[The skull and the dentofacial complex in extremely immature infants and very low birth weight infants].
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Cephalometry↗
Biomedical subjects
M Fujiwara
Publications and source records attributed to M Fujiwara.
Site and mechanism of growth inhibition by prostaglandins. IV. Effect of cyclopentenone prostaglandins on cell cycle progression of G1-enriched HeLa S3 cells.
HeLa S3 cells were enriched in the G1 phase of cell cycle by serum starvation and used for analysis of prostaglandin (PG) effect on cell cycle progression. Cell cycle progression was initiated by incubating the G1-enriched cells with fresh medium containing 10% fetal calf serum and analyzed in the presence of 40 nM colcemid to block renewal of the cycle. When progression of control cells was analyzed under these conditions, time-dependent decrease in the number of G1 phase cells and increase in that of G2/M phase cells were observed during the 24-hr incubation. Cells in S phase increased transiently during this period. Proportions of cells in G1 and G2/M phases were 65 and 15% of the total cells at 0 hr and 10 and 80% at 24 hr, respectively. When the cells were treated with either PGA2 or 9-deoxy-delta 9,12-13,14-dihydroprostaglandin D2 (delta 12-PGJ2) for more than 3 hr, inhibition of G1 phase progression became evident 3 to 6 hr after the PG addition. Progression through S phase was slowed but not arrested with the PG treatment. When cells treated with PGA2 were washed and transferred to fresh medium, G1 phase progression was resumed and transition to S phase was observed about 6 hr after the wash. However, the arrest by delta 12-PGJ2 was irreversible and no recovery was observed with washing of the cells treated with this PG. The sensitivities of cells to PG in different phases of cell cycle were compared by treating G2/M phase cells with delta 12-PGJ2.(ABSTRACT TRUNCATED AT 250 WORDS)
Cell Cycle↗
[A study on ceftriaxone in the perinatal period].
Ceftriaxone (CTRX), a new cephem antibiotic with high activity against Gram-positive and Gram-negative bacteria, was investigated pharmacokinetically in 30 mothers in the perinatal period. The obtained results are summarized below. 1. The maximum CTRX level in the maternal serum was 135 micrograms/ml between 20 and 25 minutes after an intravenous administration of 1 g of CTRX. 2. The transfer of CTRX into the umbilical cord serum and the amniotic fluid was very good. CTRX levels in these fluids were about 20% and 10% of the maternal serum level, respectively. 3. No side effect was observed in mothers or neonates. 4. CTRX is a useful antibiotic for perinatal infections.
Abortion, Induced↗
[Three cases of severe delayed hemolytic transfusion reaction by irregular antibody after cardiac surgery].
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Adult↗
Noradrenaline turnover after left coronary artery ligation in rat heart.
The levels and the turnover of noradrenaline were measured in the left and right ventricles following left coronary artery ligation for 2 h in untreated, adrenalectomized or hexamethonium-treated rats. Noradrenaline in the left ventricles was decreased by ligation and unaffected in the right ventricles, whether of untreated, adrenalectomized or hexamethonium-treated animals. Turnover in the left ventricles, as estimated by the decrease of noradrenaline under dopamine beta-hydroxylase inhibition with bis-(4-methyl-1-homo-piperazinyl-thiocarbonyl)-disulfide (FLA-63), was unaffected by ligation whether in untreated, adrenalectomized, or hexamethonium-treated rats. Ligation accelerated turnover in the right ventricles of untreated rats or attenuated it in adrenalectomized rats and caused no changes in hexamethonium-treated rats. These results suggest that noradrenaline turnover in ischemic myocardium is not affected by regional ischemia and that such ischemia might accelerate turnover in the non-ischemic area, probably as a result of increased activity of sympatho-adrenal reflexes.
Adrenalectomy↗
Effects of alismol isolated from Alismatis Rhizoma on calcium-induced contraction in the rabbit thoracic aorta.
