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T Terada

Publications and source records attributed to T Terada.

At least 91 records · Page 5Linked to original sources
PubMed2000

Immunoreactive E-cadherin, alpha-catenin, beta-catenin, and gamma-catenin proteins in hepatocellular carcinoma: relationships with tumor grade, clinicopathologic parameters, and patients' survival.

We evaluated the immunohistochemical expression status of E-cadherin, alpha-catenin, beta-catenin, and gamma-catenin, and the relationship with tumor grade, clinicopathologic parameters, and patients' survival, in 107 surgically resected hepatocellular carcinoma (HCC), using a semiquantitative scoring system. These molecules were largely located at the cell membrane of HCC cells. Compared with expression in nontumorous liver, E-cadherin showed underexpression, whereas alpha-, beta-, and gamma-catenins showed overexpression in most HCC. E-cadherin expression significantly correlated inversely with HCC histological grade, being the highest in well-differentiated HCC. In contrast, alpha-, beta-, and gamma-catenins' expression significantly correlated positively with HCC grade, being the highest in poorly differentiated HCC. Significant positive correlations were found between gamma-catenin high expression and capsular invasion or presence of satellite nodules, and between beta-catenin high expression and vascular invasion. Kaplan-Meier examination of patients' survival indicated that HCC patients with underexpression of E-cadherin, alpha-catenin, and gamma-catenin, and patients with overexpression of beta-catenin, had poor survival rates. These results suggest that E-cadherin is downregulated while the 3 catenins are upregulated in HCC, that E-cadherin expression inversely correlates with HCC grade while the 3 catenins' expression positively correlates with HCC grade, and that HCC patients with downregulation of E-cadherin, alpha-catenin, and gamma-catenin and HCC patients with upregulation of beta-catenin have poor prognosis.

Adolescent↗
PubMed2000

Protein expression of double-stranded RNA-activated protein kinase in thyroid carcinomas: correlations with histologic types, pathologic parameters, and Ki-67 labeling.

There have been no reports evaluating double-stranded RNA-activated protein kinase (PKR) in thyroid carcinomas. Therefore, we investigated the protein expression of PKR and its correlations with several pathologic parameters and Ki-67 labeling in 86 thyroid carcinomas, using a semiquantitative scoring method. Western blot analysis showed a specific band of 68 kDa corresponding to PKR molecular weight in 9 selected fresh samples. In immunohistochemistry of archival samples, PKR was expressed in 77 of 86 (90%) cases. The positive rate and PKR score were significantly higher in papillary carcinoma (75 of 80, 94%, PKR score = 4.47 +/- 2.17) than in nonpapillary carcinomas (2 of 6, 33%, PKR score = 1.50 +/- 2.81). Nontumorous thyroid showed no or faint "baseline" PKR expression. There were no significant differences between the PKR score and tumor size, tumor invasion, capsular invasion, or lymph node metastasis. However, there were significant differences between the PKR score and vascular invasion or presence of satellite tumor nodules, the PKR score being higher in cases with more vascular invasion and in cases with satellite tumor nodules than in cases without them. Ki-67 labeling showed a reverse correlation with the PKR score, being the highest in cases with low PKR scores. These results suggest that follicular cells newly express PKR during thyroid carcinogenesis, that PKR is more expressed in papillary carcinoma than in nonpapillary carcinoma, that PKR expression may be associated with high vascular invasion and satellite nodules, and that PKR expression is linked to low cell proliferative activity.

Adenocarcinoma, Follicular↗
PubMed2000

Freezability of boar spermatozoa is improved by exposure to 2-hydroxypropyl-beta-cyclodextrin.

