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Biomedical subjects

T Takagi

Publications and source records attributed to T Takagi.

At least 253 records · Page 14Linked to original sources
PubMed1998

Toward information extraction: identifying protein names from biological papers.

To solve the mystery of the life phenomenon, we must clarify when genes are expressed and how their products interact with each other. But since the amount of continuously updated knowledge on these interactions is massive and is only available in the form of published articles, an intelligent information extraction (IE) system is needed. To extract these information directly from articles, the system must firstly identify the material names. However, medical and biological documents often include proper nouns newly made by the authors, and conventional methods based on domain specific dictionaries cannot detect such unknown words or coinages. In this study, we propose a new method of extracting material names, PROPER, using surface clue on character strings. It extracts material names in the sentence with 94.70% precision and 98.84% recall, regardless of whether it is already known or newly defined.

Information Storage and Retrieval↗
PubMed1998

[Staging classification of malignant lymphoma].

Ann Arbor staging classification is used for staging of Hodgkin's disease. Recommendation by Cotswolds meeting is now widely accepted. For Non-Hodgkin's lymphoma, however, Ann Arbor staging classification can be available only for nodal lymphoma. Specified staging classifications will be suitable in extranodal Non-Hodgkin's lymphoma.

Hodgkin Disease↗
PubMed1998

[Assessment of coronary flow reserve in patients with hypertrophic cardiomyopathy using transthoracic color Doppler echocardiography].

Abnormal coronary flow pattern and coronary vasodilator reserve have been identified in patients with hypertrophic cardiomyopathy (HCM) using invasive techniques. The characteristics of coronary flow velocity and coronary flow reserve were evaluated by noninvasive-recording of coronary flow velocity in the distal portion of the left anterior descending coronary artery in 7 patients with HCM and 7 normal subjects using transthoracic color Doppler echocardiography. Coronary flow velocity was measured at rest and during intravenous infusion of adenosine triphosphate (0.15 mg/kg/min). Diastolic peak velocity, diastolic mean velocity, the time from the beginning of diastole to peak velocity (TVP) and velocity half time from peak velocity was measured in each group. Coronary flow reserve was obtained as the ratio of hyperemic mean velocity to resting mean velocity. TVP was significantly prolonged in the patients with HCM compared with the normal subjects (159 +/- 38 vs 103 +/- 54 msec, p < 0.05). Velocity half time was significantly shorter in the patients with HCM compared with the normal subjects (304 +/- 138 vs 451 +/- 109 msec, p < 0.05). Although diastolic mean velocity during hyperemia was not different between the 2 groups (62 +/- 8 vs 70 +/- 19 cm/sec), diastolic mean velocity at rest was significantly higher in the patients with HCM than in the normal subjects (39 +/- 6 vs 26 +/- 7 cm/sec, p < 0.01). Therefore, coronary flow reserve was significantly lower in the patients with HCM than in the normal subjects (1.6 +/- 0.4 vs 2.7 +/- 0.4, p < 0.001). There was a good correlation between diastolic mean velocity and the ratio of interventricular septal to posterior left ventricular wall thickness (y = 0.024x + 0.46, r = 0.75). Transthoracic assessment of coronary flow velocity using color Doppler echocardiography reveals that coronary flow reserve is reduced in patients with HCM because of increased baseline resting diastolic mean velocity.

Cardiomyopathy, Hypertrophic↗
PubMed1998

[Trends in genome informatics].

Genome Informatics is not only a new area of computer science for genome projects but also a new approach of life science. As the genome projects proceed, genome informatics is becoming more important to bio-industry as well as life science. The major subjects are as follows; Database technologies for integration of various kinds of biological data Knowledge discovery from the integrated databases Interpretation and analysis of DNA sequence data with the databases Computer technologies for simulating life system with knowledge extracted from the databases in order to check the validity of the knowledge In this article, the history and trend of development of computer technologies for the subjects are described except for computer simulation.

Animals↗
PubMed1998

[Successful treatment with CPT-11 and adriamycin for hemophagocytic syndrome associated with intravascular lymphomatosis].

A 75-year-old man was admitted because of non-Hodgkin's lymphoma (histology undetermined) of the rib. A complete remission was achieved after CHOP therapy and irradiation. One year later, high fever, thrombocytopenia and liver dysfunction developed. Bone marrow aspirate revealed a hypoplastic marrow with hemophagocytic histiocytes, and a diagnosis of hemophagocytic syndrome (HPS) was made. Although no lymphomatous lesions were detected, HPS due to relapsed lymphoma was strongly suspected. The patient received MEVP therapy including etoposide and prednisolone, but without any improvement. Soon after the initiation of CPT-11 and adriamycin (ADM) therapy, all symptoms of HPS disappeared. This combination chemotherapy was repeated over a three-week span, and the patient remained in partial remission for the next 10 months. In November 1997, a tumor developed in the paranasal sinus, and the patient died three months later. The autopsy disclosed many B lymphoma cells filling the small vessels of almost all organs, and a final diagnosis of intravascular lymphomatosis (IVL) was made. These findings indicate that combination CPT-11 and ADM therapy is effective for cases of IVL accompanied by HPS that are refractory to conventional chemotherapies.