We examined the inhibitory effects of alismol, a sesquiterpenoid isolated from Alismatis Rhizoma, on vascular contractions induced by high concentrations of K+ and Ca2+, and on 45Ca2+ retention in normal and in high K+-containing medium. Alismol affected neither the resting tension nor the 45Ca2+ retention in normal medium, but it inhibited sustained contraction and increased 45Ca2+ retention induced by high K+ concentrations. Alismol did not affect norepinephrine-induced contractions in normal medium, nor phasic contractions in Ca2+-free medium. These results suggested that alismol inhibited mainly Ca2+ influx through a voltage-dependent Ca2+ channel.
Animals↗
Effects of anoxia and ischemia on uptake2 of catecholamines in perfused rat heart.
The effects of 30 min periods of either anoxia or ischemia (stop-flow) on the uptake2 of isoprenaline and on the production of O-methyl-isoprenaline, a major metabolite of isoprenaline formed by catechol-O-methyltransferase (COMT), were examined in the perfused rat heart. After either glucose deprivation or anoxia, the uptake2 of isoprenaline in hearts subsequently perfused with isoprenaline and 3',4'-dihydroxy-2-methyl-propiophenone, a COMT inhibitor, was similar to control values. However, uptake2 was decreased following either anoxia in association with glucose deprivation or ischemia. In the absence of the COMT inhibitor, neither glucose deprivation nor anoxia alone had any effect on the production of [3H]3-O-methyl-isoprenaline from [3H]isoprenaline, but both anoxia together with glucose deprivation and stop-flow ischemia decreased it. These findings indicate that both anoxia coupled with glucose deprivation and ischemia inhibit both uptake2 and COMT activity and suggest that such inhibition may be responsible for the high concentration of catecholamines released locally following myocardial infarction.
Animals↗
Effects of barbiturates on the inhibitory action of GABA on excitatory response of the stomach to stimulation of vagal afferent fibers in cat.
Effects of barbiturates on the inhibitory action of GABA to the hexamethonium-resistant excitatory response of the stomach to stimulation of the vagal afferent fibers were studied in cats. Inhibition of the hexamethonium-resistant excitatory response by GABA were compared under alpha-chloralose, alpha-chloralose-phenobarbital (PhB), and alpha-chloralose-pentobarbital (PB)-anesthesia in cats. The ID50 of GABA on the hexamethonium-resistant excitatory response was not significantly affected by PhB, but reduced by PB. Both picrotoxin and bicuculline antagonized the effects of GABA. The present experiments demonstrated that PB potentiated the inhibitory effect of GABA on the hexamethonium-resistant excitatory response of the stomach, and suggested that the potentiation by PB may be due to activation of GABA-receptor-ionophore complex.
Afferent Pathways↗
ADP-ribosylation by type C1 and D botulinum neurotoxins: stimulation by guanine nucleotides and inhibition by guanidino-containing compounds.
We recently reported that type D botulinum neurotoxin ADP-ribosylates a specific protein of Mr 21,000 in membrane fractions of various tissues (Ohashi, Y. and Narumiya, S. (1987) J. Biol. Chem. in press). We examined similar enzyme activities in other types (types A, B, C1 and E) of botulinum neurotoxins. Of these, only type C1 toxin showed the activity similar to type D toxin and ADP-ribosylated the same Mr 21,000 protein in membranes of mouse brain. No enzyme activities were detected in type A, B and E toxins under the present experimental conditions. GTP stimulated ADP-ribosylation by the two toxins in a concentration dependent manner from 10 nM to 100 microM. The maximum stimulation was about 6 fold. GDP was 10 times less potent than GTP and achieved similar maximum at 1 mM, while GMP, ADP and ATP had little effect. Several guanidino-containing compounds dose-dependently inhibited the activities of both toxins. The IC50 values were 8.5, 14.5 and 45 mM for agmatine, L-arginine methyl ester and guanidine, respectively.
Adenosine Diphosphate Ribose↗
Preferential synthesis of diacyl and alkenylacyl ethanolamine and choline glycerophospholipids in rabbit platelet membranes.
