[Infertility in couples. Analytic study of 430 cases].
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Adolescent↗
Biomedical subjects
A Baba
Publications and source records attributed to A Baba.
Angiotensin II subtype 1 receptor modulates epinephrine release from isolated rat adrenal gland.
To elucidate the role of subtypes of the angiotensin (AT) II receptor in epinephrine release from the adrenal gland, the effects of AT II subtype 1 (AT1) receptor and AT II subtype 2 (AT2) receptor antagonists on AT II-induced modulation of epinephrine release were examined. Seven-week-old Wistar rats were used in this study. The left adrenal gland was perfused in a retrograde fashion. The effects of AT II on basal epinephrine release and epinephrine release by electrical stimulation were examined before and after treatment with CV-11974 (CV), an AT1 receptor antagonist, or PD123319 (PD), an AT2 receptor antagonist. AT II increased epinephrine release from the adrenal gland. CV almost completely suppressed AT II-induced increases in epinephrine release. In contrast, PD had no significant effects on AT II-induced increases in epinephrine release. These results suggest that AT II increases epinephrine release from the adrenal medulla via the AT1 receptor.
Adrenal Glands↗
Screening for bacteriuria in Malaysian school children.
Urinary tract infection is the most common of bacterial infections. Screening children for asymptomatic bacteriuria to prevent pyelonephritis and renal scarring is widely recommended. In Malaysia no such attempt has been made to establish the prevalence of asymptomatic bacteriuria. Bacteriuria was screened among 44,816 healthy school children from three different districts in Kelantan. There were 23,132 boys and 21,684 girls. The prevalence of bacteriuria was 0.12% after second screening. Higher prevalence was seen in other reports.
Bacteriuria↗
Inhibitory effect of idazoxan on forskolin-stimulated adenylate cyclase activity through 5-hydroxytryptamine1A receptors.
The binding affinity of the alpha 2-adrenoceptor antagonist idazoxan (CAS 79944-56-2) to 5-hydroxytryptamine1A (5-HT1A) receptors and its effect on the forskolin-stimulated adenylate cyclase activity in the rat hippocampus were examined. Idazoxan had moderate affinity for the 5-HT1A receptors. It inhibited the forskolin-stimulated adenylate cyclase activity to the same extent as 5-HT. The 5-HT1A receptor antagonist spiperone shifted the concentration-response curve of idazoxan to the right in a parallel manner. These results indicate that idazoxan is a 5-HT1A agonist.
8-Hydroxy-2-(di-n-propylamino)tetralin↗
Teratogenic effects of various di-n-butyltins with different anions and butyl(3-hydroxybutyl)tin dilaurate in rats.
In our previous study, di-n-butyltin diacetate has been shown to cause malformations such as cleft mandible, ankyloglossia, fused ribs, etc. in rat fetuses after oral treatment of maternal rats on day 8 of gestation. In this study, teratogenic effects of five di-n-butyltin compounds with different anions and also butyl(3-hydroxybutyl)tin dilaurate (3-OHDBTL) were examined in Wistar rats. Anion groups of these compounds were as follows: diacetate (DBTA), dichloride (DBTC), maleate (DBTM), oxide (DBTO) and dilaurate (DBTL). On day 8 of gestation, pregnant rats were treated orally with these compounds at 80 mumol/kg, or with 3-OHDBTL at 80 or 160 mumol/kg. Cesarean sections were performed on day 20 of gestation and fetuses were examined for their external and skeletal anomalies. Types of the observed malformations were similar to those in the previous study with DBTA except 3-OHDBTL, though the incidence of fetuses with malformations was different. In the DBTC-treated group, skeletal anomalies were predominant to external ones, especially with the higher incidence of fused ribs than in the other groups. In the 3-OHDBTL-treated group, no external and skeletal anomalies were observed at 80 mumol/kg and cleft lower lip and ankyloglossia were observed in only one fetus, but peaked mandible (the tip of lower jaw with acute angle) was specific at 160 mumol/kg. From these results, the di-n-butyl group rather than anionic group was found to be important in the teratogenicity of di-n-butyltin compounds as well as in the other kinds of toxicities and 3-OHDBTL, one of the main metabolites of DBTL, is not the critical substance of teratogenicity because of a very low teratogenic potency.
Animals↗
Autoradiographic localization of CCK-8 binding sites in the rat brain: effects of chronic methamphetamine administration on these sites.
