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Biomedical subjects

T Aramaki

Publications and source records attributed to T Aramaki.

At least 19 recordsLinked to original sources
PubMed1992

Purification and properties of a decapping enzyme from rat liver cytosol.

A decapping enzyme has been purified about 2400-fold from rat liver cytosol. The decapping enzyme was shown to be fairly homogeneous by sodium dodecyl sulfate polyacrylamide gel electrophoresis. The enzyme had an apparent molecular weight of 110,000 and consisted of two equal subunits. The enzyme hydrolyzed m7Guo5'PPP5'Ado to m7GMP and ADP. Analysis of the products produced from radioactively capped oligonucleotides and intact mRNA having 3H-cap suggests that the enzyme can hydrolyze capped mono- to pentanucleotides (m7Guo5'PPP5'N (where N = 1-5 nucleotides)) but not intact mRNA. The existence of methyl group at the N7 position of guanosine moiety of cap structure was necessary for the action of the decapping enzyme. This was confirmed by the comparison of the rates of hydrolysis of m7Guo5'PPP5'Ado by the enzyme in the presence of various nucleotides. The activity of enzyme was slightly stimulated by Na+, K+, NH4+, Ca2+ and polyamines. Mg2+ and Mn2+ were without effect on the enzyme activity.

Animals↗
PubMed1992

Long-term haemodynamic effects of a 4-week regimen of nipradilol, a new beta-blocker with nitrovasodilating properties, in patients with portal hypertension due to cirrhosis. A comparative study with propranolol.

To study the long-term effects of pharmacological combination therapy, a comparison was made of the haemodynamic changes in patients with cirrhosis and portal hypertension following a 4-week treatment of propranolol or nipradilol, a new nonselective beta-blocker with nitrovasodilating effect. Nipradilol (12 mg/dag, n = 12) significantly diminished wedged hepatic venous pressure (WHVP, 25 +/- 16%), the hepatic venous pressure gradient (HVPG, 20 +/- 12%), and estimated hepatic blood flow (EHBF, 18 +/- 16%). Propranolol (30 mg/day, n = 11) also caused a significant reduction in WHVP (22 +/- 21%) and HVPG (24 +/- 21%), but not in EHBF. The percentage of portal pressure reduction and the frequency of nonresponders did not differ between the nipradilol and propranolol groups. Both agents reduced heart rate by approx. 20%. Nipradilol, however, did not cause a significant reduction in cardiac index (CI) versus a 14% reduction by propranolol. Pulmonary capillary wedge pressure and central venous pressure, an index of preload, were decreased slightly in the nipradilol group. When nonresponders were excluded, there was a significant correlation of the percentage of reduction between WHVP and CI or systemic vascular resistance, in the nipradilol group. These results indicate that nipradilol may have potent hypotensive effects on portal hypertension, similar but not superior to propranolol. Nipradilol, at the dosage used in the present study, did not appear to exert a nitrovasodilating effect to enhance the portal pressure reduction induced by beta-blocking action.

Adrenergic beta-Antagonists↗
PubMed1992

Formation of PhIP in a mixture of creatinine, phenylalanine and sugar or aldehyde by aqueous heating.

A mixture of 100 mM creatinine and 100 mM L-phenylalanine was heated at 60 or 37 degrees C in the presence of sugar or aldehyde. A mutagen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) formed in the model system was determined by reversed-phase HPLC. Any sugars tested induced the formation of PhIP when heated at 60 degrees C, though PhIP was not detected in a mixture without sugar. Among the sugars tested, D-erythrose and D-glyceraldehyde were more productive than pentose (D-arabinose and D-ribose) and hexose (D-glucose and D-galactose) in the yield of PhIP. Moreover, PhIP was formed even when a mixture of creatinine, L-phenylalanine and D-glucose or D-ribose was incubated at 37 degrees C for a long time. Both formaldehyde and acetaldehyde also induced the formation of PhIP, though PhIP was not detected in a mixture without sugar or aldehyde even when heated at 100 degrees C. These results indicate that PhIP can be formed at low-temperature heating and that either sugar or aldehyde is essential for PhIP formation in the model system. Our data also suggest that aldehydes may be a key reactant in the formation of PhIP in aqueous heating of the mixture of creatinine and L-phenylalanine.

