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Biomedical subjects

K Terada

Publications and source records attributed to K Terada.

At least 91 records · Page 5Linked to original sources
PubMed1999

H-NMR and mass spectral study of a D-enriched acetylenic norlignan, asparenyol, from cultured cells of Asparagus officinalis.

A suspension of cultured cells of Asparagus officinalis fed L-phenyl-D5-alanine-2,3,3-D3 (D5-phe) and DL-phenylalanine-3,3-D2 (D2-phe) yielded D-enriched asparenyol, 4-[5-(4-methoxyphenoxy)-3-penten-1-ynyllphenol (1). A H-NMR spectral study indicated that incorporation of deuterium atoms into the chains of the products was restricted to the C-9 position. The molecular ion regions of the MS of D-enriched metabolites, 1(D8-200), 1(D8-100) and 1(D8-50), obtained from feeding experiments using 200 mg, 100 mg and 50 mg of Ds-phe, respectively, coincided with the theoretical spectra. This confirmed that a single phenylalanine molecule supplies the nine carbon atoms in the -CH=CH-CH2-O-C6H4-O- moiety of 1. The biosynthetic sequence forming 1 as a norlignan class of metabolite is considered.

Cells, Cultured↗
PubMed1999

Laparoscopy in gynecologic surgery.

Laparoscopy has been utilized in gynecologic surgery for over 20 years. With the introduction of video monitoring and the development of new endoscopic instruments, the role of laparoscopy has greatly expanded. Laparoscopy is an invaluable tool in the management of the cancer patient. Current use focuses primarily on the diagnosis and staging of intraabdominal and pelvic malignancies. However laparoscopy is also utilized as an adjunct to therapeutic resection and palliation. The following is a brief discussion of the role of laparoscopy in the management of gynecologic cancer.

Adult↗
PubMed1999

[Clinical results of supratentorial astrocytoma grade II].

At present, there is no consensus concerning the treatment of low-grade gliomas. The authors conducted a retrospective review of surgically treated, histologically verified cases of supratentorial astrocytomas of grade II to evaluate the results of current treatment methods. Thirty-seven patients, 23 males and 14 females, treated from April, 1977 through March, 1997 were analyzed. Median patient age was 36 years (range 2-69 years). All patients were diagnosed by surgical specimens. Thirty were fibrillary, and three were gemistocytic astrocytomas. There were 13 total resections, 7 subtotal resections, 10 partial resections. Of the remaining 7, diagnosis was obtained by stereotactic biopsy. Twenty patients were irradiated and two received chemotherapy. Follow-up information was obtained for 33 patients. The follow-up time ranged from 4 months to 246 months (mean, 9 years). Overall survival rates at 5 and 10 years for the entire treated group were 71% and 57% respectively. Total and subtotal resections were significantly associated with longer survival time, the 5- and 10-year survival rates were 93% and 67%, respectively. They were 40% and 40% in patients with partial resection or needle biopsy. Patients with gemistocytic astrocytoma had a poor prognosis with a median survival of 44.5 months. The influence of radiotherapy was not obvious: 92 and 69% of patients were alive at 5 and 10 years respectively without radiotherapy. The extent of surgery and histological type were by far the most important factors in predicting length of survival. The importance of an accurate histologic diagnosis and a gross total resection is emphasized.

Adolescent↗
PubMed1999

[Detection of anti-IgA alloantibody in a case of non-hemolytic transfusion reaction].

A 59-year-old man with myelodysplastic syndrome exhibited unticaria, dyspnea, fever, and hypotension immediately after the start of platelet concentrate (PC) transfusion on the 15th day of hospitalization. On the 17th and 21st day of hospitalization, the patient exhibited severe unticaria resembling that of erythroderma after the start of PC transfusion. Anti-IgA IgG antibody was detected by enzyme-linked immunosorbent assay (ELISA) on the 28th day of hospitalization. Anti-IgA (purified from pooled human plasma) was detected by Western blotting. The patient's IgA level was normal. No antibodies against HLA or platelet-specific antigens were detected in serum. The patient had no reaction to administration of washed PC. These findings suggest that anti-IgA antibody might have been responsible for the nonhemolytic transfusion reaction in this patient.

