Exact solution and spectral flow for twisted Haldane-Shastry model.
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Journal Article↗
Biomedical subjects
T Fukui
Publications and source records attributed to T Fukui.
Prevalence of biotin-binding immunoglobulin in patients with allergic and autoimmune diseases.
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Adolescent↗
Structure of the multifunctional loops in the nonclassical ATP-binding fold of glutathione synthetase.
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Adenosine Triphosphate↗
Specialty choice and understanding of primary care among Japanese medical students.
To assess specialty choice and understanding of primary care among Japanese medical students, all students from seven Japanese medical schools (three public and four private) were surveyed, using a written questionnaire. A total of 3377 students provided data for the study. Of the students surveyed, 89.8% wanted to become clinicians, and 79.3% wanted to have general clinical ability. About half of the respondents, 54.9%, replied that they had some, or great, interest in primary care, but it was found that their understanding of primary care was inadequate. Almost half (56.3%) of the students answered that they had some idea of what a general practitioner did. This proportion was nearly the same through all years of medical school. While 1245 (36.9%) students (most of them in the fifth or sixth year) replied that they had received some clinical training while working in hospitals, only 203 (6.0%) students had worked in private clinics (the sites where most primary care is still provided), and 129 (3.8%) students had experience in providing home visits and home care. An even greater number, 64.3%, replied that they had inadequate information about the career options available to them. The study found that although many Japanese medical students want to obtain broad clinical competence, their understanding of primary care is insufficient. In order to increase the number of primary care providers the system of medical education in Japan must provide primary care doctors to act as role models, and must make available information about postgraduate primary care programmes. These programmes need to be increased, as do rewarding positions for programme graduates.
Career Choice↗
Primary progressive apraxia in Pick's disease: a clinicopathologic study.
A 62-year-old right-handed man gradually experienced increasing difficulty with speech and manual dexterity. He had apraxia of speech, buccofacial apraxia, and complex limb apraxia as well as terminal dementia. At autopsy, focal cortical atrophy, neuronal loss, and neuropil rarefaction in the second and third cortical layers were most prominent in the left opercular, lower precentral, superior parietal, and left temporal pole. Numerous Pick bodies were diffusely present in the temporal and posterior frontal lobes and, to a lesser degree, in the superior parietal lobule. This report demonstrates an association between the distribution of Pick's pathology and several apraxic impairments.
Apraxias↗
Allelotype analysis in mouse hepatocellular carcinomas; frequent homozygous deletion of mouse homolog of p16/CDKN2 gene on chromosome 4 in culture.
Because allelotype analysis of many tumors has been important in the identification of new tumor suppressor genes, here we have analyzed hepatocellular carcinomas (HCCs) derived from F1 hybrid mice between C3H and MSM in detail. The analysis showed no allelic loss in primary HCCs, while the loss was detected in tumor cell lines established from HCCs. Recently, a candidate tumor suppressor gene termed p16/CDKN2, which was located near the interferon gene cluster on human chromosome 9p21, was identified by virtue of its frequent homozygous deletion in cell lines derived from many different tumor types. Since frequent allelic imbalances in the D4MIT9 locus and loss of heterozygosity in the alpha-interferon gene which was located near the mouse homolog of p16/CDKN2 (mouse p16) gene were detected in tumor cell lines, we investigated homozygous deletion of the mouse p16 gene by the comparative multiplex PCR method. The analysis revealed frequent homozygous deletion of the gene in thirteen of the tumor cell lines (13/25, 52%), but not in primary HCCs (0/25, 0%). These data indicate that gene deletions including the mouse p16 gene on chromosome 4 in tumor cell lines occur during the culture and that allelic imbalances are uncommon in mouse primary HCCs. Our results suggest that mouse p16 plays an important role in mouse hepatocarcinogenesis in vivo in progression or immortalization in vitro.
Alleles↗
Estimation of the prevalence of non-insulin dependent diabetes mellitus in a rural area of Japan.
The objective of this paper is to describe a method of estimating the prevalence of non-insulin dependent diabetes mellitus (NIDDM) in a community. We first counted subjects with previously diagnosed NIDDM and those newly diagnosed by use of the 75-gram oral glucose tolerance test (OGTT). We then used the OGTT data to predict the prevalence of NIDDM at different levels of fasting plasma glucose (FPG) among the subjects who did not undergo the OGTT. Data were derived from 3,614 residents aged 20 years and older in a rural area where population-based screening for NIDDM was performed using FPG or post-prandial plasma glucose (PG). Of the 318 participants who underwent an OGTT in 1992, 35 (11.0%) were judged to have NIDDM by the 2-hour PG criterion. We applied the above-described method to the 1,179 subjects who had anFPG but failed to undergo the OGTT. The estimated prevalence of NIDDM, which included the previously diagnosed group, the newly diagnosed group and the expected group, was calculated. The estimated prevalence of diabetes in this population aged 20 years and older turned out to be 6.1% (95% CI: 5.3-6.9). As a validation study, the same method was applied to 220 subjects who did not undergo the OGTT in 1992 but did so in 1994. The actual prevalence of NIDDM among these subjects was compared to the prevalence expected from the 1992 data by our method. The actual value was within the 95% confidence interval of the expected value.
