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K Takeda

Publications and source records attributed to K Takeda.

At least 361 records · Page 20Linked to original sources
PubMed1999

Assessment of coronary flow reserve with fast cine phase contrast magnetic resonance imaging: comparison with measurement by Doppler guide wire.

Fast cine phase contrast magnetic resonance imaging (fast cine phase contrast MRI) can measure phasic coronary flow velocity in humans. The purpose of this study was to compare the coronary flow velocity reserves measured by MR IMAGING with those obtained by Doppler guide wire. Nineteen patients with ischemic or valvular heart disease were studied. Fast cine phase contrast MR images of the left anterior descending (LAD) artery were acquired during breath-hold time in the basal state and after administration of dipyridamole. Flow velocity in the LAD artery was also measured with Doppler guide wire before and after venous injection of dipyridamole in all subjects. Flow velocity in the coronary artery measured with MR IMAGING in the basal state (12.5 +/- 4.9 cm/sec) was significantly lower than that obtained with Doppler guide wire (32.4 +/- 12.1 cm/sec, P < 0.01). However, MR assessments of coronary flow velocity reserve showed a good linear correlation with those measured by Doppler guide wire (r = 0.91). In conclusion, fast cine phase contrast MR imaging is a useful technique, which can provide a noninvasive assessment of flow reserve ratios in patients with coronary artery disease. J. Magn. Reson. Imaging 1999;10:563-568.

Blood Flow Velocity↗
PubMed1999

MR measurement of coronary blood flow.

The functional significance of coronary arterial stenosis can be evaluated by measuring the pharmacological flow reserve. Magnetic resonance (MR) imaging has a unique potential for noninvasive measurement of coronary blood flow and flow reserve in the native coronary artery and bypass graft. Restenosis after coronary balloon angioplasty and stenting in the left anterior descending artery can be detected noninvasively with serial MR measurements of the coronary flow reserve. Further refinement of the MR pulse sequences to improve spatial and temporal resolutions may permit accurate quantification of blood flow volume and flow reserve in all major coronary arterial branches. MR assessments of blood flow volume and flow pattern allow noninvasive detection of significant stenosis in the coronary artery bypass graft as well. By integrating MR blood flow measurement in the coronary sinus and cine MR assessment of left ventricular myocardial mass, altered myocardial micro-circulation in patients with diffuse myocardial diseases, such as hypertrophic cardiomyopathy and cardiac transplant, has been documented. J. Magn. Reson. Imaging 1999;10:728-733.

Animals↗
PubMed1999

Structural relationship of lambda-type light chains with AL amyloidosis.

Three human amyloidogenic Bence Jones proteins, NIG76 VlambdaII, NIG204 VlambdaI, and NIG250 VlambdaV, were characterized. In a comparative study, three amino acids, Ser-25a, Thr-68, and Val-95, were found to be common to amyloidogenic proteins of the VlambdaII subgroup. NIG204 had an insertion of Pro residue following position 30 (30a). Proteins having an insertion at this position are invariantly amyloidogenic. NIG250 had a characteristic VlambdaV VL domain, with Mcg+ and KERN+ CL domain isotypes. Following the protein DEL, this is the second example of this subgroup. No common residue is found in the other subgroup proteins but unique substitutions do occur. It would seem that any substitution that causes an alteration in the protein conformation may lead to its being more prone to association with the amyloid processes.

Amino Acid Sequence↗
PubMed1999

Apoptosis in a canine model of acute Chagasic myocarditis.

Histologic, ultrastructural and nick end labeling studies were made to evaluate the occurrence of apoptosis in the hearts of dogs with acute myocarditis due to experimental infection with T. cruzi. The best results for the detection of apoptosis by nick end labeling were obtained by a method combining the use of terminal deoxynucleotidyl transferase, CoCl2 and fluorescein-conjugated deoxyuridine triphosphate, followed by counterstaining of DNA with 4'6-diamidino-2-phenylindole (DAPI) and examination by laser scanning confocal fluorescence microscopy. Apoptosis was found in: (1) cardiac myocytes; (2) endothelial cells of capillaries and venules: (3) immune effector cells, including macrophages, interstitial dendritic cells (antigen-presenting cells) and granular and agranular lymphocytes, and (4) intra- and extracellular forms of T. cruzi. The apoptosis in myocytes and endothelial cells affected cells that were not infected by T. cruzi and was probably caused by the release of toxic mediators of inflammation. The apoptosis of immune effector cells could be related either to the subsidence of inflammation or to modulation (and even failure) of the immune response. The finding of apoptosis in T. cruzi confirms the results of other studies showing that this phenomenon occurs during the differentiation of trypomastigotes in vitro. Thus, apoptosis constitutes an important and multifactorial event in the pathogenesis of acute Chagasic myocarditis.