Antibodies, Anti-Idiotypic↗
PubMed1999

[Effect of low-dose sulpiride on dopamine metabolism in rat nucleus accumbens and locomotor activity: studies with intracerebral dialysis].

Changes in the concentration of dopamine (DA) and its metabolites, 3, 4-dihydroxyphenyl-acetic acid (DOPAC) and homovanillic acid (HVA), were determined sequentially in freely moving rats by using a brain dialysis method. The purpose of this study was to investigate the relationship between changes in the dopamine metabolism in the nucleus accumbens and locomotor activities following low-dose (5 mg/kg) sulpiride administration. The DA content in the dialysis fluid rose significantly 4 to 6 h after sulpiride administration. The DOPAC content rose significantly 6 h after sulpiride administration. The HVA content did not show a significant change. A slight increase of locomotor activity was found, but it was not statistically significant. The elevation of DA release in nucleus accumbens by sulpiride might relate to the clinical efficacy of low-dose administration of this drug for mood disorders.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Inhibitory effects of ursodeoxycholic acid on N-methylnitrosourea-induced colon carcinogenesis and colonic mucosal telomerase activity in F344 rats.

Bile acids are known to promote colon carcinogenesis. However, one study showed that ursodeoxychlic acid (UDCA) prevented azoxymethane-induced rat colon tumorigenesis. The aim of the present study with 3 sets of experiments was to explore the inhibitory effect of UDCA supplemented in the diet on colon carcinogenesis induced by the intrarectal administration of N-methylnitrosourea (MNU) in F344 rats. In experiment I, 5 rats per group were fed a diet supplemented with 0% (control), 0.4%, 0.08% or 0.016% UDCA or chenodeoxycholic acid (CDCA) for 5 weeks after receiving 3 intrarectal doses of 4 mg MNU in week 1. The formation of colonic aberrant crypt foci (ACFs, preneoplastic lesions) at week 6 showed a 24% and 23% reduction in the 0.4% and 0.08% UDCA groups, respectively, as compared to the control group, while it increased for the 0.4% and 0.08% CDCA groups, and was unaffected in the 0.016% UDCA and CDCA groups. In experiment II based on the results of experiment I, all rats received an intrarectal dose of 2 mg MNU 3 times a week for 3 weeks, and then were administered with 0%, 0.4% or 0.08% UDCA for 27 weeks. At week 30, the incidence of colon tumors in the UDCA groups was significantly lower than that in the control group: 20/50 (40%) and 9/25 (36%) vs. 17/25 (68%). The number of large-sized ACFs with 4 or more ACs showed a 47% and 59% reduction in the normal-appearing mucosa in the UDCA groups as compared to the control group, while the number of small-sized ACFs with 1-3 ACs was similar in all groups. The normal-appearing mucosa showed a noticeable level of telomerase activity (semiquantitative PCR-based TRAP assay) in the control group, and significantly reduced levels in the UDCA groups compared to the control group: 19.8 and 32.7 vs. 71.0 TPG unit in mean value. The colon tumors showed a high level of enzyme activity in both the control and UDCA groups. In experiment III, 6 rats per group were fed a diet supplemented with 0%, or 0.4% UDCA or CDCA for 5 weeks after receiving 3 intrarectal doses of 4 mg MNU in week 1. Two control groups did not receive any treatment with MNU and bile acids. The MNU-treated groups showed significantly elevated levels of colonic mucosal telomerase activity at week 6 as compared to the control group (6.5 TPG unit in mean value). It was noted that both UDCA and CDCA administration reduced the enzyme activity as compared to the group with MNU treatment alone: 24.7 and 25.2 vs. 40.1 TPG unit in mean value. Thus, the present study suggested that orally administered UDCA inhibited the growth of ACFs and the development of carcinomas in the colon of rats treated with MNU. Also, UDCA may suppress MNU-induced telomerase activation in normal-appearing but ACF-containing colon mucosa, and its mechanism appears to be different from that responsible for the anti-tumor promoting action of UDCA.