The effects of chronic methamphetamine (MAP) administration (at a dose of 4 mg/kg for 14 days) on [3H]pCCK-8 binding sites in the rat brain were investigated by an in vitro quantitative receptor autoradiographic technique. The number of [3H]pCCK-8 binding sites was significantly reduced in layers III and IV of the medial frontal, anterior, and posterior cingulate cortices, in layers II-IV of the retrosplenial cortex, in layers III-VI of the dorsal insular cortex, and in the reticular nucleus of the thalamus, compared to these numbers in a control group of rats that received physiologic saline. Further, chronic methamphetamine administration led to a significant increase in the number of these binding sites in layer I of the entorhinal cortex. These findings indicate the CCK peptides in the limbic lobe may be closely related to the development of the behavioral changes associated with methamphetamine sensitization. In addition, these results provide supporting evidence for the involvement of the limbic system in the pathophysiology of schizophrenia.
Animals↗
Selective induction of alpha 1 isoform of (Na+ + K+)-ATPase by insulin/insulin-like growth factor-I in cultured rat astrocytes.
Treatment of cultured rat astrocytes with insulin increased (Na+ + K+)-ATPase activity expressed per protein or DNA by 1.6- to 2.1-fold, but did not affect Mg(2+)-ATPase and adenylate cyclase activities. Insulin treatment increased protein and DNA contents under the conditions, while it did not cause morphological differentiation as determined by a microscopic inspection. Insulin-like growth factor-I (IGF-I) had a similar effect on the enzyme activity in astrocytes: the effect of insulin was observed at supraphysiological concentrations, while that of IGF-I was observed at physiological concentrations. Insulin and IGF-I both stimulated DNA synthesis at the concentrations that caused an increase in enzyme activity. The effect was blocked by tyrosine kinase inhibitors such as genistein and herbimycin A and by cycloheximide. Western blot analysis showed that alpha 1 and alpha 2 isoforms of (Na+ + K+)-ATPase were present in cultured astrocytes and that insulin and IGF-I increased the content of the alpha 1 isoform but did not that of the alpha 2 isoform. Two components of ouabain inhibition were observed in the enzyme purified partially from cultured astrocytes, and treatment of the cells with IGF-I increased the ratio of the low-affinity component of the inhibition, indicating a selective increase in the activity of the alpha 1 isoform. These results indicate that insulin increases (Na+ + K+)-ATPase activity through an activation of IGF-I receptors and the increase is due to the selective induction of the alpha 1 isoform in cultured astrocytes.
Adenylyl Cyclases↗
Inhibitory glutamate response on cyclic AMP formation in cultured astrocytes.
We examined the effects of glutamate receptor agonists on cyclic AMP (cAMP) formation in cultured astrocytes. L-Glutamate reduced the cAMP formation induced by either isoproterenol (IC50 7 microM) or forskolin without affecting the basal level. Glutamate agonists reduced the cAMP formation in astrocytes with the following rank order of potency: L-glutamate > trans-(+/-)-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD) = quisqualate. Pretreatment of astrocytes with pertussis toxin resulted in a partial reduction of the glutamate response and a complete attenuation of the t-ACPD response. These results suggest that astrocytes have another type of metabotropic glutamate receptor which inhibits adenylate cyclase through pertussis toxin-sensitive G-proteins.
Adenylate Cyclase Toxin↗
Endothelins modulate dibutyryl cAMP-induced stellation of cultured astrocytes.
Effect of endothelin-3 (ET-3) on dibutyryl cAMP (DBcAMP)-induced stellation of rat cerebral cultured astrocytes was examined. Treatment with 1 mM DBcAMP, 10 microM forskolin, 100 microM isoproterenol and 500 nM phorbol 12-myristate 13-acetate changed protoplasmic cultured astrocytes into process-bearing ones. ET-3 (1 nM) completely prevented the astrocytic stellation induced by these agents. The effect of ET-3 showed a dose-dependence, where IC50 value and maximal effective dose were 49 pM and about 0.1 nM, respectively. ET-1 and sarafotoxin (SRTX) S6b prevented the DBcAMP-induced astrocytic stellation with potencies similar to that of ET-3. ET-3 (1 nM) did not affect the cAMP accumulation after DBcAMP treatment in cultured astrocytes. Stellate astrocytes were reversed to the protoplasmic type cells by addition of 1 nM ET-3 in the presence of DBcAMP. ET-1 and SRTX similarly reversed the astrocytic stellation. ET-3 reversed the astrocytic stellation in the absence of extracellular Ca2+. Pre-loading of BAPTA-AM, a permeable Ca2+ chelator, on stellate astrocytes had no effect on the reversal by ET-3. ET-3 did not increase intracellular free Ca2+ concentration ([Ca2+]i) of most astrocytes tested at 0.1 nM. A high concentration (100 nM) of ET-3 increased astrocytic [Ca2+]i which was negated by Ca(2+)-free and BAPTA-AM loading. These results suggest that ETs modulate morphological changes in astrocytes through cAMP- and Ca(2+)-independent mechanisms.