Animals↗
PubMed1999

Sarcoplasmic reticulum Ca2+ regulatory protein gene expression in human right atrium under hemodynamic overload.

Sarcoplasmic reticulum (SR) Ca2+-adenosine triphosphatase (ATPase) mRNA expression is reduced in the failing human myocardium. However, it is not known whether SR Ca2+-regulatory protein gene expression is altered in human myocardial tissue subjected to pressure overload or volume overload. We sought to determine whether SR Ca2+-regulatory protein gene expression is altered in human atrial tissue subjected to mechanical overload. We obtained right atrial myocardial tissue (about 250mg) at open-heart surgery from three groups of patients: no hemodynamic overload to the right atrium (control group; 12 patients), atrial septal defect (ASD group; 8 patients), and tricuspid regurgitation (TR group; 7 patients). We measured the myocyte size, the area of interstitial fibrosis, SR Ca2+,-ATPase, and ryanodine receptor mRNA abundance. The isolated cardiocyte area and the percent area of interstitial fibrosis were in the order TR > ASD > control (P < 0.05). The SR Ca2+-ATPase mRNA level in TR was significantly decreased (P = 0.004) compared with the control, whereas in the ASD group it did not differ significantly from control. There were no significant differences in ryanodine receptor mRNA levels among the three groups. SR Ca2+-ATPase gene expression was downregulated in human atrial tissue with TR but not in ASD, which might have resulted from the differences in the degree and/or the type of hemodynamic overload to the myocardium.

Adolescent↗
PubMed1999

Expression of mRNA encoding tissue-nonspecific alkaline phosphatase in human dental tissues.

Tissue-nonspecific-type alkaline phosphatase (TNSALP) is found in the bone, liver, kidney, and other tissues, and its gene consists of 12 exons with the coding sequence beginning in the second exon. Recently, a noncoding first exon was identified in the liver message (liver type) which differed from that of the previously known osteoblast-derived cDNA sequence (bone type). Although these two mRNAs produce an identical protein, they have different promoter regions. It is known that ALPs in dental pulp and periodontal ligament are classified into TNSALP by their enzymatic and immunological properties, but little is known about the expression of ALP mRNAs and the transcriptional mechanisms. In order to examine the expression of their mRNA type, specific oligonucleotide primers corresponding to two types of mRNAs of human TNSALP were designed and amplified by reverse transcription-polymerase chain reaction (RT-PCR). It was found that bone-type mRNA was expressed in the human dental tissues such as dental pulp, periodontal ligament, and dental sac, whereas liver-type mRNA was not expressed. Thus, it was concluded that the human dental tissues express the bone-type isozymes and are regulated by the same transcriptional mechanism as in the bone.

Alkaline Phosphatase↗
PubMed1999

Liver transplantation for primary sclerosing cholangitis.

Although the development of interventional radiology and biliary surgical techniques has prolonged the survival time of patients with primary sclerosing cholangitis, liver transplantation remains the only effective treatment for patients with primary sclerosing cholangitis with liver cirrhosis. Several prognostic survival models have been establised for this disease, and the efficacy of actual liver transplantations has been reported in comparison with these survival models. One- and 5-year actuarial patient survivals after liver transplantation for primary sclerosing cholangitis were shown to be greater than and approximately equal to 90%, respectively. An association with cholangiocarcinoma is the most adverse factor affecting survival after liver transplantation for primary sclerosing cholangitis, while the association of inflammatory bowel disease or previous bili-ary surgery does not adversely affect the outcome of the liver transplantation. Recurrent sclerosing cholangitis is an important issue for posttransplant patients with primary sclerosing cholangitis, and occurs in 10%-20% of such patients. Although our understanding of recurrent sclerosing cholangitis is still in the early stages, its potential occurrence indicates the need for a longer follow-up period after liver transplantation.

Bile Duct Neoplasms↗
PubMed1999

Hypophosphorylation of pRB and repression of cyclin D3 and cdc25A during the granulocytic differentiation of human myeloblastic leukemia ML-1 cells.

Recently we succeeded in inducing synergistic differentiation toward granulocytes in human myeloblastic leukemia ML-1 cells by treatment of ATRA in combination with GM-CSF. To research the mechanism of this differentiation process, we examined expression of cell cycle-related genes that are concerned with cell growth and differentiation. We detected change to the hypophosphorylated form of pRB and down-regulation of cyclin D3 and cdc25A during induced differentiation. Furthermore, these marked alterations were hardly detected in ML-1 cells treated with ATRA or GM-CSF alone. These results suggest that hypophosphorylation of pRB and repression of cyclin D3 and cdc25A are induced synergistically by treatment with ATRA plus GM-CSF in ML-1 cells.

