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Biomedical subjects

M Imai

Publications and source records attributed to M Imai.

At least 253 records · Page 14Linked to original sources

Isolation and characterization of rat CYP11B genes involved in late steps of mineralo- and glucocorticoid syntheses.

We isolated and characterized four forms of rat CYP11B genes, which were tentatively named CYP11B1, -B2, -B3, and -B4. Genomic Southern analyses indicated that the members of the rat CYP11B gene subfamily were confined to these four genes; among them, CYP11B1 and -B2 encoded steroid 11 beta-hydroxylase and aldosterone synthase, respectively, while CYP11B3 was a gene highly homologous to CYP11B1 without a known expression product. By being devoid of a region spanning two exons conserved in the other three, CYP11B4 was presumably a pseudogene. In the nucleotide sequences, CYP11B1, -B3, and -B4 showed 95-96 and 93-100% identities in the coding and 0.5-kilobase 5'-flanking regions, respectively. However, the homology between the nucleotide sequences of one of the three and CYP11B2 was rather low, about 90 and 50% in the coding and 0.5-kilobase 5'-flanking regions, respectively. As a whole, CYP11B2 rather than CYP11B1, -B3, or -B4 was more homologous to CYP11B genes of other animals such as cow and human. In transient transfection experiments using mouse adrenocortical Y1 cells and chloramphenicol acetyltransferase gene constructs, the 0.5-kilobase 5'-flanking region of CYP11B1 had a 4- and 10-fold higher promoter activity than the corresponding regions of CYP11B2 and -B3, respectively. The possible presence of a suppressive element(s) was noted in the upstream of the 0.5-kilobase region of CYP11B1. Although a variant of cAMP-responsive element, which was present in rat CYP11B2 and all known CYP11B genes of other animals, was modified in rat CYP11B1 and -B3 genes, dibutyryl cAMP stimulated all the promoter activities of the 5'-flanking regions of the rat genes by 3-fold.

Amino Acid Sequence↗

Extracellular production of human hepatitis B virus preS2 antigen as hybrid proteins with Bacillus subtilis alpha-amylases in high-salt-concentration media.

To produce PreS2 antigen of human hepatitis B virus extra-cellularly in Bacillus subtilis, it was fused with the COOH-termini of B. subtilis alpha-amylases of 522 (Amy+), 467 (Amy+) and 443 (Amy-) amino acids. Among them, alpha-amylase-A467, which has 467 amino acids, was a relatively stable carrier when the cells were cultured in Luria-Bertani (LB) medium. The alpha-amylase-A443-PreS2 hybrid protein (Amy-) was quickly degraded. The alpha-amylase-A522-PreS2 hybrid was most efficiently produced when a B. subtilis transformant of a protease-super-deficient mutant was cultured in the presence of 0.5 M sodium sulphate. The production of A522-PreS2 hybrid protein under such conditions reached 5-10 mg/l and was eight, and 200-500 times higher than those obtained by the transformants of an alkaline/neutral protease-deficient mutant of B. subtilis, and a wild-type strain, in LB medium, respectively.

Bacillus subtilis↗

Mechanisms of calcium transport across the basolateral membrane of the rabbit cortical thick ascending limb of Henle's loop.

Although net Ca2+ absorption takes place in the thick ascending limb of Henle's loop, detailed mechanisms are unknown. Because it has been reported that the Ca2+ entry step across the luminal membrane is mediated by Ca2+ channels inserted by stimulation with parathyroid hormone, we studied the mechanism of Ca2+ transport across the basolateral membrane of rabbit cortical thick ascending limb (CTAL) perfused in vitro by using microscopic fluorometry of cytosolic Ca2+ ([Ca2+]i) with fura-2. The resting [Ca2+]i in this segment was 49.8 +/- 4.5 nmol/l. Neither Na+ removal from the bathing solution nor addition of ouabain (0.1 mmol/l) to the bath increased [Ca2+]i, indicating that a Na+/Ca2+ exchanger in the basolateral membrane may not contribute in any major way to [Ca2+]i of CTAL. To confirm our technical accuracy, similar protocols were conducted in the connecting tubule, where the existence of a Na+/Ca2+ exchanger has been reported. In this segment, Na+ removal from the bath increased cell Ca2+ from 148.6 +/- 6.4 nmol/l to 647.6 +/- 132.0 nmol/l, confirming the documented fact. [Ca2+]i in the CTAL was markedly increased when 1 mmol/l NaCN was added to the bath in the absence of glucose. Calmodulin inhibitors (trifluoperazine or W-7) increased [Ca2+]i. When the bath pH was made alkaline, [Ca2+]i was also increased. This response was abolished when Ca2+ was eliminated from the bath, indicating that the Ca2+ entry across the basolateral membrane is dependent on bath pH. Increase in [Ca2+]i induced by an alkaline bath was inhibited by increased the bath K+ from 5 nmol/l to 50 mmol/l, suggesting that the Ca2+ entry system is voltage-dependent.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Aberrant tissue specific expression of the transgene in transgenic mice that carry the hepatitis B virus genome defective in the X gene.

