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H Takeda

Publications and source records attributed to H Takeda.

At least 397 records · Page 22Linked to original sources
PubMed1994

Beta-adrenergic stimulation disassembles microtubules in neonatal rat cultured cardiomyocytes through intracellular Ca2+ overload.

Catecholamine cardiotoxicity is attributable in part to Ca2+ overload. To test whether the cytoskeletal structures of microtubules in cardiomyocytes are reversibly injured by catecholamine through excessive Ca2+ influx, morphological changes in the microtubules of neonatal rat myocytes were studied by immunohistochemical technique during exposure to norepinephrine (NE). In intact myocytes, microtubules appeared as a filamentous network throughout the cytoplasm and around the nucleus. NE exposure (10 mumol/L) for > 30 minutes elicited microtubular disassembly in a duration-dependent fashion without any irreversible change in sarcomere structure, and this abnormality recovered within 24 hours after cessation of stimulation. Microtubular disruption scores obtained by semiquantitative assessment were significantly increased in a dose-dependent manner (10.8 +/- 4.0 in the control condition, 23.4 +/- 4.7 at 60 minutes with 10 mumol/L NE), whereas they were significantly attenuated by pretreatment with propranolol (100 mumol/L; score, 11.8 +/- 3.3) but not with phentolamine (100 mumol/L; score, 26.4 +/- 4.8). Isoproterenol (1 mumol/L) and denopamine (10 mumol/L) mimicked the effects of NE, but phenylephrine did not, indicating that NE-induced microtubular disassembly is mediated by beta 1-adrenergic receptor stimulation. This beta-adrenergic receptor-mediated insult was significantly attenuated by a decrease in Ca2+ concentration in the medium from 2 to 0.5 mmol/L and by pretreatment with diltiazem (1 mumol/L). In contrast, microtubular disassembly was induced by an increase in Ca2+ concentration in the medium and an administration of the Ca2+ ionophore A23187, even without beta-adrenergic receptor stimulation. Involvement of intracellular hypoxia and activation of Ca(2+)-calmodulin-dependent kinase or Ca(2+)-dependent neutral protease were excluded from possible mechanisms; however, inhibition of tubulin polymerization by excessive Ca2+ influx during beta-adrenergic receptor stimulation may be primarily involved. We conclude that microtubular structures that support cellular integrity are reversibly injured by beta-adrenergic receptor stimulation through excessive Ca2+ influx.

Adrenergic beta-Agonists↗
PubMed1994

A characteristic change in ventilation mode during exertional dyspnea in patients with chronic heart failure.

Although exertional dyspnea is an important symptom limiting daily lives in patients with chronic heart failure, there is no objective assessment of this symptom. To characterize the exertional dyspnea, ventilatory responses to exercise were studied in relation to exertional dyspnea. Gas exchange data were obtained during a maximal bicycle exercise in 43 patients with chronic heart failure and 20 normal subjects. In addition to standard ventilatory variables, the ventilation mode was assessed from the tidal volume-ventilation rate (VT-f) relationship. The exercise was performed again after sublingual administration of 5 mg of isosorbide dinitrate. In normal subjects, the f and VT increased almost proportionally with exercise intensity. In 17 (85 percent) of 20 patients with exertional dyspnea, the VT-f relationship abruptly lost linearity at the onset of exertional dyspnea. This change resulted from an inadequate increase in VT and a further increase in f. In 8 of these 17 patients, isosorbide dinitrate improved exertional dyspnea with normalization of the VT-f relationship; however, in 9 patients whose dyspnea was not improved, the abnormal VT-f relationship was unaltered. Only 2 (9 percent) of 23 patients without exertional dyspnea showed the abnormal VT-f relationship. Other ventilatory variables were not different between patients with and without dyspnea. Thus, exertional dyspnea is characterized by simultaneous appearance of rapid and shallow ventilation. The VT-f relationship appears to be a simple and useful objective assessment of exertional dyspnea in patients with chronic heart failure.

Dyspnea↗
PubMed1994

[Influence of physical responses due to controlled frequency breathing during exercise].

