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Biomedical subjects

A Honda

Publications and source records attributed to A Honda.

At least 217 records · Page 12Linked to original sources
PubMed1984

Arachidonic acid metabolic pathways in the rabbit pericardium.

Minced rabbit pericardium actively converts [1-14C]arachidonic acid into the known prostaglandins (6-[1-14C]ketoprostaglandin F1 alpha, [1-14C]prostaglandin E2 and [1-14C]prostaglandin F2 alpha) and into several unidentified metabolites. The major metabolite was separated by C18 reverse-phase high-pressure liquid chromatography (HPLC) and identified by gas chromatography-mass spectrometry (GC-MS) to be 6,15-[1-14C]diketo-13,14-dihydroprostaglandin F1 alpha. The other nonpolar metabolites were 15-[1-14C]hydroxy-5,8,11,13-eicosa-tetraenoic acid (15-HETE), 11-[1-14C]hydroxy-5,8,12,14-eicosatetraenoic acid (11-HETE) and 12-[1-14C]hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE). Arachidonic acid metabolites actively produced by the pericardium could influence the tone of surface blood vessels on the myocardium.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1984

Interaction of Trimeresurus flavoviridis phospholipase A2 and its fragment with calcium ion.

Dimeric T. flavoviridis phospholipase A2 has been studied in terms of the interaction with essential Ca2+ by equilibrium gel filtration, ultraviolet difference spectroscopy, fluorescence measurements, and chemical modifications with p-bromophenacyl bromide. The subunit bound to Ca2+ with a 1:1 molar ratio and no cooperative binding was observed. The hypochromic effect produced upon the binding of Ca2+ is due to perturbation of (a) specific tryptophan residue(s) located in the vicinity of the active site and appears to be characteristic of this enzyme. On the basis of the pH dependence of the dissociation constants, it has been found that the alpha-amino group (pKa 8.7) controls the binding of Ca2+. Deprotonation of the alpha-amino group is possibly accompanied by conformational transition to the active form which is able to bind Ca2+. This is in contrast to the case of bovine pancreatic phospholipase A2 in which Asp-49 (pKa 5.2) is responsible for the metal ion binding (Fleer et al. (1981) Eur. J. Biochem. 113, 283-288). Des-octapeptide(1-8)-phospholipase A2 (L-fragment) was found to be capable of binding Ca2+ under the control of a group with a pKa of 7.6. This pKa value was similar to an apparent pKa of 7.5 determined for the histidine residue in the active site of the native enzyme by way of p-bromophenacyl bromide modification. It appears that the N-terminal (octapeptide) sequence affects the binding mode of Ca2+, possibly because of conformational transition arising from its removal. The reinvestigation showed that the N-terminal octapeptide sequence is Gly-Leu-Trp-Gln-Phe-Glu-Asn-Met.

Animals↗
PubMed1984

In vitro and in vivo detection of infectious pancreatic necrosis virus in fish by enzyme-linked immunosorbent assay.

A double antibody enzyme-linked immunosorbent assay (ELISA) was used to detect infectious pancreatic necrosis virus (IPNV). The ELISA detected VR299 strain of IPNV at a dose of 10 to 20 ng of purified IPNV protein or 10(4) TCID50 in tissue culture fluid. Specificity of ELISA was demonstrated by an ELISA inhibition test. The ELISA did not detect infectious hematopoietic necrosis virus. Normal cell culture fluid and virus-non-inoculated rainbow trout (Salmo gairdneri Richardson) homogenate did not react in the test system. The IPNV was detected in rainbow trout fry inoculated with IPNV. Although infective virus titer in fish decreased rapidly 1 week after inoculation, IPNV antigen was detected by ELISA for 15 days. The IPNV antigen was detected in the fish tissue after inactivation of infective virus. The ELISA is a rapid and reliable method for the diagnosis of IPNV infection.

Animals↗
PubMed1984

Pharmacological manipulation of canine cyclooxygenase and thromboxane synthetase in vivo: differential renal and platelet recovery rates.

