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Biomedical subjects

T Takeda

Publications and source records attributed to T Takeda.

At least 739 records · Page 41Linked to original sources
PubMed1992

Effects of arginine vasopressin, angiotensin II and endothelin-1 on the release of brain natriuretic peptide in vivo and in vitro.

1. The stimulatory effects of the vasoactive peptides arginine vasopressin (AVP), angiotensin II (AII) and endothelin-1 (ET-1) on the release of brain natriuretic peptide (BNP) were investigated in anaesthetized rats and in cultured rat atrial and ventricular cardiocytes. 2. A bolus injection of AVP induced a dose-dependent increase in plasma immunoreactive (ir)-BNP concentration in rats. AII induced a rapid and transient elevation in the ir-BNP level, while the increase produced by ET-1 was long-lasting. The elevation of the plasma ir-BNP concentration after stimulation by these three vasoconstrictors appeared to be paralleled by the elevation in mean blood pressure. 3. In the in vitro study, the rat atrial and ventricular cardiocytes both secreted ir-BNP into the medium in a time-dependent manner. ET-1 clearly stimulated the secretion of ir-BNP in both atrial and ventricular cardiocytes. In contrast, AVP and AII had no stimulatory effect in vitro. 4. Reverse-phase high performance liquid chromatography of the rat plasma and culture medium revealed a single major ir-BNP component that corresponded to synthetic rat BNP-45. 5. These observations indicate that AVP, AII and ET-1 stimulate the release of ir-BNP (probably rat BNP-45) through a change in blood pressure. In addition, ET-1 may also induce ir-BNP release through direct stimulation. As a cardiac hormone secreted from ventricles as well as atria, rat BNP may play a role in the regulation of blood pressure against the pressor effects of AVP, AII and ET-1.

Anesthesia↗
PubMed1992

Reassessment of the prevalence of heat-stable enterotoxin (NAG-ST) among environmental Vibrio cholerae non-O1 strains isolated from Calcutta, India, by using a NAG-ST DNA probe.

A collection of 521 environmental isolates of Vibrio cholerae which were previously examined by the suckling mouse assay and found to be negative for the heat-stable enterotoxin NAG-ST were reassessed by a recently developed DNA probe for NAG-ST. A total of 12 (2.3%) of the isolates hybridized with the NAG-ST probe. By using a cholera toxin (CT) DNA probe, the CT gene was detected in six of the strains in the collection, although none of the isolates of V. cholerae non-O1 hybridized with both of the toxin probes. All of the NAG-ST and CT probe-positive strains were hemolysin positive. Thirty-fold-concentrated supernatants of the three representative NAG-ST DNA probe-positive V. cholerae non-O1 strains gave positive fluid accumulation ratios in the suckling mouse assay even after heating (100 degrees C for 5 min) and also inhibited the binding of a NAG-ST monoclonal antibody to the bound NAG-ST in a competitive enzyme-linked immunosorbent assay (ELISA). Likewise, all six CT probe-positive V. cholerae non-O1 strains produced in vitro CT when examined by the CT bead ELISA. HindIII digest patterns of chromosomal DNA from the representative NAG-ST gene-positive strains were visually indistinguishable. Between the groups of NAG-ST probe-positive strains examined, there was a variation in the hybridizable fragments, with one group of strains exhibiting a hybridizable fragment similar to that of the NRT 36 reference strain; a smaller HindIII fragment hybridized with the NAG-ST probe in the other group of strains.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Evaluation of the bead enzyme-linked immunosorbent assay for detection of cholera toxin directly from stool specimens.

