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T Takano

Publications and source records attributed to T Takano.

At least 217 records · Page 12Linked to original sources
PubMed1998

Acute nephrotoxic serum nephritis in complement knockout mice: relative roles of the classical and alternate pathways in neutrophil recruitment and proteinuria.

BACKGROUND: The importance of complement in the pathophysiology of renal disease is still being appreciated. To further address the role of this mediator system, we evaluated the influence of absolute deficiency of C3 and C4 on acute nephrotoxic serum nephritis (NSN). METHODS: Selective 'knockout' of C3 and C4 was routinely confirmed in null mice by ELISA. NSN was induced by intravenous injection of a sheep anti-rat nephrotoxic serum that cross-reacts with murine glomerular antigens. Deposition of heterologous immunoglobulin in wild-type glomeruli was associated with rapid complement deposition and neutrophil infiltration, and followed by the development of proteinuria. RESULTS: Neutrophil infiltration was markedly inhibited in C3-deficient mice indicating a role for complement in PMN recruitment. In contrast, C3 deficiency afforded only partial protection against proteinuria. NSN was studied further in C4 null mice to probe the relative roles of the classical and alternate pathway in disease pathophysiology. C3 and C4 deficiency were associated with equivalent inhibition of PMN recruitment and proteinuria. CONCLUSIONS: In aggregate, the data support a major role for complement in PMN recruitment in this model and point to complement-independent mechanisms of proteinuria in antibody-mediated glomerulonephritis. These 'knockout' mice should prove valuable for defining the complement-activated mediator systems that regulate leukocyte recruitment and tissue injury in renal diseases.

Acute Disease↗
PubMed1998

Characterization of developmental changes in EEG-gamma band activity during childhood using the autoregressive model.

BACKGROUND: We characterized developmental changes in the EEG-gamma band during childhood using the autoregressive (AR) model, which was previously developed and described in our laboratory. METHODS: The subjects comprised 707 healthy children ranging in age from 3 to 12 years. Electroencephalographs (EEG) were recorded from Fp1, Fp2, C3, C4, O1 and O2, monopolar leads referenced to the ear during quiet wakefulness (eyes closed). One 10 s artifact-free segment was selected from each record, digitized, then analyzed by AR and component analysis, which estimated the component wave and power spectrum. RESULTS: Component waves obtained from all EEG leads were divided into eight groups, which comprised approximately 2, 5, 10, 17, 25, 30, 40 and 47 Hz peaks. The gamma band (peak wave 40 Hz; range 35-45 Hz) was a major EEG component throughout childhood. Different developmental characteristics of the gamma band power were exhibited in each lead. The power increased significantly (P < 0.01) between 3 and 4 years of age in all leads reaching a peak at 4-5 years of age, especially in the frontal region. CONCLUSIONS: These developmental characteristics might be related to the information processing and cognitive function, which is enhanced at 4-5 years of age, especially in the frontal region.

Child↗
PubMed1998

Characterization of two Chinese hamster ovary cell lines expressing the COOH-terminal domains of sterol regulatory element-binding protein (SREBP)-1.

Sterol regulatory element-binding proteins (SREBPs) regulate transcription of genes encoding enzymes in the cholesterol biosynthetic pathway and the LDL receptor. These proteins are synthesized as membrane-bound precursors and processed to generate the NH2-terminal domains, mature transcription factors. We established two Chinese hamster ovary (CHO) cell lines, CHO-421 expressing the truncated hamster SREBP-1 (amino acids 421-1133) with two transmenbrane domains and CHO-557 expressing another truncated SREBP-1 (amino acids 557-1133) without any transmembrane domains, to investigate the fate of the COOH terminus after cleavage of the NH2-terminal mature SREBP. The cell fractionation experiments revealed that the two proteins, regardless of the absence of transmembrane domains in the SREBP (557-1133), similarly localized in the nuclear envelope and the microsomal membrane fractions, suggesting that these proteins appear to be tightly bound to a membrane protein(s) localizing on the nuclear and endoplasmic reticulum (ER) membranes. Although we predicted that overexpression of the COOH-terminal domains, which were thought to be involved in the regulation of SREBP processing, would result in disruption of the SREBP-dependent transcriptional regulation of several genes, the mRNA levels for 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) synthase in these two cell lines were regulated in a sterol-dependent manner. Pulse-chase experiments revealed that the SREBP (421-1133) was relatively rapidly degraded (t1/2 = 4-6 hr) and that the intracellular cholesterol level did not affect the half-life time. The degradation of the SREBP (421-1133) was not suppressed by the treatment of a calpain inhibitor, N-acetyl-leucyl-leucyl-norleucynal (ALLN), which blocks the proteolysis of some proteins within or near the ER. In CHO-557 cells the SREBP (557-1133) was much more rapidly degraded (t1/2 = 1-2 hr), suggesting that the cytosolic COOH-terminal domain is accessible to the enzymatic attacks from the cytoplasm. Taken together, overexpression of the COOH-terminal domains does not affect the regulation of SREBP processing and the domains are rapidly turned over by the cytosolic proteolytic process distinct from the ALLN-sensitive ER degradative pathway.

