery efficiencies of PCDCs. The main advantage of GIMG is the capability to obtain even more detailed knowledge of the behavior and fate of solid pharmaceutical formulations during GI passage.
Human promyelocytic leukemia HL-60 cells are well known to differentiate into granulocytes or monocytes in the presence of some agents such as DMSO or PMA, respectively. Differentiated HL-60 cells become resistant to some apoptotic stimuli including anticancer drugs or irradiation though undifferentiated cells significantly respond to these stimuli. TRAIL (TNF-related apoptosis-inducing ligand) which is also known as Apo2 ligand (Apo2L), a new member of TNF family, can induce apoptosis in some tumor cells but not in many normal cells. We show here that apoptosis is well induced in HL-60 cells by TRAIL, but susceptibility to TRAIL is reduced during granulocytic differentiation by DMSO. We also suggest some possible mechanisms by which granulocytic differentiated cells become resistant to TRAIL-induced apoptosis. First, in granulocytic differentiated cells, expression of antagonistic decoy receptors for TRAIL (TRAIL-R3/TRID/DcR1/LIT and TRAIL-R4/TRUNDD/DcR2) were enhanced. In addition, expression of Toso, a cell surface apoptosis regulator, seemed to block activation of caspase-8 by TRAIL via enhanced expression of FLIPL in granulocytic differentiated cells. These findings suggest that differentiated cells are resistant using plural mechanisms against various apoptosis-inducing stimuli rather than undifferentiated cells.
The Bacillus subtilis clpX and clpP genes are the sites of pleiotropic mutations that adversely affect growth on a variety of media and impair developmental processes such as sporulation and competence development. ClpX is necessary for the post-exponential induction of genes that require the sigmaH form of RNA polymerase for transcription. Both ClpX and ClpP are required for the activation of sigmaA-dependent transcription of the srf operon that encodes surfactin synthetase and the regulatory peptide ComS, required for the development of genetic competence. Transcription of srf is activated by the two-component regulatory system ComPA in response to the peptide pheromone, ComX, which mediates cell density-dependent control. A clpX mutant, although able to produce ComX, is unable to respond to the pheromone. A mutant allele of comP, encoding a product whose activity is independent of ComX, is not able to suppress clpX with respect to srf expression, suggesting that ClpXP acts at the level of ComA-dependent activation of srf transcription initiation. Suppressor mutations of clpX (cxs-1 and cxs-2) were isolated in screens for pseudorevertants exhibiting high levels of srf expression and sigmaH-dependent transcription respectively. One mutation, cxs-1, suppressed a clpP null mutation with respect to srf transcription, but did not overcome the block conferred by clpP on competence development and sporulation. Both cxs-1 and cxs-2 mutations map to the region of the rpoA gene encoding the RNA polymerase alpha C-terminal domain (alphaCTD). The reconstruction of the cxs-1 and cxs-2 alleles of rpoA confirmed that these mutations confer the suppressor phenotype. These findings provide further support for the hypothesis that ClpX and ClpP might be intimately associated with transcription initiation in B. subtilis.
The expression of thrombospondin-1 (TSP-1) and its role in gliomas have not been well examined. In the present study TSP-1 expression in a panel of malignant glioma cell lines and the expression of TSP-1 and transforming growth factor (TGF-beta) proteins in low-grade and malignant glioma tissues were investigated. Reverse transcription-polymerase chain reaction analysis showed that nine of nine malignant glioma cell lines expressed TSP-1 mRNA, and seven of nine glioma lines expressed TSP-2 mRNA. Production and secretion of TSP-1 were examined in the T98G glioblastoma cell line by western blot analysis. Total TSP-1 protein content in the supernatant was 10 times higher than that in the cell lysate. Secretion of TSP-1 was examined in these glioma cell lines by western blot analysis. All glioma lines secreted significant levels of TSP-1. Bioassay showed that all tumor lines had the capacity to activate latent TGF-beta. Localization of TSP-1, TGF-beta1, -beta2, and -beta3 was examined immunohistochemically in surgically resected glioma tissues, including 11 glioblastomas, six anaplastic astrocytomas, and eight astrocytomas. Most glioblastomas expressed high levels of both TSP-1 and TGF-beta. Anaplastic astrocytomas expressed moderate levels of TSP-1 and TGF-beta. Most malignant gliomas expressed various levels of TGF-beta1, -beta2, and -beta3. The expression of both proteins, however, was weak in low-grade gliomas. Normal brain tissues around the tumors were negatively or very weakly positively stained for TSP-1 and TGF-beta. These results indicate that most malignant glioma cells express TSP-1 in vitro and in vivo, and the expression of TSP-1 and TGF-beta in vivo correlates with the histologic malignancy of glioma. Overexpression of both TSP-1 and TGF-beta may increase the biologic malignancy of malignant gliomas, through generating the active form of TGF-beta in tumor tissues.
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Hepatic lesions in 25 sika deer (Cervus nippon Temminck) aged 1-15 days, affected by selenium-deficiency cardiomyopathy, were examined histopathologically. Characteristic pathological findings, induced by stagnation of the plasma proteins of the cytoplasm, consisted of vacuolar degeneration of hepatocytes, formation of hyalin droplets, and ceroid-lipofuscinosis. Electron microscopically, these changes were closely associated with degeneration of the endoplasmic reticulum and mitochondria. Peroxisomes, which were observed around the vacuoles, were regarded as a reactive result of membrane disturbance caused by a decrease in glutathione peroxidase (GSH-Px)
We examined both knees in 60 patients with nontraumatic osteonecrosis of the femoral head with three-dimensional MRI. We found osteonecrosis of the patella in 9 patients (10 knees) and osteonecrosis of the femoral or tibial condyles/metaphyses in 35 patients (61 knees). In the patella, the necrosis was located in the proximal half and tended to develop in patients with other necrotic lesions in the knee.