The purpose of this study was to examine the influence of respiratory responses due to controlled frequency breathing (CFB) during steady state cycle ergometric exercise (50% of Peak VO2, 60rpm) and to compare their responses between long distance (L), badminton (B), Swimming (S) and untrained (C; Control) group. Twenty-two (n = 6; L, B, C.n = 4; S) female university students were forced to take CFB for 1 min every 3 min during 20 min exercise. The breathing frequencies (BR) were 10, 12, 15, 20 and 30 frequencies in a minute. They were represented by CFB10, CFB12, CFB15, CFB20 and CFB30 respectively. In addition, CFB5, and 40 were given in a separate series. Ventiratory volume (VE) decreased significantly, (P < 0.05) when BR decreased less than about 50% of normal breathing (NB), CFB15 in (B) and (C). It showed to be less than CFB12 in (S), and CFB10 in (L). According to the decrease of VE, tidal volume and O2 pulse increased during CFB10 and 15 in all groups to maintain a constant O2 consumption for a given workload. End tidal partial pressure of O2 (PETO2) significantly decreased during less than CFB15 in (B) and (C), during CFB10 in (L). PETCO2 increased during less than CFB15 in (B), less than CFB12 in (L) and (C). However in (S) during every CFB, neither PETO2 nor PETCO2 changed significantly. Talking about the main differences shown between the four groups, (S) and (L) significantly exceeded (C) in maintaining of VE during CFB. However, in consideration of a ratio of the frequency of CFB to that of NB, (L) could maintain VE against more strictly controlled of breathing than other groups. (B) showed similar tendencies as (C) about some responses. It is considered that these differences in respiratory responses to CFB may result from difference of the duration and the level of breathing control that were forced during their daily training rather than whether their breathing frequency during each exercise is high or low.

Adult↗
PubMed1994

Mechanisms of CBF augmentation during hypoxia in cats: probable participation of prostacyclin, nitric oxide and adenosine.

To elucidate the mechanisms of CBF augmentation during hypoxemic hypoxia, we applied continuous monitoring of CBF and metabolism to examine the participation of prostacyclin, nitric oxide (NO), and/or adenosine in these mechanisms. Cats (n = 32) were anesthetized and ventilated artificially. Cerebrovascular reactivity to hypoxia was assessed by changes in CBF, brain tissue oxygen and carbon dioxide tensions, and mean arterial blood pressure (delta CBF, delta BrPO2, delta BrPCO2, and delta MABP) during a 3-min inhalation of 10% O2 + 90% N2 before and after the intracarotid administration of (1) indomethacin (1 mg/kg, a cyclooxygenase inhibitor, n = 11), (2) L-NG-monomethyl-arginine (LNMMA, 1 mumol/kg/min, an inhibitor of nitric oxide synthesis, n = 11), and (3) caffeine (20 mg/kg, an adenosine antagonist, n = 10). BrPO2 decreased significantly in all groups during the produced hypoxemic hypoxia. CBF significantly increased in this state before the administration of indomethacin, LNMMA, or caffeine, whereas it contrastively did not significantly increase after the administration of indomethacin or caffeine. In addition, CBF significantly decreased under hypoxia during the administration of LNMMA. Taken together, these results suggest that prostacyclin (PGI2), nitric oxide (NO), and adenosine may jointly participate in CBF augmentation during hypoxia.

Adenosine↗
PubMed1994

[Clinical results of percutaneous pyeloplasty for ureteropelvic junction obstruction: 5 years follow-up].

We performed percutaneous endopyeloplasty on 20 patients between February, 1988 and July, 1993. Eighteen patients had primary and two had secondary ureteropelvic junction (UPJ) obstructions. There were 15 female and 5 male patients, whose ages ranged from 14 to 77, with an average of 43.6. The length of the follow-up after pyeloplasty ranged from 4 to 69 months with an average of 28.7 months. Among the 20 patients, there were 4 high insertion type cases, a bifid renal pelvis in one case and one case combined with a renal stone. Incisions were made with a hook-shaped cold knife and Ono's transpelvic extraureteral approach was used in most patients. Catheters were placed at the upper and the lower of renal pelvis in the patient with a bifid renal pelvis. In the case with a renal stone, pyeloplasty was successively performed after percutaneous nephrolithotomy in a single session. An endopyelotomy stent (14 Fr) was indwelled for 6 weeks in all patients except one. All patients had a low grade fever and abdominal pain for a few days after their operations, but there were no major complications. In nineteen patients (95%), the symptoms improved and their obstructive patterns disappeared or improved during follow-up. Complete ureteral stricture was found in one case at the removal of the stent and open pyeloplasty was performed. Percutaneous endopyeloplasty is a safe and useful technique, but further evaluation and/or better techniques are needed for avoiding recurrence of obstruction.

Adolescent↗
PubMed1994

[Bacterial adhesion and biofilm].

Specific and non-specific adhesion of bacteria to tissue were described. In today, non-specific absorption of bacteria and tissue will be well understood by DLVO-theory in colloidal chemistry. After the adhesion, glycocalyx was produced from the adhesive bacteria around their bodies, under the condition of a weak interaction with host cells. Each bacterium aggregate with approximate bacterium through glycocalyx and then bacterial biofilm is formed on the surface of tissue or surface of medical devices that is entered in living bodies. Bacterial biofilm has strong resistance for attack of antimicrobial agents, phagocytes and immunoglobulin. Clinical characteristic of biofilm diseases is intractable and infectious repeating, because the sessile bacteria are often released from bacterial biofilm and they often cause infection.