Aspirin (acetylsalicylic acid) was chronically infused i.v. into dogs at a low dose (0.1 mg/kg/hr) using a surgically implanted Alzet osmotic pump. The time course for inhibition of cyclooxygenase and for its recovery after removal of the pump were followed in washed platelet preparations and in kidney medulla microsomes using [14C]arachidonic acid metabolism. Chronic acetylsalicylic acid infusion inhibited platelet cyclooxygenase 60% after 1 day of treatment and 95% after 3 days. Recovery of platelet arachidonate metabolism after removal of the osmotic pump was very rapid (T 1/2 = 0.9 days). Renal cyclooxygenase was also completely inhibited after 3 days but showed a slower recovery rate (T 1/2 = 2.8 days). Therefore, canine platelets, unlike human platelets, recover more rapidly from acetylsalicylic acid inhibition than do the kidneys. We have also established a whole blood method to study the effective time course of thromboxane synthetase inhibitors. The relative potencies for inhibiting platelet thromboxane synthetase after i.v. bolus administration of the agents studied was OKY-1581 greater than OKY-046 = dazoxiben much greater than Ro 22-7878. The effective half-life of OKY-1581, OKY-046 and dazoxiben was 2 hr while the half-life of Ro 22-7878 was 0.5 hr.

Animals↗
PubMed1983

Alterations of glycosaminoglycans synthesized by chick embryo cartilage treated with 6-amino-nicotinamide.

Treatment of day-4 chick embryos with 6-aminonicotinamide (6-AN) impairs limb chondrogenesis and produces micromelia. However, treatment of day-10 chick embryos with 6-AN does not produce micromelia. In the present study, the glycosaminoglycan (GAG) biosynthesis in the cartilage isolated from the day-10 chick embryos treated with 6-AN in vitro and in the cartilage from the day-11 chick embryos treated with 6-AN in ovo at day-10 was examined. In the epiphyseal cartilage treated in vitro, the radioactivity incorporated into the GAG fraction was significantly decreased and the 35S/3H ratio in the GAG fraction and the molecular size of GAG chain were also decreased. However, the percent distribution of delta Di-0S was almost unchanged. In the epiphyseal and diaphyseal cartilage treated in ovo at day-10, the alteration in GAG biosynthesis was not observed except the reduction of the molecular size of GAG in epiphyseal cartilage. Furthermore, the biosynthetic activity of GAG in the process of recovery/repair was also examined using the micromelial cartilage isolated from day 11-chick embryos given 6-AN in ovo at day-4. In the diaphyseal cartilage, the radioactivity incorporated into the GAG fraction and the 35S/3H ratio were increased, whereas the percent distribution of delta Di-0S was almost unchanged. These results indicate that treatment of day-4 chick embryos with 6-AN produces the rebound phenomena in the diaphyseal cartilage isolated at day-11.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Aminonicotinamide↗
PubMed1983

Limb deformity induced in chick embryo by hydroxyurea.

After a dose of 800 micrograms of hydroxyurea (HU) was administered to day-4 chick embryos in ovo, the limb deformity including micromelia was observed. We examined the teratogenic mechanism of the action for HU by using histochemical and biochemical techniques. The present study provides histological evidence for the cell death and the depression of cell proliferation just after the treatment with HU and the retardation in periosteal ossification during the process of repair and/or recovery from cell death. On the other hand, the incorporation of [3H]glucosamine and [35S]sulfate into glycosaminoglycan was inhibited at day-7 and day-9, when the embryos are in the process of repair and/or recovery. The cartilage specific proteoglycan, an index of chondrogenesis, appeared at day-7, but the ratio of cartilagenous proteoglycan/noncartilagenous proteoglycan in the treated limbs was depressed. These results suggest that the slight retardation in chondrogenesis and/or the incomplete function of chondrocyte were induced by the treatment with HU in chick embryos. It is considered from above observation that the retardation in chondrogenesis and osteogenesis caused during the repair and/or recovery process of cell death brought about the limb deformity; shortening, thinning and bending of hind limbs.

Animals↗
PubMed1983

[Experience in treatment of Mycoplasma pneumoniae with acetylspiramycin].

