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Yoshihiro Takeuchi

Publications and source records attributed to Yoshihiro Takeuchi.

33 records · Page 2Linked to original sources
PubMed2004

Peters' anomaly with bilateral perisylvian polymicrogyria and abdominal calcification.

We report a neonatal case of Peters' anomaly with bilateral perisylvian polymicrogyria and abdominal calcification. The male infant was born after a normal labor. Bilateral central corneal opacities with iridocorneal strands indicated Peters' anomaly. The X-ray and abdominal computed tomography demonstrated multiple calcifications beneath the diaphragma around the liver and the spleen. TORCH serology was negative. Intracranial calcification was not detected. Brain magnetic resonance imaging demonstrated bilateral perisylvian polymicrogyria. Abdominal calcification was suspected to be related to vascular disruption. Bilateral perisylvian polymicrogyria has been thought to result from ischemic events such as intrauterine hypotension or vascular occlusions. Based on these considerations, we conclude that a vascular disruption sequence may an important pathogenetic mechanism of Peters' anomaly.

Abdomen↗
PubMed2004

Radial and tangential neuronal migration disorder in ibotenate-induced cortical lesions in hamsters: immunohistochemical study of reelin, vimentin, and calretinin.

To investigate the mechanisms of radial and tangential neuronal migration disorders, immunohistochemical expressions of reelin, vimentin, and calretinin were examined in brain lesions induced by ibotenate (an agonist of the N-methyl-D-aspartate [NMDA] complex receptor) in hamsters. Thirty-four newborn hamsters were subjected to intracerebral injections of ibotenate, and 12 animals served as the control. These hamsters were examined at 1, 2, 3, 5, and 7 days after injections. The cortical lesions observed after ibotenate injections had a strong resemblance to the following neuronal migration disorders: (1) microgyria, (2) focal subcortical heterotopia, and (3) leptomeningeal glioneuronal heterotopia. In microgyria, the radial glial fibers were sparsely distributed, but in leptomeningeal glioneuronal heterotopia, vimentin-positive fibers extended into this abnormal neural tissue. Calretinin-immunoreactive neurons and fibers were present along the lesion forming the microgyria and abnormal neuronal arrangement. Focal subcortical heterotopia also included a small number of calretinin-expressing neurons originating from the subplate neuronal population. These results imply that the neuronal migration disorders produced by ibotenate show not only the migrational arrest of neurons but also interference from the termination of the migration process. We also suggest that the heterotopic neurons constituting the focal subcortical heterotopia originate in the lateral or medial ganglionic eminence of the ventral telencephalon, probably caused by the abnormal tangential neuronal migration.

Animals↗
PubMed2004

Expression and regulation of RB1CC1 in developing murine and human tissues.

RB1-inducible coiled-coil 1 (RB1CC1) is a novel molecule implicated in the regulation of RB1 (retinoblastoma 1) expression. However, information about the RB1CC1 gene is limited and its function remains somewhat obscure. The present study analyzes the expression and promoter activities of RB1CC1 in developing murine and human tissues. Rb1cc1 was abundantly expressed from an early stage of the mouse embryo throughout development. Immunohistochemical analyses revealed that Rb1cc1 was ubiquitous in the mouse, rather than in the human embryo, especially in the musculoskeletal system, heart and neural tissues. Promoter activity was highest in a region located about 300 bp immediately upstream of exon 1 in both the mouse and human RB1CC1 genes, suggesting that this region is a core promoter. The promoter activity of RB1CC1 was generally higher in mice than in humans, and suppressive with intron 1, especially in humans. These results suggested that more Rb1cc1 is expressed throughout developing murine than in human tissues, and that RB1CC1 expression is controlled more stringently by modification at intron 1 in humans than in mice.