Adult↗
Partner notification program and possibility of including it in the HIV prevention strategies in Japan.
This article discusses the possibility of implementing partner notification program as a part of HIV prevention strategy in Japan. Relevant factors, like HIV seroprevalence, general population attitudes toward HIV, legislation, resources, barriers, behavioral changes, cost and effectiveness are analyzed in Japanese perspectives. Effectiveness of this program is also predicted based on the two informal contact tracing program in Japan. At the same time a review was made on the global perspectives of partner notification program and operational procedures are also outlined. Published literatures were investigated regarding prevalence of new HIV infection among the partners who underwent testing (11-39%), cost per new HIV positive case found (US $810-3,205), and secondary infection rate (11-20%) in Japan. Having considered all relevant factors we recommend that the partner notification program be implemented, initially in a limited area, then all over Japan. Further analysis on cost-benefit of this program remains to be done.
Adult↗
Studies on fatigue of night duty workers at a newspaper office.
Fatigue of night duty workers in different divisions of a newspaper office was investigated by physiological methods such as the Blinker, Flicker and grip methods. The relationship between fatigue and hematological parameters such as hemoglobin (Hb), the hematocrit (Ht), serum-free amino acid levels, and indices of liver function such as the GOT and GPT levels were also examined. The composing and press room workers mainly complained of the subjective symptom of muscle fatigue, while workers in the photo-engraving and editorial departments mainly complained of mental fatigue. The overall rate of fatigue in the newspaper office was about 38.1%, but varied from one division to another, being especially high in the photo-engraving and editorial departments. The subjects with fatigue had low levels of serum GOT and GPT and high levels of serum-gluconeogenic amino acids, such as aspartic acid, glutamic acid, prolin, glycine, and alanine. These altered levels of serum-free amino acids and GOT and GPT seemed to be due to increased secretion of adrenal corticoid hormone caused by the stress of fatigue.
Adult↗
Prolonged exposure to agonist results in a reduction in the levels of the Gq/G11 alpha subunits in cultured vascular smooth muscle cells.
Recent studies have shown that G proteins are a potential regulatory site in the transmembrane signaling cascade. The aim of this study was to examine the effects of prolonged agonist exposure on expression of the Gq class of G protein alpha subunits (G alpha q/G alpha 11) in cultured rat vascular smooth muscle cells (VSMC). Treatment with 100 nM angiotensin II (Ang II) led to a substantial sustained down-regulation of cellular levels of immunologically detectable G alpha q/G alpha 11 by 50% within 6 hr. The effect of Ang II was dose dependent with an EC50 of 2 nM and was specifically blocked by the vascular type-1 Ang II receptor-specific antagonist losartan. The Ang II-induced reduction in cellular levels of G protein alpha subunits was specific for G alpha q/G alpha 11. The calcium ionophore ionomycin or activators of ubiquitous protein kinases (phorbol-12-myristate-13-acetate, forskolin, and 8-bromo-cGMP) did not mimic the effects of Ang II. However, [Arg8]vasopressin also induced a significant loss in cellular G alpha q/G alpha 11 levels. Ang II-induced G alpha q/G alpha 11 down-regulation was reversed by prevention of cellular receptor processing with phenylarsine oxide or chronic potassium depletion. The effects of Ang II on G alpha q/G alpha 11 levels were inhibited when protein kinase C activity was abolished. G alpha q mRNA levels were down-regulated by 30% after 4-hr incubation with Ang II, in part by transcriptional regulation. Although a short term vasopressin pretreatment had no effect on inositol-1,4,5-trisphosphate (IP3) generation in response to subsequent Ang II stimulation, a partial heterologous desensitization of the IP3 response was induced after a long term vasopressin pretreatment, which concurrently down-regulated cellular G alpha q/G alpha 11 levels. Homologous desensitization of IP3 generation on a second Ang II stimulation was observed after both a short and long term Ang II pretreatment. In conclusion, prolonged exposure to Ang II induces down-regulation of cellular G alpha q/G alpha 11 levels in intact VSMC. The effect of Ang II appears to be mediated by the signaling pathway sensitive to inhibition of receptor processing. The present study raises the possibility that agonist-induced G alpha q/G alpha 11 down-regulation participates in the mechanism of long term desensitization of the G alpha q/G alpha 11-mediated signaling system in VSMC.
