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Biomedical subjects

K Kadowaki

Publications and source records attributed to K Kadowaki.

At least 109 records · Page 6Linked to original sources
PubMed1992

Atrial and brain natriuretic peptides enhance dopamine accumulation in cultured rat hypothalamic cells including dopaminergic neurons.

Dopamine accumulation in hypothalamic cells by atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) was analyzed using newborn rat hypothalamic cells in culture. Both ANP and BNP caused a dose-dependent increase in [3H]-dopamine accumulation in the cells. ANP increased [3H]-dopamine accumulation significantly within 20 min. The effects of ANP and BNP on dopamine accumulation paralleled an increase in intracellular cGMP concentration. (Bu)2-cGMP and sodium nitroprusside, a stimulator of the soluble form of guanylate cyclase, also enhanced [3H]-dopamine accumulation. ANP had no effect on efflux of [3H] radioactivity after [3H]-dopamine uptake. These results suggest that a change in cGMP is one of the intermediate steps in dopamine accumulation in hypothalamic cells by ANP and BNP.

Animals↗
PubMed1992

Cloning and nucleotide sequence of the maltopentaose-forming amylase gene from Pseudomonas sp. KO-8940.

The gene coding for the maltopentaose-(G5)-forming amylase of Pseudomonas sp. KO-8940 was cloned into Escherichia coli and its nucleotides were sequenced. It was expected that a long open reading frame composed of 1,842-bp that encoded 614 amino acid residues for secretory precursor polypeptide including the typical signal sequence with an NH2-terminal was the gene. An extract of Escherichia coli carrying the cloned G5-forming amylase gene had amylolytic activity with which produced only G5 from starch, the same as that of the donor strain enzyme. In the deduced primary structure of this enzyme, the four conserved regions of many alpha-amylases were found, and the COOH-terminal portion of this enzyme showed high homology with other raw starch digesting amylases.

Amino Acid Sequence↗
PubMed1992

Vasoactive intestinal peptide enhances dopamine accumulation in primary cell culture of rat hypothalamus.

The effect of vasoactive intestinal peptide (VIP) and PHI-27 on dopamine accumulation in cultured rat hypothalamic cells was investigated. VIP enhanced [3H]dopamine accumulation dose dependently. This effect was significant at 10(-8)-10(-5) M VIP with a concomitant increase in intracellular cyclic AMP (cAMP), and reached its plateau level at 10(-6) M VIP. VIP increased [3H]dopamine accumulation significantly within 15 min. PHI-27 and dibutyryl cAMP ((Bu)2-cAMP) also enhanced [3H]dopamine accumulation. These results suggest that VIP enhances dopamine accumulation in hypothalamic cells by increasing intracellular cAMP.

Animals↗
PubMed1992

[Secretion of atrial natriuretic peptide during artificial pacing: assessments including the influence of ventriculoatrial conduction].

Secretion of atrial natriuretic peptide (ANP) depends on the atrial wall distension which may be caused by ventricular pacing. This study was designed to assess the differences in plasma ANP level between DDD and VVI pacing. We measured ANP from venous blood samples using radio-immunoassay in patients with the sick sinus syndrome (n = 8) and atrioventricular block (n = 2) following DDD implantation. Measurement was made under control conditions during DDD and 15-180 min after the pacing mode was changed to VVI and 60 min after returning to DDD. Serum epinephrine (E), norepinephrine (NE), renin (R) and aldosterone (A) levels were also measured prior to and every 30 min after pacing mode changes. The plasma ANP concentration changed from 71.3 pg/ml (normal value) with DDD to 126.8 (15 min), 180.6 (30 min), 221.8 (60 min), 219.2 (90 min), 270.1 (120 min), 145.4 (150 min) and 115.1 pg/ml (180 min) with VVI. It increased markedly, then gradually decreased. It returned to the control value (66.6 pg/ml) in 60 min with DDD, and it reached the peak level with VVI within 60-120 min, and the peak was significantly higher than that for DDD. The increase related to the retrograde ventriculoatrial conduction during VVI pacing. There was no significant change in the NE, E, R and A concentrations. Systolic blood pressure decreased 15 mmHg in VVI and returned to normal by DDD. These results indicated that plasma ANP levels is elevated by VVI pacing, though it was not explained by ventricular pacing alone.

Aged↗
PubMed1992

[Histological evidence of prolonged coronary artery spasm in a necropsy case of recurrent myocardial infarction].

A 69-year-old male had acute inferior infarction during an operation of an aneurysm of the abdominal aorta and died from multiple organ failure 3 weeks after the operation. His initial coronary angiogram (CAG) showed no significant stenosis, but repeated CAG showed that the patients had developed a prolonged spasm in the mid-portion of the right coronary artery. Histologically, we observed eccentric luminal narrowing with atheromatous plaque where the spasms had been demonstrated, and a "waving form" of elastic fibers accompanied by intimal thickening in the opposite site of the atheromatous plaque. These findings suggest that organic stenosis may be underestimated angiographically because of compensatory enlargement of the non-atheromatous site in some patients with coronary artery spasm, and prolonged spasms may augment organic stenosis by following intimal thickening.