Animals↗
PubMed1998

Functional analysis of human mitochondrial receptor Tom20 for protein import into mitochondria.

The mitochondrial import receptor translocase of the outer membrane of mitochondria (Tom20) consists of five segments, an N-terminal membrane-anchor segment, a linker segment rich in charged amino acids, a tetratricopeptide repeat motif, a glutamine-rich segment, and a C-terminal segment. To assess the role of each segment, four C-terminally truncated mutants of the human receptor (hTom20) were constructed, and the effect of their overexpression in COS-7 cells was analyzed. Expression of a mutant lacking the tetratricopeptide repeat motif inhibited preornithine transcarbamylase (pOTC) import to the same extent as the wild-type receptor. Thus, overexpression of the membrane-anchor and the linker segments is sufficient for the inhibition of import. Expression of either the wild-type receptor or a mutant lacking the C-terminal end of 20 amino acid residues stimulated import of pOTC-green fluorescent protein (GFP), a fusion protein in which the presequene of pOTC was fused to green fluorescent protein. On the other hand, expression of mutants lacking either the glutamine-rich segment or larger deletions inhibited pOTC-GFP import. In vitro import of pOTC was inhibited by the wild-type hTom20 and the mutant lacking the C-terminal end, but much less strongly by the mutant lacking the glutamine-rich segment. On the other hand, import of pOTC-GFP was little affected by any of the forms of hTom20. In binding assays, pOTC binding to hTom20 was only moderately decreased by the deletion of the glutamine-rich segment, whereas pOTC-GFP binding was completely lost by this deletion. Binding of pOTCN-GFP a construct that contains an additional 58 N-terminal residues of mature OTC, resembled that of pOTC. All of these results indicate that the region 106-125 containing the glutamine-rich segment of hTom20 is essential for binding and import stimulation in vivo of pOTC-GFP and for inhibition of in vitro import of pOTC. The results also indicate that this region is important for mitochondrial aggregation. The different behaviors of pOTC and the pOTC-GFP chimera toward hTom20 mutants is explicable on the basis of the conformation of the precursor proteins.

Animals↗
PubMed1998

Bcl-2 is located predominantly in the inner membrane and crista of mitochondria in rat liver.

Bcl-2 is now recognized as a potent inhibitor of apoptotic cell death. It has been reported that Bcl-2 is located in the mitochondria, endoplasmic reticulum, and nuclear membrane in some cell lines, and it is not expressed in normal human and rat liver. An earlier study showed that Bcl-2 is an inner mitochondrial membrane protein. On the contrary, the following investigations using immunoelectron microscopy demonstrated that Bcl-2 resides predominantly in the mitochondrial outer membrane. In this study, using a cryo-sectioning immunogold labeling technique and immunoblotting, we carefully determined the subcellular localization of Bcl-2. Here we report that Bcl-2 is expressed in normal rat liver, and it is located predominantly in the inner membrane and crista rather than in the outer membrane of mitochondria.

Animals↗
PubMed1998

Absence of IgD-CD27(+) memory B cell population in X-linked hyper-IgM syndrome.

The present study analyzed peripheral blood B cell populations separated by IgD and CD27 expression in six males with X-linked hyper-IgM syndrome (XHIM). Costimulation of mononuclear cells from most of the patients induced no to low levels of class switching from IgM to IgG and IgA with Staphylococcus aureus Cowan strain (SAC) plus IL-2 or anti-CD40 mAb (anti-CD40) plus IL-10. Measurable levels of IgE were secreted in some of the patients after stimulation with anti-CD40 plus IL-4. Costimulation with SAC plus IL-2 plus anti-CD40 plus IL-10 yielded secretion of significant levels of IgG in addition to IgM, but not IgA. The most striking finding was that peripheral blood B cells from all of the six patients were composed of only IgD+ CD27(-) and IgD+ CD27(+) B cells; IgD- CD27(+) memory B cells were greatly decreased. IgD+ CD27(+) B cells from an XHIM patient produced IgM predominantly. Our data indicate that the low response of IgG production in XHIM patients is due to reduced numbers of IgD- CD27(+) memory B cells. However, the IgG production can be induced by stimulation of immunoglobulin receptors and CD40 in cooperation with such cytokines as IL-2 and IL-10 in vitro.