The control mechanisms for the transgene expression in mice that carry the hepatitis B virus genome defective in the polymerase and X genes were analyzed. Ten lines of transgenic mouse were established, and in seven lines the surface and e antigens were detected in the serum. In transgenic mice from five lines examined, the transgene was markedly expressed in a broad spectrum of tissues including the kidney, heart, brain, muscle and intestine, but only poorly in the liver. In the kidney and heart the 3.5 kb and 2.1 kb mRNAs were expressed, whereas only the 0.8 kb and 4.0 kb mRNAs were detected in the testis and brain, respectively, suggesting that each of the mRNAs was transcribed through a different control mechanism. The surface, e and core antigens accumulated in the kidney and heart. DNA was hypomethylated at a region closely downstream of the enhancer in the liver, kidney and heart, and a DNase I hypersensitive site was detected upstream of the enhancer in these tissues. In the testis, however, the whole transgene was hypomethylated and the DNase I hypersensitive site was closer to the enhancer. These differences may be relevant to the preferential expression of the 0.8 kb mRNA in the testis, but cannot explain the inefficiency of transgene expression in the liver. Our observations suggest that the X protein is required for efficient expression of the viral gene in the liver but not in other tissues.

Animals↗

Dextrorphan attenuates the behavioral consequences of ischemia and the biochemical consequences of anoxia: possible role of N-methyl-d-aspartate receptor antagonism and ATP replenishing action in its cerebroprotecting profile.

The acute anti-ischemic and anti-anoxic effects of dextrorphan (DX) were compared with those of dizocilpine (MK-801) in a variety of animal models, and in vivo and in vitro testings under anoxic conditions. DX reduced the incidence of death in ischemic mice and improved the rotarod performance of mice with brain ischemia. The ischemically-impaired memory of mice treated with DX markedly improved, as shown in the step-through type passive avoidance test, Morris water maze and in the habituation of exploratory behavior test. MK-801 likewise improved the water maze performance of the ischemically-impaired mice, but to a lesser extent. The step-through type passive avoidance performance of ischemic mice was not improved by MK-801. In the passive avoidance task with normal mice, DX, like MK-801, produced anterograde amnesia at doses higher than those needed to attenuate the behavioral effects of ischemia. DX, intravenously or centrally administered, markedly and dose-dependently reduced the incidence of death in mice receiving potassium cyanide (KCN). DX lessened the reduction in adenosine triphosphate (ATP) and increased lactate contents in mice dosed with KCN and also lessened the reduction in ATP in the TCA cycle and oxidative phosphorylation reactions caused by KCN (0.58 mmol/l), whereas MK-801 failed to show any effect on ATP formation pathways in vivo and in vitro, and failed to protect mice against KCN-induced lethal toxicity in vivo. In the in vitro studies, DX increased the adenylate kinase activity of the rat brain homogenate. DX was found to be a cerebroprotectant with anti-ischemic and anti-anoxic actions, the effects probably stemming from its N-methyl-d-aspartate receptor antagonistic property in cooperation with its ATP replenishing action.

Adenosine Triphosphate↗

Hypertensive crisis during the resection of an adrenal tumor in primary aldosteronism.

Primary aldosteronism is one of the few causes of hypertension which is subject to total surgical treatment, but a hypertensive crisis can occur during the resection of the adrenal tumor. We undertook this study to evaluate the relationship between hormonal factors and a hypertensive crisis during surgery. Sixteen patients with primary aldosteronism who were scheduled for the resection of an adrenal tumor were participated in this investigation. Hormonal factors and hemodynamic variables were evaluated before induction of anesthesia, after induction of anesthesia, 30 minutes after the incision, during tumor manipulation, during resection, and immediately after surgery. During tumor manipulation, a hypertensive crisis occurred in six patients (hypertensive group; HG) but not in any others (non-hypertensive group; NHG). There were no differences in hormonal levels, except epinephrine, during tumor manipulation between HG and NHG. Hemodynamic evaluations revealed an increase of systemic vascular resistance during the hypertensive crisis. We conclude that the hypertensive crisis during the manipulation of an adrenal tumor is caused by the rapid release of epinephrine from the manipulated adrenal gland.

