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Biomedical subjects

T Takano

Publications and source records attributed to T Takano.

At least 253 records · Page 14Linked to original sources

Serial magnetic resonance imaging findings of Rasmussen's encephalitis--case report.

A 12-year-old boy presented with Rasmussen's encephalitis. Serial magnetic resonance (MR) imaging one year after the onset of seizure showed no abnormality. T2-weighted imaging detected a high intensity lesion in the left frontal cortex when the frequency of seizures increased 11 months later. MR imaging showed the lesion rapidly spread into the white matter, then gradually regressed after biopsy and immunoglobulin therapy, and mild focal atrophy of the left frontal lobe in spite of recurrence of seizures 3 months after the therapy. Histological examination of the biopsy sample showed the characteristic findings of Rasmussen's encephalitis. Five months after the biopsy, another new high intensity lesion was detected next to the previous one, although his seizures were well controlled at that time. Although the extent of the high intensity lesion did not correlate with the frequency of seizures, such sequential changes in MR imaging appearance seemed to reflect the course of this disease.

Anti-Inflammatory Agents↗

Maturation factor for the activation process of an extracellular proteinase in Lactobacillus helveticus CP790.

A maturation factor that was needed for activation of an extracellular proteinase was partially purified from Lactobacillus helveticus CP790 by DEAE-Sepharose column chromatography, followed by gel filtration using HPLC. The protein had the ability to accelerate the conversion of proproteinase to active enzyme but had no proteolytic activity toward casein that had been treated with fluorescein isothiocyanate. The proteinase activities in the proproteinase fraction and the maturation protein fraction were not affected by preincubation of either fraction separately. However, when the mixture of the proproteinase and the maturation protein was incubated, the conversion of the proproteinase to active enzyme was accelerated, and proteinase activity increased. The production of some proteins that were specific to the active fractions was highest at the midlog phase of cell growth, which corresponded to the period of maximum proteinase activity. The results suggest that the proproteinase is activated to the mature enzyme not by an autocatalytic process but by the help of a maturation protein.

Caseins↗

Effect of topical tranilast and corticosteroids on subepithelial haze after photorefractive keratectomy in rabbits.

BACKGROUND: Tranilast (trade name Rizaben), an anti-allergic drug with anti-inflammatory effects, is thought to inhibit synthesis of extracellular matrix of fibroblasts through the suppression of TGF-beta. We evaluated the effect of topical tranilast on the subepithelial haze that developed after excimer laser keratectomy and its effect was compared with that of betamethasone eye drops METHODS: Excimer laser keratectomy (phototherapeutic keratectomy mode) was performed with the Nidek EC-5000 excimer laser on 16 rabbit corneas (eight rabbits). From the second postoperative day, topical 2% tranilast was instilled in the right eye and the control solution in the left eye, four times daily. Until the fourth week after the operation, we measured the densitometric values of scattered light intensity of the subepithelial haze with an anterior ocular analyzer, EAS-1000 (Nidek). At the fifth postoperative week, light and electron microscopy and immunohistochemistry with an antibody to TGF-beta were also performed. RESULTS: Densitometric values of the subepithelial haze in the corneas treated with 2% tranilast were slightly less than those of the subepithelial haze in the control corneas. However, the values of the subepithelial haze in the betamethasone-treated corneas were significantly less than those in control corneas. Histochemical examinations revealed that topical tranilast had a small effect on the subepithelial haze after excimer laser keratectomy in rabbits. CONCLUSION: Topical 0.1% betamethasone can limit the amount of subepithelial haze and tranilast may inhibit development of subepithelial haze by the suppression of TGF-beta.

Administration, Topical↗

Overexpression of nestin and vimentin in the ependyma of spinal cords from hydrocephalic infants.

