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Biomedical subjects

K Takeda

Publications and source records attributed to K Takeda.

At least 577 records · Page 32Linked to original sources
PubMed1997

[Antihypertensive therapy and heart diseases].

The one of the most important goal of antihypertensive therapy is to prevent and improve the hypertensive heart disease including cardiac hypertrophy and ischemic heart disease. The regression of cardiac hypertrophy by treatment reduce the risk of cardiovascular events. ACE inhibitor (ACEI) may be the most powerful among antihypertensive agents to regress hypertrophy. Ca-antagonist and ACEI can improve the impaired coronary flow reserve by microvascular circulation. Recently, the evidences have been accumulated that the release of nitric oxide (NO) from the coronary artery of hypertension is reduced. "TREND" study proved that ACEI can improve this decreases in the clinical study. For the heart failure, ACEI is a effective drugs, and Ca-antagonist and beta-blocker also have been getting good results.

Adrenergic beta-Antagonists↗
PubMed1997

Acute hemorrhagic gastritis associated with acetazolamide intoxication in a patient with chronic renal failure.

Acetazolamide (Diamox) is a carbonic anhydrase inhibitor commonly used in patients with glaucoma in order to reduce intraocular pressure. Acetazolamide (AZ) is mostly excreted in the urine, therefore, the blood levels of AZ often tend to increase in patients with chronic renal failure. We experienced a case of chronic renal failure in a patient suffering from acute hemorrhagic gastritis associated with AZ intoxication. A 66-year-old female with chronic renal failure was referred to our hospital because of drowsiness and an acute deterioration of renal function. She had been treated with AZ, 500 mg per every day for eleven days for the treatment of glaucoma. Laboratory studies showed leukocyturia, thrombocytopenia, severe anemia, and tarry stools. The serum concentration of AZ was elevated to a maximum of 76.5 mg/ml. She was thus diagnosed as having AZ intoxication. On further examination, acute extensive hemorrhagic gastritis was also found by gastroscopy. Despite of the administration of intensive therapies, she died of disseminated intravascular coagulation (DIC) and septic shock due to bone marrow depression 6 days after admission. It is generally known that excessive blood levels of AZ inhibit not only the gastric juices but also prostaglandin levels and HCO3- excretion in the gastric mucosal barrier. We thus concluded that an excessive dose of AZ had probably destroyed the gastric mucosal barrier or thrombocytopenia due to bone marrow disorder and thus eventually led to the development of hemorrhagic gastritis. As far as we know, this is the first case report of acute hemorrhagic gastritis associated with AZ intoxication. Even though AZ tends to strongly bind to plasma protein and its clearance is generally poor by hemodialysis (HD), in our patient, HD was observed to be rather effective since the clearance of AZ was 45.8 ml/min on HD and 66 ml/min on direct hemoperfusion (DHP). DHP often reduces the number of platelets, also DHP needs a lot of heparin, therefore, we should have performed HD alone instead of DHP. In patients with an impaired renal function, AZ should therefore be administered very carefully in order to avoid an accumulation of the drug. In addition, HD alone should be used to remove any excessive amounts of AZ from the blood.

Acetazolamide↗
PubMed1997

[Relationship between iodine-123-beta-methyl-p-iodophenyl-pentadecanoic acid washout ratio and oxygen consumption in normal and ischemic myocardium].

The relationship between oxygen consumption and iodine-123-beta-methyl-p-iodophenyl-pentadecanoic acid (123I-BMIPP) washout at rest and after exercise was investigated in normal and ischemic myocardium. Sixteen healthy volunteers and 14 patients with ischemic heart disease were examined. After injection of 111MBq of 123I-BMIPP, serial single photon emission computed tomography imaging was performed to evaluate washout ratio after 30 min and 1 hour of rest and after exercise. In the volunteers, the mean washout ratio was 3.3 +/- 3.5% after 1 hour of rest and increased during exercise. The exercise washout ratio showed a better correlation with net pressure rate product (net PRP: cumulative values of PRP during exercise) than with the peak PRP. The exercise washout ratio showed a strong correlation with the net PRP in the range from 180 to 300 x 10(3) mmHg. beat/min and a plateau of 10-15%. In the nine ischemic patients with net PRP > or = 300 x 10(3) mmHg.beat/min, the exercise washout ratio values were significantly elevated in normal segments relative to ischemic segments (10.1 +/- 1.9% vs 4.7 +/- 2.9%, p < 0.001). In the five ischemic patients with net PRP < 300 x 10(3) mmHg.beat/min, washout ratio at rest and after exercise did not differ significantly between normal and ischemic segments. 123I-BMIPP washout ratio increased with increased oxygen consumption during exercise in normal myocardium but not in ischemic myocardium. The patient must exercise before fatty acid metabolism can be compared between normal and ischemic myocardium.

