Search PubMed⌕ Search

Biomedical subjects

T Terada

Publications and source records attributed to T Terada.

At least 55 records · Page 3Linked to original sources
PubMed2001

Expression of c-fos, heat shock protein 70, neurotrophins, and cyclooxygenase-2 mRNA in response to focal cerebral ischemia/reperfusion in rats and their modification by magnesium sulfate.

The marginal area surrounding a region of ischemic brain tissue, designated as the penumbra, is of interest as a potential area for the rescue of neurons from cell death. Despite its clinical importance, relatively little is known about the molecular events leading to changes in brain cells in the penumbra following ischemia. In the first part of this study, we used in situ hybridization to investigate the temporal and spatial expression of c-fos, heat shock protein 70 (HSP70), neurotrophins and inducible cyclooxygenase-2 (COX-2) in the rat brain following a 2-h occlusion of the middle cerebral artery (MCA) with reperfusion. In the penumbra and surrounding cortex, upregulation of c-fos, brain-derived neurotrophic factor (BDNF), and COX-2 mRNAs was observed, while expression of HSP70 mRNA was restricted to the penumbra. This spatial discrepancy of mRNA expression suggests that different mechanisms are involved in the regulation of c-fos/BDNF/COX-2 and HSP70 expression. Intravenous infusion of magnesium sulfate (25 mg/kg) decreased both the infarct volume and upregulation of these mRNAs, suggesting its therapeutic potential.

Animals↗
PubMed2001

Fate of the mutated IgG2 heavy chain: lack of expression of mutated membrane-bound IgG2 on the B cell surface in selective IgG2 deficiency.

IgG2 deficiency is clinically characterized by sinopulmonary infections caused by pneumococcus and Hemophilus. We reported homozygous one-base insertion (1793insG) in the C(gamma)2 gene in two Japanese siblings in whom serum IgG2 levels were under detection limits. The 1793insG was present in exon 4, just upstream from the alternative splice site for M exons; the result being a complete amino acid change in transmembrane and cytosolic parts of membrane-bound gamma2 heavy chain (m gamma 2HC). To determine why this mutation caused selective and complete IgG2 deficiency, we constructed expression vectors of normal and mutant membrane-bound chimeric IgG heavy chain cDNAs. Stable transformants, Ag8N-L and Ag8M-L, expressing either normal and mutant chimeric IgG heavy chain with light chain respectively were obtained using P3X63Ag8653 as recipient cells. Of the Ag8N-L, 22.1% were surface IgG+; however, none of the Ag8M-L were surface IgG+. Addition of an anti-human IgG antibody induced cell death of Ag8N-L and we considered that the expressed chimeric IgG protein on Ag8N-L might function as the Ig receptor for signal transduction. However, Ag8M-L did not express mutant IgG on its surface nor did it secrete this mutant into culture medium. The mutant chimeric IgG protein was rapidly degraded within Ag8M-L. Thus, the mutated IgG2 heavy chain in our patient could not be expressed on the cell surface because of loss of the transmembrane domain and the evolutionally conserved cytoplasmic domain. In humans, B cells expressing surface IgG are indispensable for secretion of IgG.

Amino Acid Sequence↗
PubMed2001

Phosphatidylinositol 3-kinase in cumulus cells and oocytes is responsible for activation of oocyte mitogen-activated protein kinase during meiotic progression beyond the meiosis I stage in pigs.

The roles of phosphatidylinositol 3-kinase (PI 3-kinase) during meiotic progression beyond the meiosis I (MI) stage in porcine oocytes were investigated. PI 3-kinase exists in cumulus cells and oocytes, and the PI 3-kinase inhibitor, LY294002, suppressed the activation of mitogen-activated protein (MAP) kinase in denuded oocytes during the beginning of the treatment. However, in denuded oocytes cultured with LY294002, the MAP kinase activity steadily increased, and at 48 h of cultivation MAP kinase activity, p34(cdc2) kinase activity, and proportion of oocytes that had reached the meiosis II (MII) stage were at a similar level to those of oocytes cultured without LY294002. In contrast, LY294002 almost completely inhibited the activation of MAP kinase, p34(cdc2) kinase activity, and meiotic progression to the MII stage in oocytes surrounded with cumulus cells throughout the treatment. Treating cumulus oocyte complexes (COCs) with LY294002 produced a significant decrease in the phosphorylation of connexin-43, a gap junctional protein, in cumulus cells compared with that in COCs cultured without LY294002. These results indicate that PI 3-kinase activity in cumulus cells contributes to the activation of MAP kinase and p34(cdc2) kinase, and to meiotic progression beyond the MI stage. Moreover, gap junctional communications between cumulus cells and oocytes may be closed by phosphorylation of connexin-43 through PI 3-kinase activation in cumulus cells, leading to the activation of MAP kinase in porcine oocytes.