A highly sensitive bead enzyme-linked immunosorbent assay (bead ELISA) for detection of cholera toxin (CT) was evaluated for direct detection of CT from stool specimens of patients with acute secretory diarrhea. Of the 75 stool samples examined, 59 yielded biochemically, and serologically confirmed strains of Vibrio cholerae O1. The bead ELISA was positive for CT in stool supernatants in 50 (84.7%) of the 59 samples from which V. cholerae O1 was isolated. In addition, the bead ELISA was positive for three stool specimens which were negative by culture. The free CT present in 48 of the 50 stool samples positive by culture for V. cholerae O1 and for CT by bead ELISA was completely absorbed by anti-CT immunoglobulin G. All of the 59 strains of V. cholerae O1 biotype eltor isolated in this study produced in vitro CT. The concentration of CT present in the bead ELISA-positive stool samples ranged between 26 pg/ml and greater than 100 ng/ml. This evaluation study demonstrates that the bead ELISA is a sensitive and simple method for direct detection of CT in nonsterile stool samples, and we recommend routine use of this assay for detection of CT in stool samples and culture supernatants in clinical and reference laboratories.

Cholera Toxin↗
PubMed1992

Effect of heparin on pulmonary fibroblasts and vascular cells.

BACKGROUND: There is a large increase in mast cell numbers in fibrotic lung tissue, suggesting that mast cells may play a part in the pathogenesis of pulmonary fibrosis. Glycosaminoglycans, such as heparan sulphate, that are structurally related to heparin (a mast cell product) are part of the extracellular matrix and known to regulate cell growth. Basic fibroblast growth factor is a heparin binding growth factor produced by endothelial cells. METHODS: A study was carried out to examine the effect of heparin, basic fibroblast growth factor, and mast cell products on the proliferation of normal human lung fibroblasts and the effect of adding heparin on the proliferation of lung fibroblasts and pulmonary vascular cells incubated with basic fibroblast growth factor. RESULTS: Heparin at low concentration (0.03, 0.3-1.0 micrograms/ml) stimulated the proliferation of normal human lung fibroblasts in culture whereas a higher concentration (100 micrograms/ml) had an inhibitory effect. Mast cell products also stimulated the proliferation of fibroblasts, and the effect was decreased by pretreatment with heparinase or protamine. Heparin enhanced the growth of both fibroblasts and pulmonary vascular cells induced by low concentrations of basic fibroblast growth factor. CONCLUSIONS: Mast cells in fibrotic lung tissue may regulate fibroblast proliferation by releasing heparin. These results suggest that endothelial cells may interact with mast cells and modulate fibroblast growth by release of basic fibroblast growth factor.

Animals↗
PubMed1992

Heparin suppresses endothelin-1 action and production in spontaneously hypertensive rats.

Previous studies have shown that chronic subcutaneous administration of heparin significantly reduces blood pressure in hypertensive rats. The intracellular mechanisms of how heparin prevents smooth muscle cell proliferation remain unclear. This study was designed to examine whether heparin affects endothelin-1 action and production, to further elucidate the mechanism of the antihypertensive effect of heparin. Four-week treatment with heparin (300 U/day sc) significantly decreased blood pressure in spontaneously hypertensive rats (SHR; 199 +/- 8 vs. 164 +/- 9 mmHg; P < 0.001) and completely blunted pressor response to endothelin-1 in SHR. Heparin treatment did not decrease blood pressure response nor did it attenuate blood pressure responses to endothelin-1 in Wistar-Kyoto rats (WKY). Heparin significantly suppressed endothelin-1-induced increase in intracellular calcium concentration and inositol 1,4,5-trisphosphate level in cultured vascular smooth muscle cells in a dose-dependent manner and endothelin-1 release from cultured endothelial cells. These inhibitions were significantly more pronounced in SHR than in WKY. In conclusion, our findings indicate that the antihypertensive effect of heparin is mediated, at least in part, by the inhibition of endothelin-1 action on vascular smooth muscle cells and endothelin-1 production from endothelial cells.

Animals↗
PubMed1992

Radiolucent bone cysts and the type of dialysis membrane used in patients undergoing long-term hemodialysis.