Aged↗
PubMed1997

The structure and function of the actin-binding domain of myosin light chain kinase of smooth muscle.

In addition to its kinase activity, the myosin light chain kinase (MLCK) of smooth muscle has an actin binding activity through which it can regulate the actin-myosin interaction of smooth muscle (Kohama, K., Okagaki, T., Hayakawa, K., Lin, Y., Ishikawa, R., Shimmen, T., and Inoue, A. (1992) Biochem. Biophys. Res. Commun. 184, 1204-1211). In this study, we have analyzed the actin binding activity of MLCK and related it to its amino acid sequence by producing native and recombinant fragments of MLCK. Parent MLCK exhibited both calcium ion (Ca2+) and calmodulin (Ca2+/CaM)-sensitive and Ca2+/CaM-insensitive binding to actin filaments. The native fragment, which consists of the Met1-Lys114 sequence (Kanoh, S., Ito, M., Niwa, E., Kawano, Y., and Hartshorne, D. J. (1993) Biochemistry 32, 8902-8907), and the recombinant NN fragment, which contains this 1-114 sequence, showed only Ca2+/CaM-sensitive binding. An inhibitory effect of the NN fragment on the actin-myosin interaction was observed by assaying in vitro motility and by measuring the actin-activated ATPase activity of myosin. The recombinant NN/41 fragment, which is constructed without the Met1-Pro41 sequence of the NN fragment, lost both the actin binding activity and the inhibitory effect. We confirmed the importance of the 1-41 sequence by using a few synthetic peptides to compete against the NN fragment in binding to actin filaments. The experiments using recombinant fragments and synthetic peptides also revealed that the site for CaM-binding is the Pro26-Pro41 sequence. The site for the Ca2+/CaM-insensitive binding, which is shown to be localized between the Ca2+/CaM-sensitive site and the central kinase domain of MLCK, exerted no regulatory effects on the actin-myosin interaction.

Actins↗
PubMed1997

mRNA capping enzyme is recruited to the transcription complex by phosphorylation of the RNA polymerase II carboxy-terminal domain.

Capping of mRNA occurs shortly after transcription initiation, preceding other mRNA processing events such as mRNA splicing and polyadenylation. To determine the mechanism of coupling between transcription and capping, we tested for a physical interaction between capping enzyme and the transcription machinery. Capping enzyme is not stably associated with basal transcription factors or the RNA polymerase II (Pol II) holoenzyme. However, capping enzyme can directly and specifically interact with the phosphorylated form of the RNA polymerase carboxy-terminal domain (CTD). This association occurs in the context of the transcription initiation complex and is blocked by the CTD-kinase inhibitor H8. Furthermore, conditional truncation mutants of the Pol II CTD are lethal when combined with a capping enzyme mutant. Our results provide in vitro and in vivo evidence that capping enzyme is recruited to the transcription complex via phosphorylation of the RNA polymerase CTD.

Binding Sites↗
PubMed1997

Properties of a Mixed Micellar System of Sodium Dodecyl Sulfate and Octylglucoside

Properties of a binary mixed surfactant system of a nonionic surfactant, octylglucoside, and an anionic one, sodium dodecyl sulfate, were investigated by measurement of the surface tension of their aqueous solutions containing 20, 75, and 150 mM sodium chloride. Changes in the critical micelle concentration with the composition of the two surfactants thus determined were analyzed according to the conventional regular solution theory for mixed micelles as well as with reference to Maeda's formulation for ionic/nonionic mixed micelles (H. Maeda, J. Colloid Interface Sci. 172, 98 (1995)). For the three salt concentrations, the properties of the mixed micellar system were found to be well described by the above theories, and the parameters in Maeda's formulation, B1 and B2, which are equivalent to the interaction parameter in the conventional theory of regular solution approach were determined. The effect of salt concentration on the properties of the mixed micellar system is discussed. Copyright 1997 Academic Press. Copyright 1997Academic Press

Journal Article↗
PubMed1997

Automated assessment of mitral regurgitant volume and regurgitant fraction by a newly developed digital color Doppler velocity profile integration method.

