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A Baba

Publications and source records attributed to A Baba.

At least 55 records · Page 3Linked to original sources
PubMed1996

Expression pattern of messenger RNAs for prostanoid receptors in glial cell cultures.

Expression level of messenger RNAs (mRNAs) for prostanoid EP3, FP, and TP receptors was investigated in cultured rat astrocytes, oligodendrocytes, and microglia, as well as in meningeal fibroblasts, rat glioma C6 cells, rat pheochromocytoma PC12 cells, whole brain, and several peripheral tissues by reverse transcriptase-polymerase chain reaction. Cultured astrocytes and oligodendrocytes expressed mRNAs for 3 prostanoid receptors examined. In contrast, cultured microglia and pheochromocytoma PC12 cells expressed EP3 and TP receptor mRNAs, but not FP receptor mRNA. Glioma C6 cells expressed only TP receptor mRNA among 3 prostanoid receptors with the same expression level as that in astrocytes. Cultured meningeal fibroblasts expressed 3 receptor transcripts, and their expression levels were lower than those in astrocytes. Expression level of mRNA for each prostanoid receptor in cultured glial cells was higher than that in whole brain. These observations suggest that each prostanoid has its specific roles in each glial cell type of the brain.

Animals↗
PubMed1996

Inhibition of vanadate-induced astrocytic stress fiber formation by C3 ADP-ribosyltransferase.

Mechanisms of vanadate-induced actin reorganization were examined in cultured astrocytes. Treatment of protoplasmic astrocytes with 0.5 mM dibutyryl cAMP (DBcAMP) caused the disappearance of stress fibers (SFs) and focal adhesions (FAs) accompanied with cellular stellation. A subsequent addition of 1 mM orthovanadate (VO4(3-) reorganized SFs and FAs in DBcAMP-treated cells. The newly formed FAs had increased phosphotyrosine levels. VO4(3-) reorganized SFs and FAs in stellate astrocytes induced by 5 microM cytochalasin B, 50 microM ML-9 and 20 microM W-7. Cytoplasmic microinjection of 20 micrograms/ml C3 ADP-ribosyltransferase of C. botulinum, which inactivates rho proteins, caused disappearance of SFs. The effect of C3 enzyme on SFs was not reversed by a subsequent addition of VO4(3-). These results suggest that rho proteins are involved in vanadate-induced reorganization of cytoskeletal actin.

ADP Ribose Transferases↗
PubMed1996

Endothelin-induced cytoskeletal actin re-organization in cultured astrocytes: inhibition by C3 ADP-ribosyltransferase.

We investigated signal transduction mechanisms of endothelin (ET) receptor-mediated actin re-organization of rat cultured astrocytes. Staining of filamentous actin (F-actin) showed that stress fibers were a prominent cytoskeletal actin structure in protoplasmic astrocytes. A treatment with 0.5 mM dibutyryl cAMP (DBcAMP) caused cytoplasmic retraction and disappearance of stress fibers of astrocytes. A subsequent addition of 1 nM ET-3 after the DBcAMP treatment expanded the cytoplasm and stimulated stress fiber formation. ET-1, sarafotoxin S6b, and [Ala1,3,11,16]-ET-1 had similar effects. Pre-treatment with 0.1 microgram/ml pertussis toxin (PTX) and chelation of cytosolic Ca2+ did not affect astrocytic stress fiber formation by ET-3. ET-3 stimulated stress fiber formation in stellate astrocytes induced by 50 microM ML-9, 20 microM W-7, and 5 microM cytochalasin B (CB). Cytoplasmic microinjection of C3ADP-ribosyltransferase of C. botulinum (C3 enzyme), which impairs the interaction between rho proteins and the effectors, prevented ET-3-induced stress fiber formation and cytoplasmic expansion in DBcAMP-and CB-treated cells. Effects of ET-1 and sarafotoxin on stress fiber formation were also prevented by C3 enzyme. On the other hand, injection of C3 enzyme did not affect increase in cytoplasmic Ca2+ levels induced by ET-3. These results suggest that rho proteins are involved in the ET receptor-mediated actin re-organization of astrocytes.

ADP Ribose Transferases↗
PubMed1996

Protective effect of taurine against reperfusion injury in cultured rat astrocytes.

