Chronic eosinophilic leukemia with unique chromosomal abnormality, t(5;12) (q33;q22).
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
T Murayama
Publications and source records attributed to T Murayama.
Bladder hypersensitivity of interstitial cystitis complicated by allergic diseases.
Explore the source record for details and available documents.
Asthma↗
Involvement of noradrenaline transporters in S-nitrosocysteine-stimulated noradrenaline release from rat brain slices: existence of functional Na(+)-independent transporter activity.
Noradrenaline (NA) can be released by both exocytosis and by the membrane transporter responsible for transmitter uptake. Previously, we reported that S-nitrosocysteine (SNC), an S-nitrosothiol, stimulated [3H]NA release from the rat hippocampus. In this study, we investigated the involvement of the NA transport system in SNC-stimulated NA release from rat brain (cerebral cortex and hippocampus) slices. [3H]NA release by SNC in normal Na(+) (148 mM)-containing buffer from both slices was slightly, but significantly, inhibited by 1 microM desipramine, an NA transporter inhibitor. [3H]NA release in low Na(+) (under 14 mM)-containing buffer was inhibited by over 50% by desipramine. [3H]NA release by tyramine from both slices in normal and low Na(+) buffer was almost completely inhibited by desipramine. [3H]NA uptake into cerebral cortical slices was observed in low Na(+) buffer at 20-30% of normal Na(+) buffer levels. [3H]NA uptake in both normal and low Na(+) buffers was inhibited by desipramine and by SNC. Although [3H]NA uptake in normal Na(+) buffer was almost completely inhibited by 500 microM ouabain, the uptake in low Na(+) buffer was resistant to ouabain. These findings suggest the existence of a functional Na(+)-independent NA transport system and that SNC stimulates NA release at least partially via this system in brain slices.
Adrenergic Uptake Inhibitors↗
Kinetic analysis of cytokine gene expression in patients with GVHD after donor lymphocyte infusion.
Patients who receive a donor lymphocyte infusion (DLI) for the treatment of relapsed leukemia after allogeneic BMT (alloBMT) often developed GVHD. To determine whether cytokines might have a role in GVHD, an intensive kinetic analysis of in vivo cytokine gene expression was performed on PBMC from three such patients. Expression of IL-1beta, IL-2, IFN-gamma, IL-4, IL-5, IL-8, IL-10, IL-12, TNF-alpha, and IL-2Ralpha was examined using a sensitive semi-quantitative reverse transcription (RT)-PCR assay system. Six normal controls were also analyzed for comparison. Expression of type 1 T helper (Th1) cytokines, IL-2 and IFN-gamma was greatly increased in all three patients. In particular, the changes in IL-2 gene expression correlated well with disease progression, suggesting that IL-2 has a critical role in the development of GVHD. Although the pattern of type 2 T helper (Th2) cytokine gene expression differed in each patient, the expression of IL-4 was inversely related to expression of Th1 cytokines. These results suggest that Th1 dominates in the development of human clinical GVHD.
Adult↗
Prognosis of conservative therapy of advanced interstitial cystitis: experience of five cases.
BACKGROUND: It is generally believed that surgical procedures, particularly the more invasive ones, should be reserved for patients who fail to respond to conservative therapy by several established modalities. We studied whether conservative therapy was applicable to patients with interstitial cystitis (IC) in which an individual's awake bladder capacity decreases to 100 mL or less with vesicoureteral reflux (VUR). METHODS: Five cases that satisfied the criteria proposed by the National Institutes of Health were examined. The maximum awake bladder capacity was 50-100 mL (average, 74 mL). The bladder capacity under anesthesia was 70-300 mL (average, 199 mL). Only conservative treatments were carried out. RESULTS: The observation period ranged from 3 to 16 years with an average of 9 years. The awake bladder capacity ranged from 200 to 300 mL (average, 250 mL). The symptom index total score, which was previously 18.5, decreased to 5.5 and the problem index total score, which was previously 14.3, decreased to 3.5. Symptoms of bladder irritation improved. In four cases, VUR disappeared as the bladder capacity increased. Vesicoureteral reflux persisted in one case although its severity decreased and there was no fever. CONCLUSION: The patients treated with conservative therapy were able to maintain an awake bladder capacity that was sufficient for acceptable quality of life and their symptoms of bladder irritation improved. This suggests that we should regenerate the original remaining bladder using conservative therapy, even if IC is in a late stage.
