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Biomedical subjects

M Kawabata

Publications and source records attributed to M Kawabata.

At least 109 records · Page 6Linked to original sources
PubMed1999

Characterization of kintoki bean (Phaseolus vulgaris) alpha-amylase inhibitor: inhibitory activities against human salivary and porcine pancreatic alpha-amylases and activity changes by proteolytic digestion.

The effects of some experimental parameters on alpha-amylase inhibition by an alpha-amylase inhibitor from kintoki bean were examined. The rate of inhibition against pancreatic alpha-amylase increased with a rise in temperature to 50 degrees C, but the inhibition of salivary alpha-amylase reached a maximum above 35 degrees C. Although an increase in NaCl concentration to 1.5 M caused an increase in the inhibitory activities against both amylases, these inhibitory activities tended to decrease above 1.5 M NaCl. The effects of proteolytic digestion on the amylase inhibitory activity were also studied. The inhibitor was slightly inactivated by pepsin digestion for 2 h. Although the inhibitor rapidly lost the inhibitory activity by chymotrypsin digestion within 2 h, it was quite resistant to proteolytic digestion by trypsin.

Animals↗
PubMed1999

[Lyme disease].

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Animals↗
PubMed1999

[Clinical investigation of 15 patients with pulmonary cryptococcosis--clinical comparison of HTLV-I carriers and non-carriers].

We investigated 15 pulmonary cryptococcosis patients. The group had a mean age of 51.7 years, and 6 (40%) of the patients were women. Cryptococcosis was primary in 13 patients and secondary in 2 (diabetes mellitus and smoldering adult T-cell leukemia). Eight patients were asymptomatic and 9 patients were detected by medical examinations. Dry cough was the most common symptoms. On chest radiographs, 5 patients showed solitary nodules, 4 patients showed infiltrative shadows, and 4 patients showed multiple nodules. The right lower lobe was the predominant location of solitary nodules, and the left upper and middle lung fields were the predominant locations of infiltrative shadows. Transbronchial lung biopsy was the method of diagnosis for 9 patients, and open lung biopsy for the others. Eleven patients were treated with fluconazole, and the mean treatment period was 7 months. Four patients underwent, resection procedures only, and experienced no recurrence. Five patients were positive for HTLV-I (one had smoldering ATL) and 5 were negative. Eighty percent of the HTLV-I positive patients had some symptoms and 80% of the HTLV-I negative patients were asymptomatic. HTLV-I positive patients showed various pulmonary shadows and 80% of the HTLV-I negative patients showed solitary nodules. The pulmonary lesions in HTLV-I positive patients were more extensive than those in HTLV-I negative patients (p < 0.05). We postulate the possible existence of subtle immunological abnormalities, including abnormalities of cellular immunity, in HTLV-I carriers.

Aged↗
PubMed1999

[Vulvitis].

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Diagnosis, Differential↗
PubMed1999

[Exogenous lipoid pneumonia induced by inhalation of insecticide].

We report a case of exogenous lipoid pneumonia induced by insecticide. A 67-year-old man was admitted to our hospital with complaints of dyspnea cough, hemoptysis, and shivering 6 hours after inhaling an insecticide. A chest radiograph on admission disclosed consolidation in the right upper lobe. Chest computed tomography showed nodular infiltrates associated with ground-glass opacities. Bronchoalveolar lavage fluid was hemorrhagic and showed neutrophilia. Pathological examination of transbronchial lung biopsy specimens showed numerous vacuolated macrophages in alveolar spaces. Electron microscopy demonstrated lipid droplets in the cytoplasm of these macrophages. These findings together yielded a diagnosis of exogenous lipoid pneumonia induced by insecticide. In addition, we experimentally induced a similar form of lipoid pneumonia in rats by intratracheal instillation of the same insecticide.

Aged↗
PubMed1999

[Multiple pulmonary nodules due to ticlopidine-induced pneumonitis].