Animals↗
PubMed2003

TRAIL/Apo2L ligands induce apoptosis in malignant rhabdoid tumor cell lines.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) is a potent inducer of apoptosis in various cancer cells, whereas normal cells are not sensitive to TRAIL-mediated apoptosis. Four TRAIL/Apo2L receptors (DR4, DR5, DcR1, and DcR2) have been identified. DR4 and DR5 have a death domain, whereas DcR1 and DcR2 are called decoy receptors because of their incomplete or lack of a death domain. Malignant rhabdoid tumor (MRT) is an aggressive neoplasm showing a poor prognosis because of its resistance to chemotherapeutic agents. In this study, we examined whether TRAIL could induce apoptotic cell death in MRT cell lines. We found that although half of the MRT cell lines examined were sensitive to TRAIL/Apo2L, Western blot analysis revealed that the expression of DcR2 was low in TRAIL-sensitive MRT cells. We examined the effect of doxorubicin on the expression levels of TRAIL receptors and its enhancement on the susceptibility of MRT cell lines to TRAIL. Western blot and flow cytometric analyses revealed that doxorubicin significantly increased the expression of DR5, and somewhat up-regulated the expression of DR4 and DcR2. Moreover, doxorubicin, NF-kappaB inhibitor (SN50), and PI3-kinase/Akt inhibitor (wortmannin, LY294002) enhanced the susceptibility of MRT cell lines to TRAIL/Apo2L-induced apoptosis. These results suggest that TRAIL/Apo2L may provide the basis for clinical trials of TRAIL-based treatment to improve the outcome of MRT patients.

Animals↗
PubMed2003

A pediatric patient with sporadic dentatorubral pallidoluysian atrophy.

We report a 10-year-old girl with the juvenile type of dentatorubral pallidoluysian atrophy. There were no affected family members, suggesting a sporadic case. Deoxyribonucleic acid analysis for the dentatorubral pallidoluysian atrophy gene was performed, and the CAG trinucleotide repeat numbers in this patient were 61/15. Gene analysis of the patient's parents was not performed. The molecular mechanisms of the occurrence of sporadic cases have not been clarified.

Adult↗
PubMed2003

Ring chromosome 14 with localization-related epilepsy: three cases.

Three patients showing epileptic seizures and with mosaicism of ring chromosome 14 and monosomy for chromosome 14 are described. Patients were a 17-year-old boy, karyotype 46, XY, r(14)(p12q32.33)/45, XY, -14, a 7-month-old boy, karyotype 46, XY, r(14)(p11.2q32.33)/45, XY, -14, and a 10-month-old boy, karyotype 46, XY, r(14)(p12q32.31)/45, XY, -14. Microcephaly and alopecia were observed in the first patient. However, few dysmorphic features were found typical of ring 14 chromosome. He had exhibited complex partial seizures with secondary generalization at age 3 months and had mild motor and mental retardation. Both other patients had atonic seizures followed by staring, perioral cyanosis, and respiratory arrest at age 7 or 8 months. Both also showed mild developmental delay and had a few minor anomalies compatible with ring 14 chromosome. Interictal spikes were observed in the second patient in the right occipital region, whereas an interictal encephalogram of the third patient showed sporadic spikes in the left central region. In all three cases, seizures were resistant to common antiepileptic drugs.

Adolescent↗
PubMed2003

Malignant rhabdoid tumor shows a unique neural differentiation as distinct from neuroblastoma.