Animals↗
PubMed1998

Purulent pericarditis with tamponade caused by Salmonella enteritidis.

The incidence of purulent pericarditis has declined. However, mortality remains high. We describe a case of purulent pericarditis with tamponade caused by Salmonella enteritidis, and emphasize the importance of early recognition, prompt institution of appropriate antibiotic therapy, and early surgical drainage for survival.

Adult↗
PubMed1998

Effect of nasal continuous positive airway pressure on pulmonary edema complicating acute myocardial infarction.

Cardiogenic pulmonary edema is a frequent cause of reparatory failure. We investigated the effects of nasal continuous positive airway pressure (CPAP) in patients with severe pulmonary edema associated with acute myocardial infarction. Twenty-nine consecutive patients were divided into 3 groups: firstly, 7 intubated patients who received mechanical ventilation at study entry comprised the intubation group. The rest of the patients were randomly assigned to either of the following 2 groups: 11 patients who received oxygen plus CPAP delivered by a nasal mask (CPAP group), and 11 patients who received oxygen only via face mask (oxygen group). All patients in the intubation group had cardiogenic shock. Two patients (18%) in the CPAP group and 8 patients (73%) in the oxygen group required mechanical ventilation with endotracheal intubation (p=0.03). The hospital mortality rate in the CPAP group (9%) was significantly lower than the oxygen group (64%, p=0.02). The pulmonary artery wedge pressure and heart rate were significantly lower in the CPAP group than in the oxygen group 24 h after study entry (p<0.05 and p<0.01). The mean pulmonary artery pressure 48 h after study entry was 18+/-5 mmHg in the CPAP group and 25+/-8 mmHg in the oxygen group (p<0.05). The PaO2/FiO2 ratio increased in the intubation group (168+/-69 to 240+/-57, p<0.05) and the CPAP group (137+/-17 to 253+/-67, p<0.01) 24 h after study entry. Arterial plasma endothelin-1 concentrations decreased significantly earlier in the CPAP group than in the oxygen group (p<0.05). In patients without cardiogenic shock, nasal CPAP lead to an early improvement in oxygenation and hemodynamics, and decreased the mortality rate. Early and active respiratory management is recommended in patients with pulmonary edema associated with acute myocardial infarction.

Aged↗
PubMed1998

Classification of Lactobacillus helveticus strains by immunological differences in extracellular proteinases.

Polyclonal antibodies against an extracellular proteinase of Lactobacillus helveticus CP53 were raised. The antibodies reacted with a 170-kDa enzyme with activity and a 53-kDa protein that seemed to be a degradation product of the 170-kDa proteinase from results of immunoblotting. The antibodies reacted also with a 45-kDa extracellular proteinase of L. helveticus CP790. However, monoclonal antibodies to the CP790 proteinase did not react with the proteinase of L. helveticus CP53. Seventeen strains of L. helveticus were tested for immunological reactivity with the two kinds of antibodies. The strains all had the same reactivity as either strain CP53 or strain CP790. Eleven strains with the 45-kDa proteinase were identified as L. helveticus biovar jugurti because they did not ferment maltose, four other strains with the 170- and 53-kDa proteins were identified as L. helveticus biovar helveticus because they fermented maltose. The remaining two strains dit not fit this pattern; they had both the 170- and 53-kDa proteins, but classification by their sugar utilization showed them to be L. helveticus biovar jugurti.