Administration, Intravesical↗
Comparison of transthoracic Doppler echocardiography and natriuretic peptides in predicting mean pulmonary capillary wedge pressure in patients with chronic atrial fibrillation.
The purpose of this study was to assess whether transthoracic Doppler echocardiography and serum natriuretic peptide levels could predict mean pulmonary capillary wedge pressure (PCWP) in patients with chronic atrial fibrillation. We examined mitral flow velocity and pulmonary venous flow (PVF) velocity patterns in 32 patients with chronic atrial fibrillation. Plasma A-type and B-type natriuretic peptide (ANP, BNP, respectively) levels in the peripheral vein were measured. Significant correlations were observed between mean PCWP and the following: peak velocity (r = 0.51) and deceleration time (r = -0.65) of the mitral flow; peak velocity (r = 0.64) and deceleration time (r = -0.80) of the PVF; BNP (r = 0.60); and ANP (r = 0.36). Stepwise multiple linear regression analysis selected PVF deceleration time and mitral flow deceleration time as independent predictors of PCWP. A cutoff value of PVF deceleration time of < or =150 ms and a mitral flow deceleration time of < or =100 ms predicted a mean PCWP of > or =18 mm Hg, with a sensitivity of 100% and 80% and a specificity of 96% and 85%, respectively. In conclusion, PVF deceleration time and mitral flow deceleration time obtained from transthoracic Doppler echocardiography are more accurate predictors of mean PCWP than values obtained with natriuretic peptides in patients with chronic atrial fibrillation.
Aged↗
Overexpression of p27(Kip1) by doxycycline-regulated adenoviral vectors inhibits endothelial cell proliferation and migration and impairs angiogenesis.
Formation of new blood vessels in the adult animal (i.e., angiogenesis) is an important event for tissue repair and for tumor growth and metastasis. Angiogenesis involves the migration and proliferation of endothelial cells. We have investigated the role of the growth suppressor p27(Kip1) (p27) on endothelial cell function in vitro and angiogenesis in vivo. We have generated Ad-TetON, a replication-deficient adenovirus that constitutively expresses the reverse tet-responsive transcriptional activator, and Ad-TRE-p27, which drives expression of p27 under the control of the tet response element. Western blot analysis demonstrated doxycycline-dependent overexpression of p27 in human umbilical vein endothelial cells (HUVECs) coinfected with Ad-TetON and Ad-TRE-p27, which resulted in a marked inhibition of DNA replication and cell migration in vitro. Inducible overexpression of p27 in cultured HUVECs inhibited the formation of tubelike structures and, when applied in a murine model of hind limb ischemia, reduced hind limb blood flow recovery and capillary density. These findings thus underscore a novel role of p27 in regulating endothelial cell migration in vitro and angiogenesis in vivo, suggesting a novel anti-angiogenic therapy based on inducible p27 overexpression.
Adenoviridae↗
Role of oxidized LDL in atherosclerosis.
A critical event in the early stages of atherosclerosis is the focal accumulation of lipid-laden foam cells derived from macrophages. In various cholesterol-fed animal models of atherosclerosis, localized attachment of circulating monocytes to arterial endothelial cells appeared to precede the formation of foam cells. It is suggested that monocyte recruitment into early lesions depends on the endothelial adhesiveness for monocytes and lymphocytes. In vivo and in vitro experiments have identified molecules, such as ICAM-1, VCAM-1, and P-selectin, that can support the adhesion of monocytes and lymphocytes. Moreover, oxidized LDL, lysophosphatidyl-choline, and oxidized fatty acids induce the expression not only of these adhesion molecules but also of scavenger receptors, such as CD-36, SR-A, and LOX-1. Recently, we isolated and characterized the novel receptors for oxidized LDL, namely, LOX-1 and SR-PSOX. Expression of LOX-1 is found on endothelial cells, smooth muscle cells, and macrophages, whereas SR-PSOX is expressed on macrophages. In this paper the significance of oxidized LDL and its receptors, LOX-1 and SR-PSOX, in terms of atherogenesis is discussed.