Antibiotics of tetracycline and macrolide groups are mainly used in treatment of Mycoplasma pneumonia. In this study, acetylspiramycin (ASPM), an antibiotic of macrolide group, was given to 15 cases of Mycoplasma pneumoniae who visited this institute during the period from January, 1980 to March, 1981, and its clinical effects and side effects were investigated. The therapeutic effects were evaluated by days to the normal body temperature, to improvement in cough and to improvement in X-ray findings. The increase in serum antibody value was adopted as the diagnostic index of Mycoplasma infection. The patients who entered into this study were 7 males and 8 females, ranged from 19 to 60 years of age with an average of 36.3 years. The daily dose of ASPM was 600 to 1,200 mg (potency), and the mean administration period was 18.1 days. The results obtained were as follows. 1. The temperature fell to the normal within 2 to 7 days. 2. Cough disappeared in 2 days at shortest and in 55 days at longest. The mean period of cough disappearance was 14.5 days. 3. In 10 cases who could be followed up, shadows in X-ray films disappeared in 3 days at shortest and in 40 days at longest. The mean period to shadow disappearance was 18.6 days. 4. As regards clinical effects, marked improvement was obtained in 2 cases, improvement in 9, slight improvement in 4, and no change in 0 (improvement rate: 73.3%). 5. As a side effect, nausea was found in 1 case, but it was improved by discontinuance of administration.

Adult↗
PubMed1982

Comparative study on glycosaminoglycan-sulfotransferases in rat costal cartilage and chick embryo cartilage.

1. The comparative features of glycosaminoglycan-sulfotransferase system in rat costal cartilage and chick-embryo cartilage were examined. Some different properties of glycosaminoglycan-sulfotransferases in the cartilage of both the animals have been observed. 2. This study shows that rat costal cartilage contains more 4-sulfotransferase than 6-sulfotransferase and that that reverse situation pertains to chick-embryo cartilage, although both the rat and chick-embryo cartilage contain two sulfotransferase species. 3. Our preliminary experiments by use of rat sulfotransferases and chick endogenous acceptor or of chick sulfotransferases and rat sulfotransferases and chick endogenous acceptor or of chick sulfotransferases and rat endogenous acceptor suggest that sulfotransferases in a given tissue play a central role in determining which sites of the N-acetylgalactosamine moiety of chondroitin sulfates occurring in the tissue are sulfated.

Animals↗
PubMed1982

The teratogenic mechanism of 6-aminonicotinamide on limb formation of chick embryos: abnormalities in the biosynthesis of glycosaminoglycans and proteoglycans in micromelia.

After a dose of 10 micrograms of 6-aminonicotinamide (6-AN) was administered to day-4- chick embryo in ovo, micromelia was obviously observed in the hind limbs of 7-day chick embryos. We examined the teratogenic mechanism of 6-AN by using the normal or micromelial hind limbs (buds) from day 5 to day 7, with special attention to the biosynthesis of glycosaminoglycan (GAG) and proteoglycan as an index of limb chondrogenesis. The present study provides evidence for abnormalities in the levels of GAG or proteoglycan biosynthesis in the micromelial hind limbs (buds). 1) Both [35S]sulfate and [3H]glucosamine incorporation into GAG per 10 limbs or mg DNA of the micromelia were inhibited, suggesting a decrease of GAG synthesis. 2) The micromelial limbs synthesized low-sulfated chondroitin sulfate (chondroitin) as judged by the 35S/3H ratio, the proportion of unsulfated disaccharide (delta Di-0S), and the result of cellulose acetate electrophoresis, although there were no significant differences in the approximate molecular size of 35S-chondroitin sulfates synthesized between the normal and micromelial limbs. 3) PAPS-synthesizing activity in the micromelial limbs was markedly inhibited, and this may result in the production of low-sulfated proteoglycan. 4) The transition from mesenchymal- to cartilage-specific proteoglycan synthesis did not appear in the micromelial limbs as judged by the sedimentation profiles. 5) 6-AN caused marked reductions in the oxygen consumption and ATP level of the micromelial limbs, thereby causing the defect in PAPS formation. We suggest that these 6-AN-induced sequential molecular defects (the reduction of respiratory activity, ATP and PAPS level, and concomitant interference with GAG and proteoglycan biosynthesis) in the limbs (buds) during the critical period of limb morphogenesis must be major factors resulting in the cartilage growth retardation or disorder, i.e., micromelia.

6-Aminonicotinamide↗
PubMed1981

Severe retinal vascular lesions in systemic lupus erythematosus.

Retinal lesions in systemic lupus erythematosus (SLE) are usually closely related to the patient's general condition and occur frequently in severe states such as renal or central nervous system involvement. However, improved treatment of SLE has reduced retinal involvement, and it is rare today to observe severe retinal lesions in patients with SLE. We report two cases of severe retinal vascular lesions in SLE patients who developed otherwise unremarkable systemic manifestations and laboratory findings.

Adult↗