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Biomedical subjects

K Akimoto

Publications and source records attributed to K Akimoto.

At least 73 records · Page 4Linked to original sources
PubMed1997

[Mid-term follow-up results of coil embolization for patent ductus arteriosus].

Mid-term follow-up results of coil embolization for patent ductus arteriosus (PDA) were evaluated in 19 patients aged from 2 years 9 months to 13 years (median: 5 years and 10 months) who underwent coil embolization for PDA. The minimum diameter of PDA ranged from 1.0 to 3.5 mm (mean 2.3 +/- 0.8 mm). Coil embolization was performed by the retrograde approach in 16 patients and the anterograde approach in 3, using a Gianturco coil in 11 and a Jackson detachable coil system in 8. Sixteen patients underwent single coil embolization and three patients received two coils simultaneously with detachable coil systems. Follow-up evaluation was performed with color flow mapping and pulsed Doppler echo to identify residual shunt or acquired left pulmonary artery stenosis after embolization at 1 day, 1 week, 1, 3, 6 and 12 months, and every 6 months thereafter. In two patients, a coil had migrated into the distal left pulmonary artery immediately after implantation, and could be safely retrieved. Minimum residual shunt was found in six patients (32%) on the day after the procedure. Spontaneous closure was noted in all patients within 6 months. Recanalization of completely occluded PDA was observed in one patient at 1 month after embolization. However, spontaneous closure of the residual shunt was found at 1 year and 6 months of follow-up. There was no evidence of acquired left pulmonary artery stenosis during the follow-up period (14.5 +/- 5.8 months). Coil embolization is an effective and safe therapy for PDA. Small residual shunt may be observed immediately after the coil embolization, but will close spontaneously during the follow-up. Recanalization occurred after complete coil occlusion, so careful follow-up with color flow mapping is mandatory.

Adolescent↗
PubMed1997

[Preventative effect of a whey hydrolyzed formula (Nestle, NAN H.A.) on the development of allergic symptoms in infants].

We examined the prevent effect of a whey hydrolyzed formula (NAN H.A.) on the development of allergic disease from new born infants. A hundred thirty three pregnant women were divided into the NAN H.A. group and the control group. Mothers, who agreed to use the whey hydrolyzed formula to their infant, were classified into the NAN H.A. group. We examined laboratory date such as IgE levels of these infants as well as clinical symptoms for evaluating of the preventive effect of NAN H.A. The serum IgE levels from infants of the NAN H.A. group were lower than those of the control group. The incidance of the infants who showed allergic clinical symptoms was significant lower in the NAN H.A. group. The odds ratio to skin symptom at 3 years of age with multiple logistic regression was 5.32 between the control group and the NAN H.A. group (p < 0.05). It was 6.68 between mother's history of allergy was positive and negative (p < 0.02). These results suggest that NAN H.A. can prevent the development of allergic symptoms in infants.

Child, Preschool↗
PubMed1996

Application of percutaneous transluminal coronary angioplasty to coronary arterial stenosis in Kawasaki disease.

BACKGROUND: Percutaneous transluminal coronary angioplasty (PTCA) has rarely been performed on patients with coronary lesions that result from Kawasaki disease. In this study, we retrospectively evaluated the effectiveness of PTCA in five patients with coronary arterial stenosis that resulted from Kawasaki disease and reviewed previous reports for possible indicators of PTCA effectiveness. METHODS AND RESULTS: Five patients, ranging in age from 2 to 16 years (median 8 years) underwent conventional PTCA for localized stenosis. The lesion targeted for PTCA was located in the middle right coronary artery of three patients and in the left anterior descending artery in two patients. In four of the five patients, PTCA was angiographically effective, with stenosis rates improving from 84 +/- 10% to 33 +/- 11% (P<.05). When the previously reported cases of six similar patients were taken into consideration, the only predictor of successful PTCA seemed to be the time elapsed between the onset of Kawasaki disease and performance of this procedure. CONCLUSIONS: In cases in which patients show significant localized stenosis as a result of Kawasaki disease, PTCA should be attempted within 6 to 8 years of the onset of the disease. Additionally, intravascular ultrasound imaging was found to be a useful tool for evaluating internal morphology before and after PTCA. In older patients with coronary calcification, other alternatives to PTCA, such as the use of a rotablator or an atherectomy catheter, should be considered.

