Search PubMed⌕ Search

Biomedical subjects

K Takeda

Publications and source records attributed to K Takeda.

At least 505 records · Page 28Linked to original sources
PubMed1998

Increased lung uptake of iodine-123-MIBG in diabetics with sympathetic nervous dysfunction.

UNLABELLED: Scintigraphy with 123I-MIBG and 201TI was compared in patients with various diseases including diabetes mellitus, with and without sympathetic nervous dysfunction. This study was done to assess lung uptake of these tracers semiquantitatively. METHODS: Thirty-eight patients with diabetes mellitus, seven patients with dilated cardiomyopathy (DCM), 12 patients with hypertrophic cardiomyopathy (HCM) and eight healthy subjects were studied. Sympathetic nervous dysfunction was observed in 13 of the 38 diabetic patients. Simultaneous imaging with 123I-MIBG and 201TI was performed. The ratio of lung to total injected dose count and washout rate in the lung were calculated from dynamic images acquired in the initial 2 min and static images acquired at 15 min and at 4 hr after injection of the tracers. RESULTS: Lung uptake of 123I-MIBG at 4 hr was significantly increased in the diabetic group as compared with those in the other groups. In diabetic patients with sympathetic nervous dysfunction, the lung uptake ratio of 123I-MIBG at 4 hr was significantly higher than that in the diabetic patients without sympathetic nervous dysfunction, due to decreased clearance of 123I-MIBG from the lung. On the other hand, increased lung uptake of 201TI was observed in DCM patients at both 15 min and 4 hr. There was no significant difference between lung uptake of 201TI in diabetic patients and that in healthy subjects. CONCLUSION: Lung uptake of 123I-MIBG was increased and lung washout of 123I-MIBG was decreased in diabetic patients with sympathetic nervous dysfunction, while lung uptake of 201TI was not altered. lodine-123-MIBG scintigraphy of the lung may provide information on sympathetic nervous activity in diabetic patients. It is a promising method for studying the kinetics of norepinephrine in the lung because MIBG is taken up in the lung by the same mechanism as norepinephrine.

3-Iodobenzylguanidine↗
PubMed1998

[Anesthetic management involving difficult intubation in a child with Gaucher disease].

Gaucher disease is the most common of the glycolipid storage disorders caused by the deficiency of glucocerebrosidase, an enzyme which hydrolyzes glucocerebroside to glucose and ceramide. Accumulation of the substrate leads to multiorgan dysfunction involving the brain, spleen, liver, lymph node and bone marrow. In anesthetic management, gastroesophageal reflux leading to recurrent aspiration, pancytopenia and airway difficulties due to trismus, neck extension and upper airway infiltration with glucocerebroside must be considered. We report a case of a 9-year-old boy presenting developmental delay, mild pancytopenia, splenomegary gastroesophageal reflux. He was scheduled for measurement of intra-esophageal pressure, total splenectomy and Nissen fundoplication. Preoperative examination showed trismus and opisthotonic posturing. We predicted difficult airway maintenance and assessed his airway with airway radiograph. Airway narrowing was not shown. For this difficult airway, we made a special mask that has an introducer port for fiberbronchoscope. For the first time, we tried to insert a laryngeal mask, but the insertion was difficult due to trismus and narrowed oral cavity. Then, we used this special mask for the next time. Tracheal intubation was much safer by using this mask for fiberoptic intubation. In Gaucher disease, preoperative assessment of airway difficulties and preparation for this situation are necessary and anesthesiologist must be concerned about aspiration and airway difficulties.

Anesthesia, Inhalation↗
PubMed1998

[Influence of wall thickness on asynergy during exercise two-dimensional echocardiography in patients with old myocardial infarction].

The relationship between left ventricular wall motion worsening (new asynergy; newly developed or worsened asynergy) in the affected part of old myocardial infarction during exercise two-dimensional echocardiography and the wall thickness at diastole was evaluated in 20 patients with more than 51% diameter stenosis in only the infarcted related artery using symptom-limited graded supine bicycle exercise test and two-dimensional echocardiography. End-diastolic wall thickness at normal part of the wall (WtdN) and infarcted parts (WtdI) on the parasternal short-axis view at the papillary muscle level at rest were measured and the wall thickness ratio, WtdI/WtdN x 100(%), was calculated. The rate pressure product at the time when new asynergy appeared and the appearance time of new asynergy after starting exercise were measured in seconds. Mean values for the 20 patients were wall thickness ratio of 75.7 +/- 10.0% (mean +/- SD), new asynergy appearance time of 219 +/- 116 sec after exercise and rate pressure product of 14,209 +/- 2,997 mmHg. beat/min. Smaller wall thickness ratio was associated with lower rate pressure product levels (r = 0.696, p < 0.01) and shorter appearance time of new asynergy (r = 0.772, p < 0.01). There was no significant correlation between the percentage diameter stenosis of the infarct-related artery and appearance time of new asynergy or rate pressure product. New asynergy appeared at a specific infarcted part of the wall, and thinner walls were associated with shorter appearance time of new asynergy with lower rate pressure product levels, regardless of the severity of stenosis of the infarct-related artery.