The relationship between the types of dialysis membrane used and the prevalence and severity of radiolucent bone cysts (which are a main radiological feature of dialysis amyloidosis) was studied in 30 patients on hemodialysis for more than 10 years. One of them was treated exclusively with cuprophane; the other 29 were dialyzed with cuprophane, and then treated with polyacrylonitrile AN 69. In 12 of the 30 patients, radiolucent bone cysts (at least 5 mm in diameter in the wrists and at least 10 mm in the shoulders or hips) were observed. The patients with bone cysts spent significantly more time on cuprophane dialysis and significantly less time on AN 69 dialysis than the group of patients without bone cysts. Nine of the 14 patients who had been treated with cuprophane for more than 8 years had bone cysts; whereas bone cysts were observed in only 2 of the 12 patients dialyzed for more than 8 years with AN 69. The frequency of bone cysts was significantly different for each of the two groups. There was, however, no significant difference in the total duration of dialysis between the two groups. The severity of the cystic bone lesions correlated positively with the duration of dialysis using cuprophane and negatively with the duration of dialysis using AN 69. These findings suggest that the development of osteoarticular amyloidosis may be related to the type of dialysis membrane used. Hemodialysis using AN 69 membranes may prevent, or at least postpone the development of dialysis amyloidosis.

Bone Diseases↗
PubMed1992

Pathogenesis of widened AP-SP complex in cases of cerebellopontine angle tumors.

Pathogenesis of widened AP-SP complexes often noted in electrocochleograms (ECochGs) in cases of cerebellopontine angle tumors remains unclear. As acoustic neuromas usually originate from the vestibular nerve, some changes in this nerve might be involved in producing the broadened waveform. Effects of lidocaine on the AP-SP complex were investigated in guinea pigs by injecting this compound into the root exit zone of the vestibular nerve, where the cochlear efferent fibers run together. The AP-SP complex in response to clicks and tone bursts was recorded at the bony wall of the scala vestibuli in the basal turn of the cochlea. Inactivation of the efferent cochlear fibers resulted in a marked widening of the waveform, independent of the interstimulus intervals (ISIs). This broad wave was composed of a DC shift which was quite similar to the envelope curve of the acoustic stimuli. Although the effect of activity of the efferent cochlear fibers on negative summating potential (SP) has not been reported in detail, the authors concluded that the broad waveform observed in ECochGs in cases with cerebellopontine angle tumors was caused by enhanced negative SP due to inactivation of efferent cochlear fibers.

Animals↗
PubMed1992

Accelerated secretion of brain natriuretic peptide from the hypertrophied ventricles in experimental malignant hypertension.

Plasma concentrations of immunoreactive (ir) atrial (ANP) and brain (BNP) natriuretic peptides were measured in the prehypertensive and hypertensive phases in spontaneously hypertensive rats (SHR) and in the malignant phase of hypertension caused by deoxycorticosterone acetate (DOCA)-salt in SHR. The secretory rate of ANP and BNP were examined in the perfusion of isolated beating heart before and after atrial removal. Plasma irANP and irBNP in mature SHR were higher than those of control Wistar-Kyoto (WKY) rats, whereas ANP and BNP values in young SHR did not differ from those of control WKY rats. DOCA-salt treatment for 8 weeks markedly increased blood pressure, ventricular weight, and plasma irANP and irBNP in SHR. ANP and BNP values were positively correlated with ventricular weight in DOCA-salt SHR. The secretory rate of ANP and BNP from the perfused whole heart were much higher in DOCA-salt SHR than other rat groups. A large amount of BNP was secreted from the hypertrophied ventricles in DOCA-salt SHR. In contrast, ANP was mainly secreted from the atrium in all rat groups. High-performance liquid chromatography profiles of extract in plasma showed that a major component of irANP and irBNP corresponded to synthetic rat ANP-(1-28) and rat BNP-45, respectively. Results suggest that both rat ANP-(1-28) and rat BNP-45 are markedly increased in plasma in DOCA-salt-induced malignant hypertension of SHR and that the major source of circulating BNP is the hypertrophied ventricles in this model.