Adolescent↗
PubMed1996

EGF or PDGF receptors activate atypical PKClambda through phosphatidylinositol 3-kinase.

Overexpression of a TPA-insensitive PKC member, an atypical protein kinase C (aPKClambda), results in an enhancement of the transcriptional activation of TPA response element (TRE) in cells stimulated with epidermal growth factor (EGF) or platelet-derived growth factor (PDGF). EGF or PDGF also caused a transient increase in the in vivo phosphorylation level and a change in the intracellular localization of aPKClambda from the nucleus to the cytosol, indicating the activation of aPKClambda in response to this growth factor stimulation. These immediate signal-dependent changes in aKPClambda were observed for a PDGF receptor add-back mutant (Y40/51) that possesses only two of the five major autophosphorylation sites and binds PI3-kinase, and were inhibited by wortmannin, an inhibitor of PI3-kinase. Furthermore, an N-terminal fragment of the catalytic subunit of PI3-kinase, p110alpha, inhibited aPKClambda-dependent activation of TRE in Y40/51 cells stimulated with PDGF. Overexpression of p110alpha resulted in an enhancement of TRE expression in response to PDGF and the regulatory domain of aPKClambda inhibited this TRE activation in Y40/51 cells. These results provide the first in vivo evidence supporting the presence of a novel signalling pathway from receptor tyrosine kinases to aPKClambda through PI3-kinase.

Amino Acid Sequence↗
PubMed1996

Platelet-derived growth factor activates protein kinase C epsilon through redundant and independent signaling pathways involving phospholipase C gamma or phosphatidylinositol 3-kinase.

Protein kinase C (PKC), a major cellular receptor for tumor-promoting phorbol esters and diacylglycerols (DGs), appears to be involved in a variety of cellular functions, although its activation mechanism in vivo is not yet fully understood. To evaluate the signaling pathways involved in the activation of PKC epsilon upon stimulation by platelet-derived growth factor (PDGF) receptor (PDGFR), we used a series of PDGFR "add-back" mutants. Activation of a PDGFR mutant (Y40/51) that binds and activates phosphatidylinositol 3-kinase (PI 3-kinase) caused translocation of PKC epsilon from the cytosol to the membrane in response to PDGF. A PDGFR mutant (Y1021) that binds and activates phospholipase C gamma (PLC gamma), but not PI 3-kinase, also caused the PDGF-dependent translocation of PKC epsilon. The translocation of PKC epsilon upon stimulation of PDGFR (Y40/51) was inhibited by wortmannin, an inhibitor of PI 3-kinase. Activation of PKC epsilon was further confirmed in terms of PKC epsilon-dependent expression of a phorbol 12-tetradecanoate 13-acetate response element (TRE)-luciferase reporter. Further, purified PKC epsilon was activated in vitro by either DG or synthetic phosphatidylinositol 3,4,5-trisphosphate. These results clearly demonstrate that PKC epsilon is activated through redundant and independent signaling pathways which most likely involve PLC gamma or PI 3-kinase in vivo and that PKC epsilon is one of the downstream mediators of PI 3-kinase whose downstream targets remain to be identified.

Cell Compartmentation↗
PubMed1996

Inhibitory effects of alkyl gallate and its derivatives on fatty acid desaturation.

Alkyl gallate, which is known as an antioxidant, intensively inhibited delta 5 and delta 6 desaturation in both rat liver microsomes and an arachidonic acid-producing fungus Mortierella alpina 1S-4. The rat liver microsomal delta 5 and delta 6 desaturases were inhibited by gallic acid esterified with alcohols with various numbers of carbons, suggesting that the necessary structure in an esterified alcohol for the inhibition is not so strict. Among the three hydroxy groups in gallic acid, the m-hydroxy group was shown to be the necessary structure. Kinetic analyses revealed that propyl gallate is a noncompetitive inhibitor of delta 5 desaturase (Ki = 2.6.10(-5)M) and delta 6 desaturase (Ki = 1.7.10(-4) M). These data indicate that alkyl gallate is a new type of desaturase inhibitor and different from known natural inhibitors, i.e., sesamin and curcumin.