Malignant rhabdoid tumors (MRT) show a multiphenotypic diversity, including a neural phenotype. To elucidate the difference in neural characteristics between MRT and neuroblastoma, we examined the expression of synapsin I, neuron-restrictive silencer factor (NRSF), neurofilament medium-size (NF-M) and chromogranin A (CGA) in five MRT cell lines (TM87-16, STM91-01, TTC549, TTC642 and YAM-RTK1) and five neuroblastoma cell lines under differentiation-induction with 12-O-tetradecanoylphorbol-13-acetate (TPA). Our results showed TM87-16 and TTC642 cells, expressed synapsin I and NF-M before TPA induction, had a neural phenotype. After differentiation-induction, only TM87-16 cells expressed CGA. Among all neuroblastoma cells, expression of NF-M and CGA was stable at a high level throughout TPA-induced differentiation. In TM87-16 and TTC642 MRT cells, synapsin I mRNA promptly increased after TPA differentiation, with the peak level at 6 h, and thereafter, synapsin I mRNA rapidly decreased in a time-dependent manner. The decreased expression of synapsin I correlated with an increased expression of NRSF during differentiation-induction. In contrast, in some neuroblastoma cells, a significant up-regulation of synapsin I was observed concurrently with a down-regulation of NRSF. The inverse relationship between NRSF and synapsin I expression in TM87-16 and TTC642 MRT cells was opposite to that of neuroblastoma cells. Our results showed that the neural characteristics of these MRT cells are fairly distinct from those of neuroblastoma cells. These MRT cells appeared to have only limited capability for neural differentiation, and were still in an extremely early stage of neural differentiation.

Cell Differentiation↗
PubMed2003

Expression of pericyte, mesangium and muscle markers in malignant rhabdoid tumor cell lines: differentiation-induction using 5-azacytidine.

Malignant rhabdoid tumor (MRT) has been considered to have multiphenotypic diversity characteristics. Some MRTs exhibit a neural phenotype. However, it is still unclear whether MRT cells can display a skeletal muscle, smooth muscle or smooth muscle-like cell phenotype, like those of pericytes and mesangial cells. To determine if MRTs exhibit skeletal muscle cell or smooth muscle-like cell phenotypes, six MRT cell lines (TM87-16, STM91-01, TTC549, TTC642, YAM-RTK1 and TTC1240) were examined for markers of skeletal muscle (MyoD, myogenin, myf-5, myf-6, acetylcholine receptor-alpha, -beta and -gamma), smooth muscle (alpha-smooth muscle actin, SM-1 and SM22), and smooth muscle-like cells, such as pericytes (angiopoietin-1 and -2) and mesangial cells (megsin), using conventional RT-PCR, semi-quantitative PCR, western blotting and immunocytochemistry before and after differentiation-induction with 5-azacytidine. alpha-Smooth muscle actin and SM22 were detected in all six MRT cell lines, while MyoD and myf-5, crucial markers for skeletal myogenic determination, were not. The TM87-16 cell line expressed SM-1 and angiopoietin-1. TTC1240 also expressed angiopoietin-1. Interestingly, STM91-01 expressed megsin, a novel marker for mesangial cells, in addition to angiopoietin-1. Our results indicated that some MRTs exhibited smooth muscle and/or smooth muscle-like cell phenotypes and some renal MRTs might be of mesangial origin. Recently, smooth muscle and also smooth muscle-like cells have been considered to be of neuroectodermal origin. MRT can thus considered to belong to the category of primitive neuroectodermal tumors (PNETs) in the broad sense.

Antimetabolites, Antineoplastic↗
PubMed2002

Malignant rhabdoid tumor shows incomplete neural characteristics as revealed by expression of SNARE complex.

To elucidate the biological differences in neural phenotype between malignant rhabdoid tumor (MRT) and neuroblastoma cell lines, we examined the expression of solube N-ethylmaleimide-sensitive fusion protein attachment protein receptor (SNARE) complex proteins in MRT cell lines under differentiation induction with 12-O-tetradecanoylphorbol-13-acetate (TPA). Six MRT cell lines (TM87-16, STM91-01, TTC642, TTC549, YAM-RTK1, and TTC1240) and six neuroblastoma cell lines (IMR-32, NH12, SCCH26, TGW, NB-1, and NB-NR) were used in this study. Expression of SNAREs: the vesicle SNARE (synaptotagmin, synaptophysin, and synaptobrevin-2) and the target SNARE (syntaxin 1A, SNAP-25A/B) was examined. Our results showed that in MRT cells, only two cell lines (TM87-16, TTC642) expressed the vesicle SNARE and the target SNARE with the exception of SNAP-25B, while all neuroblastoma cells expressed the entire SNARE complex. During differentiation, synaptotagmin was upregulated in these two MRT cell lines. Interestingly, synaptophysin was downregulated in these MRT cell lines in contrast with the neuroblastoma cell lines. SNAP-25B was not expressed in MRT cells after differentiation with TPA. MRT cells having a neural phenotype morphologically looked like neuroblastoma cells after treatment with TPA. However, the expression of SNARE complex was incomplete in MRT cells. Our results suggest that the biological characteristics of MRT cells with neural phenotype are distinct from those of neuroblastoma cells.