Animals↗
Enhancement of phenylephrine-induced contraction in the isolated rat aorta with endothelium by H2O-extract from an Oriental medicinal plant Leonuri herba.
Leonuri herba (I-mu-ts'ao, the Chinese motherwort) is an ancient Chinese traditional herb. Although the pharmacological effects of extracts of Leonuri herba have been shown in platelets and uteri, the effect on the vascular system has not been determined. In the present study, we investigated the effects of extracts of Leonuri herba on the contraction of the isolated rat aorta. Although the H20-extract (0.3-3 mg/ml) by itself showed a limited effect, the extract enhanced phenylephrine-induced contraction of the aorta with endothelium, but not without endothelium. The H20-extract, like N(G)-nitro-L-arginine methyl ester (L-NAME, an inhibitor of nitric oxide synthase), significantly inhibited the relaxation induced by acetylcholine in the aorta with endothelium. The inhibitory effect of H20-extract on the relaxation decreased by co-addition with 1 mM L-arginine. The vasoconstrictive effect of H20-extract was not due to leonurine, which is a constituent in Leonuri herba and shows uterotonic activity. Intravenous injection of the H20-extract (1.5 mg/kg) to rats caused an increase in blood pressure for 5 min, like L-NAME (1.35 mg/kg). These findings suggest that there is a component(s) in Leonuri herba, which shows a vasoconstrictive activity in rat aorta in vitro and in vivo and has similar pharmacological profile to that of L-NAME.
Animals↗
Gastric acid secretion by central injection of dynorphin A-(1-17), an endogenous ligand of kappa-opioid receptor, in urethane-anesthetized rats.
Gastric acid secretion has been proposed to be regulated by opioid receptors in the central nervous system (CNS). Previously, we reported that central injection of synthetic agonists of kappa-opioid receptors stimulated gastric acid secretion in rats, and the secretion by the agonists was inhibited by norbinaltorphimine (an antagonist of kappa-opioid receptor). In the present study, we investigated the effect of dynorphin A-(1-17), an endogenous ligand of kappa-opioid receptor on the gastric acid secretion in the perfused stomach of urethane-anesthetized rats. Injection of dynorphin A-(1-17) (0.1-1 microg per rat) into the lateral cerebroventricle (LV) stimulated the secretion in a dose-dependent manner. The effect of dynorphin A-(1-17) was almost completely inhibited by the LV injection of norbinaltorphimine (10 microg) and in vagotomized rats. Although some studies of dynorphin A-(1-17) after central injection showed non-opioid effects such as the involvement of N-methyl-D-aspartate (NMDA) receptor, the effect of dynorphin A-(1-17) was not inhibited by a selective antagonist of the NMDA receptor ((+/-)-3-(2-carboxypiperazin-4-yl)-1-propylphosphonic acid, 10 microg). The LV injection of naloxone benzoylhydrazone (a kappa3-opioid receptor agonist, 100 microg) also stimulated the secretion in norbinaltorphimine-sensitive manner. These findings showed that both an endogenous ligand dynorphin A-(1-17) and a synthetic kappa3-opioid receptor agonist stimulated gastric acid secretion via kappa-opioid receptors in the CNS of rats in vivo.
Anesthesia↗
[Three cases of small intrapulmonary lymph nodes coincidental with primary lung cancer].