Animals↗
PubMed1996

Expression of avian glypican is developmentally regulated.

An avian cDNA homologue of human and rat glypicans has been cloned from a stage 17 chicken heart cDNA library and used to analyze the distribution of this proteoglycan during development by Northern analysis and whole mount in situ hybridization. At stages 7-12, strong signals were detected in the cephalic region of the neural folds, rostral portion of paraxial mesoderm, and newly formed epithelial somites. At stages 20-25, strong expression was observed in the mantle zone of the telencephalon, the apical epidermal ridge and proximal region of developing limb. Transcripts also were found in the truncus arteriosus and arteriovenous-canal region of the heart, but not in the myocardium. This distribution pattern suggests that the avian glypican may be involved in the morphogenesis of limb, somite, heart, and brain. The expression of glypican also overlaps FGFs in limb bud, FGF receptors in heart and somite, and NGF receptors in forebrain. The affinity of heparan sulfate proteoglycans for growth factors and the distribution of the avian glypican are consistent with a role for this molecule in growth factor-mediated signals.

Amino Acid Sequence↗
PubMed1996

Effect of dietary n-9 eicosatrienoic acid on the fatty acid composition of plasma lipid fractions and tissue phospholipids.

n-9 Eicosatrienoic acid (ETrA), also known as Mead acid, is a minor fatty acid in essential fatty acid (EFA)-sufficient healthy subjects but is found at increased levels in EFA deficiency. This study examined the influence of dietary ETrA from a biological source on plasma and tissue ETrA. A synthetic fat-free diet was prepared to which was added Mut 48 oil which contains 19% ETrA (wt%) as well as other n-9 fatty acids. Blends of vegetable oils were used to achieve overall diets with 5% fat (wt%) and varying amounts of ETrA at two different dietary levels of linoleic acid (LA), approximately 4.4 and 19% of total fatty acids. These diets were fed to 5-week-old Dark Agouti rats for four weeks. Plasma lipid fractions and liver, spleen, and peritoneal exudate (PE) cells were analyzed for fatty acid composition. ETrA was present at up to 20% total fatty acids in plasma triglyceride, cholesterol ester, and phospholipid fractions. ETrA also accumulated to substantial levels in phospholipids of liver and spleen (up to 15% of total fatty acids) and PE cells (up to 11%). ETrA was found in plasma and tissue phospholipids in proportion to the amount of ETrA present in the diet. The incorporation was reduced in diets with higher LA content compared to diets containing similar amounts of ETrA but lower LA. All rats remained apparently healthy, and histological survey of major organs revealed no abnormality. While the long-term implications for health of ingestion of diets rich in ETrA remain to be established, rats appear to tolerate high levels of dietary ETrA without adverse effects. Dietary enrichment with ETrA warrants further investigation for possible beneficial effects in models of inflammation and autoimmunity, as well as in other conditions in which mediators derived from n-6 fatty acids can affect homeostasis adversely.

8,11,14-Eicosatrienoic Acid↗
PubMed1996

Effect of cycloheximide on the expression of LPS-inducible iNOS, IFN-beta, and IRF-1 genes in J774 macrophages.

The effect of cycloheximide (CHX) on the gene expression for inducible NO synthase (iNOS), interferon (IFN)-beta, and IFN regulatory factor (IRF)-1 was examined in LPS-stimulated J774 macrophages. LPS caused increased expression of mRNAs specific for iNOS, IFN-beta, and IRF-1 with different kinetics. Addition of CHX resulted in inhibition of the LPS-induced iNOS gene expression and parallel decrease in NO production. In contrast, expression of IFN-beta and IRF-1 genes in response to LPS was potentiated in the presence of CHX. These results indicate that de novo protein synthesis is not required for IFN-beta and IRF-1 gene expression and that ongoing protein synthesis including IFN-beta and IRF-1 may be involved in the induction process of iNOS in mouse macrophages.

Animals↗
PubMed1996

Dominant negative effect of the truncated p110 subunit of phosphatidylinositol-3 kinase.