Cell Differentiation↗
PubMed1999

Clinical efficacy of portal vein stent placement in patients with hepatocellular carcinoma invading the main portal vein.

BACKGROUND/AIMS: Hepatocellular carcinoma frequently invades the portal veins, and when it invades the main portal vein, the patient's prognosis is extremely poor. This study was undertaken to evaluate the clinical efficacy of stent placement into the portal vein in these patients. METHODS: Twenty-one patients with hepatocellular carcinoma invading the main portal vein were studied. Stents were placed in the portal veins to compress tumor thrombi after percutaneous transhepatic portography. RESULTS: Stents were successfully placed in the portal veins in all patients. Portal venous pressure significantly decreased from 25.3 +/- 7.4 mmHg to 22.4 +/- 6.6 mmHg (p < 0.0001) immediately after stent placement, leading to improvement in gastroesophageal varices, melena and ascites. Although a pseudoaneurysm of the hepatic artery related to portal vein puncture developed in one patient, there were no major complications in the other 20 patients. Blood flow through the stent was maintained during the survival period in 15 patients. The mean stent patency period was 12.4 months. Fifteen patients underwent transcatheter arterial chemoembolization without major complications after stent placement. The survival rate was 64.2% at 6 months and 29.2% at 1 and 2 years, respectively. The mean survival period was 13.7 months. CONCLUSION: Stent placement into the portal vein is a relatively safe and feasible procedure. It improves portal hypertension, expands treatment options, and helps to prolong the survival period in patients with hepatocellular carcinoma invading the main portal vein.

Aged↗
PubMed1999

Fast magnetic resonance imaging of the heart.

Fast MR imaging techniques have multiple applications for evaluation of cardiac disease. Cine MRI and MR tagging have been shown to be highly accurate and reproducible in evaluating regional and global myocardial function. Segmented k-space cine MRI and echo-planar imaging (EPI) can considerably improve time efficiency and thereby the clinical utility of these techniques. Double IR fast spin-echo sequences enable breath-hold acquisition of T2 weighted MRI with good suppression of the blood signal. Myocardial perfusion can be assessed with fast dynamic MRI after administration of contrast media. Multi-shot EPI improves temporal resolution and also provides full coverage of the left ventricle. Substantial progress has been made in respiratory gated 3D coronary artery MR angiography with navigator echoes. The newer approaches for coronary arterial imaging including breath-hold three-dimensional segmented EPI and high resolution spiral MRI may further improve clinical usefulness of coronary MR angiography. Assessment of coronary blood flow and flow reserve with phase contrast MRI has the potential for the non-invasive evaluating of the presence and significance of stenosis in the native coronary artery and bypass grafts. Fast cardiac MRI may emerge as a cost effective modality for comprehensive assessments of both cardiac morphology, function, blood flow and perfusion.

Coronary Circulation↗
PubMed1999

Long-term follow-up arterial chemoembolization combined with transportal ethanol injection used to treat hepatocellular carcinoma.

PURPOSE: This study was undertaken to evaluate the long-term efficacy of transcatheter hepatic arterial chemoembolization (TACE) combined with transportal ethanol injection (TPEI) in patients with hepatocellular carcinoma (HCC). MATERIALS AND METHODS: Twenty-six patients with unresectable HCC underwent TPEI 2-6 weeks after TACE. The size of the main tumor ranged from 2.0 to 9.0 cm (mean, 4.5 cm). Ethanol (10-65 mL) was injected via a percutaneous transhepatic approach into the portal vein, perfusing the segment to be treated. TACE was repeated after TPEI in 18 patients. RESULTS: The combined therapy was technically successfully in all 26 cases; however, irreversible hepatic failure developed in two (8%) patients. Recurrent disease occurred either from the treated lesion (four patients) or apart from the treated liver segment (five patients) in nine of 21 patients (43%) followed up for a mean of 34 months. The survival rates were 87%, 72%, 72%, 63%, 51, and 51% at 1, 2, 3, 4, 5, and 6 years, respectively. Resected and autopsied specimens showed complete necrosis in seven of nine main lesions and severe parenchymal damage in the treated liver segment. CONCLUSION: In selected patients, combined treatment with TACE and TPEI is safe and effective, decreasing recurrence rate in the treated segment, and resulting in a 51% 6-year survival.

Aged↗
PubMed1999

Enhanced Th1 activity and development of chronic enterocolitis in mice devoid of Stat3 in macrophages and neutrophils.

We have generated mice with a cell type-specific disruption of the Stat3 gene in macrophages and neutrophils. The mutant mice are highly susceptible to endotoxin shock with increased production of inflammatory cytokines such as TNF alpha, IL-1, IFN gamma, and IL-6. Endotoxin-induced production of inflammatory cytokines is augmented because the suppressive effects of IL-10 on inflammatory cytokine production from macrophages and neutrophils are completely abolished. The mice show a polarized immune response toward the Th1 type and develop chronic enterocolitis with age. Taken together, Stat3 plays a critical role in deactivation of macrophages and neutrophils mainly exerted by IL-10.