Acetaldehyde↗
PubMed1991

[The effect of extract from human tubercle bacilli (SSM) on HBeAg positive type B chronic hepatitis].

UNLABELLED: The effect on the HBeAg/anti-HBe system of SSM (specific substance Maruyama), an extract from human tubercle bacilli, was evaluated in patients with HBeAg positive type B chronic hepatitis. SUBJECTS AND METHODS: Twenty-five (25) HBeAg positive patients with biopsy-proven chronic hepatitis were injected subcutaneously with SSM solution twice a week for two years. Fifteen (15) comparable patients served as untreated controls for one year. HBeAg and anti-HBe were measured by the RIA method. RESULTS: (1) In the group receiving SSM injections, HBeAg disappeared in 8 out of 25 patients (32.0%) one year after the treatment and in 15 out of 23 (65.2%) within two years. Seroconversion from HBeAg to anti-HBe occurred in 5 of the 25 patients (20.0%) after one year and in 7 out of 23 (30.4%) within two years. Of the 15 untreated controls, HBeAg disappeared in 3 patients (20%), and seroconversion from HBeAg to anti-HBe occurred in 1 (6.7%) within one year. (2) In the SSM group, the HBeAg cut off index decreased significantly (p less than 0.01), from 5.2 +/- 1.9 during the pretreatment period to 2.7 +/- 2.3 twelve months after the treatment. (3) In the SSM group, a transient rise in sGOT and sGPT was observed in some patients three to nine months after starting the treatment. HBeAg disappeared in all these patients. (4) No notable side effects were observed in any of the patients treated with SSM. CONCLUSION: These results indicate that SSM treatment improves the HBeAg/anti-HBe system in patients with HBeAg positive chronic hepatitis.

Adolescent↗
PubMed1991

A new experimental animal model of portal hypertension. Intrahepatic portal obstruction by injecting DEAE-cross-linked dextran microspheres into the portal vein in the rabbit.

We proposed a new experimental animal model for portal hypertension in the female Japanese white rabbit by an intraportal injection of DEAE-cross-linked dextran microspheres (100 +/- 25 microns in diameter). Histology of the liver revealed portal obstruction by the injected microspheres in almost all portal triads, resulting in a foreign body granuloma. A sustained elevation of the portal pressure by a mean of 36.7% as compared with the basal value was observed for at least eight weeks in association with the portal-systemic collateral circulation demonstrated by portography, the radioisotope labeled microsphere method and histological examination of the esophagus and the liver. The elevation in portal pressure in the eighth week was associated with an increase in the portal blood flow determined at the main portal trunk. This was in accordance with the forward theory of the pathogenesis of portal hypertension. Since this model appears to show the two main conditions characteristic of portal hypertension persistent elevation of portal pressure and both extra- and intrahepatic portal collaterals, mimicking those in humans, portal obstruction by injecting DEAE-cross-linked dextran microspheres into the portal vein of the rabbit could provide a versatile model for portal hypertension.

Animals↗
PubMed1991

[Etiologic and pathophysiological characteristics of cirrhosis of the elderly].

To evaluate the etiologic and pathophysiological characteristics of the aged cirrhotics, a total of 219 cirrhotic patients who admitted to our department between 1975 and 1989 was divided into the three age groups; less than or equal to 49 (Group A, n = 70), 50-59 (Group B, n = 77) and greater than or equal to 60 (Group C, n = 72) years and compared. The frequency of female patients was significantly higher in Group B and C than Group A, respectively. The age-related variation in etiologies of cirrhosis was analyzed among patients between 1975 and 1989, as well as those observed in 1990, when the assay for antibody to hepatitis C virus (anti-HCV) was available. Compared with Group A, patients with Group C had a lower incidence in HBsAg positive and alcoholic cases. The incidence in cases of unknown cause increased with age and in the elderly over 70 anti-HCV negative cases were found in approximately 45 per cent, the incidence being significantly higher than that of the 50-to-59 year age group. Of the Group C patients 10.6 per cent had gastrointestinal bleeding, which was significantly lower in frequency as compared with 28.6 per cent of Group A. In contrast, the frequency of the other symptoms including jaundice, ascites and encephalopathy did not differ with age. Among various liver function indices the value of gamma-GTP was significantly lower and that of cholesterol was significantly higher in Group C than in Group A, although albumin tended to decline with age. When the extent of endoscopic findings of esophageal varices were compared between the elderly over 60 and the under 60s, the former included the less advanced cases than the latter. The hemodynamic studies revealed that the portal pressure and hepatic blood flow did not differ among the three age groups, but the cardiac index reduced and total systemic vascular resistance increased with age. Regarding the cause of death, the frequency of gastrointestinal bleeding was lower in Group B and C than in Group A. From these results it may be concluded that an approximately half of cirrhosis of the elderly occurs for no known cause other than HBV, HCV and alcohol, and that the frequency of gastrointestinal bleeding as well as the extent of esophageal varices appear to decline with age.