Effects of p110, the catalytic subunit of PI-3 kinase, on induction of TPA response element-driven promoter by EGF was examined. The induction was enhanced by co-expression of the wild type of p110. The truncated p110 mutants containing the binding site for p85 but missing the catalytic activity repressed the induction. A mutant with no binding activity to p85 did not show this effect. These results suggest that PI-3 kinase is involved in signal transduction of EGF and that the truncated p110s capable of binding to p85 serves as a dominant negative reagent for PI-3 kinase.

Animals↗
PubMed1996

Dietary (n-9) eicosatrienoic acid from a cultured fungus inhibits leukotriene B4 synthesis in rats and the effect is modified by dietary linoleic acid.

Eicosatrienoic acid (ETrA) is the (n-9) homologue of (n-6) arachidonic acid (AA) and (n-3) eicosapentaenoic acid (EPA). ETrA can be synthesized endogeneously, but tissue levels are normally undetectable except in essential fatty acid (EFA) deficiency. An ETrA-rich oil extracted from a cultured fungus was used to prepare diets which had varying levels of ETrA (0-8 g/kg diet) in combination with one of two levels of linoleic acid (LA, 2.2 or 9.5 g/kg diet). All diets were sufficient in essential fatty acids. Groups of rats were fed these diets for 4 wk after which leucocyte fatty acid content and leukotriene B4 (LTB4) synthesis were measured. The influence of dietary LA on ETrA accumulation in cells was studied and correlations with LTB4 synthesis determined. ETrA was efficiently incorporated into peritoneal exudate cell (PEC) phospholipids with no evident saturation being observed with levels up to 10 mol/100 mol total fatty acids in peritoneal exudate cells. Cellular ETrA levels were lower (P < 0.001) in rats fed the higher level of LA. ETrA accumulation in peritoneal exudate cells correlated (r(2) = 0.63, P < 0.05) with reduced LTB4 synthesis which was attributable to LTA hydrolase inhibition. Thus, dietary ETrA from a biological source can accumulate in leucocytes and suppress inflammatory eicosanoid synthesis. The findings justify further studies into the biochemical and anti-inflammatory effects of dietary ETrA, which could be incorporated into palatable food additives.

8,11,14-Eicosatrienoic Acid↗
PubMed1996

Polyanion induced preferential multinucleation in macrophages at a low level of TNF-alpha secretion.

When rat bone marrow macrophages were incubated with acetyl lignin (EP3) in the presence of a 10% solution of fetal bovine serum, the macrophages secreted tumor necrosis factor (TNF-alpha) in a dose-dependent manner. This was followed by macrophage multinucleation. EP3 was found to have a significant effect on TNF-alpha secretion at a minimum dose of 5 micrograms/ml and produced no significant further increase at levels above 50 micrograms/ml, while multinucleation was most active at 10 micrograms/ml. However, multinucleation did not occur at higher concentrations of EP3 (50 micrograms/ml and 100 micrograms/ml). Secretion of TNF-alpha was significantly reduced in the absence of fetal bovine serum, whereas multinucleation was very active, starting after 6 h of incubation. At concentrations of 100 micrograms/ml, sulfonyl lignin (LS) and dextran sulfate (DS) only induced low levels of TNF-alpha secretion from macrophages, but induced active multinucleation. The multinucleation induced by addition of LS or DS was inhibited by further addition of EP3. Thus, macrophage multinucleation was most active when a low level of TNF-alpha was secreted from the macrophages.

Animals↗
PubMed1996

Angiographic assessment of the stretch-recoil-gain relation after balloon coarctation angioplasty and its relation to late restenosis.

The effects of stretch and immediate recoil after balloon angioplasty were evaluated in 21 patients with coarctation of the aorta who underwent balloon coarctation angioplasty. A total of 28 procedures were performed in these patients, who ranged in age from 1 month to 17 years with a mean of 4.3 years. The systolic pressure gradient and coarcted diameter changed significantly from 42 +/- 22 to 14 +/- 9 mmHg (P < 0.0001) and from 4.0 +/- 1.7 to 6.1 +/- 2.0 mm (P < 0.001), respectively. Immediate recoil was responsible for the loss of 33% of the potentially achievable coarcted dimension. Recoil was determined mainly by the degree of arterial stretch. Gain increased exponentially with an increase in stretch. There was a narrow range of % stretch (60-80%) within which an effective diameter gain could be obtained. Both gain and stretch were the best predictors for late restenosis: patients with a larger immediate gain and stretch developed more restenosis. These results suggest that the stretch-recoil-gain relationship may be clinically important for evaluating the best predictor of late restenosis after balloon coarctation angioplasty.