The influence of 2-hydroxypropyl-beta-cyclodextrin (HBCD) exposure on post-thaw spermatozoa prior to freezing using acrosome integrity and the parameters of motility was studied. Acrosomal status was monitored by means of FITC-labelled peanut agglutinin, and the motility parameters were assessed using a computer-assisted sperm motility analysis (CASA) system. The spermatozoa were exposed to HBCD over a period of 3 h, during which the cells were slowly cooled from 25 to 5 degrees C, and then frozen into pellets. The percentage of frozen thawed spermatozoa with intact acrosomes in 40 mM HBCD group was approximately three-fold higher than that of the control. The motility and progressive motility values of the frozen-thawed spermatozoa were found to increase significantly with increased HBCD concentrations. On the other hand, further addition of cholesterol-3-sulfate to the BF5 extender containing 20 mM HBCD resulted in a drastic decrease in the percentage of spermatozoa with intact acrosomes, and decreased motility and progressive motility, suggesting that cholesterol-sulfate probably counter-acted the protective action of HBCD. In conclusion, the results of the present study indicate that HBCD protected boar spermatozoa against freeze-thaw damage, possibly by means of stimulating the efflux of membrane cholesterol.

2-Hydroxypropyl-beta-cyclodextrin↗
PubMed2000

Physiological and pharmacological implications of peptide transporters, PEPT1 and PEPT2.

The H+/peptide co-transporters PEPT1 and PEPT2 mediate the cellular uptake of small peptides and peptide-like drugs from the glomerular filtrates. In the present study, we investigated the physiological and pharmacological implications of both transporters. (i) Comparison of the substrate affinity of PEPT1 and PEPT2 indicated that PEPT2 had higher affinity than PEPT1 for most substrates. (ii) The transport characteristics of beta-lactam antibiotics in the renal brush border membrane vesicles were well correlated with those in a PEPT2-expressing transfectant. These results suggested that PEPT2 predominantly contributed to reabsorption of beta-lactam antibiotics in the kidney at therapeutic concentrations. (iii) In rats with chronic renal failure, glycylsarcosine (Gly-Sar) uptake by the renal brush border membranes vesicles was maintained, whereas Na+-dependent glucose uptake was markedly reduced. It is therefore speculated that the function of peptide transporters is tolerant to chronic renal failure.

Absorption↗
PubMed2000

Functional expression of novel peptide transporter in renal basolateral membranes.

We examined the peptide transport activity in renal basolateral membranes. [(14)C]glycylsarcosine (Gly-Sar) uptake in rat renal cortical slices was saturable and inhibited by excess dipeptide and aminocephalosporin cefadroxil. When several renal cell lines were screened for the basolateral peptide transport activity, Madin-Darby canine kidney (MDCK) cells were demonstrated to have the greatest transport activity. [(14)C]Gly-Sar uptake across the basolateral membranes of MDCK cells was inhibited by di- and tripeptide and decreased with decreases in extracellular pH from 7.4 to 5.0. The Michaelis-Menten constant value of [(14)C]Gly-Sar uptake across the basolateral membranes of MDCK cells was 71 microM. The basolateral peptide transporter in MDCK cells showed several different [(14)C]Gly-Sar transport characteristics in growth dependence, pH profile, substrate affinity, and sensitivities to chemical modifiers from those of the apical H(+)-peptide cotransporter of MDCK cells. The findings of the present investigation indicated that the peptide transporter was expressed in the renal basolateral membranes. In addition, from the functional characteristics, the renal basolateral peptide transporter was suggested to be distinguishable from known peptide transporters, i.e., H(+)-peptide cotransporters (PEPT1 and PEPT2) and the intestinal basolateral peptide transporter.

4-Chloromercuribenzenesulfonate↗
PubMed2000

Trypsinogen expression in colorectal cancers.

The purpose of this study was to evaluate the trypsinogen expression in human colorectal cancers. We observed the trypsinogen-1 mRNA expression in five of ten human colorectal cancer cell lines by reverse transcriptase-polymerase chain reaction (RT-PCR), and gelatinolytic activity in conditioned medium of cancer cells at acidic pH by gelatin zymography. Furthermore, trypsinogen protein expression was observed in 68 out of 154 (44.2%) surgical specimens of colorectal cancer immunohistochemically. However, there was no statistically significant relationship between the trypsinogen expression and the clinicopathological findings. These findings suggest that trypsinogen might be involved in cancer invasion and metastasis throughout the cancer progression.

Colorectal Neoplasms↗
PubMed2000

PPARgamma ligand (thiazolidinedione) induces growth arrest and differentiation markers of human pancreatic cancer cells.