Animals↗
Cytochalasin B inhibits phosphoinositide hydrolysis in rat hippocampal slices.
The effect of cytochalasin B on phosphoinositide (PI) hydrolysis was examined in rat hippocampal slices. Pretreatment of the slices with cytochalasin B caused a significant decrease in PI hydrolysis elicited by carbachol, norepinephrine, or by high K+. This effect was cytochalasin B dose- and time-dependent and was not mimicked by cytochalasin D, vinblastine, colchicine, or phloretin. In contrast, in [3H]inositol-prelabeled hippocampal membranes, cytochalasin B did not affect PI hydrolysis elicited by GTP gamma S and GTP gamma S plus carbachol. Similar result was obtained using the membranes prepared from the slices pretreated with cytochalasin B. The inhibitory effect of cytochalasin B on the carbachol-response was observed in SK-N-SH human neuroblastoma cells, but not in cultured rat astrocytes. These results indicate that cytochalasin B inhibits PI hydrolysis in neuron-specific manner and that its action may be an indirect cellular mechanism other than interaction with cytoskeleton elements.
Animals↗
Aneurysmal dilatation of ductus arteriosus during lipo-prostaglandin E1 therapy for diaphragmatic hernia.
We report a case of congenital diaphragmatic hernia in which aneurysmal dilatation of ductus arteriosus developed after lipo-prostaglandin E1 (PGE1) therapy for persistent fetal circulation. After surgery Lipo-PGE1 was used at a dosage of 5 ng/kg per minute from days 2-9 during which aneurysmal dilatation (7 mm in diameter) developed and remained thereafter. Ductus arteriosus ligation was then performed. Lipo-PGE1 may promote ductus arteriosus dilatation in cases of persistent fetal circulation.
Alprostadil↗
Pretreatment of rat brain slices with ouabain decreases chloride-dependent L-glutamate transport in synaptic membrane.
Possible roles of (Na(+)-K+)-ATPase on regulation of Cl(-)-dependent L-glutamate (L-Glu) transport in rat synaptic membrane were examined. Pretreatment of rat cerebral slices with 20 micrograms/ml veratrine, 56 mM K+ and 20 microM monensin increased Cl(-)-dependent L-[3H]-Glu uptake into membrane vesicles prepared from the slices. Pretreatment with (Na(+)-K+)-ATPase inhibitors, 100 microM ouabain, 100 microM strophanthidin, 100 microM vanadate and K(+)-free medium, decreased the uptake by 25-30%, while 5 microM A23187 and 10 microM ruthenium red had no effect. Ouabain (100 microM) caused the maximal effect in 10-20 min of incubation. The effect of (Na(+)-K+)-ATPase inhibitors was reversible and characterized by a decrease in Vmax of the uptake. Addition of 5 microM ouabain abolished the increases in the uptake induced by either veratrine, 56 mM K+ or monensin. Dose-inhibition curve of ouabain on the increased Cl(-)-dependent L-[3H]-Glu uptake was bi-phasic; ouabain at 0.5-5 microM selectively diminished the stimulatory effect of veratrine and inhibited the basal uptake at higher concentrations. Veratrine had no effect on L-[3H]-Glu uptake in 5 microM strophanthidin containing or K(+)-free medium. These results suggest the involvement of (Na(+)-K+)-ATPase in the veratrine-induced increase in Cl(-)-dependent L-Glu transport in rat brain synaptic membranes.
Animals↗
Postprandial change in canine blood viscosity.
1. Postprandial variation in blood viscosity was studied in beagle dogs. 2. Blood viscosity increased following feeding. This change was caused by haematocrit elevation, which resulted mainly from splenic contraction. 3. Haemoconcentration, plasma viscosity and erythrocyte deformability did not contribute to the postprandial increment in blood viscosity.
Animals↗
Phloretin as an antagonist of prostaglandin F2 alpha receptor in cultured rat astrocytes.