We report three cases of intrapulmonary lymph nodes coincidental with primary lung cancers. In the first case, a 56-year-old man had a small subpleural nodule in the right lower lobe associated with adenocarcinoma of the right upper lobe. The small nodule was 10 mm in diameter and was difficult to differentiate radiologically from intrapulmonary metastasis. Wedge resection of this small nodule was performed. Histologic examination of the nodule revealed an intrapulmonary lymph node with anthracotic pigmentation. A right upper lobectomy for adenocarcinoma was performed, and was completely curative. The second patient, a 77-year-old woman, had adenocarcinoma in the right lower lobe diagnosed by transbronchial biopsy. Computed tomography (CT) revealed a small nodule 5 mm in diameter in the right upper lobe. Histologic examination of the small wedge-resected nodule revealed a lymph node. Lower lobectomy was performed with completely curative results. In the third case, a 63-year-old man was admitted for investigation of a mass shadow in the right upper lobe. CT showed a small nodular shadow in the right middle lobe, confirmed histologically to be lymphoid tissue, in addition to the original mass, which was diagnosed by transbronchial biopsy as squamous cell carcinoma. Upper lobectomy was performed and proved to be curative. Small intrapulmonary lymph nodes are very difficult to diagnose by methods other than surgical resection. When a small intrapulmonary nodule is detected in a patient with primary lung cancer, the presence of an intrapulmonary lymph node must be considered. If radiological characters compatible with an intrapulmonary lymph node are found and there is no other metastasis indicating poor prognosis, it should be considered as a possible indication for surgical resection.
Aged↗
Role of the diurnal variation of urinary pH and urinary calcium in urolithiasis: a study in outpatients.
BACKGROUND: We previously reported that the urinary excretion of calcium and the diurnal variation of urinary pH were important for stone formation in hospitalized inpatients with hospital standard diet. Because almost all urinary stones are formed in outpatients with ambulatory free diet, it is essential to investigate these factors in outpatients. METHODS: We examined the urinary excretion of calcium, oxalate, uric acid, phosphate and magnesium in 96 male outpatients and 142 male inpatients. We also studied the relationship between the stone composition and the diurnal variation of urinary pH in 32 male outpatients (five uric acid stones (UA), 13 pure calcium oxalate stones (CaOX) and 14 mixed calcium oxalate and calcium phosphate stones (CaOX-CaP)) and 53 male inpatients (nine UA, 15 CaOX and 29 CaOX-CaP). RESULTS: There was a significant difference in the urinary excretion of calcium among outpatients with UA, CaOX and CaOX-CaP (133 +/- 96 vs 219 +/- 97 vs 268 +/- 102 mg per day, P < 0.05). In outpatients with UA, urinary pH was constantly low throughout the entire day. In contrast, outpatients with CaOX and those with CaOX-CaP had diurnal variation of urinary pH that was low in the early morning, followed by elevation in the daytime and was lowered in the night. The pHs in the early morning, afternoon and night were significantly higher in outpatients with CaOX-CaP than in those with CaOX. CONCLUSION: The diurnal variation of urinary pH and the urinary calcium are important for stone formation.
Adult↗
[Cytopenia associated with low dose pulse methotrexate in the treatment of rheumatoid arthritis].
OBJECTIVES: To assess the associated risk factors of methotrexate (MTX)-induced cytopenia in rheumatoid arthritis (RA). METHODS: We followed 420 patients started on MTX for RA. We evaluated the frequency and clinical significance of patients with cytopenia related to MTX therapy. RESULTS: The prevalence of patients remaining in the follow-up in the MTX treatment was 21% at 60 months. eighty-seven patients (21%) continued treatment. The treatment termination in MTX was 28% for toxicity, 78 (19%) for no effect, 70 (17%) for relapse and 116 (28%) for toxicity and 69 (16%) for other reasons. A total of 10 patients with cytopenia related to MTX therapy were identified among them. The prevalence of cytopenia, including leukopenia (n = 6), thrombocytopenia (n = 3) and pancytopenia (n = 1), estimated to be 2.4% in MTX treated RA patients. Patients with cytopenia received 2.5-8 mg/w over a mean duration of 60.0 months (10-119 months). nine of 10 patients received NSAIDs with MTX therapy. The presence of renal abnormality (Cr > 1.2 mg/d) was in 3 cases, age over 70 years old in 4 patients, body weight under 50 kg in 8 patients, mean corpuscular volume (MCV) over 100 fl in 2 patients. High MCV value (over 94 fl) was in 7 patients, 6 of whom had some symptoms including fever (n = 3) and oral mucosa/lip abnormalities (n = 3). Low MCV value (under 84 fl) was in 3 patients, who had no symptom but arthralgia and no renal abnormality. And they were younger and received MTX in shorter period than high MCV group. CONCLUSIONS: In patients with high MCV (over 94 fl), most hematological toxicities seen during the course of MTX therapy can be predictable. But, some patients may develop unpredictable hematological reaction. We need to monitor hematological examination frequently and observe patients closely for the appearance of hematological toxicity throughout the presctiption period of MTX irrespective of the duration of treatment.
