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Biomedical subjects

J Kobayashi

Publications and source records attributed to J Kobayashi.

At least 433 records · Page 24Linked to original sources
PubMed1988

Eudistomin derivatives, novel phosphodiesterase inhibitors: synthesis and relative activity.

The preparations of novel phosphodiesterase inhibitors, 8-acetoxy-5-iodo-6-methoxypyrido[3,4-b]indole, 5,7-dibromo-6-hydroxypyrido[3,4-b]indole, 5,7-dichloro-6-hydroxypyrido[3,4-b]-indole and 8-acetoxy-5-bromo-6-methoxypyrido[3,4-b]indole, are described together with concentrations giving 50% inhibition against cyclic AMP phosphodiesterase, i.e. 3 X 10(-6), 3 X 10(-6), 7 X 10(-6) and 1 X 10(-5) M, respectively. The relative potency of these eudistomin derivatives is discussed in terms of the chemical structures compared with those of other inactive eudistomins and derivatives.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1988

Infantile muscle glycogen storage disease: phosphoglucomutase deficiency with decreased muscle and serum carnitine levels.

We report a 5-month-old boy with recurrent vomiting, lethargy, and poor weight gain. He had profound metabolic acidosis and nonketotic dicarboxylic aciduria. The serum and muscle carnitine levels were significantly low (60% and 10% of the control means, respectively), suggesting that the patient had a systemic carnitine deficiency syndrome. The patient showed apparent clinical improvement on oral carnitine administration. A quadriceps muscle biopsy revealed a slight increase in intrafiber lipid droplets and mild accumulation of glycogen in the subsarcolemmal portion. An anaerobic glycolysis in vitro study showed a block after glucose-1-phosphate and before glucose-6-phosphate. Direct measurement of individual glycolytic enzymes in muscle of the patient demonstrated a marked decrease in phosphoglucomutase (PGM) activity (13% of the control mean). The specific defect of PGM activity in this patient suggests that the block in the anaerobic glycolytic pathway is the primary abnormality. PGM deficiency can be added as a newly recognized cause of secondary systemic carnitine deficiency syndromes.

Carnitine↗
PubMed1988

Silver-banded karyotypes of the rainbow trout and the brook trout and their hybrids: disappearance in allotriploids of Ag-NORs originated from the brook trout.

Silver-banded karyotypes of the rainbow trout Salmo gairdneri, the brook trout Salvelinus fontinalis, and their hybrids were described. Diploid-type and triploid-type hybrids were obtained. Triploid-type hybrids had two maternal genomes of the rainbow trout and one paternal genome of the brook trout. The rainbow trout had one pair of M or SM with Ag-NORs near the satellite. In the brook trout, Ag-NORs were observed in four pairs of chromosomes, but each cell had different number of chromosomes with Ag-NORs. In all observed cells of triploid-type hybrids, Ag-NORs originated from the brook trout were not recognized, whereas those from the rainbow trout were found.

Animals↗
PubMed1988

[Study on luteal insufficiency by the two-step LH-RH test].

To clarify both the releasing function and the self-priming effect of LH-RH on gonadotropins of the anterior pituitary gland, two step administration of 100 micrograms of synthetic LH-RH at a 60 minutes interval (two step LH-RH test) was carried out in 29 women with luteal insufficiency, 10 women in luteal phase just after spontaneous abortion, 12 women in puerperium and 24 women with normal menstrual cycles. Native LH, FSH and their subunits were measured by radioimmunoassay and serum progesterone (P), estradiol (E2) and prolactin (PRL) were also measured before administration of LH-RH. By defining hormone release (1st peak level-0' level) as delta 1, self-priming effect (2nd peak level-60' level) as delta 2 and delta 2/delta 1 as delta 1 delta 2 ratio, in the luteal insufficiency group, especially in the cases with lower of serum P and E2, delta 1 was significantly higher and the delta 1 delta 2 ratio was lower than those in the control group. In the abortion group, delta 1 and delta 2 were similar to those in the control group, indicating rapid recovery of the anterior pituitary function. In the puerperium group (approximately 1 month after delivery), delta 1 was higher and the delta 1 delta 2 ratio was lower than those in the control group. This suggests that the puerperium is more or less similar to the period of luteal insufficiency. The results also indicate that the two step LH-RH test can be one of the useful methods for the study of luteal insufficiency in terms of the pituitary gonadotropin synthesis and release.