Recent development of the automated cardiac flow measurement (ACFM) method has provided automated measurement of stroke volume and cardiac output by spatial and temporal integration of digital Doppler velocity profile data. The purpose of this study was to evaluate the clinical usefulness of the ACFM method using digital color Doppler velocity profile integration in the assessment of mitral regurgitant volume and regurgitant fraction from measurements of both aortic outflow and mitral inflow volumes. We calculated both aortic outflow and mitral inflow volumes from the apical approach with the ACFM and pulsed Doppler (PD) methods in 20 patients with isolated mitral regurgitation. Mitral regurgitant volume and regurgitant fraction were calculated by the following equation: mitral regurgitant volume = (mitral inflow volume) - (aortic outflow volume), % regurgitant fraction = (mitral regurgitant volume)/(mitral inflow volume) x 100. Mitral regurgitant volume and regurgitant fraction were compared with that determined by the PD method. Mitral regurgitant volume measurement by the ACFM method showed a good correlation with that measured by the PD method (r = 0.90, y = 0.77x + 11.6, SEE = 9.0 ml); the mean differences between PD and ACFM measurements was -1.7 +/- 12.5 ml. Regurgitant fraction estimated by the ACFM method correlated well with that of the PD method (r = 0.92, y = 0.98x + 2.1, SEE = 8.8%). The mean difference for the measurement of regurgitant fraction between the PD and ACFM methods was 0.8 +/- 6.6%. Total time required for mitral regurgitant volume calculation in 1 cardiac cycle by the ACFM method was significantly shorter than that of the PD method (126 +/- 15 seconds vs 228 +/- 36 seconds, p <0.01). In conclusion, the newly developed ACFM method is simple, quick, and accurate in the automated assessment of mitral regurgitant volume and regurgitant fraction.

Adult↗
PubMed1997

Domain structures and immunogenic regions of the 90-kDa heat-shock protein (HSP90). Probing with a library of anti-HSP90 monoclonal antibodies and limited proteolysis.

Domain structures of the 90-kDa heat-shock protein (HSP90) have been investigated with a library of anti-HSP90 monoclonal antibodies (mAbs) and by limited proteolysis with trypsin and chymotrypsin. Thirty-three mAbs were obtained by immunization with bacterially expressed human HSP90alpha and HSP90beta isoforms. Among them, ten and three mAbs reacted specifically with HSP90alpha and HSP90beta, respectively. Immunoblotting and enzyme-linked immunosorbent analyses revealed that major immunogenic domains were located at two restricted regions of HSP90alpha, i.e. amino acids 227-310 (designated Region I) and 702-716 (Region II), corresponding to a highly charged region and a region near the C terminus, respectively. Taken together with the characteristics of the amino acid sequences, these two immunogenic regions appeared to be exposed at the outer surface of HSP90. We further investigated the domain structures of HSP90 by limited proteolysis in combination with N-terminal sequencing and immunoblotting analyses. Tryptic cleavages of HSP90alpha at low concentrations revealed the existence of major susceptible sites at Arg400-Glu401, Lys615-Ala616, and Arg620-Asp621. Proteolysis at higher trypsin concentrations caused successive cleavages only toward the N-terminal direction from these sites, and Region I was included in the region selectively deleted during this process, thereby further suggesting its surface location. From these results, we propose three domain structures of HSP90 consisting of amino acids 1-400, 401-615, and 621-732. Differences in the protease sensitivity and immunogenicity further suggest that every domain is composed of two subdomains. This is the first study describing the domain structures and the immunogenic regions of HSP90.

Amino Acid Sequence↗
PubMed1997

Phasic coronary flow characteristics in patients with constrictive pericarditis: comparison with restrictive cardiomyopathy.

BACKGROUND: Phasic coronary flow characteristics have been reported in patients with aortic valve disease and hypertrophic cardiomyopathy. The purpose of this study was to assess the differences in coronary flow characteristics between patients with constrictive pericarditis and those with restrictive cardiomyopathy. METHODS AND RESULTS: The study populations consisted of 7 case patients with constrictive pericarditis, 8 with restrictive cardiomyopathy, and 11 control subjects with chest pain and normal coronary arteries. Five minutes after injection of 3 mg of isosorbide dinitrate, phasic coronary flow velocity patterns were analyzed in the proximal segment of the angiographically normal left anterior descending coronary artery at rest using a 0.014-in, 15-MHz Doppler guidewire. Coronary flow reserve was obtained from the ratio of adenosine-induced (0.14 mg x kg(-1) x min(-1) I.V.) hyperemic/baseline time-averaged peak velocity. Although in case patients with constrictive pericarditis and restrictive cardiomyopathy maximal hyperemic time-averaged peak velocity (21+/-8 and 31+/-17 versus 60+/-19 cm/s, respectively; P<.001) and coronary flow reserve (1.3+/-0.4 and 1.6+/-0.6 versus 3.6+/-0.4, respectively, P<.001) were significantly lower than in control subjects, there were no significant differences in these indexes between the two groups of case patients. Velocity half-time of diastolic flow velocity corrected by square root(RR), which indicates deceleration of diastolic flow, in the groups of case patients with constrictive pericarditis and restrictive cardiomyopathy was significantly less than that in control subjects (6.2+/-2.6 and 10.6+/-1.5 versus 16.9+/-2.7, respectively; P<.001); this was also significantly smaller in constrictive pericarditis than restrictive cardiomyopathy (P<.001). This index <9.5 could distinguish constrictive pericarditis from restrictive cardiomyopathy with a sensitivity of 86% and a specificity of 88%. Furthermore, time from the beginning of diastole to diastolic peak velocity corrected by square root(RR) indicating acceleration of diastolic flow velocity in constrictive pericarditis was significantly less than that in restrictive cardiomyopathy and control subjects (2.8+/-1.2 versus 4.8+/-0.8 and 4.4+/-0.6, respectively; P<.001). CONCLUSIONS: Although coronary flow reserve is limited in both constrictive pericarditis and restrictive cardiomyopathy because of restriction of hyperemic response, rapid acceleration and more rapid deceleration of diastolic flow velocity are more characteristic in constrictive pericarditis than in restrictive cardiomyopathy.