Aged↗
PubMed1992

[A case of acute myocardial infarction following intracoronary thrombi caused by coronary artery spasm].

A 65-year-old man underwent coronary angiography (CAG) after 10 hours from the onset of myocardial infarction. We observed large Thrombi at the filling defect in the proximal site and mid-portion of the right coronary artery. CAG showed that they had disappeared completely without residual stenosis on the 4th day. In addition to this segmental spasms developed spontaneously at the proximal site of a thrombus accompanied by ST elevation, but these spasms recovered after intracoronary infusion of isosorbide dinitrate on the 26th day CAG. Thus, our case indicates that acute myocardial infarction may be caused by secondary coronary artery thrombosis and accompanying coronary artery spasm.

Aged↗
PubMed1992

[Recovery of left ventricular wall motion in early periods by successful reperfusion following myocardial infarction].

To study the time course and recovery of left ventricular (LV) function after reperfusion therapy (PTCR or PTCA), we recorded 2 D E in 1, 3, 5, 7, 14, 28 days following myocardial infarction in 41 cases with complete occlusion of left anterior descending artery. LV volumes and regional wall motion were analyzed by the centerline method (100 chords) between a reperfused (R) and a non-R group. LV end-diastolic volumes of R increased from 3 to 7 days were smaller than those in non-R. LV end-systolic volume of R decreased during the same periods were also smaller than those of non-R. Besides global ejection fractions of R were larger significantly (p less than 0.05) than those of non-R. Moreover mean percent fractional shortening of infarct-related chords from anteroseptum (-15) to lateral wall (61-80) in R improved more than those in non-R. In conclusion, LV function following myocardial infarction can be assessed by quantitative 2D echo and improved early, and become constant 7 days after successful reperfusion therapy.

Aged↗
PubMed1991

Ca2(+)-dependent regulation of the spectrin/actin interaction by calmodulin and protein 4.1.

The Ca2(+)-dependent regulation of the erythroid membrane cytoskeleton was investigated. The low-salt extract of erythroid membranes, which is mainly composed of spectrin, protein 4.1, and actin, confers a Ca2+ sensitivity on its interaction with F-actin. This Ca2+ sensitivity is fortified by calmodulin and antagonized by trifluoperazine, a potent calmodulin inhibitor. Additionally, calmodulin is detected in the low-salt extract. These results suggest that calmodulin is the sole Ca2(+)-sensitive factor in the low-salt extract. The main target of calmodulin in the erythroid membrane cytoskeleton was further examined. Under native conditions, calmodulin forms a stable and equivalent complex with protein 4.1 as determined by calmodulin affinity chromatography, cross-linking experiments, and fluorescence binding assays with an apparent Kd of 5.5 x 10(-7) M irrespective of the free Ca2+ concentration. Domain mapping with chymotryptic digestion reveals that the calmodulin-binding site resides within the N-terminal 30-kDa fragment of protein 4.1. In contrast, the interaction of calmodulin with spectrin is unexpectedly weak (Kd = 1.2 x 10(-4) M). Given the content of calmodulin in erythrocytes (2-5 microM), these results imply that the major target for calmodulin in the erythroid membrane cytoskeleton is protein 4.1. Low- and high-shear viscometry and binding assays reveal that an equivalent complex of calmodulin with protein 4.1 regulates the spectrin/actin interaction in a Ca2(+)-dependent manner. At a low Ca2+ concentration, protein 4.1 potentiates the actin cross-linking and the actin binding activities of spectrin. At a high Ca2+ concentration, the protein 4.1-potentiated actin cross-linking activity but not the actin binding activity of spectrin is suppressed by Ca2+/calmodulin. The Ca2(+)-dependent regulation of the spectrin/protein 4.1/calmodulin/actin interaction is discussed.

Actins↗
PubMed1991

The rice mitochondrial nad3 gene has an extended reading frame at its 5' end: nucleotide sequence analysis of rice trnS, nad3, and rps12 genes.

The nucleotide sequences of the tRNASer (trnS), pseudo-tRNA, NADH dehydrogenase subunit 3 (nad3), and ribosomal protein S12 (rps12) genes from rice mitochondrial DNA (mtDNA) were determined. Both trnS and nad3 were confirmed to be single copy genes by Southern blot analysis. The nad3 and rps12 genes were arranged in tandem, and the two were co-transcribed. The order of the above four genes in rice mtDNA differed from the linear order observed for the wheat and maize genes. In rice mitochondria, the trnS and pseudo-tRNA genes were found upstream of the cytochrome c oxidase subunit I gene, instead of the nad3 and rps12 genes as observed in maize and wheat. Additionally, while the rice nad3 and rps12 genes remain paired, they too are in a different sequence environment from the wheat and maize genes. The apparent split of the two pairs of genes indicates the occurrence of a mitochondrial intramolecular recombinational event. Another peculiarity is that the sequence upstream of the translational initiation codon of the rice nad3 gene is different from that of the wheat and maize versions. The ATG initiation codon of wheat and maize nad3 is replaced by TTG in the rice nad3. A subsequent deduction of the amino acid sequence, accompanied by a primer extension analysis, indicates that the predicted rice NAD3 protein has an additional 37 amino acid residues at its N-terminus compared to the wheat and maize NAD3 proteins. cDNA sequence analysis showed no introns or the occurrence of RNA editing at the newly replaced TTG codon.