Blotting, Western↗
PubMed2002

Cytotoxic edema and interleukin-6 in hypertensive encephalopathy.

We report a female, 10 years of age, with juvenile rheumatoid arthritis accompanied by hypertensive encephalopathy. The patient developed a cytotoxic brain lesion, as revealed by the high signal intensity on diffusion-weighted magnetic resonance imaging, which corresponded to the hypoperfusion area on single-photon emission computed tomography scan using (99m)Tc-ethylcysteinatedimer. Cerebrospinal fluid interleukin-6 activity was elevated when the hypertensive encephalopathy revealed active central nervous system disease, and its activity decreased when the encephalopathy recovered from the central nervous system manifestations. We speculated that the cytotoxic edema and associated parenchymal damage in hypertensive encephalopathy were closely related to the intrathecal overproduction of interleukin-6.

Brain↗
PubMed2002

Estrogen receptor expression and estrogen receptor-independent cytotoxic effects of tamoxifen on malignant rhabdoid tumor cells in vitro.

Recent studies have shown that the antiestrogen tamoxifen (TAM) can be used in the treatment of malignant neoplasms other than breast cancer. In the present study, we investigated the expression of estrogen receptor (ER) in six malignant rhabdoid tumor (MRT) cell lines. Alterations in MRT cell growth in response to estrogen or antiestrogens (4-hydroxytamoxifen (4-OHT), TAM, and ICI 182 780) were also investigated. RT-PCR and western blotting showed that ER-alpha was expressed in three of the six MRT cell lines. While 17-beta-estradiol (E2) did not significantly alter MRT cell line proliferation, the hydroxylated tamoxifen metabolite 4-OHT significantly inhibited the growth of all 6 MRT cell lines. However, the steroidal antiestrogen ICI 182 780 did not alter the proliferation of any of the MRT cell lines. 4-OHT induced apoptosis in both ER-alpha-negative and ER-alpha-positive MRT cell lines, as assessed by nuclear morphology and DNA fragmentation. Neither growth inhibition nor induction of apoptosis due to 4-OHT was blocked by the addition of excess E2. Our data suggested that 4-OHT induced cytotoxic effects against MRT cells, and that these effects were independent of ER expression.

Apoptosis↗
PubMed1999

Hypothalamic aggression area under serotonergic control in mouse-killing behaviour of rats.

The serotonergic system participates in the modulation of aggressive behaviour. We examined the neuronal substrate underlying serotonergic control of aggressive behaviour in rats using a transplantation technique. Fetal serotonergic neurons transplanted into the hypothalamus restored inhibition of mouse-killing behaviour (muricide), in rats with raphe lesions induced by a serotonergic neurotoxin, 5,7-dihydroxytryptamine. Immunohistochemical and neurochemical studies indicated that the recovery of serotonergic innervation in the lateral hypothalamic area by the raphe grafts brought about the inhibition of muricide. The extension of serotonergic fibres into the lateral hypothalamic area from the grafted serotonergic neurons is strongly related to inhibition of muricide. These results indicate the possibility that serotonergic neurons regulate muricide through the inhibition of the activity of the lateral hypothalamic area neurons.

Journal Article↗