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Biomedical subjects

K Takeda

Publications and source records attributed to K Takeda.

At least 397 records · Page 22Linked to original sources
PubMed1999

Second lung adenocarcinoma after combination chemotherapy in two patients with primary non-Hodgkin's lymphoma.

We report a rare complication of a secondary malignant solid tumor in two patients with non-Hodgkin's malignant lymphoma who developed lung adenocarcinoma after treatments with combination chemotherapies. The first was a case of primary malignant lymphoma of the cervical spinal cord which had been previously treated with radiation to the spinal lesion and combination chemotherapies and entered complete remission. The patient was further treated for relapse with autologous bone marrow transplantation preconditioned with high-dose chemotherapy. Lung adenocarcinoma developed 5.5 years after the initial diagnosis. The second case of malignant lymphoma of lymph nodes did not respond to conventional combination chemotherapies and did not enter remission. Lung adenocarcinoma developed 1 year after the initial diagnosis. The two patients died of lung carcinoma. The clinical profiles of these cases are presented and the causal relationship of primary malignant neoplasms to the second malignant neoplasms is discussed.

Adenocarcinoma↗
PubMed1999

Genomic structure and expression of the medaka fish homolog of the mammalian guanylyl cyclase B.

We have isolated a 3.9-kbp-long cDNA and approximately 93 kbp long genomic DNA encoding a membrane guanylyl cyclase (designated OlGC1) from the medaka fish Oryzias latipes, and determined their nucleotide sequences. The open reading frame for the OlGC1 cDNA predicts a protein of 1,055 amino acids. Phylogenetic analysis indicates OlGC1 to be a medaka fish homolog of mammalian guanylyl cyclase B (GC-B), a member of the natriuretic peptide receptor family. Northern blot analysis demonstrated 3.9 kb OlGC1 transcripts in the eye and brain, while reverse transcription-polymerase chain reaction (RT-PCR) analysis showed OlGC1 transcripts in a number of adult peripheral organs as well as embryos during early stages of development. The OlGC1 gene consists of 22 exons with an exon/intron organization similar to that of the human and rat GC-A genes, except that OlGC1 has several very large introns. The OlGC1 gene has no apparent TATA box or CAAT box in the region 1.2 kbp upstream of the putative transcription initiation point, but several consensus sequences for cis-regulatory elements, including an NF-IL6-binding element, a shear stress responsive element, and multiple GM-CSF-binding elements, are present in that region.

Amino Acid Sequence↗
PubMed1999

Molecular cloning of cDNA encoding a novel microphthalmia-associated transcription factor isoform with a distinct amino-terminus.

Microphthalmia-associated transcription factor (MITF) is a basic helix-loop-helix-leucine zipper protein, and plays an important role in the development of various cell types, such as neural-crest-derived melanocytes and optic-cup-derived retinal pigment epithelium. Three isoforms of MITF with distinct amino-termini have been described. These include melanocyte lineage-specific MITF-M, heart-type MITF-H, and the recently identified MITF-A. Here we identify a fourth isoform, MITF-C, with a unique amino-terminus of 34 amino acid residues, which shares about 43% sequence identity with putative transactivation segments of two previously identified leukemogenic factors, ENL and AF-9. Reverse transcription-polymerase chain reaction analysis revealed that MITF-C mRNA is expressed in many cell types, including retinal pigment epithelium, but is undetectable in melanocyte-lineage cells. In contrast, MITF-A and MITF-H mRNAs are coexpressed in all cell types examined. Transient cotransfection assays suggested that MITF-C, like other MITF isoforms, functions as a transcriptional activator of certain target genes, but its transactivation specificity for the target promoters is different from those of other MITF isoforms. Therefore, isoform multiplicity provides MITF with differential expression patterns as well as functional diversity.

Amino Acid Sequence↗
PubMed1999

Three-dimensional coronary magnetic resonance angiography with injection of extracellular contrast medium.