Animals↗
PubMed2001

Dynamic changes of connexin-43, gap junctional protein, in outer layers of cumulus cells are regulated by PKC and PI 3-kinase during meiotic resumption in porcine oocytes.

Mammalian oocytes are surrounded by numerous layers of cumulus cells, and the loss of gap junctional communication in the outer layers of cumulus cells induces meiotic resumption in oocytes. In this study, we investigated the dynamic changes in the gap junctional protein connexin-43 in cumulus cells during the meiotic resumption of porcine oocytes. The amount of connexin-43 in all layers of cumulus cells recovered from cumulus-oocyte complexes was increased after 4-h cultivation. However, at 12-h cultivation, the positive signal for connexin-43 immunoreactivity was markedly reduced in the outer layers of cumulus cells. When these reductions of connexin-43 were blocked by protein kinase C (PKC) or phosphatidylinositol (PI) 3-kinase inhibitor, networks of filamentous bivalents (i.e., advanced chromosomal status) were undetectable in the germinal vesicle of the oocyte. After 28-h cultivation, when the majority of oocytes were reaching the metaphase I (MI) stage, the connexin-43 in the inner layers of cumulus cells was phosphorylated, regardless of mitogen-activated protein (MAP) kinase activation. These results suggest that the initiation of meiotic resumption, namely, the formation of networks of filamentous bivalents in germinal vesicle, is associated with the reduction of gap junctional protein connexin-43 in the outer layers of cumulus cells via the PKC and/or PI 3-kinase pathway. Moreover, the connexin-43 in the inner layers of cumulus cells is phosphorylated during meiotic progression beyond the MI stage, regardless of MAP kinase activation in cumulus cells surrounding the oocyte.

Animals↗
PubMed2001

Inhibition of phosphatidylinositol 3-kinase or mitogen-activated protein kinase kinase leads to suppression of p34(cdc2) kinase activity and meiotic progression beyond the meiosis I stage in porcine oocytes surrounded with cumulus cells.

In this study, the effects of U0126 that inhibits the activity of mitogen-activated protein (MAP) kinase kinase (MEK), and LY294002, which is a phosphatidylinositol (PI) 3-kinase inhibitor, on meiotic progression beyond the metaphase I (MI) stage in porcine oocytes were examined. Cumulus-oocyte complexes (COCs) were cultured for 22 h with 50 microM LY294002 or 10 microM U0126 following cultivation for the initial 22 h. MAP kinase activity in oocytes cultured with LY294002 or U0126 was significantly lower than that in control oocytes cultured for up to 44 h. U0126 and LY294002 significantly decreased p34(cdc2) kinase activity and the proportion of oocytes reaching the MII stage compared to those in control oocytes. Oocytes denuded after COCs had been cultured for 22 h were cultured further for 22 h with U0126 or LY294002. In the denuded oocytes, U0126 suppressed MAP kinase activity, p34(cdc2) kinase activity, and meiotic progression to the MII stage; however, LY294002 did not significantly affect the activity of these kinases and meiotic progression. These results suggest that increasing MAP kinase activity in oocytes via the PI 3-kinase signaling pathway in cumulus cells is involved in the stimulation of maturation promoting factor, leading to meiotic progression beyond the MI to MII stage in porcine oocytes.

Animals↗
PubMed2001

Nucleotide sequence of the precore/core gene and X gene of hepatitis B virus DNA in asymptomatic hepatitis B virus carriers who are negative for serum hepatitis B core antibody.