Adult↗
PubMed1997

Systemic lupus erythematosus in a patient with remitting minimal change nephrotic syndrome.

Minimal change nephrotic syndrome (MCNS) developed in a 17-year-old female and spontaneously remitted. One month later the nephrotic syndrome relapsed. Prednisolone therapy, 60 mg/day, was started and resulted in a full remission within a week and the prednisolone dose was subsequently tapered. Seven months later, when 10 mg/day of prednisolone was being administered, she developed erythematous rash with photosensitivity and polyarthralgia without exacerbation of the nephrotic syndrome, and fulfilled four of the American College of Rheumatology criteria for classification of systemic lupus erythematosus (SLE). Avoidance of direct sunlight ameliorated the erythematous rash and the polyarthralgia disappeared even though the prednisolone dose was decreased further. This is the first reported case of SLE developed in a patient with remitting MCNS.

Adolescent↗
PubMed1997

[A neuropsychological study on a patient with the resection of the right lateral frontal lobe].

We report a patient who underwent a resection of the right lateral frontal lobe after a venous thrombosis of the superior sagittal sinus. The patient showed inertia, obsessive-compulsive behavior and disinhibition two weeks after the operation and hyperlogia and hypergraphia four weeks later, all of which disappeared within six weeks. General intelligence, language and memory were consistently preserved, though the scores of the performance IQ and the visual memory were relatively decreased. A few months after the operation emotional and personality change such as impatience and apathy became evident. We suggest that the right lateral prefrontal area is concerned with personality and behavior and that the widespread resection holds general intelligence, language and memory within normal range but relatively decreases non-verbal cognitive function that requires manual responses.

Cerebral Infarction↗
PubMed1997

Comparison of lumen area after PTCA by IVUS and QCA.

The coronary lumen area just after percutaneous transluminal coronary angioplasty (PTCA) was assessed by intravascular ultrasonography (IVUS) with 4.3 F cardiovascular imaging systems (CVIS) and quantitative coronary angiography (QCA) with Kontron CARDIO 500. Altogether 34 lesions were divided into two groups by IVUS findings using Nissen's circular shape factor (CSF), which was defined by the (calculated perimeter/observed perimeter), expressing lumen eccentricity. The eccentric group (CSF < or = 0.92) was 22, and concentric group (CSF > 0.92) was 12. The minimum lumen diameter by IVUS and QCA (both edge-detection and densitometric methods) correlated in both the eccentric and concentric groups. As for the lumen area, only the QCA densitometric method in the concentric group correlated with the lumen area determined by IVUS. Despite using QCA, it is almost impossible for angiography to determine the lumen area just after PTCA if an eccentric lesion with a tear or dissection had occurred.

Aged↗
PubMed1997

[Trend of aging on the number of teeth investigated through a survey of dental health representation in a simple equation by using a kinetic method and its application].

A survey of dental health was conducted on 6,933 residents (aged 61.8 +/- 11.1) in 4 villages Nara Prefectural Uchiyoshino Health Center administers. Examinees were divided into 7 ages groups. The mean value of present teeth at each age group was calculated. Age dependency of number of teeth was investigated with a kinetic model based on the following premise. 1. Changes between age groups can be treated as a time series occurrence. 2. Number of missing teeth can be estimated as 29 - that of present teeth. Results show that the rate of decrease of the number of present teeth is of a first order in itself and the number of missing teeth. It can be mathematically expressed as follows: -dX/dt = k.X.(29 - X).......eq. (1). in which X = number of present teeth, 29 - x = number of missing teeth k = rate constant, t = time. From this simple relationship the following are suggested 1. Tooth loss is caused by the interaction of present teeth and sites where teeth are lost. 2. Integration of eq. (1) yields ln¿(29 - X)/X¿ = 29.k.t + a.......eq. (2). in which 0 < X < 29, t = time from the youngest age group (20-29), a = constant. It appears that, from eq. (2), the dental health of a community is determined by two coefficients, 29.k and a. 3. Helping a person realize his present and future dental state and to motivate action for prevention of tooth loss by showing him his rate of decrease, "tooth age" and the predicted number of teeth a certain years later calculated from eq. (1) and eq. (2), can be of great value. 4. Eq. (2) is transformed to X = 29/¿exp(29.k.t + a) + 1¿, which represents the reverse S-shaped curve of the age dependency of the number of teeth. 5. Applying this method to cohort analysis will enable forecast of the trend of the number of teeth.

