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Biomedical subjects

H Murakami

Publications and source records attributed to H Murakami.

At least 667 records · Page 37Linked to original sources
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

Cloning, expression, and sequence homologies of cDNA for human carbonic anhydrase II.

A cDNA clone for human carbonic anhydrase (CA) II was isolated from a kidney lambda gt10 library. Expression of the cDNA insert in Cos-7 cells produced an immunoprecipitable product and enzymatically active carbonic anhydrase. The cDNA insert is 1551 bp in length and contains an open reading frame which encodes a 260-amino-acid polypeptide. The deduced amino acid sequence is identical to that reported for human CA II. The protein coding region of this cDNA for human CA II shows 81 and 70% nucleotide identity with cDNAs for CA II from mouse and chick, respectively. Even the long 3'-untranslated region of the cDNA for human CA II (703 bp) is 64 and 42% identical to those of CA II from mouse and chick, showing remarkable conservation of the CA II cDNAs in amniotes. The protein coding region of the human CA II cDNA is 64 and 65% identical with those of human CA I and CA III, which are thought to have arisen from a common precursor by gene duplication.

Amino Acid Sequence↗
PubMed1987

A genetically engineered P450 monooxygenase: construction of the functional fused enzyme between rat cytochrome P450c and NADPH-cytochrome P450 reductase.

A hybrid cDNA encoding a fused enzyme consisting of rat cytochrome P450c and rat NADPH-cytochrome P450 reductase was constructed by combining the cytochrome P450c cDNA with the cDNA fragment encoding the protease-solubilized moiety of the NADPH-cytochrome P450 reductase. The hybrid cDNA was inserted between the yeast alcohol dehydrogenase I promoter and terminator of the expression vector pAAH5 to yield expression plasmid pAMP19. Saccharomyces cerevisiae AH22 cells transformed with the expression plasmid pAMP19 produced a 130-kD protein reactive with both anti-cytochrome P450c Ig and antireductase Ig. The yeast cells containing the fused enzyme exhibited about four times higher monooxygenase activity toward 7-ethoxycoumarin than those containing rat cytochrome P450c alone. The fused enzyme was purified from the yeast microsomal fraction by sequential chromatography with DEAE-cellulose and 2',5'-ADP Sepharose 4B columns. The preparation had an apparent molecular weight of 130 kD and the same sequence of the 10 amino-terminal amino acids as that of rat cytochrome P450c. Spectral properties of the fused enzyme indicated the presence of a protoheme, flavin adenine dinucleotide, and flavin mononucleotide in the molecule. The reaction mechanism of the fused enzyme followed first-order kinetics. These results clearly indicate that the fused enzyme is a new self-catalytic P450 monooxygenase. Trypsin treatment of yeast microsomes containing the fused enzyme suggested that the P450 moiety is embedded in the microsomal membrane with the reductase moiety lying on the cytoplasmic side.

Animals↗
PubMed1987

Interaction of insulin-like growth factor I with porcine thyroid cells cultured in monolayer.

The interaction of insulin-like growth factor I (IGF-I) with porcine thyroid cells cultured in monolayer was studied. Specific binding of [125I]iodo-IGF-I to thyroid cells was a reversible process dependent on the time and temperature of incubation. A steady state was achieved in 18 h at 4 C and averaged 14.2 +/- 2% (mean +/- SD)/10(6) cells. Binding of [125I]iodo-IGF-I was inhibited by unlabeled IGF-I; half-maximal inhibition occurred at concentrations of 2-5 ng/ml. Multiplication-stimulating activity (rat IGF-II) and pork insulin had relative potencies of 1:20 and 1:300 compared with IGF-I. Scatchard analysis of binding data revealed a single class of IGF-I receptors with a Ka of 4.3 X 10(10) M-1, 49,000 binding sites were estimated per cell. Affinity cross-linking and autoradiography demonstrated the presence of type I IGF receptors. Thyroid cells also had specific receptors for insulin, but specific binding of [125I]iodoinsulin (2.03 +/- 0.03%/10(6) cells) was much lower than that of [125I]iodo-IGF-I. Preincubation of thyroid cells with IGF-I or insulin caused a concentration-dependent decrease in [125I]iodo-IGF-I binding due to an apparent loss of receptors. Preincubation with epidermal growth factor, fibroblast growth factor, platelet-derived growth factor, or TSH did not alter subsequent binding of [125I]iodo-IGF-I. Low concentrations of IGF-I stimulated DNA synthesis and proliferation of thyroid cells and acted synergistically with epidermal growth factor. Multiplication-stimulating activity and insulin had relative potencies in stimulating DNA synthesis comparable to their abilities to inhibit the binding of [125I]iodo-IGF-I to thyroid cells, suggesting that their effects are mediated primarily by IGF-I receptors. Preincubation with IGF-I did not alter cAMP responsiveness to TSH. We, thus, demonstrated the presence of functional and regulated IGF-I receptors on porcine thyroid cells.

Animals↗
PubMed1987

Comparison of the inhibitory effects of cilostazol, acetylsalicylic acid and ticlopidine on platelet functions ex vivo. Randomized, double-blind cross-over study.