Adult↗
PubMed1998

Highly selective separation of rhodopsin from bovine rod outer segment membranes using combination of divalent cation and alkyl(thio)glucoside.

The micellization process of bovine rod outer segment (ROS) membranes is investigated utilizing a series of neutral detergents. It is found that when alkyl(thio)glucosides with an appropriate hydrophillic-lipophilic balance (e.g. octylthioglucoside) are used in combination with a divalent cation, rhodopsin is selectively extracted from ROS membranes at a specific detergent-to-membrane ratio. This allows remarkable purification of rhodopsin by a single-step solubilization, because the residual membranes are heavily aggregated in the presence of divalent cation and are therefore easily sedimented by low-speed centrifugation. The absorption spectrum of the supernatant reproducibly exhibits an A280/A500 value of 1.6, an excellent value that could rarely be obtained by chromatographic purification. The degree of purification also depends on the type of divalent cation included in the solubilization solution; specific binding of IIB-series cations (Zn2+ and Cd2+) to ROS membranes is suggested to play an important role in the solubilization process. The present result represents a unique example of selective solubilization of a specific membrane protein from highly aggregated membranes.

Animals↗
PubMed1998

Echocardiographic evaluation in long-term continuous ambulatory peritoneal dialysis compared with the hemodialysis patients.

In dialysis patients, the prevalence of severe left ventricular (LV) hypertrophy and systolic failure, important predictors of cardiovascular morbidity and mortality, has been reported to be very high. Therefore, we investigated cardiac function in 17 long-term CAPD patients (dialysis duration: 76.5 +/- 13.2 months; L-CAPD) by echocardiography and pulsed Doppler, and then compared with 16 short-term CAPD patients (dialysis duration: 28.9 +/- 11.9 months; S-CAPD), 21 long-term hemodialysis patients (dialysis duration: 165.1 +/- 52.7 months; L-HD), and 22 short-term hemodialysis patients (dialysis duration: 71.3 +/- 28.9 months; S-HD), except for the cases with diabetes mellitus, ischemic heart disease, cardiac surgery or overt congestive heart failure. We selected 13 normotensive patients with normal kidney function as normal control group matched for sex and age (Control). Concerning with L-CAPD, S-CAPD, L-HD, and S-HD, these four groups were matched for age and original diseases. We examined blood pressure (BP), cardiothoracic rate (CTR), antihypertensive (AHT) drugs and laboratory data. Wall thickness, left atrium, ventricular chamber size, ejection fraction (EF) and left ventricular mass (LV mass) [Devereux et al. 1986] were measured by echocardiograph. Peak early diastolic flow velocity (E), peak atrial filling velocity (A), A/E ratio and deceleration time of peak early diastolic flow velocity (DT) were calculated by analyzing transmitral flow, recorded by pulsed Doppler. BP control, CTR and EF were significantly worse in L-CAPD than in other patient groups. A/E as one of parameters for cardiac diastolic function was significantly higher in L-CAPD than in HD patients. LVMI (LV mass index: LV mass/body surface area) was significantly higher in L-CAPD than in other groups. LVMI in CAPD patients was shown to be significantly worse as time goes. Volume control by itself without AHT drugs could achieve good BP control in the long-term CAPD patients who were changed to maintenance hemodialysis because of peritoneal sclerosis. We concluded that LV hypertrophy and systolic dysfunction tend to progress in CAPD patients as time goes on. Also it is suggested that the cause of cardiac dysfunction in CAPD patients was mainly based on poor BP control probably due to overhydration, and therefore, appropriate volume control in CAPD patients is especially important.

Antihypertensive Agents↗
PubMed1998

[Assessment of ischemic heart disease by dipyridamole stress electrocardiographic gated myocardial single photon emission computed tomography with technetium-99m tetrofosmin].