Adult↗
PubMed1991

[Estimation of portal pressure using the theory of quantification].

An attempt was made to estimate noninvasively portal pressure (PP) in patients with chronic liver disease, using the theory of quantification, a kind of multivariate analysis. Forty-one patients with liver cirrhosis and 22 patients with chronic hepatitis in whom hepatic venous catheterization had been performed were studied. Seventeen parameters (age, sex, mean blood pressure, red blood cell count, platelet count, prothrombin time, lactate dehydrogenase, alkaline phosphatase, total bilirubin, albumin, gamma-globulin, indocyanine green retention at 15 min, blood urea nitrogen, hepatomegaly, splenomegaly, ascites and edema) were selected for the estimation of PP. The estimated PP correlated significantly with the data obtained by hepatic venous catheterization with a high correlation coefficient of 0.835 (p less than 0.01). An investigation using the theory of quantification was also undertaken to determine which of the 17 parameters selected above was most useful in estimating PP. Among the 17 parameters indocyanine green retention at 15 min, red blood cell count, prothrombin time, hepatomegaly and splenomegaly seemed to contribute significantly to the estimation of PP. When the formula was applied to 31 successive patients with chronic liver disease (external samples), the correlation between the estimated and measured PP was 0.455 (p less than 0.01). These results indicate that the formula is clinically useful in estimating PP in patients with chronic liver disease.

Adult↗
PubMed1991

Reduction in hepatic venous pressure gradient as a consequence of volume contraction due to chronic administration of spironolactone in patients with cirrhosis and no ascites.

The effect of plasma volume contraction induced by a 4-wk administration of spironolactone or furosemide on the hepatic venous pressure gradient was evaluated in consecutively allocated patients with cirrhosis and no ascites. In the spironolactone group (n = 15), the hepatic venous pressure gradient decreased significantly (p less than 0.005), by 21.8%, with a significant contraction of circulating plasma volume (p less than 0.01). Although there were no statistically significant correlations between the change in hepatic venous pressure gradient and changes in circulating plasma volume or in simultaneously determined systemic hemodynamics, a significant negative correlation (r = -0.74, p less than 0.01, n = 12) between the hepatic venous pressure gradient change and the post-treatment plasma aldosterone levels was found. However, in the furosemide group (n = 10), the hepatic venous pressure gradient and circulating plasma volume did not significantly decrease. Our data demonstrated a significant reduction in the hepatic venous pressure gradient on a chronic administration of spironolactone, which may have been due to volume contractions in patients with cirrhosis and no ascites.

Adult↗
PubMed1990

Regional differences in peripheral circulation between upper and lower extremity in patients with cirrhosis.

In 42 patients with compensated cirrhosis and 31 control subjects, blood flow (BF) and vascular resistance (VR) were measured at the forearm and calf, using a pneumoplethysmograph. In some of the subjects deep-body temperature (DBT) was also measured by the zero heat flow method. In cirrhosis, BF and DBT were significantly higher and VR was significantly lower in the forearm than in the calf. Corresponding differences were not observed in control subjects. When these indices of the forearm were compared between cirrhosis and controls, BF and DBT were significantly higher and VR was significantly lower in cirrhosis than in controls. In cirrhotics in whom the gradient between forearm BF and calf BF was 1 ml.dl-1.min-1 or more (forearm greater than calf), the vascular response of the forearm to cold stimulation was reduced, whereas in the remaining patients and in controls the forearm BF and VR responded significantly. These results suggest that there is a regional difference in peripheral circulation in cirrhotics, partly with participation of impaired sympathetic nervous activity, which may account for the selective distribution observed in the clinical manifestations of vascular spider, palmar erythema, and warm hand, inclined toward the upper extremities or the upper part of the body.