Adult↗
The immediate early gene 1 product of human cytomegalovirus is sufficient for up-regulation of interleukin-8 gene expression.
We previously observed that human cytomegalovirus (CMV) infection induced a massive production of a chemokine with potent neutrophil chemotactic activity, interleukin-8 (IL-8). Hence, we examined the effect of CMV immediate early (IE) gene products on IL-8 production by the human astrocytoma cell line, U373MG. Transient or stable transfection with a CMV IE1 gene expression vector, but not with a IE2 gene expression vector, significantly augmented IL-8 protein secretion and IL-8 mRNA expression. Luciferase activity was enhanced in U373MG cells when the cells were cotransfected with CMV IE1 and chimeric firefly luciferase reporter genes driven by the transcriptional regulatory region of the human IL-8 gene. Moreover, IE1 gene-mediated enhancement of luciferase activity was abolished by the introduction of mutations into the AP-1 or NF-kappa B factor binding elements in the regulatory region of the IL-8 promoter. Furthermore, electrophoretic mobility shift assays demonstrated that CMV IE1 gene products induced the formation of NF-kappa B or AP-1 complexes. Finally, Western blotting analysis demonstrated that the CMV IE1 gene product increased the amount of NF-kappa B complexes translocated into the nucleus. Collectively, CMV IE1 gene expression may be sufficient to activate AP-1 and NF-kappa B, resulting in IL-8 gene expression.
Base Sequence↗
Changes in expressions of proinflammatory cytokines IL-1beta, TNF-alpha and IL-6 in the brain of senescence accelerated mouse (SAM) P8.
The senescence-accelerated mouse (SAM) is known to be a murine model for accelerated aging. The SAMP8 strain shows age-related deterioration of learning and memory at an earlier age than control mice (SAMR1). In the present study, we investigated the changes in expressions of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in the brain of SAMP8. In the hippocampus of 10 months old SAMP8, the expression of IL-1 mRNA was significantly elevated in comparison with that of SAMR1. In both strains of SAMs, increases in IL-1beta protein in the brain were observed at 10 months of age compared with 2 and 5 months. The only differences found between the strain in protein levels were at 10 months and were elevations in IL-1beta in the hippocampus and hypothalamus, and in TNF-alpha and IL-6 in the cerebral cortex and the hippocampus in SAMP8 as compared with SAMR1. However, lipopolysaccharide-induced increases in the expression of these cytokines in brain did not differ between SAMP8 and SAMR1. Increases in expression of proinflammatory cytokines in the brain may be involved in the age-related neural dysfunction and/or learning deficiency in SAMP8.
Aging↗
Selectively suppressed Ca2+-induced Ca2+ release activity of alpha-ryanodine receptor (alpha-RyR) in frog skeletal muscle sarcoplasmic reticulum: potential distinct modes in Ca2+ release between alpha- and beta-RyR.