Abortion, Spontaneous↗
PubMed1987

Mode of inhibition of brain Na+,K+-ATPase by agelasidines and agelasines from a sea sponge.

The Na+,K+-ATPase from brain or kidney and sarcoplasmic reticulum (SR) Ca2+-ATPase were inhibited potently by agelasidine C (Agd-C) and agelasine B (Ags-B), the bioactive principles of sea sponge, while Agd-C and Ags-B exerted less potent inhibition of heart Na+,K+-ATPase. The ionized moiety in Agd-C and the long nonpolar side chains in Ags-B play important roles in their inhibitory action. The inhibition of Na+,K+-ATPase by Agd-C or Ags-B was virtually reversed by diluting with the inhibitor-free solution. Kinetic analysis of the inhibitory effects of Agd-C and Ags-B indicates that the inhibition of pig brain Na+,K+-ATPase is parabolic and noncompetitive with respect to ATP. This may indicate that the inhibition of Na+,K+-ATPase results from the binding of two molecules of Agd-C or Ags-B to one enzyme. The sigmoidal behavior (n = 1.3-1.4) in the K+ activation curve for Na+,K+-ATPase was strikingly intensified (n = 2.1) by Agd-C, whereas it was almost eliminated (n = 1.1) by Ags-B. These results suggest that the cooperative interaction between K+-binding sites on the enzyme was dramatically altered.

Animals↗
PubMed1987

The mechanism of inhibition of light-chain phosphorylation by purealin in chicken gizzard myosin.

The actin-activated Mg2+-ATPase activity of dephosphorylated chicken gizzard myosin reconstituted with actin, tropomyosin, myosin light-chain kinase (MLCK) and calmodulin was inhibited completely by purealin, 20 microM, whereas the activity of the phosphorylated and dephosphorylated myosin was not affected. Purealin inhibited the phosphorylation of myosin light chains caused by MLCK and calmodulin (IC50, 5 microM). On the other hand, purealin had no effect on myosin phosphorylation induced by Ca2+ -independent MLCK. The calmodulin-stimulated phosphodiesterase activity was inhibited by purealin (IC50, 7 microM) at concentrations very close to those that inhibit myosin phosphorylation. Kinetic analysis revealed a competitive mode of inhibition of calmodulin-stimulated phosphodiesterase activity by purealin. These results suggest that purealin acts as a calmodulin antagonist in reconstituted actomyosin from chicken gizzard, resulting in inhibition of light chain phosphorylation and the actin-activated ATPase activity of myosin.

Adenosine Triphosphatases↗
PubMed1987

Purealin, a novel activator of skeletal muscle actomyosin ATPase and myosin EDTA-ATPase that enhanced the superprecipitation of actomyosin.

1. Purealin, a novel bioactive principle of a sea sponge Psammaplysilla purea, activated the superprecipitation of myosin B (natural actomyosin) from rabbit skeletal muscle. The maximum change in the turbidity increased with increasing purealin concentrations and was three times the control value in the presence of 50 microM purealin. 2. The ATPase activity of myosin B was also elevated to 160% of the control value by 10 microM purealin. On the other hand, purealin inhibited the myosin ATPase in the presence of 10 mM CaCl2 and 0.5 M KCl (Ca2+-ATPase), and the concentration for the half inhibition was 4 microM. 3. On the other hand, purealin activated the myosin ATPase in the presence of 5 mM EDTA and 0.5 M KCl (EDTA-ATPase). The maximum activation by 10 microM purealin was 160% of the control value. 4. Furthermore, similar results concerning the modification of ATPase activities by purealin were obtained in myosin subfragment-1 instead of myosin. 5. These results suggest that purealin activates the superprecipitation of myosin B by affecting the myosin heads directly. It is also an interesting observation that there is a correlation between the activities of the myosin EDTA-ATPase and actomyosin ATPase of myosin B.