A 54-year-old man had been treated with Ticlopidine for antithrombotic therapy after a myocardial infarction. Six months after the start of Ticlopidine, pruritic skin rash developed. After 8 months, chest X-ray films revealed multiple nodules, and the patient was admitted to our hospital. Laboratory data indicated liver dysfunction and sputum eosinophilia. Transbronchial biopsy specimens disclosed intraluminal organization and alveolar septal thickening with lymphocyte infiltration. After cessation of Ticlopidine, the cutaneous lesions quickly improved, and multiple nodules completely resolved within 4 months. These findings resulted in a diagnosis of Ticlopidine-induced pneumonitis. The radiographic pattern of multiple pulmonary nodules was very rare. Sputum eosinophilia may be helpful in the diagnosis of drug-induced pneumonitis. To our knowledge, there have been no previous reports of Ticlopidine-induced pneumonitis in Japan.

Humans↗
PubMed1999

The p16-cyclin D1/CDK4-pRb pathway and clinical outcome in epithelial ovarian cancer.

A significant positive association has been reported between p16 expression and clinical outcome for epithelial ovarian cancer patients. However, there is a reciprocal correlation between genetic alterations of single members of the p16-cyclin D1/CDK4-pRb pathway (G1 pathway). Simultaneous evaluation of these four elements may produce a better prognostic factor than p16 alone. We studied the prognostic significance of the G1 pathway in 59 epithelial ovarian cancer patients undergoing surgery and platinum-based chemotherapy by immunohistochemical technique. Abnormal expression of p16 or pRb was defined by negative nuclei staining, and that of CDK4 and cyclin D1 was defined by 50% nuclear staining. An abnormal G1 pathway was indicated in cases that have at least one abnormality among these four elements. Abnormal expression of p16, pRb, and cyclin D1/CDK4 was observed in 33.9, 3.4, and 15.3% of studied cases, respectively. Abnormal G1 pathway was detected in 49.2% (29 of 59) of all cases. The patients with normal G1 pathway tended to achieve a higher complete response rate (81.0%) to chemotherapy, compared with patients with abnormal G1 pathway (55.0%); however, there was no significant difference (P = 0.1001) between the two groups. Univariate analyses identified advanced stage [hazards ratio (HR), 3.665; P = 0.0218], histological low grade (HR, 3.625; P = 0.0066), and abnormal G1 pathway (HR, 2.935; P = 0.03) as prognostic factors for overall survival. The G1 pathway might help as a prognostic factor to select high-risk patients.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1999

Chemotherapeutic malaria control as a selective primary health care activity in the Solomon Islands.

Malaria control by chemotherapy has been established in rural villages of Guadalcanal, the Solomon Islands, following field trials. As a selective primary health care activity, mobile unit teams visited villages once or twice a year to detect malaria positives and gave chloroquine and primaquine to treat the infection and interrupt the transmission. On site diagnosis was by the use of acridine orange fluorescent staining or the ICTPf commercial diagnostic kit. To avoid possible haemolytic crises, a new single step screening method of G6PD deficiency was introduced. This approach has been accepted well by villagers and proved to be an efficient and feasible control method even in remote rural villages with endemic malaria transmission. Epidemiological modelling of the situation predicts reduction of prevalence in five years.

Adult↗
PubMed1998

Polar amino acid-rich sequences bind to polyglutamine tracts.

Polyglutamine tracts are found in different proteins including transcription factors and cofactors as well as in triplet repeat disease gene products. To characterize the protein motif that binds to the polyglutamine tract, we screened a human embryonic brain cDNA library with the polyglutamine tract of Brn-2 as bait using the yeast two-hybrid method. All six isolated clones encoding polyglutamine tract binding proteins were rich in polar amino acids. Three of these clones could form polar helical structures. These observations suggest that polar amino acid-rich sequences are essential for binding to the polyglutamine tract.

Amino Acid Sequence↗
PubMed1998

Premature bifurcation of the apical dendritic trunk of vibrissa-responding pyramidal neurones of X-irradiated rat neocortex.