Animals↗
PubMed1999

Unresponsiveness of MyD88-deficient mice to endotoxin.

MyD88 is a general adaptor protein that plays an important role in the Toll/IL-1 receptor family signalings. Recently, Toll-like receptors 2 and 4 (TLR2 and TLR4) have been suggested to be the signaling receptors for lipopolysaccharide (LPS). In this study, we demonstrate that MyD88 knockout mice lack the ability to respond to LPS as measured by shock response, B cell proliferative response, and secretion of cytokines by macrophages and embryonic fibroblasts. However, activation of neither NF-kappaB nor the mitogen-activated protein (MAP) kinase family is abolished in MyD88 knockout mice. These findings demonstrate that signaling via MyD88 is essential for LPS response, but the inability of MyD88 knockout mice to induce LPS-dependent gene expression cannot simply be attributed to lack of the activation of MAP kinases and NF-kappaB.

Adaptor Proteins, Signal Transducing↗
PubMed1999

Caspase-1-independent, Fas/Fas ligand-mediated IL-18 secretion from macrophages causes acute liver injury in mice.

IL-18, produced as a biologically inactive precursor, is processed by caspase-1 in LPS-activated macrophages. Here, we investigated caspase-1-independent processing of IL-18 in Fas ligand (FasL)-stimulated macrophages and its involvement in liver injury. Administration of Propionibacterium acnes (P. acnes) upregulated functional Fas expression on macrophages in an IFNgamma-dependent manner, and these macrophages became competent to secrete mature IL-18 upon stimulation with FasL. This was also the case for caspase-1-deficient mice. Administration of recombinant soluble FasL (rFasL) after P. acnes priming induced comparable elevation of serum IL-18 in parallel with elevated serum liver enzyme levels. However, liver injury was not induced in IL-18-deficient mice after rFasL administration. These results indicate a caspase-1-independent pathway of IL-18 secretion from FasL-stimulated macrophages and its critical involvement in FasL-induced liver injury.

Amino Acid Chloromethyl Ketones↗
PubMed1999

Differential roles of TLR2 and TLR4 in recognition of gram-negative and gram-positive bacterial cell wall components.

Toll-like receptor (TLR) 2 and TLR4 are implicated in the recognition of various bacterial cell wall components, such as lipopolysaccharide (LPS). To investigate in vivo roles of TLR2, we generated TLR2-deficient mice. In contrast to LPS unresponsiveness in TLR4-deficient mice, TLR2-deficient mice responded to LPS to the same extent as wild-type mice. TLR2-deficient macrophages were hyporesponsive to several Gram-positive bacterial cell walls as well as Staphylococcus aureus peptidoglycan. TLR4-deficient macrophages lacked the response to Gram-positive lipoteichoic acids. These results demonstrate that TLR2 and TLR4 recognize different bacterial cell wall components in vivo and TLR2 plays a major role in Gram-positive bacterial recognition.

Animals↗
PubMed1999

In vitro processing of amyloid precursor protein by cathepsin D.

The formation of beta A4 amyloid in the brains of individuals with Alzheimer's disease requires the proteolytic cleavage of amyloid precursor protein. Several lines of evidence suggest that cathepsin D, the major lysosomal/endosomal aspartic protease, may be involved in this process. In this work, we used a sensitive in vitro method of detection to investigate the role of cathepsin D in the proteolytic processing of a 100-amino acid C-terminal fragment (C100) inclusive of beta A4 and cytoplasmic domain of APP. Digestion of C100 with cathepsin D resulted in cleavage at the amyloidogenic gamma-cleavage sites. This occurred preferentially at Thr43-Val44 and at Ala42-Thr43, generating full length beta A4 43 and beta A4 42 amyloid peptides, respectively. Cathepsin D was also found to cleave the substrate at the following nonamyloidogenic sites; Leu34-Met35, Thr48-Leu49 and Leu49-Val50. A high concentration of cathepsin D resulted in cleavage also occurring at Phe19-Phe20, Phe20-Ala21 and Phe93-Phe94 of the C100, suggesting that these sites are somewhat less sensitive to the action of cathepsin D. Digestion of C100 using different solublizing agents indicated that the cleavage of C100 by cathepsin D is greatly influenced by the structural integrity of the substrate. However, our results suggest that cathepsin D could generate the pathogenic beta A4 amyloid peptides from its precursor in vitro, which may indicate a role in the amyloidogenesis of Alzheimer's disease.

Alzheimer Disease↗