A randomized double-blind cross-over study was conducted to determine the inhibitory effects of acetylsalicylic acid (ASA), ticlopidine (TP) and cilostazol (OPC-13013; in the following briefly called CS), a new antithrombotic agent on platelet functions ex vivo. Nine patients with cerebral thrombosis were enrolled in this study. Patients were given each of the three drugs for one week in a complete cross-over design according to a randomization schedule, followed by a wash-out period with a placebo for one week. It was found that CS and TP significantly inhibited platelet aggregation induced by ADP. Collagen- and arachidonic acid-induced platelet aggregation was all inhibited by CS, TP and ASA. Duncan's multiple range test to compare the anti-platelet effects of the three drugs revealed that: CS greater than ASA and TP greater than ASA in inhibiting ADP-induced platelet aggregation and CS greater than TP and ASA greater than TP in inhibiting arachidonic acid-induced platelet aggregation. These results may suggest that CS is superior to ASA and TP in inhibiting platelet aggregation ex vivo.

Aged↗
PubMed1987

[A case of superior sagittal thrombosis secondary to hyperlipidemia].

A 42-year-old man was admitted to the Saiseikai Fukuoka General Hospital on March 22, 1985 with complaints of nausea, vomiting and headache which had continued for twelve days. On physical examinations, multiple subcutaneous nodules were noted in the chest, abdomen and extremities with dilated veins in the chest wall. Furthermore, the discoloration of the skin attributable to the venous occlusion was noted in the left foot. Neurological examinations failed to reveal any abnormalities except for moderate choked disc in bilateral ocular fundi. Spinal puncture revealed CSF pressure as high as 350 mmH2O with slight increase in cell numbers. CT demonstrated small intracerebral hematomas bilaterally in occipital lobes with evidence of "empty delta" sign in the superior sagittal sinus. On angiographical findings, the superior sagittal sinus was not demonstrated in venous phase and the blood was drained mainly through the paravertebral plexus and the pterygoid plexus without any abnormalities in arterial and capillary phases. Serological examination revealed a hypercoagulability and hyperlipidemia especially in LDL (Low Density Lipoprotein) and VLDL (Very Low Density Lipoprotein). On etiological considerations, all of these abnormalities seemed to be derived from the hyperlipidemia. Furthermore, multiple symmetrical lipomatosis was defined as a "lipoprotein storage disease" in which laboratory examinations revealed hyperlipidemia especially in LDL and in some subfraction of HDL. Although not a typical case, there must be some possibilities that the lipomatosis of this case is secondary to disorder of lipid metabolisms. In conclusion, all of various pathological conditions observed in this case were considered to be due to the disorder of lipid metabolism.

Adult↗
PubMed1987

[The systolic slipping mechanism of the anterior mitral leaflet in patients with the straight back syndrome].

The systolic slipping mechanism of the anterior mitral leaflet in patients with the straight back syndrome (SBS) was evaluated by two-dimensional echocardiography in 16 SBS patients and 11 normal subjects. Doppler echocardiography was performed in all subjects to detect mitral regurgitation. The site of the mitral slipping was identified in a centromedial region of the anterior mitral leaflet in these patients. The ellipsoidal index (long axis/short axis) of the left ventricle was greater in SBS patients than in normal subjects. The left ventricular wall had a characteristic motion in SBS. The lateral wall contracted well, while the posterior septum and inferoposterior wall were hypokinetic. Moreover, the anterolateral papillary muscle moved horizontally during systole, while the posteromedial papillary muscle moved anteriorly. There was a significant correlation between the distance of slipping of the anterior mitral leaflet and the PL/PM ratio (r = -0.39, p less than 0.001), where PL is the distance from the gravity point of the left ventricle to the midpoint of the anterolateral papillary muscle, and PM is that from the gravity point of the left ventricle to the posteromedial papillary muscle. Mild mitral regurgitation was identified in four cases with SBS by Doppler echocardiography, and this regurgitant jet was directed from the posterior mitral leaflet to the posterior wall of the left atrium. These results suggest that the systolic slipping of the anterior mitral leaflet in SBS might be caused by asynchronous papillary muscle motion. This might be based on the ellipsoidal left ventricle due to the short internal dimension of the thorax.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

[A case of cavernous angioma of the middle cranial fossa originating in the cavernous sinus with hyperprolactinemia].

A 43-year-old female was admitted showing abnormal feeling in the left eye region. Left facial hypesthesia and quadrantic hemianopsia of left eye were the detectable neurological findings. A plain skull x-ray film revealed a double floor and dilatation of the sella turcica. The tomogram of the sella turcica demonstrated a dilatation of superior orbital fissure. Caudocranial projection revealed a dilatation of foramen ovale. A computerized tomography scan revealed a slightly high density tumor which was enhanced slightly with a contrast medium in the parasellar region and left middle fossa. Carotid angiogram demonstrated the displacement of the left carotid fork to the upper and lateral direction. However, no other sign was found. The sinogram of cavernous sinus clearly demonstrated an indentation in the left cavernous sinus. The endocrinological tests were almost normal except for hyperprolactinemia. A trigeminal neurinoma and a pituitary tumor were suspected. The tumor was totally removed and was histologically diagnosed as a cavernous angioma. At operation it seems to be extracerebral in the middle fossa and originate in the cavernous sinus. Diagnostic problems endocrine findings and the origin are discussed.

Adult↗