The ependyma of the spinal central canal in cases of hydrocephalus shows abnormalities which vary with the aetiology of ventricular dilatation. To determine whether these ependymal changes are developmental or reactive in nature, immunohistochemical findings were compared between nine normal controls and 12 cases of hydrocephalus (three each of congenital aqueductal stenosis. Dandy-Walker malformation, Chiari type II malformation, and post-haemorrhagic hydrocephalus) using antisera to nestin, vimentin and glial fibrillary acidic protein. The main pathological findings were disruption of ependymal layer, apparent pseudostratification of ependyma, expansion, cleft or syrinx formation in relation to the central canal, and ependymal rosette formation. In normal developing fetal spinal cord, nestin and vimentin were expressed mainly in pseudostratified ependymal cells and radial fibres in the median septum. In cases with congenital hydrocephalus (congenital aqueductal stenosis. Dandy-Walker malformation, and Chiari type II malformation), nestin was overexpressed in immature ependymal cells, and strong vimentin immunoreactivity was detected in the long tract of radial fibres in the median septum. Nestin and vimentin were also expressed in small cells and their fibres which covered areas denuded of ependymal cells in cases of Chiari type II malformation and post-haemorrhagic hydrocephalus. Two conclusions are suggested by this report. First, the ependyma of the spinal central canal in congenital hydrocephalus shows a delay in maturation of radial glial cells into mature astrocytes and ependymal cells. Second, areas of ependymal denudation may be repaired by the immature glial cells derived from subependymal cells.

Ependyma↗

Autoantibody selectively inhibits binding of von Willebrand factor to glycoprotein ib. Recognition site is located in the A1 loop of von Willebrand factor.

A 20-year-old man with severe von Willebrand disease recently presented a progressive bleeding tendency, characterized recurrent subcutaneous hemorrhages and cerebral hemorrhage. Mixing and infusion studies suggested the presence of an inhibitor directed against vWF:RCo activity of von Willebrand factor (vWF) without significant inhibition of the FVIII:C. The inhibitor was identified as an antibody of IgG class. The inhibitor inhibited the interaction of vWF in the presence of ristocetin and that of asialo-vWF with GPIb while it partially blocked botrocetin-mediated interaction of vWF to GPIb. The inhibitor reacted with native vWF, the 39/34 kDa fragment (amino acids [aa] 480/ 481-718) and the recombinant vWF fragment (MalE-rvWF508-704), but not with Fragment III-T2 (heavy chains, aa 273-511; light chains, aa 674-728). A synthetic peptide (aa 514-542) did not inhibit vWF-inhibitor complex formation. We conclude that this is the first auto-antibody of class IgG from human origin that recognizes the sequence in the A1 loop of vWF, resulting in a virtual absence of functional vWF and a concomitant severe bleeding tendency although recognition site is different from the residues 514-542 which is crucial for vWF-GPIb interaction.

Adult↗

The effect of preoperative high dose methylprednisolone in attenuating the metabolic response after oesophageal resection.

OBJECTIVE: To evaluate the effect of giving glucocorticoids preoperatively for the prophylaxis of surgical stress. DESIGN: Prospective randomised study. SETTING: University hospital, Japan. SUBJECTS: 30 patients undergoing resection of oesophageal carcinoma. INTERVENTIONS: 15 patients (group 1) were randomised to be given methylprednisolone (30 mg/kg) and 15 patients (group 2) to be given saline intravenously before operation. MAIN OUTCOME MEASURES: Outcome, length of stay in the intensive care unit (ICU), metabolic response, and oxygenation. RESULTS: Patients given methylprednisolone had a mean stay in the ICU of 5.1 +/- 1.0 days compared with 8.2 +/- 4.5 days in the saline group (p < 0.01). 5 patients in the saline group compared with 0 in the methylprednisolone group developed postoperative complications (p = 0.02). Plasma norepinephrine and arginine vasopressin levels in methylprednisolone group were significantly lower than those in the saline group (p < 0.05). The PaO2:FiO2 ratio in the saline group was significantly lower than that in the experimental group (p < 0.01). CONCLUSIONS: Preoperative methylprednisolone may facilitate the postoperative management of surgical patients.