In rabbit platelet membranes, the contents of alkenylacyl phospholipids (plasmalogen) were 56% of phosphatidylethanolamine and 3% of phosphatidylcholine. This uneven distribution of plasmalogens in each phospholipid class could be attributed to the different substrate specificity of ethanolaminephosphotransferase (EC 2.7.8.1) and cholinephosphotransferase (EC 2.7.8.2). The properties of the enzymes were studied, using endogenous diglycerides and CDP-[3H]ethanolamine or CDP-[14C]choline as substrates. The newly formed phospholipids were mainly diacyl and alkenylacyl and only rarely alkylacyl type. The ratios of the labeled alkenylacyl to diacyl type of phospholipids clearly varied with the concentrations of CDP-ethanolamine or CDP-choline. When 1, 10, and 30 microM CDP-[3H]ethanolamine were used, the labeled phospholipids contained 53, 37, and 27% of the alkenylacyl type, respectively. The apparent Km for CDP-ethanolamine to synthesize alkenylacyl and diacyl types were 2.2 and 8.1 microM. On the other hand, when 1, 10, and 30 microM CDP-[14C]choline were used, the labeled lipids contained 10, 17, and 24% alkenylacyl type, respectively. The apparent Km for CDP-choline to synthesize alkenylacyl and diacyl types were 24 and 4.3 microM. Further, the syntheses of diacyl type of phosphatidylethanolamine and the alkenylacyl type of phosphatidylcholine were markedly inhibited by unlabeled CDP-choline and CDP-ethanolamine, respectively. The two enzymes had opposite substrate specificities, and ethanolaminephosphotransferase showed a high preference to plasmalogen synthesis, especially in the presence of CDP-choline.
Animals↗
Effects of extraneuronal uptake inhibitors on the positive chronotropic response to isoprenaline and on the accumulation of isoprenaline in perfused rat heart after inhibition of catechol-O-methyl transferase.
Experiments were carried out in isolated perfused rat hearts. The presence of tropolone (100 mumol/l), an inhibitor of catechol-O-methyl transferase (COMT), significantly potentiated the positive chronotropic response to isoprenaline (0.1, 1, 3 and 10 nmol/l). Two uptake2 inhibitors, 3-O-methylisoprenaline (100 mumol/l) and normetanephrine (100 mumol/l), induced a positive chronotropic response, but corticosterone (100 mumol/l) and hydrocortisone (100 mumol/l) had no such effect. 3-O-methylisoprenaline (100 mumol/l) and normetanephrine (100 mumol/l) enhanced the positive chronotropic response to isoprenaline (0.1, 1, 3 and 10 nmol/l). Corticosterone (100 mumol/l) potentiated the positive chronotropic response to isoprenaline (0.1 and 1 nmol/l). Hydrocortisone (30 mumol/l) enhanced the response to 0.1 nmol/l isoprenaline but did not affect the positive chronotropic responses to 1, 3 or 10 nmol/l isoprenaline. The addition of uptake2 inhibitors (3-O-methylisoprenaline, 100 mumol/l; normetanephrine, 100 mumol/l; corticosterone, 100 mumol/l) to the perfusion medium significantly reduced the positive chronotropic response to the perfusion with isoprenaline (3 nmol/l) and tropolone (100 mumol/l). The accumulation of 3H-isoprenaline in the heart perfused with 3H-isoprenaline (1, 10 and 100 nmol/l) was significantly increased by the presence of tropolone (100 mumol/l): the accumulation for 1, 10 and 100 nmol/l of 3H-isoprenaline was 5.07, 47.0 and 500 pmol/g, respectively. The high accumulation observed during perfusion with 3H-isoprenaline (3 nmol/l) and tropolone (100 mumol/l) was significantly decreased by the addition of an uptake2 inhibitor, 3-O-methylisoprenaline (100 mumol/l), normetanephrine (100 mumol/l) or corticosterone (100 mumol/l), but not by hydrocortisone (30 mumol/l).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Postcolumn fluorometric detection system for liquid chromatographic analysis of amino and imino acids using o-phthalaldehyde/N-acetyl-L-cysteine reagent.