RATIONALE AND OBJECTIVES: To evaluate serial changes of the signal intensity and the contrast-to-noise ratios of the coronary arteries on three-dimensional (3D) coronary magnetic resonance angiography (MRA) after an injection of extracellular contrast medium, and to demonstrate the feasibility of this method for the diagnosis of coronary artery abnormalities. METHODS: Five healthy volunteers and two patients with Kawasaki disease and an anomalous coronary artery were studied. Coronary MRAs of the left anterior descending artery and the right coronary artery were obtained using a fat-suppressed 3D MRA sequence before and 0 to 5, 10 to 15, 20 to 25, and 30 to 35 minutes after administration of Gd-DTPA-BMA. RESULTS: Administration of the contrast agent provided a significant increase in the signal intensity and contrast-to-noise ratio. Aneurysm of the left anterior descending artery in Kawasaki disease and the proximal course of the anomalous right coronary artery, which were not well depicted on precontrast 3D MRA, were clearly demonstrated after contrast injection. CONCLUSIONS: The current study demonstrated that the use of an extracellular gadolinium contrast agent can significantly improve the clinical usefulness of 3D coronary MRA.

Adolescent↗
PubMed1999

Sympathetic activation and contribution of genetic factors in hypertension with neurovascular compression of the rostral ventrolateral medulla.

OBJECTIVE: The rostral ventrolateral medulla is an important center for the regulation of sympathetic and cardiovascular activities. Reportedly, neurovascular compression of the rostral ventrolateral medulla may be causally related to essential hypertension. We aimed to determine the mechanism behind elevated blood pressure in hypertensive patients with compression of the rostral ventrolateral medulla and to investigate whether genetic factors contribute to the etiology of hypertension with compression. DESIGN AND METHODS: The study included 56 patients with essential hypertension and 25 normotensive individuals. With the use of magnetic resonance imaging, the essential hypertension group was subdivided into hypertension with compression and without compression groups. We compared plasma levels of hormones that raise blood pressure and family histories of hypertension between the two hypertension groups and the normotension group. RESULTS: Plasma norepinephrine levels, but not plasma renin activity, aldosterone, epinephrine, or vasopressin levels, were significantly higher in the hypertension with compression group (389+/-53 pg/ml) than in the hypertension without compression group (217+/-38, P<0.05) or in the normotension group (225+/-30, P<0.05). The percentage of individuals who had two hypertensive parents was significantly higher in the hypertension with compression group (39.4%) than in the hypertension without compression group (13.0%, P<0.05) or in the normotension group (8.0%, P<0.01). CONCLUSIONS: These results indicate that neurovascular compression of the rostral ventrolateral medulla might be, at least in part, causally related to essential hypertension by increasing sympathetic nerve activity. They also suggest that genetic factors might contribute to the etiology of hypertension with neurovascular compression.

Alleles↗
PubMed1999

Central effects of endothelin and its antagonists on sympathetic and cardiovascular regulation in SHR-SP.

Intracerebroventricular injections of endothelin-1 (ET-1) are reported to cause dose-related increases in sympathetic nerve activity and blood pressure in anesthetized normotensive rats. These studies were performed to determine the following: which endothelin receptor, A or B, is involved in mediating sympathetic and cardiovascular effects of ET-1 injected centrally; whether central endothelin tonically participates in blood pressure regulation in normotensive rats; and whether the altered endothelin system in the central nervous system contributes to blood pressure elevation in hypertensive rats. ET-1, ET-A antagonist (BQ-123), or ET-B antagonist (RES-701-1) was injected into the lateral cerebral ventricle (i.c.v.) of urethane-anesthetized normotensive Wistar and Wistar-Kyoto (WKY) rats, spontaneously hypertensive rats (SHRs), and stroke-prone SHRs (SHR-SPs). In Wistar rats, i.c.v. injections of ET-1 (1, 5, 10 pmol) consistently increased sympathetic nerve activity, thereby elevating blood pressure in a dose-related manner. The pressor responses induced by i.c.v. ET-1 were abolished after intravenous pretreatment with phentolamine. Neither ET-A nor ET-B antagonist, when injected centrally, altered basal levels of sympathetic nerve activity, heart rate, or blood pressure in Wistar rats. However, sympathetic activation and pressor responses induced by i.c.v. injection of endothelin were completely abolished after i.c.v. pretreatment with ET-A antagonist but were unaffected after pretreatment with ET-B antagonist. Although i.c.v. injections of ET-1 increased sympathetic nerve activity and blood pressure in WKY rats, SHRs, and SHR-SPs, the magnitudes of these responses did not differ among these three groups. In contrast, i.c.v. injections of ET-A antagonist decreased sympathetic nerve activity, blood pressure, and heart rate only in SHR-SPs, but not in WKY rats and SHRs. In addition, the depressor effects of i.c.v. ET-A antagonist in SHR-SPs were ascertained while these rats were awake. In summary, i.c.v. injections of ET-1 increased sympathetic nerve activity and blood pressure via ET-A receptors but not via ET-B receptors. Central ET might tonically activate sympathetic nerve activity to thereby contribute to blood pressure elevation in SHR-SPs, but not in WKY rats and SHRs.