The aim of this study was to examine whether a specific PPARgamma ligand can inhibit the growth of human pancreatic cancer cells through induction of terminal differentiation. PPARgamma was expressed in five human pancreatic cancer cell lines: Capan-1, AsPC-1, BxPC-3, PANC-1, and MIA PaCa-2. Treatment of these cells with a specific PPARgamma ligand, thiazolidinedione (TZD), resulted in inhibition of both cellular and clonogenic growth, and G1 cell cycle arrest. Finally, thiazolidinedione treatment resulted in induction of p21WAF-1 and increased expression of differentiation markers. These results suggest that thiazolidinedione treatment inhibits growth and induces cellular differentiation in pancreatic cancer cells and thereby reduces their development in favor of differentiated and stable cell phenotype.

Adenocarcinoma↗
PubMed2000

Epithelioid leiomyosarcoma with osteoclast-like giant cells in the rectum.

We report a rare case of rectal epithelioid leiomyosarcoma with osteoclast-like giant cells. A 71-year-old Japanese man was admitted to a hospital with melena. Results of a colonoscopy test revealed a polypoid tumor in the rectum, and a biopsy specimen from the lesion showed a sarcoma; the patient underwent rectosigmoidectomy. At gross inspection, the tumor measured 8 x 7 x 4 cm and was polypoid with ulcerations. Necrotic and hemorrhagic foci were scattered. Microscopically, the tumor consisted of 2 cell types: malignant tumor cells with epithelioid features and benign-appearing osteoclast-like giant cells. The tumor cells were polygonal and epithelioid in shape and had eosinophilic or clear cytoplasms, with scattered giant tumor cells. Immunohistochemical examination revealed that the tumor cells were positive for vimentin, muscle actin, alpha-smooth muscle actin, and desmin, whereas the osteoclast-like giant cells were positive for CD68, leukocyte common antigen, and lysozymes. We diagnosed this case as epithelioid leiomyosarcoma with osteoclast-like giant cells. To the best of our knowledge, this is the first case of rectal epithelioid leiomyosarcoma with osteoclast-like giant cells.

Aged↗
PubMed2000

Increased midkine expression in hepatocellular carcinoma.

CONTEXT: Midkine (MK) is a novel heparin-binding growth factor whose gene was identified in embryonal carcinoma cells in early stages of retinoic acid-induced differentiation. OBJECTIVE: To examine the overexpression of MK in hepatocellular carcinoma (HCC). METHODS: Seventy-seven primary HCC specimens from patients aged 17 to 72 years (63 men and 14 women) were examined. Histologically, 16 cases of HCC were classified as the well-differentiated type, 50 cases as the moderately differentiated type, and 11 cases as the poorly differentiated type. Immunohistochemical analysis was performed using a rat immunoglobulin G2a monoclonal antibody against the carboxyl terminal region of human MK. In situ hybridization was also performed on 20 HCC samples. RESULTS: We successfully applied this monoclonal antibody against MK to analyze archival paraffin sections. The cancer tissues showed a positive reaction to this antibody, in which there was an intense reaction in their cytoplasm. Approximately one third of the individuals with HCC (26/77) had tumor cells that expressed MK, and these were classified into the following types: moderately differentiated (20/50), well differentiated (3/16), and poorly differentiated (3/11). The in situ hybridization analysis revealed that the signals of MK transcripts were found in the cytoplasm of the cancer cells; the distribution and localization of the MK transcripts' signals determined by in situ hybridization analysis were similar to those obtained by immunohistochemical analysis. CONCLUSIONS: Hepatocellular carcinoma expressed increased MK at the messenger RNA and protein level.

Adolescent↗
PubMed2000

[Agenesis of the right internal carotid artery associated with complicated anastomosis of middle cerebral artery: a case report].