Adult↗
PubMed1996

Cytotoxic gammadelta or alphabeta T cells with a natural killer cell marker, CD56, induced from human peripheral blood lymphocytes by a combination of IL-12 and IL-2.

Populations of cytotoxic CD3+CD56+ cells were selectively expanded when monocyte-depleted human PBL (M(-) PBL) were cultured with 20 U/ml IL-12 and 100 U/ml IL-2. In a majority of cases, CD4-CD8- as well as CD8+ gammadelta T cells with CD56 Ag were induced, but in some cases CD4+CD56+ alphabeta T cells were selectively increased. Determination of which will increase, gammadelta or alphabeta T cells, apparently is dependent upon individuals. When M(-) PBL were stimulated with IL-12 and IL-2 in the presence of immobilized anti-CD3 Ab, CD8+CD56+ alphabeta T cells increased exclusively. When M(-) PBL were cultured by IL-2 alone, CD3+CD56- cell expansion was predominant while CD3+CD56+ cells remained a minor population. Cytotoxic activity of M(-) PBL cultured with a combination of IL-12 and IL-2 is much greater than when cultured with IL-2 alone. The cytotoxicity of activated M(-) PBL was abrogated by the depletion of either CD3+ or CD56+ cells irrespective of their gammadelta or alphabeta phenotypes. These types of cells are preferentially present in the livers of humans. The results revealed that, under certain conditions, IL-12 synergizes with IL-2 to induce potent cytotoxic T cells with CD56 Ag of humans, and suggest that these cells in the human liver are functionally similar to NK1+ alphabeta T cells in murine liver.

Biomarkers↗
PubMed1996

Ectopic expression of CHOP (GADD153) induces apoptosis in M1 myeloblastic leukemia cells.

CHOP (GADD153) is a member of the C/EBP family and a stress-induced protein. To investigate the role of CHOP in cellular growth, we expressed CHOP conditionally in M1 myeloblastic leukemia cells that do not express p53 protein. More than 60% of M1 cells died through apoptosis 72 h after CHOP induction. Site-directed mutagenesis revealed that this process requires leucine zipper domain but neither intact basic region nor trans-activation domain. CHOP-mediated apoptosis accompanied downregulation of bcl-2 mRNA and overexpression of Bcl-2 delayed the process. Our results indicate that CHOP can induce apoptosis in a p53-independent manner.

Animals↗
PubMed1996

Impaired IL-13-mediated functions of macrophages in STAT6-deficient mice.

IL-13 shares many biologic responses with IL-4. In contrast to well-characterized IL-4 signaling pathways, which utilize STAT6 and 4PS/IRS2, IL-13 signaling pathways are poorly understood. Recent studies performed with STAT6-deficient mice have demonstrated that STAT6 plays an essential role in IL-4 signaling. In this study, the functions of peritoneal macrophages of STAT6-deficient mice in response to IL-13 were analyzed. In STAT6-deficient mice, neither morphologic changes nor augmentation of MHC class II expression in response to IL-13 was observed. In addition, IL-13 did not decrease the nitric oxide production by activated macrophages. Taken together, these results suggest that the macrophage functions in response to IL-13 were impaired in STAT6-deficient mice, indicating that IL-13 and IL-4 share the signaling pathway via STAT6.

Animals↗
PubMed1996

Estimation of the malignancy of pleural effusions by electron spin resonance.

We conducted an electron spin resonance (ESR) study on human pleural effusions obtained from patients (n = 15) with and without cancer at 77 K. We detected two kinds of signals which are considered to be due to transition metal ions in metalloproteins such as Fe3+ in transferrin and Cu2+ in ceruloplasmin from their g values (g = 4.2 and 2.049) and line shapes. We found a significant difference in the signal intensity ratio, Cu2+/Fe3+, of the pleural effusions between cancer and noncancer patients by the Mann-Whitney U test (P < 0.01). The ESR study of pleural effusion enabled us to estimate its malignancy and may have future applications.

Electron Spin Resonance Spectroscopy↗
PubMed1996

Quantal release at a neuronal nicotinic synapse from rat adrenal gland.