Animals↗
PubMed1993

Simultaneous determination of bile acids in rat bile and serum by high-performance liquid chromatography.

A method for the simultaneous determination of bile acids in rat bile and serum by high-performance liquid chromatography with a post-column enzymic reaction and fluorescence detection has been developed. Without prior fractionation and alkaline hydrolysis, 26 unconjugated, glycine- and taurine-conjugated bile acids were determined. They were separated on a reversed-phase column using a linear gradient solvent system of 200 mM dibasic ammonium phosphate buffer (pH 7.9)-acetonitrile-methanol (73:19:8, v/v/v) and 20 mM dibasic ammonium phosphate buffer (pH 7.9)-acetonitrile-methanol (2:1:2, v/v/v). The limits of detection were 1-5 pmol, and calibration curves were linear for concentrations between 10 and 4000 pmol. This rapid and reliable method is effective for measuring bile acid levels in the bile and serum not only of rats but also of patients with hepatobiliary and other diseases.

Animals↗
PubMed1993

[CT findings of invaginated mesentery in adult intussusception].

The CT findings of invaginated mesentery in adult intussusception were analyzed in 12 patients (three patients with four small bowel intussusceptions and nine patients with nine large bowel intussusceptions). In all small bowel intussusceptions, the neck was located near the superior mesenteric artery and vein (SMA & SMV) and showed a medial opening, and the vessels in the neck showed a continuity to the left side of SMA & SMV. In most of the large bowel intussusceptions, the neck was located distant from SMA & SMV, and the vessels in the neck did not show continuity to SMA & SMV. The difference in CT findings between small and large bowel intussusception is attributed to the difference in mesenteric anatomy; the small bowel and its mesentery move freely in the peritoneal cavity, whereas the large bowel is partially fixed to the retroperitoneum.

Adult↗
PubMed1993

Constitutive activation of Src family kinases in mouse embryos that lack Csk.

Csk is a novel cytoplasmic protein-tyrosine kinase that has been shown to inactivate members of the Src family of protein-tyrosine kinases in vitro. To examine the function of Csk in vivo, Csk-deficient mouse embryos were generated by gene targeting in embryonic stem cells. These embryos were developmentally arrested at the 10 to 12 somite stage and exhibited growth retardation and necrosis in the neural tissues. The kinase activity of p60c-src, p59fyn, and p53/56lyn in these embryos was greatly enhanced as an apparent consequence of enhanced specific activity. The increase in kinase activity was associated with an increase in tyrosine phosphorylation of several proteins, especially those around 85 and 120 kd. Thus, these results suggest that Csk indeed acts as an indispensable negative regulator of Src family kinases in vivo.

Animals↗
PubMed1993

Cytosolic free magnesium concentration in human platelets.

Although the magnesium ion (Mg2+) is considered to play an important role in cell activation, information is limited by the lack of suitable methods for measuring cytosolic free Mg2+ concentration ([Mg2+]i). We measured [Mg2+]i in resting and activated human platelets using a new fluorescent Mg(2+)-indicator, mag-fura-2. [Mg2+]i was 0.54 +/- 0.14 mM in resting platelets from 15 healthy volunteers. [Mg2+]i was elevated to 1.33 +/- 0.44 mM and 0.92 +/- 0.37 mM in platelets stimulated with thrombin and collagen, respectively. Increased Mg2+ was considered to be derived chiefly from intracellular Mg2+ mobilization. These results suggest that platelet activation is associated with the increase in [Mg2+]i. The estimation of [Mg2+]i using this method is useful for the investigation of mechanism for various cell activation.

Blood Platelets↗
PubMed1993

Liver scintigraphy in a patient with Gaucher disease.

Liver scintigraphy including SPECT was performed in a patient with Gaucher disease and compared with other methods. Multiple photon-deficient areas in the liver and spleen were recognized, and in evaluating the reticuloendothelial system of the liver, liver SPECT image was superior to US, CT and MR images.

Adult↗
PubMed1993

99mTc-HMDP accumulation in a phyllodes tumor of the breast, a case report.

In a patient with breast tumor, 99mTc-HMDP accumulation in the tumor was recognized in evaluating bone metastasis. Surgery and histopathology revealed that the tumor was a phyllodes tumor. This scintigraphic finding was thought to be rare and phyllodes tumor should be included in differential diagnosis when 99mTc-HMDP accumulation in the breast was recognized.

Breast Neoplasms↗
PubMed1993

Acetyl-low density lipoprotein receptors on rat mesangial cells.