Adult↗

Detection of CD44 variants in fine needle aspiration biopsies of thyroid tumor by RT-PCR.

Increased expression of CD44 variants is often observed in differentiated thyroid carcinomas. To establish a method for gene diagnosis of thyroid without any additional invasions to the patients, RNA in leftover cells inside the needle used for fine needle aspiration biopsies (FNABs) was extracted to detect the expression of CD44 variants by reverse transcription-polymerase chain reaction (RT-PCR). After FNAB and preparation of sample on a slide glass for cytological examinations, RNA in leftover cells inside the needle was extracted. After reverse transcription, cDNA was amplified by PCR with specific primers for CD44. The results were compared with the cytological diagnosis. CD44 variants were detectable in all seven samples that were diagnosed as positive cytology. However, they were detected in only five of the 29 samples of negative cytology. Therefore, thyroid tumors may be more accurately diagnosed by a combination of cytological examination and detection of CD44 variants in RNA obtained by FNAB.

Adult↗

[Anesthesia for a patient with macrothrombocytopenia].

A 56-year-old female with macrothrombocytopenia was scheduled for colectomy and hepatectomy. She had not shown significant bleeding tendency. Her preoperative platelet counts were 0.5-1.6 x 10(4) microliters-1 with the use of an automated cell counter. However, microscopic examination showed platelet number ranging 0.9-3.4 x 10(4) microliters-1 and many macrothrombocytes. Therefore, platelet biomass (platelet number x platelet volume) seemed almost normal. Bleeding time was 3 minutes and platelet function was normal. She received preoperatively high dose gamma-globulin administration and intraoperatively platelet transfusion. The operation was performed under combined epidural and general anesthesia. Intra- and post-operative course was uneventful.

Anesthesia, Epidural↗

[Studies on the bottles of mineral water and the foreign plastic like substances].

The containers of mineral water and the foreign plastic substances which were found in the mineral water were investigated. Most of plastic bottles were made of polyethylene terephthalate (PET) and the caps were made of polypropylene (PP), polyethylene (PE) or aluminum. PE liners were attached to some caps. Most of the foreign plastic substances were PET while others were PE, PP, Teflon and rubber. Some bottles had a scratch on the top inside. The origin of most PET fragments was presumed to be scraped off the bottles by the lowering of the injection nozzle during the water filling process. The sources of the other substances were also determined.

Food Contamination↗

Oxidized phosphatidylcholines that modify proteins. Analysis by monoclonal antibody against oxidized low density lipoprotein.

Oxidatively modified low density lipoprotein (OxLDL) is known to be involved in atherogenesis. We have previously developed a murine monoclonal antibody, FOH1a/DLH3, which recognized oxidatively modified lipoproteins as well as foam cells in human atherosclerotic lesions (Itabe, H., Takeshima, E., Iwasaki, H., Kimura, J., Yoshida, Y., Imanaka, T., and Takano, T. (1994) J. Biol. Chem. 269, 15274-15279). The antigen of this monoclonal antibody was formed by peroxidation of phosphatidylcholine (PC), and the antigenic oxidized PC (OxPC) derivatives are thought to form complexes with polypeptides including apolipoproteins. OxLDL was measured by a sensitive sandwich enzyme-linked immunosorbent assay using the monoclonal antibody and anti-human apolipoprotein B antibody, in which antigenic OxPC competed with OxLDL. When antigenic activities of PC analogs were tested by the competition assay, 1-palmitoyl-2-(9-oxononanoyl) PC (9-CHO PC) and the hydroperoxide of egg PC potently inhibited the detection of OxLDL. 1-Palmitoyl-2-linoleoyl PC was oxidized with ferrous ion and ascorbic acid, and the antigenic products were purified from the OxPC extracts on high pressure liquid chromatography columns and subsequently analyzed by laser desorption mass spectrometry. Molecular weight determination and retention times of high pressure liquid chromatography suggest that one of these products was 9-CHO PC. Other products are thought to be 8-carbon aldehyde, dihydroxy, and ketohydroxy derivatives of PC. When a C-terminal 16-mer synthetic peptide of the 70-kDa peroxisomal membrane protein was simply incubated with 9-CHO PC, it was found to be reactive in a sandwich enzyme-linked immunosorbent assay using FOH1a/DLH3 and an anti-peptide antiserum. These results suggest that the anti-OxLDL monoclonal antibody FOH1a/DLH3 reacts with several oxidized products of PC including aldehyde derivatives of PC, which covalently modify polypeptides.