Adolescent↗
PubMed1998

Endothelial myosin light chain kinase regulates neutrophil migration across human umbilical vein endothelial cell monolayer.

Although extravasation of neutrophils is a critical step in acute inflammation, the role of the endothelial cytoskeleton in neutrophil transmigration has not been fully investigated. We used an in vitro model of neutrophil transmigration across a monolayer of HUVEC cultured on amniotic membrane. Human neutrophils were allowed to migrate across the HUVEC monolayer in response to a gradient leukotriene B4 and then the number of migrated neutrophils were counted microscopically. We also followed endothelial F-actin and myosin filament formation using rhodamine-phalloidin and anti-myosin Ab staining. Myosin light chain (MLC) phosphorylation in endothelial cells was determined by immunoprecipitation of 32P-labeled HUVEC with anti-myosin polyclonal Ab. Normally, neutrophil migration induced F-actin formation, myosin filament formation, and MLC phosphorylation in HUVEC. When HUVEC was pretreated with the myosin light chain kinase (MLCK) inhibitor, ML-9, neutrophil migration was diminished and F-actin formation, myosin filament formation, and MLC phosphorylation were inhibited. Pretreatments of HUVEC with the intracellular calcium ion chelator, bis-(O-aminophenoxyl)ethane-N, N, N', N'-tetraacetic acid acetoxymethyl ester (BAPTA/AM), and the calmodulin antagonist, trifluoperazine, had similar effects. These results indicate that a calcium/ calmodulin-dependent MLCK in endothelial cells regulates neutrophil transendothelial migration.

Actins↗
PubMed1998

Mouse forkhead (winged helix) gene LUN encodes a transactivator that acts in the lung.

Many transcription factors involved in the determination and maintenance of cell fates share DNA-binding motifs to form gene families. The most recently discovered evolutionarily conserved DNA-binding domain of 100 amino acids, termed the forkhead domain, emerged from a sequence comparison of the rat transcription factor HNF-3 alpha and the homeotic gene fork head of Drosophila. Here we describe the isolation of a new mouse forkhead gene named LUN. Of a total of five forkhead genes in the lung, the LUN gene was uniquely expressed in the bronchiolar epithelium and in type II pneumocytes. We found that the LUN protein has forkhead domain that is identical to the HFH8 gene and a C-terminal region that is very similar to the HFH8 gene. Based on the structural similarity of the two proteins, we investigated the structure-function relationship of the LUN protein in two kinds of promoters and found that regions C and D work differently as activation domains, namely that region C acts autonomously but region D cannot work without region C. These results suggest that the LUN gene may play an important role as a transactivator in the determination and maintenance of some types of cells in the lung.

Animals↗
PubMed1998

Analysis of functional domains of Wilson disease protein (ATP7B) in Saccharomyces cerevisiae.

Wilson disease is a genetic disorder of copper metabolism characterized by the toxic accumulation of copper in the liver. The ATP7B gene, which encodes a copper transporting P-type ATPase, is defective in patients with Wilson disease. To investigate the function of ATP7B, wild type or mutated ATP7B cDNA was introduced into a yeast strain lacking the CCC2 gene (delta ccc2), the yeast homologue of ATP7B. Wild type and the H1069Q mutant could rescue delta ccc2, however, the N1270S mutant could not, reflecting phenotypic variability of Wilson disease. In addition, the mutant containing only the sixth copper binding domain could rescue delta ccc2, indicating its functional importance.

Adenosine Triphosphatases↗
PubMed1998

Human supplementary motor area is active in preparation for both voluntary muscle relaxation and contraction: subdural recording of Bereitschaftspotential.