A 57-year-old female was admitted to our hospital because of headache, nausea, and vomiting. Head CT scan demonstrated subarachnoid hemorrhage. Cerebral angiography showed the absence of the right internal carotid artery, and skull base CT of the bone window level revealed the absence of the right carotid canal. The right middle cerebral artery (MCA) and anterior cerebral artery (ACA) were opacified from the left internal carotid artery. The right A1 portion was hypoplastic and the distal portion of the right M1 portion was replaced by several minute complicated anastomotic vessels connected to the right M2 portion. The right MCA territory was mainly supplied by collateral flow from the right ACA and the right posterior cerebral artery via the leptomeningeal anastomosis. These was neither aneurysm nor arteriovenous malformation. The second angiography, 1 week after the initial angiography, showed the same hemodynamic pattern and aneurysms were not found. We diagnosed the patient as agenesis of the right internal carotid artery and the etiology of subarachnoid hemorrhage was suspected to be a rupture of the anastomotic vessels between the right M1 and M2. She was discharged on the 21st hospital day without any neurological deficit.

Carotid Artery, Internal↗
PubMed2000

[Preliminary report on the efficacy and safety of brief-pulse ECT in depression].

Because there is no report on the use of brief-pulse devices in Japan, we have examined the efficacy and safety of brief-pulse electroconvulsive therapy (ECT) on four treatment-resistant depressive patients (three males and one female, 55.0 +/- 17.8 years of age). The ethical committee of the National Center of Neurology and Psychiatry approved this study and written informed consent was obtained from all of the patients. ECT was administered bilaterally twice a week using atropine, propofol, and succinylcholine (or vecronium) as anesthetic medications. The Hamilton rating scale for depression scores decreased from 30.5 +/- 11.0 to 14.8 +/- 11.5 following a course of 5-12 treatments. Memory and cognitive functioning, evaluated using the Mini-Mental State Examination, Short-Memory Questionnaire and so on, had not changed a week after the last ECT. These results further support the view that brief-pulse ECT is efficacious and safe for the treatment of depression.

Adult↗
PubMed2000

[Photodynamic diagnosis and photodynamic therapy for experimental hepatoma with ME 2906].

We studied the effects of photodynamic diagnosis (PDD) and photodynamic therapy (PDT) in confirming the existence of hepatoma, using the new photosensitizer mono-L-aspartyl chlorine 6. Japanese white rabbits were selected for abdominal incision under intravenous anesthesia, and VX 2 tumor cells were transplanted into the left liver lobe to create a hepatoma model. In the experiment, hepatoma of 1 cm in diameter (at one week after transplantation) was radiated with a semiconducter laser (664 nm, 200 J/cm2) for treatment.

Animals↗
PubMed1999

An ABC transporter homologous to TAP proteins.

Polymerase chain reaction amplification of cDNA from rat intestine revealed the expression of a novel ABC transporter, TAPL (TAP-like). Subsequently, the protein sequence was deduced from the nucleotide sequence of cDNA carrying the entire coding region. TAPL is transcribed ubiquitously in various rat tissues. The protein, with 762 amino acid residues, has potential transmembrane domains, and an ATP-binding domain in its amino and carboxyl terminal regions, respectively, and is highly homologous to TAP1 and TAP2 (transporters associated with antigen presentation/processing): pairwise comparisons with TAPL demonstrated 39 and 41% of the residues are identical, respectively. These numerical values are essentially the same as that for TAP1 and TAP2 (39%), and the hydropathy profiles of TAPL, TAP1 and TAP2 are quite similar. The similarity among these three proteins suggests that they could be derived from a common ancestral gene. Furthermore, we found that there is a potential splicing isoform, sharing the amino terminal 720 amino acid residues of TAPL.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

Sterol regulatory element-binding protein negatively regulates microsomal triglyceride transfer protein gene transcription.