The neuronal nicotinic synapse in tissue slices of the adrenal medulla was studied with whole-cell patch-clamp. Excitatory postsynaptic currents (EPSCs) were evoked by local field stimulation or occurred spontaneously especially when external [K+] was increased. EPSCs were carried by channels sharing biophysical and pharmacological properties of neuronal-type nicotinic receptors (nAChRs). A single-channel conductance (gamma) of 43-45 pS was found from nonstationary variance analysis of EPSCs. Spontaneous EPSCs were tetrodotoxin-insensitive and Ca(2+)-dependent and occurred in burst-like clusters. Quantal analysis of spontaneous EPSCs gave a quantal size of 20 pA and amplitude histograms were well described by binomial models with low values of quantal content, consistent with a small number of spontaneously active release sites. However, rare large amplitude EPSCs suggest that the total number of sites is higher and that extrajunctional receptors are involved. Our estimates of quantal content and size at the chromaffin cell neuronal nicotinic synapse may be useful in characterizing central neuronal-type nicotinic receptor-mediated cholinergic synaptic transmission.

Adrenal Medulla↗
PubMed1996

Identification of a variant A-specific neutralizing epitope on glycoprotein B (gB) of human herpesvirus-6 (HHV-6).

Based on genetic, antigenic, and growth properties, human herpesvirus-6 (HHV-6) can be classified into two groups, variant A (HHV-6A) and variant B (HHV-6B). We have mapped the HHV-6A-specific epitope on glycoprotein B (gB), which was recognized by a monoclonal antibody (MAb), 87-y-13, with a complement-independent neutralizing activity. Plasmids carrying various chimeric gB sequences formed between strains U1102 (HHV-6A) and HST (HHV-6B) and carrying sequences for a series of carboxy-terminal deletions of U1102 gB were constructed. By using the plasmids, in vitro transcription and subsequent in vitro translation were carried out. Immunoprecipitation assay of the translated products with MAb 87-y-13 revealed that MAb 87-y-13 was able to react only with in vitro translation products containing the sequence between amino acid residues 335 and 395 of U1102 gB. Amino acid sequence comparison between HHV-6A and HHV-6B in this region showed that amino acid residues 347, 387, and 393-395 were HHV-6A-specific. To determine which amino acid residue(s) was involved in recognition by MAb 87-y-13 as well as in the neutralizing activity, point mutations were introduced at those amino acid positions. Immunoprecipitation assay of the mutagenized gB with point mutations suggested that the neutralizing MAb-y-13 was involved in the recognition of the amino acid Asn at residue 347 of U1102 gB (HHV-6A). This site may play an important role in viral infection.

Amino Acid Sequence↗
PubMed1996

Structural analysis of unsaturated hexasaccharides isolated from shark cartilage chondroitin sulfate D that are substrates for the exolytic action of chondroitin ABC lyase.

The enzymatic action of highly purified chondroitin ABC lyase from Proteus vulgaris is dependent on the size of the substrate, and the enzyme does not cleave tetrasaccharides, irrespective of their sulfation profiles [Sugahara, K., Shigeno, K., Masuda, M., Fujii, N., Kurosaka, A. & Takeda, K. (1994) Carbohydr. Res. 255, 145-163]. To characterize the enzyme action in more detail, we isolated nine sulfated hexasaccharides from commercial shark cartilage chondroitin sulfate D, after partial digestion with highly purified chondroitin ABC lyase, by means of gel chromatography and HPLC on an amine-bound silica column. Structural analysis by 500-MHz H-NMR spectroscopy, and enzymatic digestion in conjunction with HPLC, demonstrated that these hexasaccharides, with the common core saccharide structure delta 4 HexA (alpha 1-3)GalNAc(beta 1-4)GlcA(beta 1-3)GalNAc(beta 1-4) GlcA(beta 1-3)GalNAc(where delta 4 HexA and GlcA represent 4-deoxy-alpha-L-threo-hex-4-enepyranosyluronic acid and glucuronic acid, respectively) bear three or four sulfate groups in different combinations. In the hexasaccharides, the D, disaccharide unit GlcA2-SO3 (beta 1-3) GalNAc4SO(3-) which is characteristic of chondroitin sulfate D, was arranged on the reducing side of the A disaccharide unit GlcA(beta 1-3)GalNAc4SO(3)-, and thus formed an A-D tetrasaccharide sequence GlcA(beta 1-3)GalNAc4SO(3)-(beta 1-4)GlcA2SO(3)-(beta 1-3) GalNAc6SO(3)-. Analysis of the degradation products of these hexasaccharides with highly purified chondroitin ABC lyase indicated that the enzyme preferentially acted on the unsaturated hexasaccharides in an exolytic fashion and removed an unsaturated disaccharide unit from the non-reducing termini, irrespective of the sulfation profiles of the hexasaccharides.