Bereitschaftspotentials (BPs) preceding muscle relaxation and contraction were compared by using subdural electrodes which were implanted onto the right medial frontal surface in two patients with supplementary motor area (SMA) seizure. The applied movement paradigm (muscle relaxation and contraction tasks) was completely the same as employed in our previous study [Terada, K., Ikeda, A., Nagamine, T. and Shibasaki, H., Electroenceph. clin. Neurophysiol., 95 (1995) 335-345]. In both patients, either negative or positive BPs were observed in the SMA-proper and supplementary negative motor area (SNMA) starting at 1.2-1.8 prior to both movements. In one patient, BP was more widespread in the relaxation task whereas more restricted to the hand area in the contraction task. In the other patient, the BPs were observed in the cortical area rostral to SNMA (pre-SMA), in addition to the SMA-proper, in both tasks. It is concluded that SMA-proper and SNMA, and probably pre-SMA as well, in humans are similarly active in preparation for both voluntary muscle contraction and relaxation.

Adult↗
PubMed1998

Restoration of holoceruloplasmin synthesis in LEC rat after infusion of recombinant adenovirus bearing WND cDNA.

Wilson's disease, an autosomal recessive disorder, is characterized by the excessive accumulation of copper in the liver. WND (ATP7B) gene, which encodes a putative copper transporting P-type ATPase, is defective in the patients. To investigate the in vivo function of WND protein as well as its intracellular localization, WND cDNA was introduced to the Long-Evans Cinnamon rat, known as a rodent model for Wilson's disease, by recombinant adenovirus-mediated gene delivery. An immunofluorescent study and a subcellular fractionation study revealed the transgene expression in liver and its localization to the Golgi apparatus. Moreover, since the synthesis of holoceruloplasmin is disturbed in the Long-Evans Cinnamon rat, the plasma level of holoceruloplasmin, oxidase-active and copper-bound form, was examined to evaluate the function of WND protein with respect to the copper transport. Consequently, the appearance of holoceruloplasmin in plasma was confirmed by Western blot analysis and plasma measurements for the oxidase activity and the copper content. These findings indicate that introduced WND protein may function in the copper transport coupled with the synthesis of ceruloplasmin and that the Golgi apparatus is the likely site for WND protein to manifest its function.

Adenosine Triphosphatases↗
PubMed1998

Copper resistant human hepatoblastoma mutant cell lines without metallothionein induction overexpress ATP7B.

Mutant human hepatoblastoma cell lines resistant to copper toxicity were isolated from mutagenized HuH7. Two copper resistant cell lines (CuR), CuR 23 and CuR 27, had reduced basal expression of metallothionein (MT) messenger RNA (mRNA) and exhibited minimal or no increase in resistance to cadmium or zinc toxicity. Copper uptake, efflux of newly transported copper, glutathione content, and efflux rate were comparable with HuH7, whereas holoceruloplasmin synthesis and secretion were slightly decreased. Subcellular distribution of copper at steady-state showed an increase in organelle and membrane fractions with a reduction in cytosol. Expression of ATP7B mRNA was fivefold increased, and ATP7B protein approximately threefold increased in both CuR 23 and 27. Another cell line, CuR 41, showed increased basal expression of MT and ATP7B mRNA but not ATP7B protein, and resistance to cadmium and zinc toxicity. Copper uptake in CuR 41 was comparable with HuH7, but initial rates of efflux of copper and glutathione were reduced. The synthesis of holoceruloplasmin but not ceruloplasmin peptide was markedly diminished in CuR 41. Subcellular distribution of copper showed an increase in cytosolic and decreased organelle and membrane-associated copper. These data suggest that cellular resistance to copper toxicity was achieved in two independent cell lines without MT induction and that the induction of ATP7B may lead to the enhanced intracellular sequestration of copper by organelles.

Adenosine Triphosphatases↗
PubMed1998

Electrophysiological studies of early stage corticobasal degeneration.

We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic-rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon-emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor-evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input from the sensory cortex.

Aged↗