Angiotensin II↗
[Successful surgical treatment for fungal endocarditis involving the aortic valve: report of a case].
A 50-year-old man who had undergone successful aortic valve replacement for fungal endocarditis was presented. He had been doing well until October 1993, when he suddenly developed shock with high fever. In two weeks he recovered from septic shock with vigorous medical treatment including intravenous administration of antibiotics. The infecting organism was not detected on repeated blood cultures. Four months later he was admitted to our hospital because of left heart failure. Although he was afebrile on admission, a two dimensional echocardiogram revealed vegetation on the aortic valve and massive aortic regurgitation. Inflammatory signs persisted and the vegetation increased in size, and therefore an aortic valve replacement was performed. A surgical specimen of the aortic valve revealed perforation in each of three cusps and vegetation on the non-coronary cusp. Pathological exploration revealed typical colonies of fungi. Following the diagnosis of fungal endocarditis, administration of an anti-fungal drug was started. His post-operative course was uneventful, and there was no evidence of recurrence with the anti-fungal medication for one year postoperatively.
Antifungal Agents↗
Serial change of mitral regurgitation after mitral valve repair: comparison of anterior with posterior leaflet lesions.
Mitral valve repair is an important operative procedure for correcting mitral regurgitation (MR). However, serial change of residual MR after operation has not been reported. Serial change of MR after mitral valve repair was evaluated by transesophageal color Doppler echocardiography (TEE). Twenty-six patients undergoing mitral valve repair for MR during 1987 to 1991 were examined by TEE just after operation, 6 months after operation, and late follow-up period (mean 3.7 years). Thirteen patients had a lesion of the anterior mitral leaflet before operation (group A). Thirteen patients had a lesion of the posterior mitral leaflet before operation (group P). The MR area was measured by TEE at each stage after operation. In group A, the MR area at late follow-up increased significantly compared with just after operation (1.1 vs 4.3 cm2, p < 0.001). In group P, the MR area at late follow-up did not increase significantly compared with just after operation (0.6 vs 1.3 cm2, p = NS). In conclusion, MR does not increase after mitral valve repair in patients with posterior mitral valve repair, but MR may increase at late follow-up after operation for anterior mitral valve prolapse.
Echocardiography↗
Processing and activation of recombinant mouse mastocytoma histidine decarboxylase in the particulate fraction of Sf9 cells by porcine pancreatic elastase.
Mature 53 kDa histidine decarboxylase (HDC) peptide is produced from a precursor 74 kDa peptide. The mechanism of specific cleavage by processing enzyme is unknown. Using the recombinant mouse 74 kDa HDC, we found that porcine pancreatic elastase specifically converted the inactive 74 kDa HDC to its active form of 53 kDa HDC.
Animals↗
Prostaglandin E2 at priming of naive CD4+ T cells inhibits acquisition of ability to produce IFN-gamma and IL-2, but not IL-4 and IL-5.
We investigated the effect of prostaglandin E2 on the acquisition of cytokine-producing ability by naive CD4+ T cells in human cord blood. Naive CD4+ T cells were stimulated for 3 days with mouse monoclonal anti-CD3 Ab, then washed and expanded in IL-2-containing medium for 3 more days. These activated T cells produced IL-2, IL-4, IL-5, and IFN-gamma upon stimulation with PMA and ionomycin. PGE2 added at priming of naive T cells inhibited the production of IL-2 and IFN-gamma, but not of IL-4 and IL-5, in a dose-dependent manner. This change in the cytokine production profile induced by PGE2 was maintained in T cells restimulated with anti-CD3 in the absence of PGE2, expanded by IL-2, and stimulated with PMA and ionomycin. The mRNA expression of IFN-gamma and IL-2, but not that of IL-4, was also decreased in these cells. Forskolin and dibutyryl cAMP had a similar effect. PGE2 must exist at an early stage of T cell activation to inhibit priming for IL-2 and IFN-gamma production. PGE2 also showed this effect, even in the presence of exogenous IFN-gamma, at the primary stimulation. These results indicate that PGE2 inhibits the acquisition of the ability to produce IL-2 and IFN-gamma by acting directly on naive T cells. Our results suggest that PGE2 plays a role in facilitating the development of the Th2-type cytokine production profile.
Animals↗
Cytochrome b-558 alpha-subunit cloning and expression in rat aortic smooth muscle cells.
Recent studies have shown that the NADPH oxidase participates in the generation of superoxide anion in non-phagocytic cells. Here we report the isolation and nucleotide sequence of a cDNA for the cytochrome b-558 alpha-subunit of the NADPH oxidase in rat vascular smooth muscle cells (VSMCs). The coding region of the cDNA was 93% homologous to mouse and 81% to human in nucleotide sequence and 96% homologous to mouse and 89% to human in the deduced amino acid sequence. Our results provide a tool with which to explore the mechanism of superoxide anion generation in rat VSMCs and other non-phagocytic cells.