We herein report that mRNA expression of microsomal triglyceride transfer protein (MTP) and its protein synthesis decline in response to sterol depletion in HepG2 cells, and we functionally characterized the MTP gene promoter in an effort to investigate the molecular mechanisms by which MTP gene transcription is regulated. Luciferase assays using truncated versions of the reporter gene revealed that the region at -124 to +33 base pairs of the human promoter contains the elements required for the suppression of transcription by sterol depletion. Enforced expression of an active form of sterol regulatory element-binding protein (SREBP)-1 (amino acids 1-487) or -2 (amino acids 1-481), both of which are activated under sterol-depleted conditions, is able to mimic sterol-mediated down-regulation. Either further truncation of the promoter region or mutation of the putative SREBP-binding sequence (5'-GCAGCCCAC-3', -124 to -116 base pairs) abolishes the sterol- and SREBP-dependent transcriptional regulation. Gel mobility shift assay showed that recombinant SREBP-2-(1-481) is able to bind the sequence. Enforced expression of a truncated form of SREBP-2 (amino acids 31-481), which acts as an inhibitor of transcription of the low density lipoprotein receptor gene because it lacks the transcriptional activation domain, also diminishes the luciferase activity, suggesting that direct binding to the promoter region might be sufficient and that the mechanism by which SREBPs inhibit MTP gene expression is distinct from that for the transcriptional stimulation of sterol-regulated genes. Although the SREBP-binding site overlaps a negative insulin-responsive element, insulin negatively regulates MTP gene expression even when the amount of the active form of SREBPs is quite low under the sterol-loaded conditions, indicating that SREBPs only slightly mediate, if at all, the insulin effects. Overall, we conclude that SREBPs are responsible for regulation of lipoprotein secretion via their control of MTP gene expression. Moreover, our results describe for the first time a novel mechanism by which SREBPs negatively regulate expression of the gene encoding the protein involved in lipid metabolism.

Base Sequence↗
PubMed1999

Novel TSC2 mutation in a patient with pulmonary tuberous sclerosis: lack of loss of heterozygosity in a lung cyst.

A Japanese patient with tuberous sclerosis (TSC), who manifested with multiple lung cysts and pneumothorax, is described. All exons of two TSC genes, TSC1 and TSC2, in peripheral blood leukocytes from the patient were analyzed by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP). A novel T-to-G transition was found in exon 19 of TSC2 at nucleotide position 2168. This mutation caused an amino acid change, L717R. There was no such mutation in any other family members or in 100 normal Japanese. An automated sequencer-assisted quantitative analysis of normal and mutated SSCP-bands revealed no loss of heterozygosity (LOH) in the lung cyst tissue of the patient.

Adolescent↗
PubMed1999

Nuclear magnetic resonance and molecular dynamics studies on the interactions of the Ras-binding domain of Raf-1 with wild-type and mutant Ras proteins.

The Ras protein and its homolog, Rap1A, have an identical "effector region" (residues 32-40) preceded by Asp30-Glu31 and Glu30-Lys31, respectively. In the complex of the "Ras-like" E30D/K31E mutant Rap1A with the Ras-binding domain (RBD), residues 51-131 of Raf-1, Glu31 in Rap1A forms a tight salt bridge with Lys84 in Raf-1. However, we have recently found that Raf-1 RBD binding of Ras is indeed reduced by the E31K mutation, but is not affected by the E31A mutation. Here, the "Rap1A-like" D30E/E31K mutant of Ras was prepared and shown to bind the Raf-1 RBD less strongly than wild-type Ras, but slightly more tightly than the E31K mutant. The backbone 1H, 13C, and 15N magnetic resonances of the Raf-1 RBD were assigned in complexes with the wild-type and D30E/E31K mutant Ras proteins in the guanosine 5'-O-(beta,gamma-imidotriphosphate)-bound form. The Lys84 residue in the Raf-1 RBD exhibited a large change in chemical shift upon binding wild-type Ras, suggesting that Lys84 interacts with wild-type Ras. The D30E/E31K mutant of Ras caused nearly the same perturbations in Raf-1 chemical shifts, including that of Lys84. We hypothesized that Glu31 in Ras may not be the major salt bridge partner of Lys84 in Raf-1. A molecular dynamics simulation of a model structure of the Raf-1 RBD.Ras.GTP complex suggested that Lys84 in Raf-1 might instead form a tight salt bridge with Asp33 in Ras. Consistent with this, the D33A mutation in Ras greatly reduced its Raf-I RBD binding activity. We conclude that the major salt bridge partner of Lys84 in Raf-1 may be Asp33 in Ras.

Amino Acid Sequence↗