A high-performance liquid chromatographic system for the determination of amino acid and imino acid was developed using a two-step reaction with sodium hypochlorite and o-phthalaldehyde/N-acetyl-L-cysteine (OPTA/AcCys) reagent. This reagent improved the sensitivity in the analysis of proline presumably because the fluorophore is more stable to hypochlorite which has been used for the oxidative cleavage of the imino linkage. The use of OPTA/AcCys facilitated the detection of imino acids at the same concentration level as that of amino acids. The detection limit for all the amino and imino acids was a few picomoles. This detection system, together with cation-exchange chromatographic separation, was applied to the determination of amino and imino acids in biological samples.
Acetylcysteine↗
Biogenic amines in the Arthus reaction.
The concentrations of serotonin, tryptamine, dopamine, and tyramine were quantitatively determined in the Arthus reaction, since the activity of histamine-N-methyltransferase (HMT), a major histamine-metabolizing enzyme that had been demonstrated to be inhibited by such biogenic amines in vitro, decreased significantly in the reaction site. The concentrations of serotonin, tryptamine, and dopamine were unchanged in dinitrochlorobenzene allergic and croton oil dermatitis except for a slight increase of tryptamine in the latter. Tyramine was unable to be demonstrated quantitatively in all specimens tested. The concentration of serotonin decreased to about 30% that of the control level until 1 hr, followed by a prominent increase to about two-fold at 6 hr after the initiation of the Arthus reaction accompanying with a concomitant decrease in HMT activity. However, the concentrations of tryptamine and dopamine were rather decreased in the reaction site, and the net decrease of two amines was far greater than the increased amount of serotonin. The decrease in HMT activity is not stoichiometrically well elucidated from these results, and therefore, the presence of other hypothetic inhibitory factors that are increased in the Arthus reaction should be suspected.
Animals↗
The immunopathology of adoptively transferred experimental allergic encephalomyelitis (EAE) in Lewis rats. Part 1. Immunohistochemical examination of developing lesions of EAE.
In order to examine developing lesions of experimental allergic encephalomyelitis (EAE) at the preclinical stage, adoptive transfer of EAE was achieved in Lewis rats using spleen cells obtained from rats previously immunized with 50 micrograms of guinea pig myelin basic protein (MBP) in complete Freund's adjuvant. After cell transfer, all the recipient rats developed severe paraparesis with minimal variation in the onset of clinical signs, which facilitated immunohistochemical examination of developing lesions of EAE in asymptomatic animals. The initial pathological finding detected in this system was an increased number of inflammatory cells (both OX19+ and OX8+ T cells and macrophages) in the subarachnoid space (SAS) which was observed on day 3 post-transfer (PT) when the recipient animals showed no neurological abnormalities. By day 4 PT, inflammatory cells were detected in the Virchow-Robin space of vessels which were continuous to the SAS. Perivascular lymphocytic infiltration was scarcely detected in the gray matter. On day 5 PT, the rats showed severe paraparesis. Inflammatory foci increased in number and were detected in both the white and gray matter. Diffuse parenchymal T-lymphocyte infiltration was also recognized at this stage. From day 6 PT onwards, inflammatory cells decreased gradually. On day 8 PT, all the rats recovered from EAE and few inflammatory cells were detected in the parenchyma and SAS. Immunohistochemical examination of T-cell subsets and Ia antigens revealed that the number of OX19+ cells was greater than that of OX8+ cells in the parenchyma and SAS at all stages examined, the distribution of OX19+ cells was almost the same as that of OX8+ cells, OX8+ cells decreased in number before clinical signs subsided, and that after the infiltration of T cells into the parenchyma, cells with dendritic morphology (microglia) expressed Ia antigens in close association with the infiltrating T cells. Adoptive transfer of MBP-sensitized spleen cells provides constant induction of EAE with minimal variation in clinical onset and severity, thus being a useful model for the examination of early events of EAE.
Albumins↗
Noradrenergic involvement in catalepsy induced by delta 9-tetrahydrocannabinol.