A hepatitis B virus (HBV) carrier who is positive for hepatitis B surface (HBs) antigen but negative for hepatitis B core (HBc) antibody despite persistent HBV infection, is designated as having hepatitis B virus 2 (HBV2). HBV2 is reported to be induced by mild-grade hepatitis. Patients with HBV2 have been reported in Taiwan and Senegal. In the present study, we determined the nucleotide (nt) sequence of the precore/core gene coding region and X gene region of the HBV DNA sequence in 7 subjects who were positive for HBs antigen and negative for HBc antibody. HBV DNA was detected by nested polymerase chain reaction (PCR). Nested PCR was carried out to amplify the precore/core and X open reading frames (ORFs) of HBV DNA. The second PCR products were sequenced, followed by investigation of nt homology. There were no deletions nor insertions in the nt sequence of the precore/core and X ORFs in the HBV DNA of these 7 patients, and mutations were found only sporadically in the 7 patients. Also, there were no common amino acid substitutions in the examined regions of the amino acid sequence of HBV in the 7 patients, and we could not find a common mutation in the examined regions of HBV DNA that could potentially contribute to the development of negativity for HBc antibody. Thus, it is suggested that negativity for HBc antibody in patients with HBV2 is due to an immune response abnormality in the host.

Adolescent↗
PubMed2001

Characterization of the mouse TFF1 (pS2) gene promoter region.

Trefoil peptides (TFFs) with a unique trefoil domain(s) are presumed to function in protection and repair of the gastrointestinal epithelial layer. Three peptide family members are differently distributed in the mouse gastrointestinal tract: TFF1/pS2 specifically in stomach, TFF2/SP mainly in stomach, pancreas and duodenum, and TFF3/ITF in intestine. We cloned and sequenced the mouse TFF1 gene 5'-upstream region by means of the genomic walking procedure. The cloned region was ligated to the luciferase reporter gene and then introduced into mouse gastric surface mucous GSM10 cells which express TFF1 and TFF2. The minimum promoter was located in the region containing the TATA-box between -39 and the transcriptional start site. Further upstream regions stimulated (-2192-- -1630bp, -641-- -243bp, -137-- -39bp) and inhibited (-1630-- -641bp, -243-- -137 bp) luciferase gene expression. These regions as well as short segments conserved in the mouse and human 5'-upstream sequences may be important for modulation of the mRNA level of the TFF1 gene.

Animals↗
PubMed2001

Bone defect associated with middle meningeal arteriovenous fistula treated by embolization--case report.

A 57-year-old male presented with a frontal bone defect associated with a middle meningeal arteriovenous fistula (AVF) manifesting as headache. The patient had a history of head injury 19 years previously. Skull radiography and computed tomography demonstrated a left frontal bone defect. Left external carotid angiography demonstrated a middle meningeal AVF at the frontal region, at the same location as the bone defect. The AVF was fed by the bilateral middle meningeal and left deep temporal arteries, and drained by the superior sagittal and ipsilateral cavernous sinuses. The minor feeding artery, the left deep temporal artery, was embolized with polyvinyl alcohol particles, then 0.4 ml of a 1:3 mixture of n-butyl cyanoacrylate and lipiodol was injected from the left middle meningeal artery. Follow-up angiography 3 months after the embolization revealed complete obliteration of the fistula. The bone defect may have been caused by erosion of the frontal bone by the pulsating effect of the feeding and draining vessels of the fistula, or by inadequate nutrition to the bone tissue because of the arteriovenous shunt.

Arteriovenous Fistula↗
PubMed2001

Effect of the factor inhibiting germinal vesicle breakdown on the disruption of gap junctions and cumulus expansion of pig cumulus-oocyte complexes cultured in vitro.

The present study was undertaken to explore the regulatory mechanisms for meiotic resumption of pig cumulus-oocyte complexes (COCs) by assessing the nuclear status of oocytes, the degree of gap junction cell-to-cell communication and cumulus expansion after culture of various numbers of COCs in 10 microl droplets of medium for 24 h. Gap junction communication was examined by confocal laser scanning microscopy after injection of a fluorescent dye, lucifer yellow, into the oocytes. When one, three or six COCs were cultured in a 10 microl droplet, germinal vesicle breakdown was observed in > 70% of oocytes; increasing the number of COCs in a droplet further actually decreased the proportion of oocytes undergoing germinal vesicle breakdown (10 COCs: 49%; 20 COCs: 21%; 40 COCs: 13%). When six COCs were cultured in a 10 microl droplet of conditioned medium (prepared previously by culturing 20 intact and oocytectomized COCs for 24 h), the proportion of oocytes undergoing germinal vesicle breakdown was significantly reduced compared with the proportion in fresh medium. An increase in the proportion of category 1 COCs (all gap junctions within cumulus cells and between cumulus cells and oocyte are functionally maintained) was achieved by increasing the number of COCs cultured in a 10 microl droplet. The addition of conditioned medium to the fresh medium at a concentration of 50% significantly inhibited cumulus expansion. From these results, it is concluded that the factors secreted by cumulus cells regulate the disruption of gap junctions and cumulus expansion, and concurrently control the incidence of germinal vesicle breakdown in pig COCs.