Anesthesia↗
PubMed1999

Specific lipid-protein interactions in a novel honeycomb lattice structure of bacteriorhodopsin.

In the purple membrane of Halobacterium salinarium, bacteriorhodopsin trimers are arranged in a hexagonal lattice. When purple membrane sheets are incubated at high temperature with neutral detergent, membrane vesicularization takes place, yielding inside-out vesicles with a diameter of 50 nm. The vesicular structure becomes unstable at low temperature, where successive fusion of the vesicles yields a crystal which is composed of stacked planar membranes. X-ray crystallographic analysis reveals that the bacteriorhodopsin trimers are arranged in a honeycomb lattice in each membrane layer and that neighbouring membranes orient in opposite directions. The native structure of the trimeric unit is preserved in the honeycomb lattice, irrespective of alterations in the in-plane orientation of the trimer. One phospholipid tightly bound to a crevice between monomers in the trimeric unit is suggested to act as a glue in the formation of the trimer.

Bacteriorhodopsins↗
PubMed1999

Role of interleukin-18 (IL-18) in mycobacterial infection in IL-18-gene-disrupted mice.

Immunity to mycobacterial infection is closely linked to the emergence of T cells that secrete cytokines, gamma interferon (IFN-gamma), interleukin-12 (IL-12), and tumor necrosis factor alpha (TNF-alpha), resulting in macrophage activation and recruitment of circulating monocytes to initiate chronic granuloma formation. The cytokine that mediates macrophage activation is IFN-gamma, and, like IL-12, IL-18 was shown to activate Th1 cells and induce IFN-gamma production by these cells. In order to investigate the role of IL-18 in mycobacterial infection, IL-18-deficient mice were infected with Mycobacterium tuberculosis and Mycobacterium bovis BCG Pasteur, and their capacities to control bacterial growth, granuloma formation, cytokine secretion, and NO production were examined. These mice developed marked granulomatous, but not necrotic, lesions in their lungs and spleens. Compared with the levels in wild-type mice, the splenic IFN-gamma levels were low but the IL-12 levels were normal in IL-18-deficient mice. The reduced IFN-gamma production was not secondary to reduced induction of IL-12 production. The levels of NO production by peritoneal macrophages of IL-18-deficient and wild-type mice did not differ significantly. Granulomatous lesion development by IL-18-deficient mice was inhibited significantly by treatment with exogenous recombinant IL-18. Therefore, IL-18 is important for the generation of protective immunity to mycobacteria, and its main function is the induction of IFN-gamma expression.

Animals↗
PubMed1999

Evaluation of a rapid immunochromatographic test for detection of antibodies to human immunodeficiency virus.