Simultaneous assessment of stress perfusion and rest function is possible with gated single photon emission computed tomography (SPECT) using stress injected technetium-99m (99mTc) tetrofosmin (TF). The feasibility of dipyridamole stress electrocardiographic gated myocardial SPECT (GSPECT) with TF was examined as an alternative to conventional stress/rest imaging. Fifty-one patients underwent stress GSPECT. 740 MBq of TF was administered 3 min after dipyridamole infusion. GSPECT acquisition was performed one hour after the injection. Additional rest SPECT was performed on another day only in patients with abnormal perfusion on stress images. Perfusion and thickening were analyzed visually on 17 segments of the left ventricle. Percentage of wall thickening (%WT) was also calculated in 17 segments of the polar map. Thirty-two of 51 patients (63%) had normal stress perfusion and normal rest thickening. Nineteen of 51 patients (37%) had abnormal perfusion on stress images. Among 157 abnormal perfusion segments of the 19 patients, 139 segments (89%) had thickening and the rest (11%) had no thickening. %WT was higher in the reversible segments with or without thickening. There was better agreement for the identification of normal segments and the presence of reversibility between stress GSPECT and the conventional stress/rest study in patients without previous myocardial infarction than in those with previous myocardial infarction (89% vs 79%). These results suggest that stress GSPECT may substitute for conventional stress/rest perfusion study in patients without previous myocardial infarction, allowing shorter examination time and lower cost. However, stress GSPECT does not replace the need for rest perfusion study in patients with previous myocardial infarction, because of underestimation of viability, but %WT may eliminate this underestimation.

Aged↗
PubMed1997

Assembly of the chimeric Na+/K+-ATPase and H+/K+-ATPase beta-subunit with the Na+/K+-ATPase alpha-subunit.

Two sets of chimeric beta-subunits were constructed from subunits of Torpedo californica Na+/K+-ATPase and pig gastric H+/K+-ATPase. Five unique restriction sites (SnaBI, EcoRV, MunI, SphI and EcoT22I) were created at equivalent positions of the respective cDNAs and were used as joining points for the construction. One set of chimeras (HxN series) was made by exchanging the 5' portion of the Na+/K+-ATPase beta-subunit cDNA with the corresponding portion of the H+/K+-ATPase beta-subunit cDNA at the respective joining point. Complementary constructs were also prepared (NxH series). In the HxN series, the chimera joined at the SnaBI site formed a stable trypsin resistant complex with the Na+/K+-ATPase alpha-subunit, which was functional with respect to ATP hydrolysis and pump current generation, although the activities were less than those of the complex with the Na+/K+-ATPase beta-subunit. Trypsin resistance decreased for the complex of the chimera joined at the EcoRV site. In the NxH series, the chimeras joined at the SnaBI site and the EcoRV site formed rather trypsin-resistant complexes, but the expressions of the alpha-subunits were below 50% of the control. The chimeras joined at the MunI, SphI and EcoT22I site formed complexes susceptible to tryptic digestion. None of the chimeras in the NxH series were functional. These results suggest that at least two regions of the Na+/K+-ATPase beta-subunit [SnaBI site(Tyr40) to EcoRV site(Ile89) and EcoT22I site(Cys176) to C-terminus)] are involved in stable assembly with the Na+/K+-ATPase alpha-subunit and that the cytoplasmic domain [N-terminus to SnaBI site(Tyr40)] is functionally replaceable with the corresponding domain of the H+/K+-ATPase beta-subunit.

Amino Acid Sequence↗
PubMed1997

Nonmuscle myosin II-B is required for normal development of the mouse heart.

We used targeted gene disruption in mice to ablate nonmuscle myosin heavy chain B (NMHC-B), one of the two isoforms of nonmuscle myosin II present in all vertebrate cells. Approximately 65% of the NMHC-B-/- embryos died prior to birth, and those that were born suffered from congestive heart failure and died during the first day. No abnormalities were detected in NMHC-B+/- mice. The absence of NMHC-B resulted in a significant increase in the transverse diameters of the cardiac myocytes from 7.8 +/- 1.8 micron (right ventricle) and 7.8 +/- 1.3 micron (left ventricle) in NMHC-B+/+ and B+/- mice to 14.7 +/- 1.1 micron and 13.8 +/- 2.3 micron, respectively, in NMHC-B-/- mice (in both cases, P < 0.001). The increase in size of the cardiac myocytes was seen as early as embryonic day 12.5 (4.5 +/- 0.2 micron for NMHC-B+/+ and B+/- vs. 7. 2 +/- 0.6 micron for NMHC-B-/- mice (P < 0.01)). Six of seven NMHC-B-/- newborn mice analyzed by serial sectioning also showed structural cardiac defects, including a ventricular septal defect, an aortic root that either straddled the defect or originated from the right ventricle, and muscular obstruction to right ventricular outflow. Some of the hearts of NMHC-B-/- mice showed evidence for up-regulation of NMHC-A protein. These studies suggest that nonmuscle myosin II-B is required for normal cardiac myocyte development and that its absence results in structural defects resembling, in part, two common human congenital heart diseases, tetralogy of Fallot and double outlet right ventricle.