Animals↗
PubMed2001

Recognition and transport characteristics of nonpeptidic compounds by basolateral peptide transporter in Caco-2 cells.

Recent studies have revealed that diverse compounds lacking peptide bonds, such as valacyclovir and delta-aminolevulinic acid (delta-ALA), can be recognized by H+-coupled peptide transporters (PEPT1 and PEPT2). In the present study, recognition and transport characteristics of nonpeptidic compounds by the basolateral peptide transporter, which is distinct from PEPTs, were compared with those by PEPT1 using the human intestinal Caco-2 cells. [14C]Glycylsarcosine uptake via PEPT1 was inhibited by all nonpeptidic compounds tested. Similarly, most nonpeptidic compounds showed an inhibitory effect on [14C]glycylsarcosine uptake by the basolateral peptide transporter, although some kinds of nonpeptidic compounds, such as valine methyl ester, did not. Direct measurements of valacyclovir and delta-ALA transport revealed that both compounds were able to be transported by the basolateral peptide transporter. Because delta-ALA has been used recently in vitro and in clinical studies as an endogenous photosensitizer for photodynamic therapy, the intestinal transport characteristics of delta-ALA were further examined. Inhibition studies and Eadie-Hofstee plot analysis suggested that delta-ALA transport across the brush-border and basolateral membranes of the intestine was mainly mediated by peptide transporters. In addition, the apical-to-basolateral transport of delta-ALA was greater than that of the opposite direction. These findings provide the first evidence that the intestinal basolateral peptide transporter can recognize and transport nonpeptidic compounds, and play a definitive role in the absorption of delta-ALA.

ATP-Binding Cassette Transporters↗
PubMed2001

[E-cadherin].

Explore the source record for details and available documents.

Animals↗
PubMed2000

Accelerated growth of hepatocytes in association with Up-regulation of cyclin E in transgenic mice expressing the dominant negative form of retinoic acid receptor.

Retinoids play an important role in pathogenesis of liver diseases. To clarify the functional role of retinoic acid (RA) in liver, we developed transgenic mice (Tg) which express the dominant negative form of retinoic acid receptor (RARE) in liver. Here, we report that proliferation of hepatocytes in RARE Tg is greatly enhanced and that cyclin E is up-regulated in RARE Tg. Liver weight, liver/body weight, and proliferating cell nuclear antigen (PCNA) labeling index in RARE Tg were significantly increased, compared to those in wild-type mice (P < 0.01, each). Cell cycle analysis showed that 2N DNA content cells and aneuploid area between 2N and 4N DNA, reflecting S phase cells, were significantly increased in RARE Tg, compared to wild-type mice (P < 0.01, each). Of G1 phase-related proteins including cyclins, cyclin-dependent protein kinases (CDKs) and cyclin-dependent protein kinase inhibitors (CKIs), cyclin E mRNA and protein was up-regulated in liver from RARE Tg by reverse transcription polymerase chain reaction and Western blot analysis. Furthermore, the immunoprecipitation with anti-cdk2 antibody, followed by Western blot analysis with anti-cyclin E antibody indicated that cyclin E/cdk2 complex is increased in liver of RARE Tg. The results of the present study suggest that cyclin E in association with cdk2 governs cell cycle progression through G1 in hepatocytes where function of RA is inhibited.

Aneuploidy↗
PubMed2000

Inhibitory effect of novel oral hypoglycemic agent nateglinide (AY4166) on peptide transporters PEPT1 and PEPT2.