Animals↗
PubMed1998

[Mobility of orbital implant covered by own sclera].

We evaluated in 7 eyes the mobility of a newly designed orbital implant made of hydroxyapatite. This orbital implant has a screw peg and is covered with a piece of sclera from the enucleated eye of the patient. The implant was well tolerated and there were no cases of proptosis during the follow-up of 1.8 +/- 0.6 years. Assuming the mobility of a healthy eye as 100%, photographic analysis showed the mobility of the anterior orbit to be 92.6% in adduction, 85.9% in abduction, 84.9% in supraduction, and 90.9% in infraduction. The mean tugging weight of the implant was, when measured by a strain gauge, 344.2 +/- 29.2 g in adduction and 327.6 +/- 33.4 g in abduction. These values corresponded to 90.4 +/- 4.4% and 89.5 +/- 5.3% respectively of those in a healthy eye. The presence of the orbital implant did not affect the electrooculogram as compared to a healthy eye. Cinematic studies using magnetic resonance imaging (MRI) showed that the constriction and extension of the extraocular muscles, which were sewn onto the orbital implant, matched that of a healthy eye.

Adult↗
PubMed1998

[Evaluation of whole blood rapid troponin T assay: cooperative study of general practitioners and office cardiologists in Tokyo].

The recently developed whole blood rapid assay for cardiac troponin T (TROP T) was evaluated by a cooperative study of general practitioners and office cardiologists in the Tokyo area (Tokyo TROP T Trial). Seventy patients with suspected acute myocardial infarction treated at 14 medical clinics were enrolled in this study. The diagnostic efficacy of troponin T was compared with that of electrocardiographic evaluations and clinical standards for diagnosis of acute myocardial infarction. Twelve of the 70 patients (17.1%) had final diagnoses of acute myocardial infarction or severe unstable angina necessitating emergency coronary intervention. Troponin T was judged as positive when simultaneously measured serum troponin T was more than 0.25 ng/ml. Sensitivity, specificity, positive predictive value, and negative predictive value were 100%, 58.6%, 33.3%, and 100% for electrocardiographic evaluation, and 58.3%, 100%, 100%, and 92.1% for troponin T, respectively. Presence of bundle branch block (11/70 cases) or previous myocardial infarction (14/70 cases) caused false positive readings on electrocardiography, and resulted in the lower positive predictive value. In contrast, troponin T was false in patients admitted within 4 hours after the onset, or patients with smaller infarct. The Tokyo TROP T Trial by general practitioners and office cardiologists concluded that the combination of electrocardiographic evaluation and use of troponin T is a rapid and efficient diagnostic method for the evaluation of patients with suspected acute myocardial infarction.

Adult↗
PubMed1998

A plaque hybridization assay for quantifying and cloning infectious human immunodeficiency virus type 1 virions.

A biological method was developed for quantifying and cloning of infectious virions of human immunodeficiency virus type 1 (HIV-1). Virus preparations were mixed with permissive cells for binding, and the cells were cast in an agarose gel. After incubation for 9 days viral particles released from infected cells propagating from each initially infected cell were transferred on nylon membrane and subjected to hybridization using a radioactive HIV-1 DNA probe. Infectious centers of HIV-1 were detected as hybridization spots on autoradiographs regardless of cytopathic effects or syncytium formation. Three different CD4+ cell lines (MT-4, MOLT-4 and U937) and peripheral blood mononuclear cells from healthy donors were used as recipient cells. Infectious virions were recovered from a portion of agarose gel corresponding to each hybridization spot. This assay is suitable for quantifying infectious HIV-1 virions with different cell tropisms and for investigating the relationship between the phenotype and genotype of HIV-1 at a clonal level.

Cell Line, Transformed↗
PubMed1998

[Management of difficult airway during induction of anesthesia in a patient with Hallermann-Streiff syndrome].