Adult↗
PubMed1997

Comparison of coronary flow reserve between focal and diffuse vasoconstriction induced by ergonovine in patients with vasospastic angina.

Decreased coronary flow reserve has been reported in patients with ergonovine-induced coronary vasoconstriction by the thermodilution method. To assess the difference of coronary flow reserve between patients with focal and diffuse vasospasm, after the vasospasm is discontinued by injection 3 mg of isosorbide dinitrate, phasic flow velocities of the diseased coronary artery were recorded at rest and during hyperemia (140 microg/kg/min of adenosine infusion intravenously) using a 0.014-inch, 15-MHz Doppler guidewire in 26 patients with ergonovine-induced coronary vasospasm (0.2-mg ergonovine injection intravenously), including 12 patients with focal (>90% stenosis), 14 patients with diffuse vasospasm (>50%), and 11 controls with normal coronary arteries without vasospasm. Although time-averaged peak velocity in cases with diffuse and focal vasospasm was not significantly different compared with that in controls at baseline (22 +/- 7, 18 +/- 5 vs 20 +/- 7 cm/s, respectively, NS), it was significantly lower in patients with diffuse vasospasm than in cases with focal vasospasm and in controls during hyperemia (43 +/- 13 vs 64 +/- 18, 61 +/- 19 cm/s, respectively, p <0.01). As a result, coronary flow reserve obtained from the ratio of hyperemic/baseline time-averaged peak velocity was significantly lower in patients with diffuse vasospasm than that in controls (1.9 +/- 0.4 vs 3.1 +/- 0.4, p <0.01), although it was not significantly different between the subjects with focal vasospasm and controls (3.5 +/- 0.7 vs 3.1 +/- 0.4, NS). Thus, coronary flow reserve is maintained normally in patients with focal vasospasm and limited in those with diffuse vasospasm. Microvascular impairment could exist further in cases with diffuse vasospasm, although similar endothelial dysfunction of the epicardial coronary artery is observed in focal and diffuse vasospasm.

Adult↗
PubMed1997

Expression of zinc transporter gene, ZnT-1, is induced after transient forebrain ischemia in the gerbil.

To elucidate the molecular mechanisms underlying neuronal death after transient forebrain ischemia, we cloned genes expressed after transient forebrain ischemia in the Mongolian gerbil by a differential display method. A gerbil homolog of rat zinc transporter, ZnT-1, which transports intracellular Zn2+ out of cells, was isolated. Its expression became detectable exclusively in pyramidal neurons of the CA1 region 12 hr after ischemia and reached a maximum from day 1 to day 2 as shown by in situ hybridization. By day 7, expression had disappeared entirely from the cells in the CA1 region, because the neurons had died. No other brain regions exhibited such a significant level of ZnT-1 mRNA expression during this period. Zn2+ was shown to accumulate in CA1 pyramidal neurons expressing ZnT-1 mRNA after the ischemia by using zinquin, a zinc-specific fluorescent dye. When primary hippocampal neurons were exposed to a high dose of Zn2+, ZnT-1 mRNA accumulated. These results suggest that the induction of ZnT-1 mRNA observed in CA1 neurons was caused by an increase in the intracellular Zn2+ concentration. It was reported recently that Zn2+ chelator blocked neuronal death after ischemia and that the influx of Zn2+ might be a key mechanism underlying neuronal death. The induction of ZnT-1 mRNA in CA1 pyramidal neurons fated to die after transient ischemia is of interest to the study of postischemic events and the molecular mechanisms underlying delayed neuronal death.

Amino Acid Sequence↗