Animals↗

A high frequency of defective vif genes in peripheral blood mononuclear cells from HIV type 1-infected individuals.

We studied the heterogeneity and intactness of the vif gene in six HIV-1-infected individuals at various clinical stages. The proviral vif sequences in peripheral blood mononuclear cells were amplified by PCR, followed by cloning and sequencing of 45 vif clones. The intraindividual diversity of the vif genes ranged from 0.45 to 3.3% and was not correlated with disease stage. Although the vif gene has been shown to be essential for infection of HIV-1 in vitro, a high frequency (31%) of defective vif genes was observed. In one patient, six vif clones carried double nonsense mutations at the same positions, five of which were clustered in the phylogenetic tree, suggesting that these vif-defective viruses may have replicated in vivo. Phylogenetic analysis revealed that the vif sequences from each individual were clustered into a separate group and that all of them belong to subtype B.

Adult↗

Sterol-dependent transcriptional regulation of sterol regulatory element-binding protein-2.

We show in this manuscript that expression of the mRNA for sterol regulatory element-binding protein-2 (SREBP-2) is regulated by the cellular sterol level in cultured HeLa cells. We have cloned the 5'-flanking region of the gene encoding human SREBP-2. Characterization of this region shows the minimum 50-base pair segment, which contains a 10-base pair sterol regulatory element 1 (SRE-1) identical to the one in the human LDL receptor promoter, confers sterol responsiveness when fused to the luciferase reporter gene. Enforced expression of the truncated SREBP-2 protein (amino acid residues 1-481) also shows that this upstream segment contains the information required for transcriptional activation. The luciferase assays using mutant versions of the reporter genes reveal that the sterol-dependent transcriptional regulation is mediated by two nearby motifs, the SRE-1 and the NF-Y binding site (the inverted CCAAT box, ATTGGC); the latter is reported to play a critical role in sterol-dependent regulation of 3-hydroxy-3-methylglutaryl-coenzyme A synthase and farnesyl diphosphate synthase genes (Jackson, S. M., Ericsson, J., Osborne, T. F., and Edwards, P. A. (1995) J. Biol. Chem. 270, 21445-21448). Gel mobility shift assays demonstrate that the transcription factor NF-Y truly binds to the ATTGGC sequence. These findings suggest that the activity of SREBP-2 is controlled not only post-translationally by proteolytic activation of the precursor protein but also transcriptionally by itself together with NF-Y.

Binding Sites↗

Genetic linkage of the sarco(endo)plasmic reticulum Ca(2+)-dependent ATPase II gene to intracellular Ca2+ concentration in the spontaneously hypertensive rat.

A cosegregation analysis of sarco(endo)plasmic reticulum Ca(2+)-dependent ATPase (SERCA) II genotype, systolic blood pressure and platelet intracellular Ca2+ concentration was performed to dissect polygenic hypertensive traits in spontaneously hypertensive rats. Backcross analysis between spontaneously hypertensive rats and normotensive. Donryu rats demonstrated the existence of an inferred single major gene locus (ht). Thrombin-stimulated intraplatelet Ca2+ concentration was significantly higher in the SERCA II homozygotes than in the heterozygotes. The SERCA II genotype did not cosegregate with the blood pressure level. The SERCA II gene was assigned to rat chromosome 12. These results suggest that the SERCA II gene on rat chromosome 12 contributes to increased thrombin-stimulated intraplatelet Ca2+ concentration and that the SERCA II gene is not identical to ht.