To elucidate whether mesangial cells have any scavenger functions for modified lipoproteins, surface binding and cholesteryl ester (CE) formation by acetyl-low density lipoproteins (acetyl-LDL) have been studied in cultured rat renal mesangial cells. Specific binding kinetics for acetyl-LDL were observed with Kd = 28.3 micrograms/ml and Bmax = 1.1 ng/micrograms cell protein at 0 degrees C. The fluorescence microscopic finding demonstrated the enhanced uptake of DiI-acetyl-LDL in mesangial cells. Incorporation of [14C]oleate into CE was enhanced to 6-fold by loading 30 micrograms/ml of acetyl-LDL on 10 micrograms/ml of [14C]oleate-bovine serum albumin conjugate as compared with the control without lipoproteins (P < 0.05). The CE formation was completely inhibited by chloroquine. The light microscopic finding demonstrated the increased CE deposition by acetyl-LDL, resulting in foam cell formation. These results indicate biochemically and morphologically that the mesangial cells take up acetyl-LDL by receptor-mediated endocytosis, and that cholesterols in acetyl-LDL are converted to CE, resulting in an increased cellular cholesterol content. In conclusion, mesangial cells may have a scavenger function similar to macrophages.

Animals↗
PubMed1993

Transient cerebral vasodilatory effect of neuropeptide Y mediated by nitric oxide.

The effects of intracarotidly injected neuropeptide Y (NPY; 0.1 micrograms/kg) on the local cerebral blood volume (CBV) and blood flow (CBF) in the parieto-temporal cortex were examined by the photoelectric method in 17 anesthetized cats. CBV reflects the cumulative crosssectional area of the cerebral microvascular beds. NPY immediately caused transient but significant increases in CBV and CBF, which lasted for less than 5 min. Thereafter, CBV returned to and remained at the control level, although CBF was decreased by 30-40% for 60 min during the monitoring period. The CBV increases after NPY were prevented by a 15-min preinjection of 0.35 mg/kg/min of NG-monomethyl-L-arginine (L-NMMA), which is a competitive blocker of nitric oxide synthesis. The CBV increases after NPY reappeared following a 15-min administration of 0.25 mg/kg/min of L-arginine, which is a precursor of nitric oxide. We conclude that NPY administered in vivo exerts a previously unreported effect of transient vasodilatation on the cerebral microvessels. This action appears to be mediated by nitric oxide, which is a major candidate as an endothelium-derived relaxing factor (EDRF).

Animals↗
PubMed1993

The mechanisms of aspirin-induced gastric mucosal injury.

We examined changes in intracellular pH with the fluorescent probe BCECF after treatment with aspirin (ASA) in gastric mucosal cells isolated from guinea pigs at various extracellular, pH levels. The cytotoxic activities of ASA and the intracellular trapping of ASA at various extracellular pH levels were also examined by colorimetric MTT assay and counting the influx of [14C](carboxyl-14C)-ASA. Under acid extracellular pH, ASA reduced intracellular pH in gastric mucosal cells and exhibited cytotoxicity. Intracellular trapping of ASA was also observed only under acidic extracellular conditions. The present study suggests that ASA causes gastric mucosal cell injury in vitro by reducing intracellular pH, resulting from intracellular trapping of ASA under acidic extracellular conditions.

Animals↗
PubMed1993

A functional in vitro model for studying the cellular and molecular basis of spinal cord injury.

Very little is understood about how spinal cord injury affects the molecular mechanisms responsible for generating locomotion. Recently, it has been shown in the spinal cord that the N-methyl-D-aspartate receptor, a specific class of excitatory amino acid receptors, plays a major role in the neurogenesis of locomotion. Paradoxically, studies of the brain and the spinal cord have shown that overeactivation of this receptor can cause excitotoxicity and subsequent cell death. The ultimate goal of these experiments was to develop an isolated brain stem/spinal cord/hind limb preparation that would allow study of issues related to excitotoxicity and the neurogenesis of locomotion. Findings indicate that: 1) exposure of the spinal cord to the excitatory amino acids produced an alternating gate of the hind limbs; 2) application of N-methyl-D-aspartate inhibitors were effective in preventing hind limb movement initiated by exposure to N-methyl-D-aspartate; 3) sensorimotor stimulation of the tail produced hind limb movement that could be evoked for periods up to 8 hours; and 4) an excitotoxic event produced substantial loss of protein and possible osmotic changes. This study represents the first step in developing a powerful model for examining the effect of spinal cord injury on molecular mechanisms responsible for the neurogenesis of locomotion both at the brain stem, spinal motor generator, or sensorimotor level. The opportunity of observing hind limb movement in this preparation represents a powerful functional bioassay for evaluating the extent of spinal cord injury.

Animals↗