Amino Acid Sequence↗
Spectroscopic studies on the mechanism of the topa quinone generation in bacterial monoamine oxidase.
Electron paramagnetic resonance (EPR), circular dichroism (CD), and optical absorption spectroscopies have been used to investigate the copper-dependent autoxidation process generating the 6-hydroxydopa (topa) quinone cofactor in the recombinant phenethylamine oxidase from Arthrobacter globiformis. The cupric ion bound to the copper/topa quinone-less, inactive enzyme is first reduced to Cu(I), as inferred from the spectroscopic features observed under strictly anaerobic conditions. Cu(I) is also detectable chemically with a Cu(I)-specific chelating agent, bathocuproinedisulfonate. Introduction of a limited amount of oxygen then leads to the formation of a paramagnetic species (g = 2.004) that is stable for over several to 10 min but vanishes swiftly upon addition of sufficient oxygen. Strikingly, the hyperfine EPR structure of the organic radical is almost identical with that of the topa semiquinolamine observed in the copper/topa quinone-containing, active enzyme anaerobically reduced with substrate. Concomitant with the generation of topa quinone exhibiting characteristic optical absorption and CD bands under fully aerobic conditions, the bound copper finally shows EPR signals typical of nonblue type II Cu(II) and optical absorption around 700 nm with negative CD above 700 nm. None of these spectral changes are evoked in the binding of Cu(II) to the Tyr382-->Phe mutant enzyme, indicating that the precursor Tyr382 to topa quinone participates in the initial reduction of bound copper and serves as the origin of the transiently formed semiquinone radical. The prosthetic cupric ion plays an essential role, by changing its redox state, in the oxidative modification of the tyrosyl phenol ring, leading to topa quinone.
Arthrobacter↗
A third type of nucleoside diphosphate kinase from spinach leaves: purification, characterization and amino-acid sequence.
A third type of nucleoside diphosphate kinase (NDP kinase III), distinct from the previously described NDP kinases I and II (Nomura et al. (1991) Biochim. Biophys. Acta 1077, 47-55), was purified from spinach leaves to electrophoretic homogeneity. NDP kinase III was judged by SDS-PAGE and by gel filtration to have molecular masses of 17 kDa and 102 kDa, respectively, suggesting that it is composed of six subunits similarly to the other spinach isoforms, NDP kinases I and II. Amino-acid sequence analysis revealed the primary structure of NDP kinase III to be comprised of 153 amino-acid residues, the sequence of which exhibited 61% and 53% homology with those of NDP kinases I and II, respectively. In the reaction catalyzed by the three isoforms, the order of Km as phosphate acceptor was determined as GDP << ADP for NDP kinase III, different from those observed for NDP kinase I (ADP << GDP) and for NDP kinase II (GDP = ADP). These results suggest that the three isoforms may have distinct roles in regulating intracellular 5'-di- and 5'-triphosphonucleotide levels in spinach leaves.
Amino Acid Sequence↗
Copper/topa quinone-containing histamine oxidase from Arthrobacter globiformis. Molecular cloning and sequencing, overproduction of precursor enzyme, and generation of topa quinone cofactor.
The gene coding for histamine oxidase has been cloned and sequenced from a Coryneform bacterium Arthrobacter globiformis. The deduced amino acid sequence consists of 684 residues with a calculated molecular mass of 75,109 daltons and shows a high overall identity (58%) with that of phenethylamine oxidase derived from the same bacterial strain. Although the sequence similarities are rather low when compared with copper amine oxidases from other organisms, the consensus Asn-Tyr-Asp/Glu sequence, in which the middle Tyr is the precursor to the quinone cofactor (the quinone of 2,4,5-trihydroxyphenylalanine, topa) covalently bound to this class of enzymes, is also conserved in the histamine oxidase sequence. To identify the quinone cofactor, an overexpression plasmid has been constructed for the recombinant histamine oxidase. The inactive enzyme purified from the transformed Escherichia coli cells grown in a copper-depleted medium gained maximal activity upon stoichiometric binding of cupric ions. Concomitantly with the enzyme activation by copper, a brownish pink compound was generated in the enzyme, which was identified as the quinone of topa by absorption and resonance Raman spectroscopies of the p-nitrophenylhydrazine-derivatized enzyme and found at the position corresponding to the precursor Tyr (Tyr-402). Therefore, the copper-dependent autoxidation of a specific tyrosyl residue operates on the formation of the topa quinone cofactor in this enzyme, as recently demonstrated with the precursor form of phenethylamine oxidase (Matsuzaki, R., Fukui, T., Sato, H., Ozaki, Y., and Tanizawa, K. (1994) FEBS Lett. 351, 360-364).
Amine Oxidase (Copper-Containing)↗