[Evaluation of arterial embolization therapy for hepatocellular carcinoma by ultrasonography (author's transl)].
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Biomedical subjects
Publications and source records attributed to J Ueda.
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The senescence-promoting substance of wormwood (Artemisia absinthium L.) as detected by the oat (Avena sativa L. cv "Victory") leaf assay has been identified as (-)-methyl jasmonate, methyl (1S, 2R)-3-oxo-2-(2'-cis-pentenyl)-cyclopentane-1-acetate, by gas-liquid chromatography-mass spectrometry and optical rotatory dispersion. Its senescence-promoting effect was much stronger than that of abscisic acid, and even at such a low concentration as 1 to 2.5 micrograms per milliliter, it could completely eliminate the anti-senescence action of 2 micrograms per milliliter kinetin. Comparing the biological activity of the (-)- with the (+/-)-forms of methyl jasmonate, it seemed that only the (-)-form was biologically active.
Effects of adenine and adenosine compounds (adenosine, AMP, ATP, cyclic AMP and dibutyryl cyclic AMP) on the contractile responses of helically cut strips of canine superior mesenteric arteries to various agonists (K+, norepinephrine, angiotensin II and Ba2+), to transmural electrical stimulation and on Ca2+ contractures of K+-depolarized strips were studied. The contractions induced by these agonists were suppressed, dose dependently, but to a different degree by these adenosine compounds, with the exception of the potentiating action of ATP on the Ba2+-induced contraction. The suppression of the effect of norepinephrine, angiotensin II and transmural stimulation was appreciably greater than that of K+ and Ba2+. Adenine was equally or more effective in inhibiting the contractions induced by these agonists than were the other adenosine compounds used. The order of relative inhibitory potency was adenine Greater Than or Equal to adenosine Greater Than or Equal to AMP = ATP Greater Than cyclic AMP = dibutyryl cyclic AMP. The ATP-induced contraction was influenced in a different manner by each adenosine compound. Adenosine and cyclic AMP did not affect the ATP-induced contraction but AMP and dibutyryl cyclic AMP in a narrow range of concentrations enhanced the contraction. On the contrary, adenine and ATP inhibited the ATP contraction, dose-dependently, resulting in tachyphylaxis, with the repeated application of ATP. The present results suggest that adenine moiety in the molecule plays an important role in the inhibitory action of adenosine compounds, and that the antagonistic action of adenosine compounds is due to their inhibitory actions on Ca2+-influx and Ca2+-release from cell stores.
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Three individual variants of acid phosphatase in chicken leucocytes were found by means of starch gel electrophoresis. The phenotype in leucocytes showed the same appearance as polymorphic forms of liver acid phosphatase in the same bird. The study of the Hardy-Weinberg distribution of the phenotypes of acid phosphatase in leucocytes also indicated that they are controlled by the same pair of codominant autosomal alleles as the phenotypes in the liver. Acid phosphatase is polymorphic in all six strains of chickens studied.
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The effects of glucagon alone or in combination with theophylline on renin section were studied in relation to renal hemodynamic responses in anesthetized dogs. The intrarenal infusion of glucagon (0.5 microgram/kg/min) increased heart rate, renal blood flow, glomerular filtration rate and urine flow without any effect on renin secretion, but at a higher dose (1.0 microgram/kg/min) it increased renin secretion significantly. Theophylline (0.1 mg/kg/min) did not affect renal hemodynamics but caused a slight increase in renin secretion after 30--60 min infusion. The combined infusion of glucagon (0.5 microgram/kg/min) with theophylline (0.1 mg/kg/min) increased renin secretion markedly, although it produced renal hemodynamic changes similar to those induced by glucagon alone. These effects were not suppressed by d,l-propranolol (1.0 microgram/kg/min). It is suggested that the increase in renin secretion caused by the combined infusion of glucagon and theophylline resulted mainly from an increase in cyclic AMP in the juxtaglomerular cells, and not from stimulation of beta-adrenoceptors.
An intrarenal infusion of glucagon resulted in an increase of glomerular filtration rate (GFR) with the same order of magnitude of renal blood flow (RBF) but did not affect the intrarenal distribution of blood flow. A superimposition of acetylcholine and glucagon decreased GFR even though RBF increased significantly. These findings indicate that the effect of glucagon on GFR depended on the selective dilation of afferent arterioles without any change in permeability of glomerular capillaries and redistribution of filtration.
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The effect of glucagon on the renal hemodynamics in the dog was examined by comparing its effect with that of secretin, a peptide with which glucagon shares a similar chemical structure. An intrarenal infusion of glucagon resulted in increases of RBF and GFR. GFR rose by approximately the same order of magnitude of RBF. The increase in GFR depended on the selective dilation of the afferent arteriole and a consequent rise in the transcapillary pressure difference. On the other hand, secretin infusion produced highly significant and proportional decreases in both afferent and efferent arteriolar resistance, resulting in no change in GFR. A superimposition of acetylcholine to glucagon decreased GFR even though RBF increased significantly. Glucagon infusion did not affect the permeability of glomerular capillary and the distribution of cortical blood flow. These findings indicate that the effect of glucagon on GFR depended on the selective dilation of afferent arteriole, and that as a result of its dilation the net filtration pressure increased without any change in permeability of glomerular capillary and a redistribution of filtration.
In anesthetized mongreal dogs, the intrarenal arterial (0.2 approximately 1.0 unit/kg-min) and the intravenous infusion (0.4 approximately 2.0 unit/kg-min) of secretin caused dose-dependent increase of RBF, accompanied by decreases of the calculated afferent arteriolar resistance (Ra) and efferent arteriolar resistance (Re), but produced no significant effect on GFR, urine flow, electrolyte excretion, osmolar clearance and free water reabsorption. The distribution of cortical blood flow was examined using the radioactive microsphere technique. The intrarenal infusion of secretin (1.0 unit/kg-min) increased renal cortical blood flow in the juxtamedullary area much more than in the superficial area, shifting the blood flow from the outer to the inner zone. Simultaneous intrarenal infusion of secretin (1.0 unit/kg-min) and glucagon (0.5 microng/kg-min) produced increases in GFR, urine flow and electrolyte excretion to a lesser degree than those induced by glucagon alone, whereas the increment in RBF and the decreases in Ra and Re were almost to the same degree as those caused by secretin alone. The present results indicate that secretin produces the dilation of afferent and efferent arterioles, resulting in an increase in RBF, with no change in GFR and urine flow, and that the effects of glucagon on renal functions are masked by secretin mainly through the effects of renal hemodynamics.
Effects of ATP and ADP on helically cut strips of canine different blood vessels were studied, in comparison with those of K+ and norepinephrine (N.E.). ATP and ADP were equally effective in causing transient contractions in contrast to sustained contractions induced by K+ and N.E.. The mesenteric, renal arteries and portal veins were sensitive to both nucleotides. The response to the nucleotides was K+ was more dependent on Ca++ and Mg++ concentrations in bathing media than that to N.E.. Treatment of the strips with EGTA in Ca++ -free media quickly abolished the contractile responses to ATP, ADP and K+. Application of 0.1 mM Cd++ attenuated the contractile responses to K+ more markedly than those to N.E., but did not affect ATP action. Verapamil at 0.5 micron inhibited the K+-induced contraction alone, and 2 mM procaine inhibited the response to N.E. alone, but rather intensified the ATP-induced contraction. It may be concluded that ATP and ADP produce a transient contraction of isolated canine blood vessels by a mechanism relating to an increased mobilization of loosely bound Ca++ in cell membranes.
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