Journal Article↗

Does a lidocaine patch reduce the pain at venous cannulation in adults?

In this study we evaluated whether a lidocaine patch reduces the pain relating to a venous cannulation in adults. The patch is consisted of the base containing 50% lidocaine on a thin polyester membrane. Its surface area is 15 cm2. Twenty-six adult patients scheduled for elective surgery (11 males and 15 females) were randomly divided into two groups according to application periods: Group A for 15 min and Group B for 30 min. Either the dorsal part of the hand or the radial side of the wrist was chosen and covered with the patch. Pain assessment was made by patients using a 0-100 point visual analog scale (VAS). In 7 patients of Group A, plasma lidocaine levels were measured 15 min after application by homogeneous enzyme immunoassay. The levels were further measured 30 and 60 min after application in 3 of those patients. The mean VAS score was 28.4 +/- 13.1 (mean +/- SD) for Group A and 51.8 +/- 15.9 for Group B, and the difference was statistically significant (P < 0.05). Plasma lidocaine levels were always below 0.2 microg.ml(-1). The results indicate that the skin was partially anesthetized by the lidocaine patch. A lidocaine patch may be useful and safely applicable for venous cannulation in adult patients.

Clinical Trial↗

Neuromuscular effects of pipecuronium during sevoflurane anesthesia compared with isoflurane and enflurane anesthesia.

We evaluated the neuromuscular effects of pipecuronium during anesthesia with equipotent concentrations of either sevoflurane, isoflurane or enflurane. Twenty-seven patients scheduled for minor elective otolaryngeal or plastic surgery were studied and randomly assigned to 3 groups, one group per anesthetic agent. Anesthesia was induced with thiamylal 5 mg.kg(-1) and the trachea was intubated with succinylcholine 1 mg.kg(-1), then anesthesia was maintained with 60% nitrous oxide in oxygen and sevolfurane, isoflurane or enflurane, depending on the group. Neuromuscular blocking effects were monitored by recording the electromyographic activity of the adductor pollicis muscle from supramaximal stimulation of the ulnar nerve at 10-s intervals. Pipecuronium 40 microg.kg(-1) was administered when electromyographic activity had reached a stable state, 30 min after succinylcholine administration. The maximum effect (% block of control) and clinical duration (time to 25% recovery) of pipecuronium were 99.1 +/- 1.4% and 63.7 +/- 14.7 min (mean +/- S.D.) for sevoflurane, 99.0 +/- 2.0% and 60.9 +/- 20.5 min for isoflurane, and 98.0 +/- 2.5% and 62.8 +/- 28.7 min for enflurane, respectively. There were no significant differences in these values between the anesthetics. Cardiovascular stimulant effects were not observed in any of the groups. We conclude that the effect of pipecuronium under seveflurane anesthesia is similar to that under isoflurane and enflurane anesthesia.

Clinical Trial↗

Regulation of cortical collecting duct function: effect of endothelin.

We recently showed that endothelin-1 (ET-1) increases cell Ca2+ in the mouse cortical collecting duct. To clarify the cellular action and target cell of ET-1, electrophysiologic techniques and cell Ca2+ measurement were applied to rabbit cortical collecting ducts perfused in vitro. When 10(-8) mol/L ET-1 was added to the bath, a transient increase followed by a sustained increase in cell Ca2+ was observed. A sustained increase in cell Ca2+ lasted 10 to 20 minutes and was associated with a decrease in lumen-negative transepithelial voltage. To confirm the target cell type of ET-1, confocal laser microscopy was used. An increase in cell Ca2+ was observed in the same cell, which also showed an increase in cell Ca2+ in response to arginine vasopressin (AVP), which indicated that the principal cell has ET-1 receptors in the basolateral membrane. When ET-1 was applied to the bath, total cellular membrane resistance (Ri) decreased initially and then gradually increased because of inhibition of the luminal Na+ channel. An initial decrease in Ri was considered an influx of Ca2+ from the basolateral membrane. To further determine the source of an increase in cell Ca2+, the effect of ET-1 was tested in the absence of external Ca2+ and in the presence of a Ca2+ channel blocker in the bath. Cell Ca2+ did not respond to ET-1 in the absence of external Ca2+, a condition in which an AVP-stimulated increase in cell Ca2+ was preserved.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Long-term palliation after systemic-to-pulmonary artery shunt using an internal mammary artery.

We report the long-term results after systemic-to-pulmonary artery shunts using the internal mammary arteries in 2 patients. The systemic-to-pulmonary artery shunts using the internal mammary arteries were created in 2 children. Both of them are doing well 11 years and 7 years after operation. This procedure could be a reasonable alternative to classic Blalock-Taussig shunt for patients with diminutive pulmonary arteries as it offered good long-term palliation.