Animals↗

Import into mitochondria of phospholipid hydroperoxide glutathione peroxidase requires a leader sequence.

An in vitro import system was used to characterize the mechanism of import of phospholipid hydroperoxide glutathione peroxidase (PHGPx) into mitochondria. Mitochondria were isolated from rat liver and incubated at 25 degrees C with [35S]methionine-labeled products of the in vitro translation of mRNA that encoded 23-kDa and 20-kDa PHGPx. 23-kDa PHGPx was imported into mitochondria in a time-dependent manner and was processed to yield the 20-kDa form of PHGPx. The 20-kDa form of PHGPx, without a leader sequence, associated weakly with mitochondria but was not imported. An analysis with an uncoupler of oxidative phosphorylation showed that a membrane potential in the mitochondria was also required for the import of PHGPx. It appears, therefore, that the leader sequence in the precursor to PHGPx is the signal for import into the mitochondria. This is the first report to indicate that the precursor to PHGPx is imported into the mitochondria via the action of a leader sequence.

Animals↗

Sequential morphologic events during apoptosis of human neutrophils. Modulation by lipoxygenase-derived eicosanoids.

Dual-laser flow cytometry, based on the properties of the DNA-binding dyes Hoechst 33342 and propidium iodide, was used, with light and electron microscopy and DNA fragmentation studies, to define the influence of lipoxygenase-derived eicosanoids on apoptosis of human polymorphonuclear neutrophils (PMN) in vitro. Apoptosis was characterized by progression through an early apoptotic phase characterized by condensation of chromatin and coalescence of nuclear lobes, to a late apoptotic phase characterized by nuclear degradation and evanescence, and secondary necrosis. Prolonged exposure of PMN to leukotriene B4 (LTB4) afforded dose-dependent inhibition of constitutive PMN apoptosis (percentage of normal and apoptotic PMN, respectively, after aging for 18 h: vehicle, 30.5 +/- 2.7% and 61.8 +/- 3.2%; LTB4 10(-7) M, 57.6 +/- 1.2% and 37.6 +/- 1.0%) and apoptosis triggered by the classic peptide chemoattractant FMLP. In contrast, apoptosis was not affected by the LTB4 precursor 5(S)-hydroxyeicosatetraenoic acid (HETE), the omega-oxidation LTB4 metabolites 20-hydroxy-LTB4 and 20-carboxy-LTB4, the cysteinyl leukotriene LTC4, the 15-lipoxygenase product 15(S)-HETE, or the lipoxygenase interaction product lipoxin A4. The anti-apoptotic effect of LTB4 was mimicked by 20,20,20-trifluoro-LTB4, LTB4-dimethylamide, and 14,15-dehydro-LTB4, and was blunted by pertussis toxin and genistein, inhibitors of G alpha i GTP-binding proteins and tyrosine kinases, respectively, but not by staurosporine, 15(S)-HETE, or lipoxin A4. This unique pharmacologic profile suggested that LTB4 attenuated apoptosis through activation of cell surface receptors and signaling events distinct from those involved with PMN trafficking, degranulation, and respiratory bursts.

Animals↗

Assignment of Alzheimer's presenilin-1 (PS-1) gene to 14q24.3 by fluorescence in situ hybridization.

Presenilin-1 (PS-1) was suggested to be localized on 14q24.3 based on linkage analysis and cDNA cloning. The final identification of PS-1 as the causal gene for Alzheimer's disease (AD) was concluded based on finding of the point mutations in the candidate cDNA linked with pedigrees with early-onset familial AD. We present evidence of its physical genome mapping of PS-1 by fluorescence in situ hybridization method.

Alzheimer Disease↗