Adenosine Triphosphatases↗
PubMed1987

Enhancement of the actin-activated ATPase activity of myosin from canine cardiac ventricle by purealin.

The effects of purealin isolated from the sea sponge, Psammaplysilla purea, on the enzymatic properties of myosin and natural actomyosin (a complex of myosin, actin, tropomyosin and troponin) from canine cardiac ventricle were studied. Purealin increased the ATPase activity of natural actomyosin and the actin-activated ATPase activity of myosin, and accelerated the superprecipitation of natural actomyosin. The Ca2+- and Mg2+-ATPase activities of myosin were inhibited by purealin, whereas the K+-EDTA-ATPase activity was increased. These results suggest that purealin binds to the myosin portion involved in actin-myosin interaction and increases the actin-activated ATPase activity of myosin.

Actins↗
PubMed1987

omega-Hydroxyemodin, a major hepatic metabolite of emodin in various animals and its mutagenic activity.

The hepatic microsomes derived from various animal species transformed emodin (1,3,8-trihydroxy-6-methylanthraquinone), an anthraquinoid pigment present in fungal metabolites and a constituent of plant medicines, into an unidentified anthraquinone h, along with 2-hydroxy-, 4-hydroxy- and 7-hydroxyemodins. TLC, UV, MS and NMR clarified this unidentified major metabolite as omega-hydroxy-emodin (1,3,8-trihydroxy-6-hydroxymethylanthraquinone). Among 7 animal species, the highest activity to produce this omega-hydroxyemodin was observed in the hepatic microsomes of guinea pig and rat, followed by mouse and rabbit. The microsomal activity to convert emodin into omega-hydroxyemodin was accelerated by the pretreatment of animals with phenobarbital, and inhibited by SKF 525A. The microsomal hydroxylation reactions of the methyl residue and the anthraquinoid nucleus of emodin were presumed to be catalyzed regiospecifically by multiple forms of cytochrome P-450. omega-Hydroxyemodin was not mutagenic to Salmonella typhimurium in the absence of S9, but exhibited mutagenicity in the presence of an activating system. This genotoxic potential was comparable to 2-hydroxyemodin, a direct-acting mutagen.

Animals↗
PubMed1987

The cytochrome P-450-dependent hydroxylation of T-2 toxin in various animal species.

Gas-liquid chromatography was used to investigate the hepatic and intestinal metabolism of T-2 toxin, a cytotoxic and immunodepressive trichothecene produced by species of Fusarium. The hepatic S-9 and microsomal fractions of various species hydroxylated T-2 toxin to form 3'-hydroxy-T-2. HT-2 toxin, a deacetylated metabolite of T-2 toxin formed by reactions involving microsomal esterases, was also hydroxylated, to 3'-hydroxy HT-2 toxin. Experiments with inhibitors and inducers of the cytochrome P-450-dependent system revealed that these two hydroxylation reactions were catalysed by the cytochrome P-450-dependent monooxygenase system. Species comparisons using rats, mice, guinea-pigs, rabbits, pigs, cows and chickens showed that the rate of the hydroxylation reaction was highest in the hepatic microsomes of guinea-pigs, followed by mice. Chickens possessed a low activity both in the hydrolysis and hydroxylation reactions. No hydroxylated metabolites were produced by the intestinal microsomes of rabbits. These two hydroxylated metabolites were far less cytotoxic to Reuber hepatoma cells than the parent compound, T-2 toxin.

Animals↗
PubMed1987

Additional aortopulmonary anastomosis for subaortic obstruction in the Rastelli-type repair for the Taussig-Bing malformation.

In the Taussig-Bing malformation, residual subaortic obstruction from a hypertrophied subaortic conus is often a problem at the time of intraventricular repair. To alleviate this problem, during a Rastelli-type repair involving an extracardiac valved conduit and an intraventricular connection from the ventricular septal defect to both aortic and pulmonary outflows, an additional side-to-side anastomosis between the ascending aorta and the proximal portion of the divided pulmonary artery can be performed, creating a supplementary outflow for the left ventricle. This method was used in 2 patients who had anteroposterior transposition of the great arteries, with 1 long-term survivor.

Aorta↗