Arm↗
PubMed1990

[Hepatic and systemic hemodynamics in compensated cirrhosis--effect of posture change].

The effect of changes in body posture on estimated hepatic blood flow (EHBF) and various hemodynamic parameters was examined in 15 patients with compensated cirrhosis. EHBF and various hemodynamic parameters were first measured with the patients in the supine position, and then again 10 min after tilting to 45 degrees. EHBF was 1089 +/- 315 ml/min at supine and 1065 +/- 328 after tilting; the difference was not significant. However, the patients were then divided into two groups according to the magnitude of the decrease in EHBF after tilting, with those showing a decrease of 10% of more assigned to group B, and those showing a decrease of less than 10% assigned to group A. It was found that ICG (R15) and BSP (R45) were significantly higher in group A. Meanwhile, among hepatic and systemic hemodynamics, wedged hepatic venous pressure, hepatic venous pressure gradient, free hepatic venous pressure, cardiac index, systolic blood pressure, systemic vascular resistance, and stroke volume were found to have changed significantly after tilting. These results suggest that posture change has no effect on EHBF in compensated cirrhotic patients.

Aged↗
PubMed1989

Portal hypertension secondary to intrahepatic arterio-portal shunt in primary amyloidosis: a case report.

Portal hypertension is a rare complication in hepatic amyloidosis. We experienced a case of a 40-year-old man with primary amyloidosis and advanced esophageal varices. Angiographic procedures clearly demonstrated portal hypertension secondary to intrahepatic arterio-portal shunting. Hepatic arterial embolization brought about a disappearance of the A-P shunt and portal hypertension, though rebleeding occurred. To our knowledge, this is the first case report in which the pathogenesis of portal hypertension in hepatic amyloidosis was elucidated.

Adult↗
PubMed1989

Pathophysiology and epidemiology of portal hypertension.

Changes in portal pressure are regulated by changes in hepatic vascular resistance, which is normally under neurohumoral control, and portal tributary blood flow. Two theories on the pathophysiology of portal hypertension have been proposed: the 'backward flow' theory, in which portal hypertension is attributable to increased resistance to portal venous flow, and the 'forward flow' theory, in which increased splanchnic blood flow maintains portal hypertension despite extreme portal-systemic shunting. The sinusoidal abnormalities caused by an accumulation of collagen in the perisinusoidal space of Disse may induce increased resistance to blood flow in various pathological conditions of the liver. Non-cirrhotic portal hypertension results from not only relatively uncommon disorders prevalent mainly in Asia and tropical countries, but also from acute and chronic phases of relatively common liver diseases. Systemic hyperdynamic circulation, characterised by an increased cardiac output and a reduced peripheral vascular resistance, and splanchnic hyperaemia may develop as consequences of portal hypertension. Although the mechanisms of these changes are not clearly understood, portal-systemic shunting as well as some vasoactive substances, including prostaglandins, may be involved. The erosive and eruptive mechanisms are the two potential explanations for variceal bleeding. In the latter, pressure should not be viewed in isolation and other additive factors such as variceal size may be involved. Several new techniques of measuring variceal pressure and blood flow may improve understanding of the actual pathophysiology of variceal bleeding. Renal haemodynamic alterations secondary to the systemic circulatory changes produced by portal hypertension may occur. The geographical pattern of prevalence in disorders associated with portal hypertension is briefly described in this paper.

Humans↗
PubMed1988

Primary biliary cirrhosis with fibrosing alveolitis.

A 65-year-old case diagnosed as primary biliary cirrhosis without definite signs of Sjögren's syndrome at age 62 developed interstitial lung disease, which was clinically, histologically, radiographically, and scintigraphically compatible with fibrosing alveolitis. Analysis of the cells in bronchoalveolar lavage fluid revealed, however, increased proportions of not only neutrophils but also lymphocytic cells, which were predominant. This case should focus attention on the association of primary biliary cirrhosis and fibrosing alveolitis.

Aged↗