In order to elucidate the role of the catecholaminergic system in the cataleptogenic effect of delta 9-tetrahydrocannabinol (THC), the effect of pretreatment with 6-hydroxydopamine (6-OHDA) or with desipramine and 6-OHDA and lesions of the locus coeruleus were investigated in rats. The cataleptogenic effect of THC was significantly reduced in rats treated with 6-OHDA and in rats with lesions of the locus coeruleus but not in rats treated with desipramine and 6-OHDA, as compared with control rats. On the contrary, the cataleptogenic effect of haloperidol was significantly reduced in rats treated with desipramine and 6-OHDA but not in rats treated with 6-OHDA or in rats with lesions of the locus coeruleus. These results indicate that noradrenergic neurons have an important role in the manifestation of catalepsy induced by THC, whereas dopaminergic neurons are important in catalepsy induced by haloperidol.
Animals↗
The involvement of neuropeptide Y in the antimuricide action of noradrenaline injected into the medial amygdala of olfactory bulbectomized rats.
The present study was designed to clarify the functional role of neuropeptide Y (NPY) in the regulation of muricide induced by olfactory bulbectomy (OB) in relation to that of noradrenaline (NA) in the medial amygdala (AME). NA injected into AME inhibited muricide dose-dependently in OB rats. NPY at doses of 5 and 10 micrograms/microliter injected alone into AME failed to suppress muricide. When NPY 10 micrograms was injected into AME in combination with the maximal non-effective dose of NA, which was determined in each rat, muricide was suppressed in 80% of OB rats. The present study has provided the first evidence suggesting that NPY may be involved in the regulation of OB-induced muricide.
Aggression↗
The role of brain catecholamines in the exhibition of muricide induced by nucleus accumbens lesions and the effect of antidepressants in rats.
Changes in brain catecholamine content after lesioning the nucleus accumbens (ACC) and the effects of antidepressants were investigated using HPLC-ECD. ACC lesion reduced dopamine (DA) in the rostral caudate-putamen (r-CP), lateral hypothalamus (LH) and central amygdala (ACE). Imipramine (IMP) and nomifensine (NOM) increased DA in r-CP, caudal (c)-CP and basolateral amygdala. Mianserin (MIAN) and zimelidine (ZIM) increased DA only in c-CP. ACC lesion did not change DOPAC. Only IMP (in c-CP) and NOM (in r-CP and c-CP) increased DOPAC. Noradrenaline (NA) was decreased in c-CP and ACE after ACC lesion. IMP and ZIM displayed no effect on NA, while NOM increased NA in LH and frontal cortex (FC) and MIAN only in FC. These results suggest an important role for DA but not NA in the exhibition of muricide after ACC lesion, and in the antimuricide effect of antidepressants.
3,4-Dihydroxyphenylacetic Acid↗
The effect of neurotransmitters on cataleptic behavior induced by PG D2 in rats.
The effects of several neurotransmitters on prostaglandin (PG) D2-induced cataleptic behavior in rats were investigated by the high bar test. Intracerebroventricular administration of PG D2 elicited cataleptic behavior in a dose-dependent manner without producing a marked change in spontaneous motor activity. The incidences of cataleptic behavior were 20% and 100% at doses of 2 nmol and 50 nmol of PG D2, respectively. Intraperitoneal pretreatment with L-DOPA (100 mg/kg), apomorphine (1 mg/kg), amantadine (0.2 mg/kg), atropine (0.5 mg/kg) or p-chlorophenylalanine (300 mg/kg) significantly decreased the cataleptic behavior induced by 50 nmol of PG D2. Conversely, simultaneous treatment with 5-hydroxy-L-tryptophan (30 mg/kg), 5-methoxy-N,N-dimethyltryptamine (5 mg/kg), imipramine (20 mg/kg) or clomipramine (10 mg/kg) markedly increased the cataleptic behavior induced by 2 nmol of PG D2. Propranolol (10 mg/kg) and phenoxybenzamine (10 mg/kg) did not affect the induction of cataleptic behavior by either 2 nmol or 50 nmol of PG D2. These results suggest that PG D2 might be involved in inducing cataleptic behavior by modulating serotonergic, cholinergic and dopaminergic systems.
Acetylcholine↗