Amino Acid Sequence↗
PubMed1991

Short-term treatment with 17-beta estradiol enhances spontaneous [3H] dopamine release from cultured rat tuberoinfundibular neurons.

The effects of 17-beta estradiol (E2) on spontaneous [3H] dopamine ([3H]DA) release was investigated using primary cultured cells from the tuberoinfundibular region of rat hypothalamus, which includes DA neurons. [3H] DA uptake by the neurons in the presence of E2 at 10(-8) mol/l was similar to that by control cells. Pretreatment with E2 at 10(-9) mol/l or more resulted in dose-dependent increase in spontaneous [3H] DA release from the cultured hypothalamic cells. The spontaneous [3H] DA release reached almost a plateau on pretreatment with E2 at 10(-9) mol/l for 6 hours. Pretreatment with 1 nM E2 also enhanced DA release induced by 10 microM ionophore A23187. These results indicate that estrogen stimulates tuberoinfundibular DA neuronal activity.

Animals↗
PubMed1991

Hepatic arterial embolization in cases of extensive celiac arterial stenosis.

Transarterial hepatic embolization was attempted in 10 and succeeded in nine patients with hepatocellular carcinoma accompanied by extensive celiac arterial stenosis. All catheterization was done through the femoral artery. In six cases, the tip of the catheter (2.5-F ball-tip microcatheter in three cases, 4-F ball-tip supple catheter in three cases) was placed in the proper hepatic artery through the pancreaticoduodenal collaterals. In three cases, a ball-tip microcatheter was injected from the guiding catheter, which was placed in a pinhole of the celiac trunk. These techniques involving flow-guided ball-tip catheters are of great value for hepatic arterial catheterization in cases of extensive celiac arterial stenosis.

Arterial Occlusive Diseases↗
PubMed1991

Tumor necrosis factor-alpha increases release of arachidonate and prolactin from rat anterior pituitary cells.

We investigated the effect of tumor necrosis factor-alpha (TNF alpha), a product of activated macrophages, on the release of arachidonate from dispersed anterior pituitary cells. Primary cultures of anterior pituitary cells from rats were preincubated with [3H]arachidonate to label their phospholipid-containing components. The cells were then washed and incubated with vehicle or test agents, and PRL release into the medium and [3H]arachidonate cleaved from phospholipid were measured. TNF alpha significantly increased the release of both PRL and [3H] arachidonate release in a time- and dose-dependent manner. Other cytokines, such as interleukin-1 alpha, interleukin-1 beta, and gamma-interferon, had no effect on [3H]arachidonate release. To define the role of calcium in TNF alpha-induced arachidonate release, dispersed pituitary cells were incubated with low calcium medium, which decreased arachidonate release in response to TNF alpha. TNF alpha potentiated the release of [3H]arachidonate and PRL promoted by phospholipase-A2 and melittin, and markedly shifted the dose-response curve to the left. Inhibitors of phospholipase-A2, such as p-bromophenacyl bromide and quinacrine, had no effect on TNF alpha-induced [3H]arachidonate and PRL release. BW755C, an inhibitor of the conversion of arachidonate to its metabolites, decreased TNF alpha-induced PRL release, while indomethacin, a prostaglandin synthesis inhibitor, had no effect on TNF alpha-induced PRL release. These data indicate that arachidonate metabolites may be involved in the process of TNF alpha-induced PRL release.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1990

A chimeric gene containing the 5' portion of atp6 is associated with cytoplasmic male-sterility of rice.

Three ATPase subunit 6 (atp6) genes of rice mitochondria were isolated, one from normal and two from cms-Bo male-sterile cytoplasms, in order to determine whether the extra atp6 gene in cms-Bo rice plays a role in cytoplasmic male-sterility (CMS). The nucleotide sequences of all three genes were determined and analysis showed a chimeric atp6 gene (urf-rmc) as well as a normal atp6 gene in cms-Bo cytoplasm, but only the normal atp6 gene in normal cytoplasm. The urf-rmc gene is completely homologous to the normal atp6 gene from at least position -426 in the 5' flanking region to position +511 downstream from the initiation codon ATG: however, the following downstream sequence shows no homology with the normal rice atp6 gene, or any other reported sequence. Introduction of the restorer of fertility gene altered transcription of the urf-rmc gene but not the atp6 gene, indicating participation of the chimeric gene in the expression of CMS. Southern blot analysis showed that the urf-rmc gene was generated by an intramolecular recombination event in mitochondrial DNA, and the homologous recombination point between the atp6 gene and the opposite ancestral sequence was identified as 5'-TTCCCTC-3'.

Adenosine Triphosphatases↗