A new immunochromatographic rapid test, Determine HIV-1/2, for the detection of antibodies to human immunodeficiency virus type 1 (HIV-1) and HIV-2 in human whole blood, serum, and plasma was evaluated. Determine HIV-1/2 is a sandwich immunoassay and uses a nitrocellulose strip with a capture site for the patient's results and a procedural control site to confirm the validity of the assay. The results can be read visually, and a positive result is indicated by the formation of a red line within 15 min after sample application. The test showed 100% sensitivity for HIV-1 with 102 whole-blood, 152 serum, and 144 plasma samples obtained from Ramathibodi Hospital, Bangkok, Thailand. The sensitivity of the test for HIV-2 was 100% with 100 serum or plasma samples obtained from Ivory Coast. The sensitivity of the test with 4 anti-HIV-1 seroconversion panels from Boston Biomedica Inc. was equivalent to or better than those of another agglutination assay with serum or plasma and the enzyme immunoassay licensed by the U.S. Food and Drug Administration. The specificity was 100% with 367 sets of whole-blood, serum, and plasma samples from Ramathibodi Hospital. This method had an analytical sensitivity for the detection of HIV-1 equivalent to or better than that of another agglutination assay with serum or plasma. This test had an analytical sensitivity for the detection of HIV-1 better than that of another immunochromatographic test with whole blood. This evaluation demonstrated the excellent performance of this immunochromatographic test with EDTA-anticoagulated whole-blood, serum, and plasma samples. We conclude that this test is suitable for use in emerging countries and is an excellent alternative to HIV antibody testing at remote sites, as well as in traditional laboratories.

AIDS Serodiagnosis↗
PubMed1999

The utility of endoscopic ultrasonography and endoscopy in the endoscopic mucosal resection of early gastric cancer.

OBJECTIVE: To clarify the usefulness of endoscopic ultrasonography (EUS) and endoscopy in the endoscopic mucosal resection (EMR) of early gastric cancer. Patients/Methods-EMR was performed in 61 patients with early gastric cancer over the past five years. The accuracy of the assessment of the depth of cancerous invasion was studied in 49 patients who had EUS before EMR. Forty eight patients were treated with endoscopy alone; in these patients, EUS and endoscopic findings correlated with the clinical course. RESULTS: Forty six patients showed no changes in the submucosal layer or deeper structures on EUS. Pathologically these included 37 patients with mucosal cancer and nine with submucosal cancer showing very slight submucosal infiltration. Three patients showed diffuse low echo changes in the submucosal layer on EUS; pathologically, these included two with submucosal cancer and one with mucosal cancer with a peptic ulcer scar within the tumour focus. Of 48 patients receiving endoscopic treatment alone, 45 showed no tumour recurrence or evidence of metastases on EUS and endoscopy. Three cases of recurrence were observed. Two of these patients had a surgical gastrectomy, and one was re-treated endoscopically. In the former cases, the surgical results correlated well with assessment by EUS and endoscopy. In addition, the latter patient who was re-treated endoscopically after evaluation with EUS and endoscopy has so far had no recurrence. CONCLUSION: The combined use of EUS and endoscopy is effective in diagnosing the depth of cancerous invasion in patients undergoing EMR as well as in clarifying changes both within and between anatomic levels during follow up.

Aged↗
PubMed1999

Hypertrophic cardiomyopathy: MR measurement of coronary blood flow and vasodilator flow reserve in patients and healthy subjects.

PURPOSE: To evaluate coronary blood flow per gram of myocardial mass and vasodilator flow reserve in patients with hypertrophic cardiomyopathy (HCM) and in healthy subjects by using breath-hold velocity-encoded cine (VEC) magnetic resonance (MR) imaging. MATERIALS AND METHODS: Twenty-nine patients with HCM and nine healthy volunteers were examined. Fast VEC MR images were obtained in an oblique imaging plane perpendicular to the coronary sinus before and after intravenous injection of dipyridamole (0.56 mg/kg). The products of mean velocity and cross-sectional area of the vessel were integrated to measure blood flow. Breath-hold cine MR images encompassing the entire left ventricle were acquired to quantify the left ventricular mass. RESULTS: In the basal state, the coronary blood flow per gram of myocardial mass was 0.74 mL/min/g +/- 0.23 in healthy subjects and 0.62 mL/min/g +/- 0.27 in patients with HCM. After administration of dipyridamole, coronary blood flow in patients with HCM increased to a level significantly less than that in healthy subjects (1.03 mL/min/g +/- 0.40 vs 2.14 mL/min/g +/- 0.51; P < .01), resulting in a severely depressed flow reserve ratio in patients with HCM compared with that in healthy subjects (1.72 +/- 0.49 vs 3.01 +/- 0.75; P < .01). CONCLUSION: Breath-hold VEC MR imaging is a noninvasive technique for evaluating coronary flow per gram of myocardial mass and coronary flow reserve.