An 18-year-old female with Hallermann-Streiff syndrome underwent the fixation of prolapsus recti. She had significant microgenia, mental retardation and pharyngeal airway stenosis. During induction of anesthesia with halothane and nitrous oxide, severe upper airway obstruction and respiratory depression occurred. The mask ventilation with jaw lift maneuver was impossible. Lowering anesthetic level restored her spontaneous breathing and airway patency. Although the direct laryngoscopic view under light anesthesia with halothane was limited to the epiglottic tip, blind orotracheal intubation using stylet was accomplish after several attempts. At the end of anesthesia, the tracheal tube was extubated after the patient had become fully awake and had recovered completely from neuromuscular blockade monitored by electromyography.

Adolescent↗
PubMed1998

Aspirin-triggered 15-epi-lipoxin A4 (ATL) generation by human leukocytes and murine peritonitis exudates: development of a specific 15-epi-LXA4 ELISA.

Aspirin (ASA) triggers the formation of 15-epi-lipoxins (15-epi-LXs or ATL [ASA-triggered LX]), which are potent bioactive eicosanoids that may contribute to the therapeutic impact of ASA. To elucidate the role of these new compounds in vivo, it is essential to establish quick and sensitive detection methods. To this end, we prepared an enzyme-linked immunosorbent assay specific for 15-epi-LXA4 that proved to be highly sensitive (IC50 approximately 50 pg, minimum detection approximately 3.5 pg) and stereoselective. The amounts of 15-epi-LXA4 generated by human neutrophils from peripheral blood of healthy volunteers using this enzyme-linked immunosorbent assay were in agreement with those values obtained by liquid chromatography. Formation of 15-epi-LXA4 was cell ratio-dependent during THP-1 (a monocytic leukemia cell line)-neutrophil interactions with ASA-treated cells, and 15-epi-LXA4 was not detected with either cell type alone. Generation of 15-epi-LXA4 was also examined in murine peritonitis with ASA administration. Exudates from ASA-treated mice showed increased production of 15-epi-LXA4 that was diminished by indomethacin, a blocker of ASA-dependent acetylation of prostaglandin G/H synthase. A cytochrome P450 inhibitor administered in the presence of ASA did not prevent 15-epi-LXA4 formation, which suggests that P450 does not significantly contribute to formation of 15-epi-LXA4 in this murine model. These results indicate that the new enzyme-linked immunosorbent assay is both sensitive and selective for 15-epi-LXA4 and that 15-epi-LXA4 is produced by human leukocyte-leukocyte interactions. In addition, 15-epi-LXA4 is generated by inflammatory exudates when ASA is administered during murine peritonitis and when prostaglandin G/H synthase is upregulated and acetylated. This assay should provide rapid means to investigate 15-epi-LXA4 generation in both cellular and animal models.

Animals↗
PubMed1998

[Potential role of primary hypercoagulability and antiphospholipid antibody as a risk factor of acute pulmonary thromboembolism].

To examine whether primary hypercoagulable states, such as protein C and protein S deficiencies and antiphospholipid antibody, are associated with an increased risk, severity and recurrence of acute pulmonary thromboembolism, the blood levels of antithrombin III, protein C, protein S, lupus anticoagulant, anticardiolipin antibodies were measured in 23 patients with acute pulmonary thromboembolism, 7 men and 16 women (mean age +/- SD, 52 +/- 5 years), admitted to Nippon Medical School Hospital from January, 1990 through December, 1997. Four patients (17.4%) had protein C deficiency, one had protein S deficiency (4.3%), 10 had lupus anticoagulant (43.5%), and 2 had anticardiolipin antibodies (8.7%). Hemodynamic evaluation by Swan-Ganz catheter and venography of the lower extremity to detect deep venous thrombi were carried out in 20 and 21 patients, respectively. There were no differences between the patients with and without primary hypercoagulable states in age (52 +/- 14 vs 52 +/- 19 years), gender, or percentage of patients with deep venous thrombi in the lower extremity (91.7% vs 88.9%). Mean pulmonary arterial pressure (38 +/- 9 vs 26 +/- 4 mmHg, p < 0.05) and total pulmonary vascular resistance (10 +/- 5 vs 6 +/- 2 Wood unit, p < 0.1) were higher in the 13 patients with primary hypercoagulable states compared with the 10 patients without primary hypercoagulable states. Recurrence of pulmonary thromboembolism tended to be higher in the 13 patients with primary hypercoagulable states compared with the 10 patients without primary hypercoagulable states (46.2% vs 10.0%, p < 0.1). These findings suggest that primary hypercoagulable states, such as protein C and S deficiencies and antiphospholipid antibody, are associated with the severity and increased risk and recurrence of acute pulmonary thromboembolism.