1. Electrophysiological and morphological experiments were performed on the pyramidal neurones of the somatosensory neocortex of the adult rat that had been exposed in utero to 200 rad of X-irradiation. Under urethane anaesthesia, evoked gross potentials, extracellular and intracellular neuronal responses, and laminar field potentials were recorded. The evoked epicortical potential to deflection of a single whisker was a long-lasting positive wave which contrasted with a biphasic positive-negative complex in unirradiated controls. Neurones were initially tested during extracellular recording for responses to whisker deflections. This was followed by intracellular injection with horseradish peroxidase (HRP), and the HRP-stained neuronal elements were visualized using diaminobenzidine as a chromagen. 2. Fifty neurones were recorded and stained through the soma. The mean response latency was 15.1 ms. Of these, thirty-six showed premature bifurcation of the apical dendrite. The angle of bifurcation of the apical dendrite was measured in the coronal plane and was found to be a function of the depth at which the soma was located and the distance between the soma and bifurcation point. It was suggested that the apical dendrites of these neurones underwent premature bifurcation due to an imbalance between the growth of neurones and skull. 3. Fifteen neurones were recorded and stained through the presumed apical dendritic shaft. The mean response latency was 19.5 ms. The electrode track left in the histological specimen pointed to the stained apical dendrite. Dendritic elements distal to the entry point were preferentially filled with HRP. In no cases were somata stained. There was, in turn, no evidence of recording from dendritic elements distal to the bifurcation since no electrode track was found to point to these elements. That dendritic spike responses may not travel beyond the bifurcation was further substantiated by laminar analysis of field potentials.

Algorithms↗
PubMed1998

Effects of lysophosphatidic acid on proliferation of stellate cells and hepatocytes in culture.

Lysophosphatidic acid (LPA) is a growth factor-like mediator for fibroblasts or smooth muscle cells produced and released by activated platelets. Platelet activation occurs with hepatic necrosis and subsequent liver regeneration and fibrosis. In the fibrosis, hepatic stellate cells proliferate with phenotypic transformation to myofibroblasts. Thus, effects of LPA on proliferation of hepatocytes and stellate cells were investigated. In cultured rat stellate cells, LPA increased DNA synthesis with enhanced MAP kinase activity. Pertussis toxin (PTX) attenuated this mitogenic action. In contrast, LPA decreased DNA synthesis by cultured rat hepatocytes induced by hepatocyte growth factor (HGF) or epidermal growth factor (EGF) without affecting protein synthesis. Enhanced MAP kinase activity by HGF or EGF was not changed by LPA. This anti-mitogenic action was attenuated by PTX. TGFbeta level in the medium was less than the level effective for inhibiting the DNA synthesis in the presence of LPA. Our results suggest that LPA might affect proliferation of hepatocytes and stellate cells in liver diseases complicating platelet activation.

Animals↗
PubMed1998

Smad proteins exist as monomers in vivo and undergo homo- and hetero-oligomerization upon activation by serine/threonine kinase receptors.

Smad proteins are signal transducers for the members of the transforming growth factor-beta (TGF-beta) superfamily. Here we show that, in the absence TGF-beta stimulation, Smads exist as monomers in vivo. Smad2 and Smad3 form homo-oligomers upon phosphorylation by the constitutively active TGF-beta type I receptor, and this oligomerization does not require Smad4. Major portions of Smad4, Smad6 and Smad7 are also present as monomers in vivo. Analysis using a cross-linking reagent suggested that the Smad2 oligomer induced by receptor activation is a trimer. Studies by gel chromatography demonstrated that the Smad2-Smad4 heteromer is not larger than the Smad2 homomer. Moreover, overexpression of Smad4 prevented Smad2 from forming a homo-oligomer. These findings suggest that Smad2 may form a homotrimer, or heterotrimers with Smad4, which are probably composed of two and one, or one and two molecules of Smad2 and Smad4, respectively, depending on the amount of each protein. Gel-mobility shift assay revealed that the Smad3 homomer and Smad3-Smad4 heteromer constitute DNA-binding complexes. Transition of the Smad proteins from monomers to oligomers is thus a critical event in the signal transduction of the TGF-beta superfamily members.

Activin Receptors, Type I↗
PubMed1998

Sequence analysis and expression of a novel mouse homolog of Escherichia coli recA gene.

Escherichia coli recA and its yeast homologs RAD51 and DMC1 play crucial roles in mitotic and/or meiotic recombination and in repair of double-strand DNA breaks. We have identified a murine novel recA-like gene (MmTRAD). The predicted 329 amino acid protein showed significant homology to mouse Rec2, Rad51, Dmc1 (or Lim15) and E. coli RecA. Northern blot analysis revealed that MmTRAD was ubiquitously transcribed in various tissues.

Amino Acid Sequence↗
PubMed1998

A single missense mutant of Smad3 inhibits activation of both Smad2 and Smad3, and has a dominant negative effect on TGF-beta signals.