The novel oral hypoglycemic agent nateglinide (AY4166) is a nonsulfonylurea insulin secretagogue, and its pharmacokinetic features include rapid absorption and elimination. As nateglinide is a dipeptide-like drug, we investigated the interaction of nateglinide with peptide transporters PEPT1 and PEPT2, which mediate the absorption of various peptide-like drugs. Nateglinide exhibited a potent inhibitory effect on [14C]glycylsarcosine uptake by the human colon adenocarcinoma cell line Caco-2 and rat PEPT-transfectants. Kinetic analysis revealed that these inhibitory effects were noncompetitive. Na(+)-coupled alanine or threonine uptake by Caco-2 cells was not inhibited by nateglinide, suggesting that the inhibitory effect of nateglinide on peptide transporters was not due to nonspecific interaction. There was little uptake of [14C]nateglinide by peptide transporters. Various sulfonylureas, such as glibenclamide, also inhibited [14C]glycylsarcosine uptake by rat PEPT-transfectants. In conclusion, nateglinide as well as sulfonylureas inhibit the transport activity of PEPT1 and PEPT2, although nateglinide itself is not transported by these transporters.

Administration, Oral↗
PubMed2000

Dephosphorylation-induced decrease of anti-apoptotic function of Bcl-2 in neuronally differentiated P19 cells following ischemic insults.

It is known that Bcl-2 has a protective effect against neuronal ischemia. Some reports speculate anti-apoptotic function of Bcl-2 depends not on the expression level but on the phosphorylation state. We found induction of apoptosis and CPP32 activation by energy impairment (3-nitropropionic acid (3-NP)-treatment or glucose-deprivation) in the neuronally differentiated P19 cells. Time course study of cell viability following ischemic insults showed that the number of viable cells decreased along with the increase in the amount of dephosphorylated Bcl-2 without obvious quantitative alteration of the protein. Then, we generated differentiated P19 cells overexpressing wild-type Bcl-2 (P19/wt. Bcl-2) or phosphorylation-negative Bcl-2 mutant (P19/mut.Bcl-2), in which alanine was substituted for serine 70. When the cell viability was examined within 24 h, P19/mut.Bcl-2 was more vulnerable to energy impairment as compared with P19/wt.Bcl-2. In addition, overexpression of wild-type Bcl-2 inhibited DNA laddering and CPP32 activation induced by the insults, while that of mutant Bcl-2 did not. These findings suggest that the phosphorylation state, as well as the expression level, of Bcl-2 plays an important role to modulate its protective effect against ischemic insults.

Animals↗
PubMed2000

Vitreous surgery simulator.

OBJECTIVE: To reduce the surgical risks to patients and expose surgeons to surgical experience and complications, we have developed a practical system of vitreous surgery using virtual-reality technology. METHODS: The system is composed of high-resolution color stereo binoculars, haptic devices, foot switches, and a high-speed graphics computer. To simulate vitreous surgery, we created several virtual patient eyes with retinal diseases such as preretinal membranes and subretinal neovascular tissue at the fovea. RESULTS: The simulator provided the trainees with an operating environment similar to an actual one, and allowed them to learn to maneuver surgical instruments and remove proliferative tissue on the retina, under the retina, or both. This system allowed surgeons to avoid iatrogenic complications through visual signs such as retinal hemorrhage when the instrument contacted the retinal surface. CONCLUSIONS: This simulator may not only be suitable for residents to learn ocular surgical techniques but may also allow veteran surgeons to develop new surgical methods and skills.

Computer Simulation↗
PubMed2000

Treatment of restenosis after percutaneous transluminal angioplasty for internal carotid artery stenosis.

The efficacy of repeated percutaneous transluminal angioplasty (PTA) and carotid endarterectomy (CEA) was examined in patients with restenosis after PTA for carotid stenosis. After percutaneous transluminal angioplasty (PTA) for 63 cases of internal carotid stenoses 13 cases of restenosis appeared. They were treated by PTA or carotid endarterectomy. The treatment was chosen by the patient after explanation of each treatment. We initially treated seven patients by repeat PTA and six by carotid endarterectomy. The degree of stenosis improved from 82% to 30% on average after repeated PTA. However, one patient in the PTA group had restenosis, and carotid endarterectomy was then performed. The other cases also had restenosis and were treated by PTA. The six cases treated by carotid endarterectomy were successfully treated without difficulty. The success rate of PTA was 5/7 (71%) in the restenosis cases. Patients with a greater residual stenosis after initial PTA had significantly more frequent restenosis. Repeat PTA and CEA both appeared effective treatment for restenosis after initial PTA, although PTA had a restenosis rate similar to that of initial PTA.

Aged↗