Aging↗
PubMed1992

Phorbol ester and atrial natriuretic peptide receptor response on vascular smooth muscle.

At least two types of receptors for natriuretic peptides have been reported: biologically active receptors coupled with guanylate cyclase (atrial natriuretic peptide [ANP]-B receptors) and clearance receptors (ANP-C receptors). To elucidate the role of protein kinase C (PKC) in the regulation of ANP-B receptors, vascular smooth muscle cells in culture were treated with phorbol ester. Incubation with receptor agonists and phorbol ester led to the desensitization of receptor-mediated cyclic guanosine monophosphate (ANP-B receptor response) in rat vascular smooth muscle cells. Although a PKC inhibitor and downregulation of PKC by long-term incubation of cells with phorbol esters blocked the phorbol ester-induced desensitization of the ANP-B receptor response, they did not block the ANP-induced desensitization of the ANP-B receptor response. In addition, when desensitization by phorbol esters was observed, ANP was still capable of desensitization. These observations suggest that the mechanism for regulating ANP-B receptor sensitivity may be both PKC-dependent and PKC-independent and mediated by phorbol esters and ANP, respectively.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

C-type natriuretic peptide inhibits thrombin- and angiotensin II-stimulated endothelin release via cyclic guanosine 3',5'-monophosphate.

We examined the inhibitory effect of porcine C-type natriuretic peptide (CNP) on endothelin-1 secretion stimulated by thrombin and angiotensin II (Ang II) in cultured porcine endothelial cells. The results were compared with the effects of atrial (ANP) and brain (BNP) natriuretic peptides. Thrombin and Ang II produced a concentration-dependent stimulation of immunoreactive endothelin-1 secretion, and porcine CNP-22 potently inhibited this stimulated secretion in a concentration-dependent manner. CNP-22 had a stronger inhibitory effect than either porcine ANP(1-28) or porcine BNP-26. In addition, CNP potently increased the cellular level of cyclic guanosine 3',5'-monophosphate (GMP), with the inhibition of immunoreactive endothelin-1 secretion in response to thrombin and Ang II being paralleled by the increase in the cyclic GMP level. The increase of cyclic GMP produced by CNP was also greater than that due to porcine ANP(1-28) or porcine BNP-26. The immunoreactive endothelin-1 in the culture medium had two components on high-performance liquid chromatography; the major one corresponded to endothelin-1 (1-21) and the minor one to big endothelin-1 (porcine 1-39). Treatment with CNP did not affect this profile. Our results suggest that CNP probably inhibits the endothelin-1 secretion stimulated by thrombin and Ang II through a cyclic GMP-dependent process. The increase of cyclic GMP levels and the inhibition of immunoreactive endothelin-1 secretion produced by CNP appear to be greater than those produced by ANP or BNP.

Angiotensin II↗
PubMed1992

Atrial and brain natriuretic peptides inhibit the endothelin-1 secretory response to angiotensin II in porcine aorta.

We have recently shown that the porcine aorta releases immunoreactive endothelin-1 in a time-dependent way. Here, we examined the inhibition by atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) of endothelin-1 secretion after stimulation with angiotensin II (Ang II) by using porcine aorta. Ang II dose-dependently stimulated immunoreactive endothelin-1 secretion. Porcine ANP-(1-28) and porcine BNP-26 both inhibited such secretion in a dose-dependent way. The addition of a cyclic guanosine 5'-monophosphate (cGMP) analogue, 8-bromo-cGMP, reduced the immunoreactive endothelin-1 secretion after stimulation with Ang II. In cultured porcine endothelial cells the inhibition by porcine ANP-(1-28) and porcine BNP-26 of immunoreactive endothelin-1 secretion after stimulation with Ang II was paralleled by an increase in the cellular cGMP level. Rat ANP-(5-25) was weaker than porcine ANP-(1-28) in inhibiting immunoreactive endothelin-1 secretion and increasing cGMP in cultured cells. There was negative correlation between the percent decrease in immunoreactive endothelin-1 and the percent increase in cGMP. Neither porcine ANP-(1-28) nor BNP-26 affected the number or sensitivity of Ang II binding sites in cultured porcine endothelial cells. These results suggest that ANP and BNP inhibit endothelin-1 secretion after stimulation with Ang II, probably through a cGMP-dependent process.