Reperfusion of cultured rat astrocytes with Ca(2+)-containing medium after exposure to Ca(2+)-free medium for a short time caused an increase in intracellular Ca2+ ([Ca2+]i), and delayed cell death (Ca2+ paradox-like injury). Exposure of astrocytes to Ca(2+)-free medium caused a marked release of taurine. Taurine (3-30 mM) reduced the reperfusion-induced increase in [Ca2+]i and attenuated the delayed glial cell death. Glycine, GABA and beta-alanine did not affect reperfusion-induced cell toxicity. The protective effect of taurine required addition at an early time during reperfusion. Ouabain and monensin mimicked reperfusion injury and their toxicity was also reduced by taurine. Taurine (3-30 mM) inhibited dose-dependently 45Ca2+ uptake stimulated by ouabain and monensin in astrocytes. These findings suggest that taurine has a protective effect against reperfusion injury via an inhibition of Na+/Ca2+ exchange activity in the reverse mode.

Animals↗
PubMed1996

Immunomodulating and articular protecting activities of a new anti-rheumatic drug, TAK-603.

We investigated the pharmacological activities of a newly synthesized anti-rheumatic drug, TAK-603. (1) In vivo: In adjuvant arthritic (AA) rats, TAK-603 inhibited the hind paw swelling and the body weight loss. The minimum effective dose was 3.13 mg/kg/day (p.o.). Histological and radiographic studies showed that TAK-603 suppressed the development of synovial lesions and joint and bone destruction. TAK-603 was also effective in AA rats when administered for the first 7 days after the adjuvant injection. It suppressed type IV allergy (25 mg/kg/day, p.o.) but had no effect on type III allergy. It had little effect in acute inflammation, analgesic and antipyretic models. These data suggest that TAK-603 acts on the immune system, especially on cellular immunity. (2) In vitro: TAK-603 suppressed the mitogen-induced proliferation of mouse lymphocytes and the ConA-induced IFN-gamma and IL-2 production by rat lymphocytes at 10(-7) to 10(-5) M. It also significantly inhibited the IL-1 induced extracellular matrix reduction in rabbit chondrocytes. It had no effects on prostaglandin E2 (PGE2) production in rat peritoneal cells. These data show that TAK-603 has the ability to suppress the immune system and protect cartilage from destruction. TAK-603 is expected to be a promising drug for rheumatoid arthritis.

Adjuvants, Immunologic↗
PubMed1996

Early reduction of neurohumoral factors plays a key role in mediating the efficacy of beta-blocker therapy for congestive heart failure.

This study examined the role played by neurohumoral factors in mediating the effects of beta-blocker therapy for congestive heart failure. Fifteen patients with congestive heart failure underwent beta-blocker therapy. Plasma norepinephrine and alpha-atrial natriuretic peptide concentrations decreased 2 weeks after initiation of beta-blocker therapy. Decrease in plasma norepinephrine level persisted for 6 months. Lymphocyte beta-adrenoceptor density increased 2 weeks after therapy but was not increased 6 months later. Left ventricular ejection fraction was unchanged 2 weeks after therapy, but it increased 6 months after introduction of beta-blockers. Plasma norepinephrine level decreased 2 weeks after the therapy in the responders (increase in ejection fraction > 0.10) but not in the nonresponders. Thus early reduction of neurohumoral factor levels preceded the late improvement of left ventricular contractile function and may therefore be partly responsible for the efficacy of beta-blocker therapy for congestive heart failure.

Adrenergic beta-Antagonists↗
PubMed1996

Involvement of Na+,K(+)ATPase in the mitogenic effect of insulin-like growth factor-I on cultured rat astrocytes.

We have previously reported that insulin/insulin-like growth factor (IGF)-I induced the alpha 1 isoform of Na+,K(+)-ATPase in cultured astrocytes. In this study the effects of insulin/IGF-I on Na+,K(+)-ATPase activity and cell proliferation were examined in astrocytes cultured under the various conditions, to test the possible involvement of the enzyme activity in the mitogenic action of IGF-I on astrocytes. Insulin increased Na+,K(+)-ATPase activity and stimulated cell proliferation in subconfluent astrocytes (cultured for 7-14 days in vitro). In contrast, these effects were not observed in confluent cells (cultured for 28 days). Furthermore, insulin stimulated neither the enzyme activity nor [3H]thymidine incorporation in astrocytes preincubated in fetal calf serum-free medium for 2 days (quiescent cells) and treated with dibutyryl cyclic AMP (differentiated cells). The increases in Na+,K(+)-ATPase activity and expression of the alpha 1 mRNA preceded the mitogenic effect. 125I-IGF-I binding experiment showed that all the cells used here had similar binding characteristics. The insulin-induced increase in enzyme activity was not affected by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), and it was observed even in Ca(2+)-free medium. The stimulation by IGF-I of [3H]thymidine incorporation was attenuated by ouabain and a low external K+ level. These findings suggest that stimulation of Na+,K(+)-ATPase activity is involved in the mitogenic action of IGF-I on cultured astrocytes.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1996

Role of Na(+)-Ca2+ exchanger in agonist-induced Ca2+ signaling in cultured rat astrocytes.