Angiography↗

Electronmicroscopic observation on the degeneration of skeletal muscles in Xenopus laevis during metamorphosis and after denervation.

We observed metamorphosis-related structural changes in the tail muscle of Xenopus laevis tadpoles during tail involution and changes in the calf muscles of adult Xenopus laevis. The specimens were treated with hydrochloric acid for extraction of the fibrous components in the connective tissues. Prior to metamorphosis, the muscle fibers appeared straight and flat. At the start of metamorphosis, they appeared crooked with uneven surfaces. Scanning electronmicroscopy revealed a marked increase in the number of macrophages and fibroblast-like cells in the muscle fibers. Transmission electronmicroscopy revealed an enlargement of the sarcoplasmic reticulum, the appearance of myelin structures and the uptake of muscle fragments by macrophages. The myofilaments in the muscle fragments were in different stages of decomposition. After denervation of the nervus ischiadicus, scanning electron-microscopy showed that the diameter of the muscles was reduced; a fine unevenness of the muscle surface could be observed. However, the cellular component in the muscle fibers was not obviously increased. Transmission electronmicroscopy showed that the sarcolemma and basal lamina were finely waved; cross striae were unclear due to a decrease in myofilaments. There are similarities in the structural changes which occur in the tail muscles of Xenopus laevis during tail involution and calf muscles after denervation, but the processes are not identical. In tadpols, nerves exert a secondary influence on structural changes of the muscles in the process of tail involution during metamorphosis.

Animals↗

Simulation of lithium transport along the thin segments of Henle's loop.

Although the renal clearance of lithium is widely used as an index of sodium and water delivery to the end of the proximal tubule, micropuncture studies of superficial nephrons suggest that lithium may be reabsorbed additionally in the loop of Henle. In order to examine the possibility of lithium transport in the thin loop segments of deep nephrons, we conducted a computer simulation study using a modification of the mathematical model reported previously. The data for the model were obtained from measurements of osmolality and electrolyte concentrations in systemic plasma and renal papillary interstitial fluid of control and furosemide-treated rats. Papillary interstitium/plasma Li+ concentration ratios were 3.23 and 1.48 in the control and the furosemide group, respectively. Assuming that solute concentration in the renal medulla increases as an exponential function, and applying phenomenological coefficients obtained from hamsters, the transport profiles of Li+ along the thin loop segments were calculated to be very similar to those of Na+. In the control group, about 82% of delivered Li+ was reabsorbed along the entire thin loop segments, with all segments contributing equally. This value may represent the highest possible capacity of the thin loop segments. In the furosemide group, Li+ reabsorption in the thin loop was reduced to 31% of delivered Li+. From these analyses, we conclude that an appreciable amount of lithium may be reabsorbed in the thin loop segments of long-looped nephrons by passive mechanisms. Furosemide inhibits Li+ reabsorption by dissipating the osmotic concentration gradient in the renal medulla.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of nafamostat mesilate on Na+ and K+ transport properties in the rabbit cortical collecting duct.

1. To determine the mechanism(s) of hyperkalemia caused by nafamostat mesilate (NM), a serine-protease inhibitor, we investigated the effects of the drug on Na+ and K+ transport properties of the collecting duct (CD) cell in the isolated and perfused cortical collecting duct from rabbit kidneys. 2. NM at 10(-4) M in the lumen, hyperpolarized the apical membrane in parallel with increases in transepithelial resistance (RT) and fractional apical membrane resistance (fRA). 3. These effects were completely inhibited by pretreatment with 50 microM luminal amiloride, whereas they were not affected by luminal addition of 2 mM Ba2+. 4. NM at 10(-4) M in the bath slightly but significantly depolarized the basolateral membrane without any changes in RT or fRA, although NM at 10(-5) M in the bath had no effect on the electrical parameters. 5. It is concluded that NM mainly acts on the apical membrane of the CD cell and inhibits the amiloride-sensitive Na+ conductance in the apical membrane.

Amiloride↗

Ultrastructure of wound healing following direct pulp capping with calcium-beta-glycerophosphate (Ca-BGP).