The effect of phloretin on prostaglandin (PG) F2 alpha-induced phosphoinositide hydrolysis and elevation of intracellular Ca2+ concentration was examined in cultured rat astrocytes. Phloretin inhibited PGF2 alpha (1 microM)-induced phosphoinositide hydrolysis in a concentration-dependent manner with an IC50 value of 16 microM. The inhibitory action of phloretin was specific for PGs. The addition of increasing concentrations of phloretin caused progressive shifts of the dose-response curves of PGF2 alpha to the right. In digitonin-permeabilized astrocytes, phloretin (100 microM) inhibited the stimulation induced by PGF2 alpha (1 microM) plus GTP gamma S (50 microM) without affecting that induced by GTP gamma S alone. PGF2 alpha at 1 microM transiently increased astrocytic intracellular Ca2+ concentration in 39% of the cells tested. The response was completely blocked by 100 microM phloretin and the calcium response recovered again after washing out phloretin. These results suggest that phloretin is an antagonist of PGF2 alpha receptor linked to phospholipase C in astrocytes.
Adenosine Triphosphate↗
[Histoire de la greffe de la cornée].
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Corneal Transplantation↗
Sex difference for tolerance of 5-HT1A receptor-mediated temperature and corticosterone responses in mice.
Repeated treatment with 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) resulted in significant attenuation of 8-OH-DPAT-induced hypothermia and adrenocorticol effect in mice of both sexes, while it did not affect the 8-OH-DPAT-induced decrease in 5-hydroxyindoleacetic acid in the hypothalamus in either sex. The attenuated responses developed more rapidly in female than in male mice, indicating sex differences in the adaptive regulation of the 5-HT1A receptor-mediated responses.
8-Hydroxy-2-(di-n-propylamino)tetralin↗
Fetal liver T cell receptor gamma/delta+ T cells as cytotoxic T lymphocytes specific for maternal alloantigens.
We have established fetal liver-derived T cell receptor (TCR) gamma/delta+, CD3+ T cell lines that are cytotoxic for maternal T cells. Fetal liver-derived lymphoid progenitors yielded predominantly TCR-gamma/delta+ cell clusters when cultured on fetal bone marrow-derived stromal cells in the presence of a cytokine cocktail under magnetic force. These tightly adherent clusters were cloned by limiting dilution and the resulting cell lines analyzed for phenotype and function. Six of eight TCR-gamma/delta lines from 8-9.5-wk gestation fetuses were V delta 2+ as compared with zero of eight lines from later stages of gestation (10 and 15 wk), where all the lines were V delta 1+. In cytotoxicity assays, these TCR-gamma/delta+, CD3+, CD4-, and CD8+ or CD8- long-term cultured lymphoid cells (LLC) were killer cells active against the class I antigens on maternal T cells. Of the cell lines, the CD8+ TCR-gamma/delta+ LLC had the highest levels of killer activity. Thus fetal liver TCR-gamma/delta+ T cells may play a crucial role in protection against invading maternal T cells generated in the feto-maternal interaction.
Cells, Cultured↗
Glucose and oxygen deprivation induces a Ca(2+)-mediated decrease in (Na(+)+K+)-ATPase activity in rat brain slices.
Exposure of rat brain cortical slices to a medium lacking in glucose, oxygen or both glucose and oxygen, resulted in a decrease of the tissue ATP content and a reduction of (Na(+)+K+)-ATPase activity in membranes prepared from the slices. These treatments also inhibited partial reactions of (Na(+)+K+)-ATPase such as Na(+)-dependent phosphorylation and K(+)-stimulated phosphatase, as well as specific binding of [3H]ouabain in membranes prepared from the slices. Glucose deprivation and hypoxia decreased (Na(+)+K+)-ATPase activity in the absence of extracellular Ca2+, but the effects were blocked by 1,2-bis(2-amino-phenoxy)ethane-N,N,N',N'-tetraacetic acid tetra-acetomethyl ester (BAPTA-AM), a chelator of intracellular Ca2+. Metabolic inhibitors mimicked the effects of glucose deprivation and hypoxia. The effect of glucose-free hypoxia was dependent on extracellular Ca2+. It was blocked by Mg2+ at high concentration, bepridil or amiloride, but not by voltage-sensitive Ca2+ channel antagonists and glutamate receptor antagonists. None of the drugs tested here, except for dithiothreitol, affected the inhibitory effect of glucose-free hypoxia on the enzyme activity. In contrast to brain (Na(+)+K+)-ATPase, the kidney enzyme was insensitive to glucose and oxygen deprivation and metabolic inhibitors which depleted the tissue ATP.
Animals↗