Animals↗
PubMed1997

Molecular cloning and characterization of the mouse apoptosis signal-regulating kinase 1.

The mouse cDNA for apoptosis signal-regulating kinase 1 (ASK)1 was isolated. The overall amino acid sequence identity between the mouse and the human ASK1 was 91.9%. A database search revealed that the kinase domain of ASK1 is evolutionally well-conserved over species among nematode, fly, mouse and human. Northern blot analysis identified a 6-kb transcript of ASK1 which is expressed in the various mouse adult tissues including heart, brain, lung, liver and kidney. Immunohistochemical analysis of mouse embryos (17 days post coitum) revealed a localized expression of ASK1 in developing skin, cartilage and bone, suggesting a possible role for ASK1 in tissue development during embryogenesis as well as cytokine-induced apoptosis.

Amino Acid Sequence↗
PubMed1997

Modulation of antigen-induced B and T cell responses by antigen-specific IgE antibodies.

Ag-specific IgE Abs not only mediate immediate hypersensitivity through mast cell activation, but also enhance in vitro Ag presentation and in vivo specific Ab responses in mice. To delineate the role of IgE Ab in the modulation of Ag-specific responses, spleen cells from OVA-sensitized BALB/C mice were cultured together with OVA-specific IgE (or IgG isotypes). OVA-dependent proliferative responses and anti-OVA IgE production were enhanced in the presence of anti-OVA IgE. A significant decrease in IFN-gamma secretion in OVA-stimulated cultures was observed in the presence of anti-OVA IgE, but no changes in IL-4 production were detected. Anti-OVA IgG isotypes or anti-TNP IgE showed no significant effect on any of these Ag-dependent responses. Addition of anti-CD23 Ab abolished these effects of anti-OVA IgE. Further, OVA-sensitized spleen cells from CD23-deficient mice responded to in vitro stimulation with OVA, but demonstrated no modulation by anti-OVA IgE. These results demonstrate that Ag-specific IgE not only augments Ag presentation and T cell proliferation, but also alters the pattern of cytokine production and increases specific IgE synthesis. These modulatory effects of Ag-specific IgE appear to be mediated by binding to Fc epsilon RII/CD23.

Adjuvants, Immunologic↗
PubMed1997

Chemical kindling induced by pentylenetetrazol changes cholecystokinin mRNA and peptide levels in rat frontal cortex.

Kindling model is useful to study the mechanism of learning and memory. Cholecystokinin (CCK) mRNA and CCK-like immunoreactivity (CCK-LI) levels in the hippocampus and frontal cortex of chemically kindled rats were determined at different time points. In the frontal cortex, chronic treatment with pentylenetetrazol (PTZ) (40 mg/kg per day for 8 days) increased CCK mRNA level at 7 days, and decreased CCK-LI level at 2 and 7 days after the last injection. However, neither CCK mRNA nor CCK-LI levels in the hippocampus changed. These results suggest that PTZ-induced kindling increases CCK mRNA expression and CCK-LI release in the frontal cortex.

Animals↗
PubMed1997

Development of eosinophilic airway inflammation and airway hyperresponsiveness in mast cell-deficient mice.

Mast cells are the main effector cells of immediate hypersensitivity and anaphylaxis. Their role in the development of allergen-induced airway hyperresponsiveness (AHR) is controversial and based on indirect evidence. To address these issues, mast cell-deficient mice (W/W v) and their congenic littermates were sensitized to ovalbumin (OVA) by intraperitoneal injection and subsequently challenged with OVA via the airways. Comparison of OVA-specific immunoglobulin E (IgE) levels in the serum and numbers of eosinophils in bronchoalveolar lavage fluid or lung digests showed no differences between the two groups of mice. Further, measurements of airway resistance and dynamic compliance at baseline and after inhalation of methacholine were similar. These data indicate that mast cells or IgE-mast cell activation is not required for the development of eosinophilic inflammation and AHR in mice sensitized to allergen via the intraperitoneal route and challenged via the airways.