We have previously demonstrated that activation of the Na(+)-Ca2+ exchanger in the reverse mode causes Ca2+ influx in astrocytes. In addition, we showed that the exchange activity was stimulated by nitric oxide (NO)/cyclic GMP and inhibited by ascorbic acid. The present study demonstrates that the Na(+)-Ca2+ exchanger is involved in agonist-induced Ca2+ signaling in cultured rat astrocytes. The astrocytic intracellular Ca2+ concentration ([Ca2+]i) was increased by L-glutamate, noradrenaline (NA), and ATP, and the increases were all attenuated by the NO generator sodium nitroprusside (SNP). SNP also reduced the ionomycin-induced increase in [Ca2+]i. The NA-induced Ca2+ signal was also attenuated by S-nitroso-L-cysteine and 8-bromo cyclic GMP, whereas it was enhanced by 3,4-dichlorobenzamil, an inhibitor of the Na(+)-Ca2+ exchanger. Treatment of astrocytes with antisense, but not sense, deoxynucleotides to the sequence encoding the Na(+)-Ca2+ exchanger enhanced the ionomycin-induced increase in [Ca2+]i and blocked the effects of SNP and 8-bromo cyclic GMP in reducing the NA-induced Ca2+ signal. Furthermore, the ionomycin-induced Ca2+ signal was enhanced by removal of extracellular Na+ and pretreatment with ascorbic acid. These findings indicate that the Na(+)-Ca2+ exchanger is a target for NO modulation of elevated [Ca2+]i and that the exchanger plays a role in Ca2+ efflux when [Ca2+]i is raised above basal levels in astrocytes.

Adenosine Triphosphate↗
PubMed1996

Involvement of Na+-Ca2+ exchanger in reperfusion-induced delayed cell death of cultured rat astrocytes.

In some cells, Ca2+ depletion induces an increase in intracellular Ca2+ ([Ca2+]i) after reperfusion with Ca2+-containing solution, but the mechanism for the reperfusion injury is not fully elucidated. Using an antisense strategy we studied the role of the Na+-Ca2+ exchanger in reperfusion injury in cultured rat astrocytes. When astrocytes were perfused in Ca2+-free medium for 15-60 min, a persistent increase in [Ca2+]i was observed immediately after reperfusion with Ca2+-containing medium, and the number of surviving cells decreased 3-5 days later. The increase in [Ca2+]i was enhanced by low extracellular Na+ ([Na+]0) during reperfusion and blocked by the inhibitors of the Na+-Ca2+ exchanger amiloride and 3, 4-dichlorobenzamil, but not by the Ca2+ channel antagonists nifedipine, Ca2+ and Ni2+. Treatment of astrocytes with antisense, but not sense, oligodeoxynucleotide to the Na+-Ca2+ exchanger decreased Na+-Ca2+ exchanger protein level and exchange activity. The antisense oligomer attenuated reperfusion-induced increase in [Ca2+]i and cell toxicity. The Na+-Ca2+ exchange inhibitors 3, 4-dichlorobenzamil and ascorbic acid protected astrocytes from reperfusion injury partially, while the stimulators sodium nitroprusside and 8-bromo-cyclic GMP and low [Na+]0 exacerbated the injury. Pretreatment of astrocytes with ouabain and monensin caused similar delayed glial cell death. These findings suggest that Ca2+ entry via the Na+-Ca2+ exchanger plays an important role in reperfusion-induced delayed glial cell death.

Amiloride↗
PubMed1996

Prostanoid receptor-mediated calcium signaling in cultured rat astrocytes.