Angiotensin II↗
PubMed1992

Heat shock decreases nuclear transport of 3,5,3'-triiodo-L-thyronine in clone 9 cells.

Thyroid hormone, T3, enters cells through an energy-dependent, saturable process and/or passive diffusion. Although the nucleus is the primary site of T3 action, exact mechanisms by which T3 is transported to nucleus are uncertain. In this report, initial cellular and nuclear uptake of T3 was determined using a rat liver cell line (clone 9), in which energy-dependent cellular T3 uptake was demonstrable. One to 5 mM sodium butyrate enhanced cellular T3 uptake with a concomitant increase in nuclear T3 uptake after 30 h. Increased cellular T3 uptake was associated with the increase in the maximum velocity of saturable cellular T3 uptake systems without affecting the Michaelis-Menten constant. Sodium butyrate, however, elicited a reduction in nuclear thyroid hormone receptor levels. On the other hand, heat shock (42 C for 60 min) reduced nuclear T3 uptake without affecting the Michaelis-Menten constant and maximum velocity of saturable cellular T3 uptake. Although nuclear receptor levels were reduced transiently after the heat shock, decreased nuclear T3 transport was not caused by the changes in the receptor levels. NADPH-dependent cytosolic T3 binding protein was undetectable in clone 9 cells before and after butyrate treatment or heat shock. In conclusion, sodium butyrate enhanced nuclear T3 uptake through the increase in cellular T3 uptake that is prerequisite to nuclear T3 transport. However, nuclear T3 uptake mechanisms independent of the cellular uptake system exist and are sensitive to heat shock. Nuclear receptors and cytosolic T3 binding proteins do not seem to be involved in the alteration of nuclear T3 uptake after sodium butyrate or heat shock. These findings suggest intracellular regulatory mechanisms of thyroid hormone transport.

Animals↗
PubMed1992

Effect of administration of thyroxine on the risk of postpartum recurrence of hyperthyroid Graves' disease.

In our previous study, we reported that the administration of T4 to patients with Graves' disease who were under treatment with methimazole (MMI) decreased the level of antibodies to thyroid-stimulating hormone (TSH) receptors and the rate of recurrence of hyperthyroidism. In this study, the effect of T4 administration on the rate of postpartum recurrence of hyperthyroidism was examined. Seventy-eight patients with Graves' disease had been treated with MMI for 1-3 yr before pregnancy, and MMI was discontinued 5-6 months after the onset of pregnancy because the levels of antibodies to TSH receptors decreased during early pregnancy. The patients were then divided into two groups. Group A (n = 40) was given T4 (100 micrograms/day) and group B (n = 38) was not given any drugs from 5 months after the onset of pregnancy until 1 yr after delivery. The levels of the antibodies to TSH receptors and serum concentrations of thyroxine-binding globulin (TBG) and T4 were not different between the two groups before and during pregnancy, although a transient increase in serum T4 and TBG concentrations were observed during the pregnancy in both groups. After delivery, levels of antibodies to TSH receptors increased in both groups. The rate of increase, however, was more rapid in group B than in group A. The levels were significantly higher in group B than A at 3, 6, 9, and 12 months after delivery. Serum T4 and TBG concentrations decreased after delivery in both groups. Serum concentrations of T4 increased after delivery in group B but not in group A. The concentration of T4 was significantly higher in group B than in group A at 9 and 12 months after delivery. Postpartum recurrence of hyperthyroidism was 5.0% in group A and 31.6% in group B, respectively, during the first year after delivery. These results suggest that administration of T4 during pregnancy and after delivery is effective in decreasing the level of antibodies to TSH receptors and to prevent the postpartum recurrence of hyperthyroidism.