Adolescent↗
PubMed1996

Inhibition of rat liver microsomal desaturases by curcumin and related compounds.

Curcumin (1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione) inhibited noncompetitively rat liver microsomal delta 5 desaturase (Ki = 36 microM) and delta 6 desaturase (Ki = 28 microM). Although curcumin has a symmetrical structure with a methylene group as the center, only half the structure is essential for the desaturase inhibition. The structure necessary for the inhibition is similar to that of alkyl gallate (H. Kawashima et al., Biochim. Biophys. Acta, in press), i.e., a 3-hydroxy group of the aromatic ring is essential for the inhibition and a free carboxyl group at the end opposite to the aromatic ring interferes with the inhibitory effect. The following structural features of curcumin are necessary for the desaturase inhibition: (i) the aromatic ring conjugated with the double bond between the 1 and 2 (or 6 and 7) positions; (ii) both 4-hydroxy and 3-methoxy groups (for both desaturase inhibitions); and (iii) only a 4-hydroxy group (for delta 6 desaturase inhibition).

Animals↗
PubMed1996

Nicardipine and nifedipine inhibit fatty acid desaturases in rat liver microsomes.

Nicardipine and nifedipine, Ca channel blockers, inhibited rat liver microsomal desaturases, though verapamil, methoxyverapamil, cinnarizine, flunarizine, and diltiazem did not. However, nicardipine and nefidipine apparently did not inhibit the fungal desaturation in Mortierella alpina 1S-4. Nicardipine inhibited rat liver microsomal delta 5 desaturase specifically (50% inhibitory concentration. 170 microM), and nifedipine inhibited delta 6 desaturase specifically (78 microM). The inhibition by nicardipine and nifedipine is uncompetitive, the Ki values for delta 5 and delta 6 desaturases being 62 and 44 microM, respectively.

Animals↗
PubMed1996

[A case of superior vena cava syndrome treated with combination radiation and CRE (CBDCA and VP-16) therapy].

Carboplatin and etoposide were reported to be excellent radiation sensitizers. We encountered a patient with SVC syndrome due to lung cancer who was successfully treated by combination carboplatin, etoposide and hyperfractionation radiotherapy. A 72-year-old man was admitted to our hospital because of remarkable face edema. Computed tomography revealed a huge lung tumor and compressed SVC due to tumor growth. Acute tumor regression was essential for this case. We performed combination chemotherapy and radiation. The regime consisted of CBDCA 300 mg (day 1 1 hr drip infusion) and etoposide 50 mg/day for 21 days by oral administration. Two daily fractionations of 1.4 Gy were delivered 5 days-a-week, with a 4 h interval between fractions (total dose 49.8 Gy). Complete response of huge tumor was attained in this case. The major side effect associated with the therapy was myelosuppression. The patient's quality of life has been remarkably improved with this therapy.

Aged↗
PubMed1996

Internal DNA deletion within the BCL-6 gene on untranslocated chromosome in non-Hodgkin's lymphoma with 3q27 abnormality.

Chromosomal translocations involving the band 3q27 are recognized as common specific cytogenetic abnormalities in B cell non-Hodgkin's lymphoma (NHL), and the BCL-6 gene, identified on 3q27 was shown to be disrupted by these translocations. Previously, we have reported biallelic BCL-6 rearrangements occurring in some patients with B cell NHL. In the present study, we describe a NHL patient with t(3;22)(q27;q11) translocation. In this patient, biallelic BCL-6 abnormalities were indicated by Southern blot analysis. Further studies revealed that one of the two independent abnormalities was a juxtaposition to the immunoglobulin (Ig) lambda gene associated with chromosomal translocation, whereas the other was an internal DNA deletion of 1.5 kb area on untranslocated chromosome 3. Deletion junctions were located within the first exon and the 5' region of the first intron. The result provides the evidence that, besides chromosomal translocation, submicroscopic local DNA recombination can cause structural alteration of the BCL-6 gene.

Base Sequence↗