We investigated prostanoid-induced intracellular Ca2+ mobilization in Ca(2+)-sensitive dye fura-2-loaded cultured astrocytes. The thromboxane (TX) A2 analog STA2 (9,11-epithio-11,12-methano-TXA2) and/or prostaglandin (PG) F2 alpha (each used at 1 microM) stimulated intracellular Ca2+ mobilization in single cultured rat type 1 astrocytes. Three response patterns were observed: only STA2-sensitive, only PGF2 alpha-sensitive, and both prostanoids-sensitive cells. The Ca2+ response was prostanoid-dose-dependent (0.1 - 1 microM) and showed a rapid spike-like Ca2+ rise that peaked within 30 sec after the stimulation by the ligand. These observations suggest that type 1 astrocytes are heterogeneous with respect to the expression of receptors for TXA2 and PGF2 alpha, which are linked to Ca2+ mobilization.

Animals↗
PubMed1996

Ouabain-induced cell proliferation in cultured rat astrocytes.

Ouabain markedly stimulated not only [3H]thymidine incorporation but also [3H]uridine incorporation into astrocytes. The effects were observed at 36-48 hr and 12-72 hr after addition of ouabain, respectively. The dose-response curves were both bell-shaped types with a peak at 10(-3) M for thymidine incorporation and 2 x 10(-3) M for uridine incorporation. Ouabain increased cell number as determined by an assay using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and by a method using a hemocytometer. Low concentration of external K+ mimicked the effect of ouabain in stimulating [3H]-thymidine incorporation, and high concentration of external K+ blocked the effect of ouabain. In contrast to astrocytes, ouabain did not stimulate [3H]thymidine incorporation into C6 glioma and fibroblast cells. The effect of ouabain on [3H]thymidine incorporation in astrocytes was dependent on external Ca2+, and it was blocked by cycloheximide. These findings indicate that prolonged Na+, K(+)-ATPase inhibition causes cell proliferation in cultured astrocytes in cell-specific and Ca(2+)-dependent manners.

Animals↗
PubMed1996

Ca2+ depletion facilitates taurine release in cultured rat astrocytes.

Removal of external Ca2+ facilitated endogenous taurine release in cultured rat astrocytes. The stimulated release was not affected by furosemide, sucrose, tetrodotoxin and 3,4-dichlorobenzamil, but partially inhibited by nifedipine. Omission of external Na+ increased basal taurine release, and the effects of Na+ removal and Ca2+ depletion on the release were additive. The Na(+)-free condition did not affect Ca2+ paradox-induced cell death in astrocytes. These findings suggest that Ca2+ depletion facilitates taurine release in a mechanism independent of volume and the Na+ gradient and that the release is not involved in Ca2+ paradox-induced delayed cell toxicity in astrocytes.

Amiloride↗
PubMed1996

Adrenal tumor producing 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone and aldosterone.

A case of adrenal tumor producing 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone and aldosterone is reported. A 55-year-old woman had hypertension, hypokalemia, low plasma renin activity and an adrenal tumor. The plasma level of aldosterone was normal, and the levels of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone were extremely high. After the tumor removal, the plasma level of aldosterone decreased and plasma levels of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone were normalized. The tumor was benign adenoma and the production of steroid hormones was under control of adrenocorticotropic hormone. The enzyme activity of 21-hydroxylation in the tumor was elevated and that of 11 beta-hydroxylation was decreased compared with the adjacent tissue.

18-Hydroxydesoxycorticosterone↗
PubMed1996

[Usefulness of the newly developed transtelephonic electrocardiogram and computer-supported response system].

The "Cardiophone System" is a system designed to expand the relationship between patients and medical services using a transtelephonic electrocardiogram and computer-assisted answering system. The transtelephonic electrocardiogram, or so-called "Cardiophone", developed by Nihon Kohden, Inc., allows the patients to carry a "Cardiophone" to record electrocardiograms during paroxysmal occurrences of palpitation, chest pain, and other symptoms. The Cardiophone may function as a terminal of the host computer at the hospital, which stores the electrocardiogram and print it as soon as the computer receives the electrocardiogram over the phone. Cardiologists can examine the electrocardiogram immediately after it is printed. Cardiologists and operators are on duty 24 hours a day. Judgments based on the electrocardiogram are made by the cardiologist on duty, and stored in the computer by the operator. The patients may listen to the judgment over the phone within 30 min of sending the electrocardiogram. In the case of potentially lethal findings on the electrocardiogram, the cardiologist on duty calls the patient directly to give a medical advice. We studied 184 outpatients who were enrolled in the Cardiophone System of our hospital. The average number of transtelephonic electrocardiograms was 10 per day. Abnormal electrocardiographic changes were observed in 42 patients, and the diagnoses were as follows: paroxysmal supraventricular tachycardia in 18 patients, paroxysmal atrial fibrillation in 17, ventricular tachycardia in 3, and angina in 7. Among seven patients in whom ST changes were documented by Cardiophone, six were diagnosed as variant angina. In several patients with diagnoses already made by Holter monitoring, the Cardiophone was used to monitor the drug effects and the correlations between symptoms and arrhythmic events. We conclude that the Cardiophone System is useful for diagnosing the causes of paroxysmal cardiac symptoms in some patients and for improving home medical services.