Tissue changes in rat incisors after direct pulp capping with calcium-beta-glycerophosphate (Ca-BGP) have been studied using light and electron microscopy. Immediately after pulp capping, Ca-BGP was converted to hydroxyapatite (HAP) at the cavity floor. At Day 1, the exposure site was covered with Ca-BGP-mediated mineralized tissue. Osteodentine had developed below this mineralized tissue at Day 3. Matrix vesicles (MV) were observed in the extracellular matrix between large cells and osteodentine. At Day 5, tubular dentine was observed below the osteodentine. Three days after the application of Ca(OH)2 in a control experiment, osteodentine had formed below the necrotic zone; however, tubular dentine was not observed at Day 5. These findings suggest that the applied Ca-BGP might be the source of Ca and inorganic phosphate (Pi) through hydrolysis by alkaline phosphatase (ALP), and that Ca-BGP-mediated mineralized tissue induces the early formation of tubular dentine.

Animals↗

Pathological mineralization in a serially passaged cell line from rat pulp.

The ultrastructure of crystal formation in association with dental pulp cells isolated from rat incisor was studied in vitro. A clone, RPC-K, was obtained and incubated with Na-beta-glycerophosphate (BGP). Growing pulp cells showed low alkaline phosphatase (ALP) activity, which began to increase with cell proliferation. Pulp cells formed cell multilayers after day 14 of culture. Mineralized tissues were observed within cell multilayers on day 28 of culture. Vesicular structures were found around degenerate and necrotic cells. Some of these vesicles contained needle-like crystals. Organic structures appeared at the periphery of mineralized tissues with a post-embedding demineralization and staining method. Electron diffraction patterns of the newly formed crystals revealed a pattern consistent with hydroxyapatite (HAP). These findings suggest that the RPC-K cell line might be useful for a model system to investigate pathological mineralization.

Alkaline Phosphatase↗

Effects of prostaglandin E2 on membrane voltage of the connecting tubule and cortical collecting duct from rabbits.

1. Effects of prostaglandin E2 (PGE2) on ion transport were examined by observing the transmural (VT) and basolateral membrane voltage (VB) in the in vitro perfused rabbit connecting tubule (CNT) and the cortical collecting duct (CCD). 2. Addition of 1 microM PGE2 to the bath induced a biphasic response of transmural voltage (VT), with initial negative VT deflection followed by positive deflection in the CNT, but monophasic negative deflection in the CCD. Because PGE2 had no affect on the basolateral membrane voltage (VB), PGE2 mainly causes changes in the apical membrane voltage. 3. Elimination of Na+ from the lumen abolished the PGE2-induced VT response in the CNT. In the presence of 10 microM luminal amiloride, PGE2 caused only an initial negative deflection without causing later positive deflection. The positive VT deflection induced by PGE2 in the CCD was also blocked by luminal amiloride. 4. Addition of ouabain (0.1 mM) to the bath completely abolished the PGE2-induced VT changes in the CNT, indicating that an intact Na(+)-K+ pump is a prerequisite for the VT response to PGE2. 5. Addition of 2 mM Ba2+ to the lumen did not affect biphasic VT response to PGE2, indicating that Ba(2+)-sensitive K+ conductance is not involved. 6. Basolateral addition of 0.1 mM 8-(4-chlorophenylthio)-cAMP inhibited only the negative VT deflection induced by PGE2. 7. The positive VT deflection was blocked by basolateral addition of 50 microM 8-(N,N-diethylamino)octyl 3,4,5-trimethoxy benzoate hydrochloride (TMB-8), an inhibitor of intracellular Ca2+ release. But elimination of luminal Ca2+ did not affect the biphasic response to PGE2. 8. These findings suggest that the initial negative VT deflection is caused by an increase in Na+ influx across the luminal membrane through an amiloride-insensitive Na+ conductive pathway, whereas the later positive deflection is caused by the inhibition of Na+ influx through the amiloride-sensitive Na+ conductive pathway. The cAMP messenger system may be responsible for the initial negative deflection, whereas an increased intercellular Ca2+ release from the store is necessary for the later positive deflection caused by PGE2. The response in the CCD is comparable to the later response in the CNT.

Amiloride↗

[Mutations of HIV-1 RT gene isolated from patients treated with AZT].

HIV-1 strains were isolated from three patients treated with AZT and from three patients not treated with AZT. Progenomes of HIV-1 RT gene were amplified by PCR and cloned to M13mp18 vecter. Four amino acid mutations in RT gene (Asp67, Lys70, Thr215, Lys219) associated with resistance to AZT were analysed. All of the 14 clones obtained from the three patients with AZT therapy had mutations at codon 215 (Thr-->Tyr or Phe). Some of the 14 clones also had other mutations at codon 67 (Asp-->Asn or Ser), codon 70 (Lys-->Arg) and codon 219 (Lys-->Glu). All of 18 clones obtained from the patients not treated with AZT have no mutation at any codon mentioned above.

Amino Acid Sequence↗