Airway Resistance↗
PubMed1997

Requirement of IL-4 and liver NK1+ T cells for concanavalin A-induced hepatic injury in mice.

Con A-induced hepatic injury of mice accompanied by elevated transaminase was inhibited after in vivo depletion of liver NK cells and NK1+ T cells with intermediate TCR by anti-NK1 Ab or anti-IL-2Rbeta Ab. However, depletion of liver NK cells alone by anti-asialo-GM1 Ab did not inhibit hepatic injury. Although depletion of NK1+ T cells inhibited Con A-induced IL-2R expression of CD4+ high TCR (TCRhigh) cells and IL-4 mRNA expression of hepatic mononuclear cells, exogenous IL-4 engendered Con A-induced hepatic injury and endowed the expression of IL-2R of CD4+ TCRhigh cells. It was also found that in vivo treatment with anti-IL-4 Ab before Con A administration inhibited Con A-induced hepatic injury. In addition, although Con A did not induce hepatic injury in MHC class I-deficient mice, exogenous IL-4 again engendered severe hepatic injury in these mice. Further, while serum TNF-alpha levels induced by Con A were greatly decreased in NK1+ T cell-depleted mice and class I-deficient mice, TNF-alpha levels were recovered by exogenous IL-4. These findings reveal that although CD4+ TCRhigh cells in the liver and their production of TNF-alpha are the direct effectors of Con A-induced hepatic injury, liver NK1+ T cells also play an important role in this hepatitis model. Con A hepatitis may serve as an experimental model for human autoimmune hepatitis.

Adjuvants, Immunologic↗
PubMed1997

Respiratory syncytial virus infection results in airway hyperresponsiveness and enhanced airway sensitization to allergen.

Viral respiratory infections can predispose to the development of asthma by mechanisms that are presently undetermined. Using a murine model of respiratory syncytial virus (RSV) infection, acute infection is associated with airway hyperresponsiveness as well as enhanced responses to subsequent sensitization to allergen. We demonstrate that acute viral infection results in increased airway responsiveness to inhaled methacholine and pulmonary neutrophilic and eosinophilic inflammation. This response is associated with predominant production of Th-1-type cytokines in peribronchial lymph node cells in vitro. Mice sensitized to ovalbumin via the airways after RSV infection developed increased airway responsiveness to methacholine and pulmonary eosinophilic and neutrophilic inflammation, associated with the predominant production of Th-2-type cytokines. Treatment of the mice with anti-IL-5 antibody abolished airway hyperresponsiveness and eosinophilic but not neutrophilic inflammation in both acutely infected mice and mice sensitized after infection. We conclude that RSV infection results in airway hyperresponsiveness in the acute phase and leads to changes in immune function that can enhance the effects of airway sensitization to antigen after infection. In both situations, airway hyperresponsiveness is closely associated with pulmonary eosinophilic inflammation. This model provides a means for further analyzing the influence of viral respiratory infections on airway sensitization and the development of altered airway responsiveness.

Allergens↗
PubMed1997

Expansion of an unusual population of Gr-1+CD3int cells in the lymph nodes and other peripheral organs of mice carrying the lpr gene.

Granulocytes and extrathymic T cells are often activated simultaneously, but they are absolutely separate populations in normal mice. However, some abnormal extrathymic T cells (i.e., CD3int cells) seen in mice carrying the lpr gene were found to express a granulocyte marker, Gr-1. Such mice include MRL-lpr/lpr mice and SCG mice. In parallel with an age-associated increase of IL-2Rbeta(low)CD3int cells which contained double-negative CD4-8- and B220+CD2- cells, Gr-1+CD3int cells increased in number in the lymph nodes and other peripheral organs. In addition to a major population of IL-2Rbeta(low)CD3int cells, there is a small population of IL-2Rbeta(high)CD3int cells which produce normal Fas mRNA and Fas molecule from the lpr gene. It was found that both IL-2Rbeta(low)CD3int and IL-2Rbeta(high)CD3int cell populations contained Gr-1+ cells. IL-2Rbeta(high)CD3int cells tended to contain a higher proportion of Gr-1+ cells than did IL-2Rbeta(low)CD3int cells. More interestingly, Gr-1+CD3int cells expressed a considerable level of mRNA of the mG-CSF receptor, similar to granulocytes. The present study thus yielded further information on an unusual property of abnormally expanding CD3int cells in mice carrying the lpr gene.

Aging↗