Adolescent↗
PubMed1996

Novel benzodioxan derivative, 5-[3-[((2S)-1,4-benzodioxan-2-ylmethyl) amino]propoxy]-1,3-benzodioxole HCl (MKC-242), with anxiolytic-like and antidepressant-like effects in animal models.

Behavioral effects of MKC-242 (5-{3-[((2>)-1,4-benzodioxan-2-ylmethyl)amino] propoxy}-1,3-benzodioxole CHl), a novel and selective serotonin 1A receptor agonist, were investigated in rats and mice and compared against those of diazepam, buspirone and tandospirone. MKC-242 (0.0625-0.25 mg/kg, p.o.) significantly increased punished drinking in water-deprived rats. The reference compounds also increased punished drinking at doses of 10 to 40 mg/kg, p.o. The increase by MKC-242 was blocked by N-tert-butyl-3-(4-(2-methoxypenyl)piperazin-1-yl) -2-phenylpropanamide, a serotonin 1A receptor antagonist. MKC-242 (0.1-0.5 mg/kg, p.o.) also increased social interaction under high light and unfamiliar conditions in rats. It had weak benzodiazepine-like side effects in mice. MKC-242 (1, 3 mg/kg, p.o.) attenuated the reduction of locomotion caused by restraint stress in rats, the same effects were observed on both buspirone (100 mg/kg, p.o.) and tandospirone (100 mg/kg, p.o.). In the forced swimming test in rats, MKC-242 (0.3-3 mg/kg, i.p.), 8-hydroxy-2-(di-n-propylamino) tetralin (1, 3 mg/kg, i.p.) and amitriptyline (30 mg/kg, i.p.) reduced immobility, although diazepam, buspirone and tandospirone did not. The reduction by MKC-242 and 8-OH-DPAT was antagonized by N-tert-butyl-3-(4-(2-methoxyphenyl)piperazin-1-yl) -2-phenylpropanamide. Moreover, the reduction was also blocked by 1-(2--pyrimidinyl)piperazine (1-PP), a common metabolite of buspirone and tandospirone. These findings suggest that MKC-242 possesses potent anxiolytic and antidepressant properties that are mediated via an activation of serotonin 1A receptors.

Animals↗
PubMed1996

[Na+ -Ca2+ exchanger].

Na+ -Ca2+ exchanger couples the translocation of Na+ in one direction with that of Ca2+ in the opposite direction, and it is considered to have an important role in Ca2+ homeostasis in several cells. There are two types of Na+ -Ca2+ exchangers (cardiac and rod outer segment types). The cardiac clone (NCX1) is modeled to have an amino-terminal cleaved signal sequence, 11 transmembrane segments, and a large hydrophilic cytoplasmic domain. Several isoforms generated by alternative splicing of NCX1 and an isoform (NCX2), a product of a different gene, are present in different tissues. This brief review focuses on the physiological importance, molecular aspects and the pathological roles of the exchanger, especially NCX1.

Amino Acid Sequence↗
PubMed1996

The value of positive nitrites in screening asymptomatic bacteriuria amongst Malaysian school children.

It is important to diagnose and treat urinary tract infection in children before renal damage has taken place. Hence a new screening procedure will be of interest. This study was conducted to evaluate the efficacy of urinary nitrite in screening for asymptomatic bacteriuria among school children compared to a more traditional method. Of the 44,816 school children investigated 240 (0.54%) students were judged to have bacteriuria ie 82 (0.19%) in boys and 158 (0.35%) in girls. Escherichia coli was the commonest organism isolated (28.75%). Urine dipstick testing for nitrite was found to have a low sensitivity and positive predictive value. While urinalysis for pyuria was noted to have a sensitivity of 77.9%, a specificity of 95.8% and a negative predictive value of 99.9%.

Bacteriuria↗