Acute Disease↗
PubMed1997

Prolonged activation of phospholipase D in Chinese hamster ovary cells expressing platelet-activating-factor receptor lacking cytoplasmic C-terminal tail.

The mechanism and role of phospholipase D (PLD) activation by platelet-activating factor (PAF) were examined with Chinese hamster ovary cells stably expressing wild-type PAF receptor (WT-H cells) and truncated PAF receptor lacking the C-terminal cytoplasmic tail (D-H cells). Treatment of D-H cells with PAF resulted in the rapid formation of Ins(1,4,5)P3, which was followed by a sustained phase for more than 10 min. In these cells, PAF-induced PLD activation lasted for more than 20 min. In contrast, PLD activation in WT-H cells was transient. PAF stimulation caused the biphasic formation of 1,2-diacylglycerol (DG) in both types of cell. The first phase was rapid and transient, coinciding with the Ins(1,4,5)P3 peak. The second sustained phase of DG formation was attenuated by butanol, which produces phosphatidylbutanol at the expense of phosphatidic acid (PA) by transphosphatidylation activity of PLD, and by propranolol, a selective inhibitor for PA phosphohydrolase catalysing the conversion of PA into DG. The DG level returned nearly to basal at 20 min after PAF stimulation in WT-H cells, whereas in D-H cells the elevated DG level was sustained for more than 20 min. The profile of translocation of protein kinase Calpha (PKCalpha) to membrane was similar to that of DG formation. In WT-H cells, PKCalpha was transiently associated with membranes and then returned to the cytosol. However, in D-H cells PKCalpha was rapidly translocated to and remained in membranes for more than 20 min. Butanol suppressed this sustained translocation of PKCalpha. Furthermore the mRNA levels of c-fos and c-jun by PAF in WT-H cells were much lower than those in D-H cells. Propranolol and butanol at concentrations that inhibited the formation of DG suppressed the PAF-induced mRNA expression of c-fos and c-jun. Taken together, the prolonged PLD activation in D-H cells confirmed a primary role for phospholipase C/PKC in PLD activation by PAF. Furthermore the results obtained here suggest that sustained PLD activation in turn leads to chronic activation and membrane translocation of PKCalpha, which might play an important role in the expression of c-fos and c-jun.

1-Butanol↗
PubMed1997

Rapid detection of specific messenger RNAs in thyroid carcinomas by reverse transcription-PCR with degenerate primers: specific expression of oncofetal fibronectin messenger RNA in papillary carcinoma.

The search for mRNAs that are specifically expressed in cancer tissues is important for gene diagnosis and therapy. However, finding such mRNAs in human cancers is usually very difficult, both because of the limited volume of RNA obtainable from the tissues and the many technical difficulties of RNA analysis. To address these problems, the present study compared mRNA from thyroid cancer tissues with those from normal and benign tissues by reverse transcription-PCR using two degenerate primers. Amplified cDNAs were separated by electrophoresis with nondenaturing acrylamide gel, then three bands that are increased in cancer tissues were selected, reamplified by PCR, and cloned into T-vector. One of the bands was determined by sequencing analysis to be oncofetal fibronectin. The expression of oncofetal fibronectin mRNA in benign and malignant tissues was examined by Northern blot and reverse transcription-PCR using specific primers of its cDNA sequence, and its increased expression was observed only in papillary and anaplastic carcinomas. Thus, the present method rapidly detected specific mRNAs in cancer tissues, and one of these, oncofetal fibronectin mRNA, is a good target for gene diagnosis of papillary carcinoma.