A missense mutation of Smad2 identified in cancer cells was reconstructed on the corresponding residue of Smad3. This mutant, Smad3D407E, was not phosphorylated by the constitutively active form of type I receptor for transforming growth factor-beta (TGF-beta), and inhibited the phosphorylation of co-expressed wild-type Smad2 and Smad3. This mutant also had a dominant negative effect on the growth inhibition of HaCaT cells and on the expression of p3TP-lux reporter gene induced by TGF-beta. However, it did not alter the phosphorylation of Smad1 induced by the constitutively active form of the bone morphogenetic protein type IA receptor. These findings showed that a single missense mutation in Smad3 could specifically block TGF-beta signals by preventing activation of both Smad2 and Smad3.

Amino Acid Sequence↗
PubMed1998

Direct fractionation of proteins in particle-containing feedstocks by a filter paper pieces-based DEAE-cellulose column chromatography. Rapid, robust and low-cost capturing procedure for protein.

Filter paper pieces-based (FPB) DEAE-celluloses was prepared for direct fractionation of proteins in particle-containing feedstocks. FPB DEAE-cellulose has a protein binding capacity equivalent to that of commercially available DEAE-cellulose. Crude extracts from porcine intestine and kiwi fruit pulp, which were unmanageable by commercially available chromatographic media due to rapid clothing, could be directly fractionated with FPB DEAE-cellulose column. In addition, effluents from an FPB DEAE-cellulose column were extensively clarified. The present approach can be used as a rapid, robust and low-cost capturing step for protein from particle-containing feedstocks.

Animals↗
PubMed1998

Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1.

Apoptosis signal-regulating kinase (ASK) 1 was recently identified as a mitogen-activated protein (MAP) kinase kinase kinase which activates the c-Jun N-terminal kinase (JNK) and p38 MAP kinase pathways and is required for tumor necrosis factor (TNF)-alpha-induced apoptosis; however, the mechanism regulating ASK1 activity is unknown. Through genetic screening for ASK1-binding proteins, thioredoxin (Trx), a reduction/oxidation (redox)-regulatory protein thought to have anti-apoptotic effects, was identified as an interacting partner of ASK1. Trx associated with the N-terminal portion of ASK1 in vitro and in vivo. Expression of Trx inhibited ASK1 kinase activity and the subsequent ASK1-dependent apoptosis. Treatment of cells with N-acetyl-L-cysteine also inhibited serum withdrawal-, TNF-alpha- and hydrogen peroxide-induced activation of ASK1 as well as apoptosis. The interaction between Trx and ASK1 was found to be highly dependent on the redox status of Trx. Moreover, inhibition of Trx resulted in activation of endogenous ASK1 activity, suggesting that Trx is a physiological inhibitor of ASK1. The evidence that Trx is a negative regulator of ASK1 suggests possible mechanisms for redox regulation of the apoptosis signal transduction pathway as well as the effects of antioxidants against cytokine- and stress-induced apoptosis.

Animals↗
PubMed1998

Interaction of Drosophila inhibitors of apoptosis with thick veins, a type I serine/threonine kinase receptor for decapentaplegic.

Decapentaplegic (Dpp) is a Drosophila member of bone morphogenetic proteins, which belong to the transforming growth factor-beta superfamily. Members of this family regulate a variety of biological processes such as cell proliferation, morphogenesis, immune response, and apoptosis. Dpp plays a critical role in many aspects of Drosophila development. Members of the transforming growth factor-beta superfamily bind to two different types of serine/threonine kinase receptors, termed type I and type II. Type I receptors act as downstream components of type II receptors in the receptor complexes. Therefore, intracellular proteins that interact with the type I receptors are likely to play important roles in signaling. Several proteins have been identified through protein-protein interaction screenings. We identified Drosophila inhibitor of apoptosis (DIAP) 1 as an interacting protein of a Dpp type I receptor, Thick veins (Tkv). DIAP1 associates with Tkv in vivo. The binding region in DIAP1 is mapped to its C-terminal RING finger region. DIAP2, another Drosophila member of the inhibitor of apoptosis protein family, also interacts with Tkv in vivo. These data suggest that DIAP1 and DIAP2 may be involved, possibly as negative regulators, in the Dpp signaling pathway, which leads to cell apoptosis.

Animals↗