Animals↗
PubMed1996

Regulation of human heme oxygenase-1 gene expression under thermal stress.

Heme oxygenase-1 is an essential enzyme in heme catabolism, and its human gene promoter contains a putative heat shock element (HHO-HSE). This study was designed to analyze the regulation of human heme oxygenase-1 gene expression under thermal stress. The amounts of heme oxygenase-1 protein were not increased by heat shock (incubation at 42 degrees C) in human alveolar macrophages and in a human erythroblastic cell line, YN-1-0-A, whereas heat shock protein 70 (HSP70) was noticeably induced. However, heat shock factor does bind in vitro to HHO-HSE and the synthetic HHO-HSE by itself is sufficient to confer the increase in the transient expression of a reporter gene upon heat shock. The deletion of the sequence, located downstream from HHO-HSE, resulted in the activation of a reporter gene by heat shock. These results suggest that HHO-HSE is potentially functional but is repressed in vivo. Interestingly, heat shock abolished the remarkable increase in the levels of heme oxygenase-1 mRNA in YN-1-0-A cells treated with hemin or cadmium, in which HSP70 mRNA was noticeably induced. Furthermore, transient expression assays showed that heat shock inhibits the cadmium-mediated activation of the heme oxygenase-1 promoter, whereas the HSP70 gene promoter was activated upon heat shock. Such regulation of heme oxygenase-1 under thermal stress may be of physiologic significance in erythroid cells.

Base Sequence↗
PubMed1996

Liver NK1.1+ CD4+ alpha beta T cells activated by IL-12 as a major effector in inhibition of experimental tumor metastasis.

We demonstrate herein evidence that IL-12-activated alpha beta T cells with intermediate TCR (NK1+ TCRint cells) in the liver inhibit metastases in the lung as well as in the liver metastases of i-v. injected tumors. IL-12 administration enhanced NK1 expression of NK1+ TCRint cells (NK1high) and increased CD4 weakly positive (CD4low) TCRint cells, while both CD4+ TCRint cells and double-negative TCRint cells were proportionally diminished. Accordingly, the major parts of NK1high TCRint cells are CD4low cells, and most of these cells are V beta 8+ cells. The cytotoxic assays of IL-12-stimulated hepatic mononuclear cells after treatment with respective Abs and complement in vitro and after sorting revealed that CD4low NK1high TCRint cells are cytotoxic effectors. When IL-12-stimulated hepatic mononuclear cells (but not splenocytes) were transferred into tumor-preinjected mice, EL-4 cell metastases in the liver as well as 3LL cell metastases in the lung were inhibited. The antimetastasis of hepatic mononuclear cells transfer was abrogated by the depletion of NK1+ cells, CD3+ cells, or CD4+ cells but not CD8+ cells before transfer. Moreover, transfer of these cells of nude mice into tumor-preinjected mice also inhibited metastases in both organs. Although NK1+ TCRint cells are nearly absent in the hepatic vein blood, a significant proportion of NK1high TCRint cells appeared by IL-12 administration. These results demonstrate that IL-12-stimulated liver NK1high TCRint cells, including extrathymic ones, are major effectors against tumor metastasis and suggest that the cells migrate and inhibit lung metastases.

Animals↗
PubMed1996

STAT3 activation is a critical step in gp130-mediated terminal differentiation and growth arrest of a myeloid cell line.

Myeloid leukemia M1 cells can be induced for growth arrest and terminal differentiation into macrophages in response to interleukin 6 (IL-6) or leukemia inhibitory factor (LIF). Recently, a large number of cytokines and growth factors have been shown to activate the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway. In the case of IL-6 and LIF, which share a signal transducing receptor gp130, STAT3 is specifically tyrosine-phosphorylated and activated by stimulation with each cytokine in various cell types. To know the role of JAK-STAT pathway in M1 differentiation, we have constructed dominant negative forms of STAT3 and established M1 cell lines that constitutively express them. These M1 cells that overexpressed dominant negative forms showed no induction of differentiation-associated markers including Fc gamma receptors, ferritin light chain, and lysozyme after treatment with IL-6. Expression of either c-myb or c-myc was not downregulated. Furthermore, IL-6- and LIF-mediated growth arrest and apoptosis were completely blocked. Thus these findings demonstrate that STAT3 activation is the critical step in a cascade of events that leads to terminal differentiation of M1 cells.

Acute-Phase Proteins↗