Adenoma↗
PubMed1997

Pressure-induced apoptosis in human lymphoblasts.

The viability of human lymphoblasts was investigated after compression at 37 degrees C for 30 min. Immediately after decompression, necrotic cells were observed and the viability decreased sigmoidally to 0 with increasing pressure from 85 to 200 MPa. Apoptotic cells began to be observed from 8 h after decompression in the case of compression at 100 MPa for 30 min at 37 degrees C. The apoptosis was confirmed to be pressure-induced by the Tunel method and by optical and electron microscopy. Cell death by both necrosis and apoptosis due to compression was accelerated in the S phase of the cell cycle.

Apoptosis↗
PubMed1997

Molecular analysis of eight biochemically unique glucose-6-phosphate dehydrogenase variants found in Japan.

We analyzed the molecular mutations of eight known Japanese glucose-6-phosphate dehydrogenase (G6PD) variants with unique biochemical properties. Three of them were caused by novel missense mutations: G6PD Musashino by 185 C-->T, G6PD Asahikawa by 695 G-->A, and G6PD Kamiube by 1387 C-->T. Predicted amino acid substitutions causing asymptomatic variants G6PD Musashino (62 Pro-->Phe) and G6PD Kamiube (463 Arg-->Cys) were located in regions near the amino or carboxyl end of the polypeptide chain, whereas an amino acid change 232 Cys-->Tyr causing a class 1 variant G6PD Asahikawa was located in the region where amino acid alterations in some class 1 variants were clustered. The other five variants had known missense mutations, namely, G6PD Fukushima, 1246 G-->A, G6PD Morioka, 1339 G-->A, and G6PD Iwate, G6PD Niigata and G6PD Yamaguchi, 1160 G-->A, which cause variants, G6PD Tokyo, G6PD Santiago de Cuba, and G6PD Beverly Hills, respectively.

Anemia, Hemolytic, Congenital Nonspherocytic↗
PubMed1997

Aspirin-triggered 15-epi-lipoxin A4 (LXA4) and LXA4 stable analogues are potent inhibitors of acute inflammation: evidence for anti-inflammatory receptors.

Lipoxins are bioactive eicosanoids that are immunomodulators. In human myeloid cells, lipoxin (LX) A4 actions are mediated by interaction with a G protein-coupled receptor. To explore functions of LXA4 and aspirin-triggered 5(S),6(R),15(R)-trihydroxy-7,9,13-trans-11-cis-eicosatetraenoic acid (15-epi-LXA4) in vivo, we cloned and characterized a mouse LXA4 receptor (LXA4R). When expressed in Chinese hamster ovary cells, the mouse LXA4R showed specific binding to [3H]LXA4 (K(d) approximately 1.5 nM), and with LXA4 activated GTP hydrolysis. Mouse LXA4R mRNA was most abundant in neutrophils. In addition to LXA4 and 15-epi-LXA4, bioactive LX stable analogues competed with both [3H]LXA4 and [3H]leukotriene D4 (LTD4)-specific binding in vitro to neutrophils and endothelial cells, respectively. Topical application of LXA4 analogues and novel aspirin-triggered 15-epi-LXA4 stable analogues to mouse ears markedly inhibited neutrophil infiltration in vivo as assessed by both light microscopy and reduced myeloperoxidase activity in skin biopsies. The 15(R)-16-phenoxy-17,18, 19,20-tetranor-LXA4 methyl ester (15-epi-16-phenoxy-LXA4), an analogue of aspirin triggered 15-epi-LXA4, and 15(S)-16-phenoxy-17,18,19,20-tetranor-LXA4 methyl ester (16-phenoxy-LXA4) were each as potent as equimolar applications of the anti-inflammatory, dexamethasone. Thus, we identified murine LXA4R, which is highly expressed on murine neutrophils, and showed that both LXA4 and 15-epi-LXA4 stable analogues inhibit neutrophil infiltration in the mouse ear model of inflammation. These findings provide direct in vivo evidence for an anti-inflammatory action for both aspirin-triggered LXA4 and LXA4 stable analogues and their site of action in vivo.

Amino Acid Sequence↗