Adolescent↗
PubMed1992

Histamine decreases the permeability of an endothelial cell monolayer by stimulating cyclic AMP production through the H2-receptor.

To determine if histamine acts directly on the vascular endothelium, the effect of histamine on the permeability of cultured human endothelial cell monolayers and the role of second messengers were examined. The addition of 10(-6) to 10(-4) M histamine to the culture medium decreased the endothelial cell monolayer permeability and increased both cyclic AMP and free-calcium levels. The decrease in permeability and the increase in cyclic AMP mediated by histamine were prevented by an H2-blocker (famotidine) while the increase in free-calcium was inhibited by an H1-blocker (diphenhydramine). These results suggest that histamine decreases the permeability of endothelial cell monolayers through the H2-receptor, and cyclic AMP plays a more important role than calcium ion as a second messenger.

Animals↗
PubMed1992

Clinical significance of reverse redistribution on thallium-201 single-photon emission computed tomography in patients with acute myocardial infarction.

To determine the clinical significance of reverse redistribution (RR), resting thallium-201 myocardial single-photon emission computed tomography was performed once or twice in 80 patients in subacute phase (1 week to 2 months) of myocardial infarction. Thirty eight patients demonstrated RR on at least one study (group RR) and 32 a fixed defect only (group FD). Group RR had significantly smaller defects than group FD. Standardizing the relation of the severity of wall motion abnormality of left ventricle on echocardiogram with that of perfusion defect, in group RR wall motion abnormality in the acute and subacute phase reflected the defect of delayed image, while that in chronic phase, which was thought to reflect the viability of myocardium in the infarct region, reflected the defect of initial image. In serial thallium-201 studies, only the defect of delayed image of group RR improved on the second study, while the defect of initial image of group RR and defect of group FD did not improve. Wall motion of group RR improved with the disappearance of RR, and when RR remained, wall motion did not improve so much. We concluded that RR was thought to be demonstrated in viable myocardium with severe wall motion abnormality.

Adult↗
PubMed1992

Extensive specifically localized myocardial calcium deposition in a hemodialysis patient.

A 51-year-old female who was hospitalized for evaluation of frequent episodes of hypotension, died unexpectedly. At autopsy, there were many fine, white granular deposits in the myocardium, which were more prominent in the subepicardium of the left ventricle than in the subendocardium. Pathologic calcification is sometimes seen in chronic hemodialysis patients and in some organs the sites of calcium deposition are quite specific. There have been few reports concerning the pattern of calcium deposition in the myocardium and, to our knowledge, the reason for this characteristic distribution is unknown. However it may relate to hydrogen ion concentration in the myocardium.

Calcinosis↗
PubMed1992

Facial nerve to facial canal cross-sectional area ratio in children.

The incidence of facial palsy among children is lower than that among adults, and the recovery rate after facial palsy among children is higher than that of adults. To investigate these differences, we compared the cross-sectional area ratio of the facial nerve to that of the facial canal in 26 pediatric temporal bone specimens with that of 10 adult temporal bone specimens. The ratios were 0.31 +/- 0.08, 0.35 +/- 0.10, and 0.18 +/- 0.12, respectively, in the labyrinthine, horizontal, and mastoid segments of pediatric specimens. The ratios for adult specimens were 0.46 +/- 0.07, 0.52 +/- 0.17, and 0.37 +/- 0.04, respectively, in the labyrinthine, horizontal, and mastoid segments. These ratios were all significantly smaller than those for the corresponding segments of the adult specimens (P < .01). The results indicate that in children there is less possibility for entrapment of the facial nerve in the facial canal, and that children require facial nerve decompression less often than adults.

Adult↗