We reported earlier that the two ryanodine receptor (RyR) isoforms (alpha- and beta-RyR) purified from frog skeletal muscle were equipotent in the Ca(2+)-induced Ca(2+) release (CICR) activity (Murayama, T., Kurebayashi, N., and Ogawa, Y. (2000) Biophys. J. 78, 1810-1824). Whether this is also the case with the native Ca(2+) release channel in the sarcoplasmic reticulum (SR), however, remains to be determined. Taking advantage of the facts that [(3)H]ryanodine binds only to the open form of the channels and that it is practically irreversible at 4 degrees C, we devised a method to separate the total binding to contributions of alpha- and beta-RyR, using immunoprecipitation with an alpha-RyR-specific monoclonal antibody. Surprisingly, the binding of alpha-RyR was strongly suppressed to as low as approximately 4% that of beta-RyR in the SR vesicles. The two isoforms, however, showed no difference in sensitivity to Ca(2+), adenine nucleotides, or caffeine. This reduced binding of alpha-RyR was ascribed to the low affinity for [(3)H]ryanodine, with no change in the maximal binding sites. Solubilization of SR with 3-[(3-cholamidopropyl) dimethylammonio]-1-propanesulfonic acid partly remedied this nonequivalence, whereas 1 m NaCl was ineffective. 12-kDa FK506-binding protein (FKBP12), however, could not be responsible for it, because FK506 treatment did not eliminate the suppression, in contrast to marked removal of 12-kDa FK506-binding protein from alpha-RyR. These results suggest that alpha-RyR in the SR may serve Ca(2+) release in a mode other than CICR, being selectively suppressed in CICR.
Amino Acid Sequence↗
Metal-to-insulator crossover in the low-temperature normal state of Bi(2)Sr(2-x)La(x)CuO(6+delta).
We measure the normal-state in-plane resistivity of Bi(2)Sr(2-x)La(x)CuO(6+delta) single crystals at low temperatures by suppressing superconductivity with 60 T pulsed magnetic fields. With decreasing hole doping, we observe a crossover from a metallic to an insulating behavior in the low-temperature normal state. This crossover is estimated to occur near 1/8 doping, well inside the underdoped regime, and not at optimum doping as reported for other cuprates. The insulating regime is marked by a logarithmic temperature dependence of the resistivity over two decades of temperature, suggesting that a peculiar charge localization is common to the cuprates.
Journal Article↗
Apoptosis induction by a dopaminergic neurotoxin, 1-methyl-4-phenylpyridinium ion (MPP(+)), and inhibition by epidermal growth factor in GH3 cells.
A dopaminergic neurotoxin, 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP), can induce dopaminergic denervation and Parkinsonism in humans. The active metabolite of MPTP is the 1-methyl-4-phenylpyridinium ion (MPP(+)). Previously we reported that MPP(+) is incorporated via the dopamine transport system and causes delayed cell death in GH3 cells, a clonal strain from the rat anterior pituitary. In this study, we investigated whether MPP(+) induces apoptosis. GH3 cells cultured with MPP(+) exhibited DNA laddering and fragmentation in a time- and concentration-dependent manner. The effect of MPP(+) was inhibited in GH3 cells treated with a pan-caspase inhibitor (100 microM ZVAD-fmk), an antioxidant (25 mM N-acetyl-l-cysteine), or epidermal growth factor (EGF; 50 ng/mL). Because EGF stimulated tyrosine phosphorylation of the EGF receptor and tyrphostin AG1478 [4-(3-chloroanilino)-6,7-dimethoxyquinazoline; 5 microM, a specific inhibitor of EGF receptor kinase] abolished EGF inhibition, involvement of EGF receptor kinase is assumed. Protein kinase C-dependent processes and Bcl-2 protein expression were shown not to be involved in EGF inhibition. MPP(+) increased cytochrome c immunoreactivity in cytosolic fractions in GH3 cells. The addition of 200 microM MPP(+) to isolated mitochondrial fractions from GH3 cells stimulated the release of a 13-kDa protein that cross-reacted with anti-cytochrome c antibody. The release was inhibited in EGF-treated GH3 cells. Our findings demonstrated that (i) MPP(+) induces apoptosis of GH3 cells via cytochrome c release and caspase activation, and (ii) apoptosis by MPP(+) can be blocked by N-acetyl-l-cysteine or EGF treatment.
1-Methyl-4-phenylpyridinium↗