Blood Flow Velocity↗
PubMed1999

Pituitary adenoma showing intermittent secretion of high molecular weight adrenocorticotropin without evidence of Cushing's disease.

A 29-year-old woman was admitted in March 1998 due to high plasma ACTH levels, amenorrhea and uncontrolled diabetes mellitus (DM) which had persisted since 1991. Plasma ACTH levels showed a wide range of changes: they were usually high (59-240 pg/ml), intermittently very high (336-942 pg/ml), and sometimes normal or low. Plasma cortisol levels were usually normal but were sometimes high when the ACTH levels were very high. However, even when the plasma ACTH levels were very high, she did not show any cushingoid features. DM was diagnosed as non-insulin-dependent DM. Plasma ACTH showed an excessive response to CRH, while cortisol showed a delayed response. Plasma cortisol showed a poor response to ACTH-(1-24). ACTH receptor gene analysis revealed no mutations in the ACTH receptor-coding region. MRI showed a nonenhancing mass on the left side of the pituitary. Cavernous sinus sampling showed a very high plasma ACTH level in the left cavernous sinus compared with the levels in the right cavernous sinus and peripheral blood. Sephadex G-75 gel filtration of plasma ACTH immunoreactivity in plasma obtained by cavernous sinus sampling showed mainly high molecular forms of ACTH, probably proopiomelanocortin and ACTH-beta-lipotropin. This case is a very rare form of pituitary adenoma showing intermittent secretion of high molecular ACTH unaccompanied by cushingoid features.

Adenoma↗
PubMed1999

Role of early continuous regional arterial infusion of protease inhibitor and antibiotic in nonsurgical treatment of acute necrotizing pancreatitis.

This paper reviewed our experience with the nonsurgical management of acute necrotizing pancreatitis (ANP) by continuous regional arterial infusion (CRAI) of protease inhibitor (nafamostat mesilate, 240 mg/day) and antibiotic (imipenem, 0.5 g every 12 h). 47 patients with ANP admitted within 7 days were treated with intensive care and CRAI for 5 days prospectively. 40 patients responded to CRAI therapy and the mortality rate in these patients was 2.5%. 7 patients (14. 9%) did not respond to CRAI. 5 of 7 nonresponders died of multiple organ failure although pancreatic necrosis was persistently sterile. The remaining 2 patients who underwent necrosectomy for infected pancreatic necrosis recovered after surgery. In 34 patients treated with CRAI in the early stage within 72 h after the onset, 31 (91.2%) responded. The mortality rate was 5.9% and the incidence of infected pancreatic necrosis was 2.9% in these 34 patients. These results demonstrated that most patients with ANP responded to conservative management combined with CRAI with nafamostat and imipenem when employed within 72 h after the onset. Early intervention of CRAI with protease inhibitor and antibiotic has a significant role in the nonsurgical management of ANP.

Adult↗
PubMed1999

A novel diamino-pyridine derivative prevents excessive leukocyte infiltration in aggravation of acute necrotizing pancreatitis.

Leukocyte infiltration in the pancreas is involved in the aggravation of acute pancreatitis from edematous phase into necrotic change, and mild disease into severe disease; however, the mechanism responsible for leukocyte accumulation is not fully understood. This study was designed to clarify the mechanism underlying leukocyte accumulation into the pancreas and to elucidate the therapeutic efficacy of a novel diamino-pyridine derivative, IS-741 on leukocyte-endothelial cell interaction using rat necrotizing pancreatitis model. The number of adherent leukocytes to pancreatic collecting venules assessed by in vivo fluorescence microscopy increased significantly in necrotizing pancreatitis animals in a time-dependent manner. The expression of CD11b on circulating neutrophils determined by flow cytometric analysis was enhanced to approximately 500% after 2 h. IS-741 attenuated the leukocyte adherence significantly, accompanied by a lower up-regulation of CD11b. These findings were further supported by the histological examination that the accumulation of leukocytes in the pancreas was remarkably inhibited by IS-741. These results suggest that the leukocyte accumulation in the early phase of acute necrotizing pancreatitis may be mediated by leukocyte-endothelial cell interaction via leukocyte integrin CD11b/18. IS-741 attenuated the leukocyte endothelial cell interaction as a consequence of its inhibitory effect on CD11b upregulation.

Animals↗
PubMed1999

Pressor response to compression of the ventrolateral medulla mediated by glutamate receptors.

The rostral ventrolateral medulla (RVLM) is considered a major center for the regulation of sympathetic and cardiovascular activities. Several clinical studies have indicated a possible causal relationship between neurovascular contact of the left RVLM and essential hypertension, and some investigators have suggested that the left RVLM is more sensitive to pulsatile compression than the right RVLM. Previously, we reported that pulsatile compression of the RVLM elevates arterial pressure by enhancing sympathetic outflow in rats; however, we have not investigated the laterality of the responses to the compression. In addition, it remains to be elucidated whether RVLM neurons are activated by compression and, if so, how they are activated. Therefore, we performed compression experiments in rats to investigate these issues. Pulsatile compression was performed on the unilateral RVLM with a pulsating probe in anesthetized and artificially ventilated rats. Pulsatile compression of the unilateral RVLM increased arterial pressure, heart rate, and sympathetic nerve activity. The pressor response to compression was inhibited significantly after local microinjection of glutamate receptor antagonists. Pulsatile compression of the RVLM increased Fos immunoreactivitiy, a marker of neuronal activation, within the nuclei of postsynaptic RVLM neurons. All results were observed symmetrically. The data indicate that the responses to pulsatile compression of the unilateral RVLM are similar on both sides. They also suggest that pulsatile compression of the RVLM increases sympathetic and cardiovascular activities by activating postsynaptic RVLM neurons through the stimulation of the local glutamate receptors in rats.

Animals↗
PubMed1999

Decreases in blood pressure and sympathetic nerve activity by microvascular decompression of the rostral ventrolateral medulla in essential hypertension.

BACKGROUND: Neurovascular compression of the rostral ventrolateral medulla, a major center regulating sympathetic nerve activity, may be causally related to essential hypertension. Microvascular decompression of the rostral ventrolateral medulla decreases elevated blood pressure. CASE DESCRIPTION: A 47-year-old male essential hypertension patient with hemifacial nerve spasms exhibited neurovascular compression of the rostral ventrolateral medulla and facial nerve. Microvascular decompression of the rostral ventrolateral medulla successfully reduced blood pressure and plasma and urine norepinephrine levels, low-frequency to high-frequency ratio obtained by power spectral analysis, and muscle sympathetic nerve activity. CONCLUSIONS: This case suggests not only that reduction in blood pressure by microvascular decompression of the rostral ventrolateral medulla may be mediated by a decrease in sympathetic nerve activity but also that neurovascular compression of this area may be a cause of blood pressure elevation via increased sympathetic nerve activity.

Blood Pressure↗
PubMed1999

Anti-CD86 (B7.2) treatment abolishes allergic airway hyperresponsiveness in mice.

Allergic sensitization in asthma develops as a consequence of complex interactions between T cells and antigen-presenting cells. We have developed several in vivo models to study allergen-specific T cell and B cell function and their relevance to allergic airway hyperresponsiveness (AHR), focusing on the role of the costimulatory molecules CD80 and CD86. Treatment of mice with anti-CD86, but not anti-CD80, significantly inhibited increased serum levels of ovalbumin (OA)-specific IgE and IgG1, airway eosinophilia, and AHR both after 10 d of OA aerosol exposure (in the absence of adjuvant) and after intraperitoneal sensitization followed by repeated airway challenges. Inhibition of AHR was associated with decreased IL-4 and IL-5 levels in the BAL fluid of sensitized mice, suggesting impaired Th2 function in anti-CD86-treated animals. This effect was not seen when mice received treatment only before allergen challenge, indicating that anti-CD86 acts through inhibition of allergic sensitization and not simply by inhibiting the influx of inflammatory cells. These data suggest that the CD86 costimulatory ligand plays a major role in the development of allergic inflammation and AHR in allergen-challenged mice. Further, this study demonstrates that T-B cell interactions during allergic sensitization are amenable to therapeutic manipulation and that selective blockade of accessory signals can be an effective means for modulating distinct T cell functions.

Animals↗