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Biomedical subjects

B Hultberg

Publications and source records attributed to B Hultberg.

At least 127 records · Page 7Linked to original sources

Plasma homocysteine and methionine tolerance in early-onset vascular disease.

In three different studies we tested the hypothesis that early-onset vascular disease is associated with impaired homocysteine metabolism which could contribute to the development of arteriosclerosis and thrombosis. In patients with occlusive vascular disease before the age of 60, a post-methionine load increase of plasma homocysteine exceeding the highest value for comparable healthy control subjects was found in 1 of 21 with myocardial infarction (5%), 14 of 37 with aorto-iliac disease (38%), and 17 of 53 with cerebrovascular disease (32%). This might indicate heterozygosity for homocystinuria due to cystathionine beta-synthase deficiency. Concentrations of serum vitamin B12 and red cell folate had an important modulating effect on plasma homocysteine concentrations in the fasting state.

Drug Tolerance↗

Enzyme immunoassay of beta-hexosaminidase isoenzymes in human urine and renal cortex with monoclonal antibodies.

Enzyme immunoassay (EIA) methods with monoclonal antibodies specific for N-acetyl-beta-D-glucosaminidase (NAG) isoenzymes A and B in human urine are presented. The proportion of NAG B obtained with the EIA methods was similar to that found with ion-exchange chromatography. In fresh human control urines, NAG B was found to be approximately 20% of the total NAG activity. A significant correlation was obtained between total NAG activity in human urine assayed with a conventional enzyme substrate method and the total NAG activity obtained as the sum of NAG A and NAG B analyzed with the EIA methods. Total NAG activity with the latter (EIA) methods showed about 30% higher values than found by the enzyme substrate method, which probably was due to inhibitors of NAG activity present in urine did not interfere with the EIA methods. The content of NAG A and NAG B in renal cortex was determined with the EIA methods. NAG B accounted for about 20% of the total NAG activity, which was similar to that found in fresh human urines.

Acetylglucosaminidase↗

Alkaline phosphatase in cholestatic and cirrhotic rats. A biochemical and histochemical study.

Alkaline phosphatase (ALP) was studied by enzyme histochemical methods and by biochemical quantitations in rat livers with chronic bile duct obstruction and experimental cirrhosis. The most evident ALP increase was histochemically found in portal tracts of rats with bile duct obstruction and localized to the walls of proliferating blood vessels. Furthermore, a slight canalicular membrane enzyme increase was histochemically found in both groups, most evident in cirrhosis, whereas the biochemical assay of ALP in serum and liver from both pathological groups showed 3 times higher values compared to controls. The portal tracts did not seem to contribute to the serum increase, since the rise of serum ALP was similar in chronic bile duct obstruction and in experimental cirrhosis without changes of the portal tracts. It is concluded that the increase ALP activity in serum from rats with bile duct obstruction and cirrhosis mainly has a hepatocytic origin.

Alkaline Phosphatase↗

Urinary excretion of N-acetyl-beta-D-glucosaminidase in normal and complicated pregnancy.

The urinary excretion of N-acetyl-beta-D-glucosaminidase activity, a sensitive indicator of renal tubular injury, was monitored during and after pregnancy. During normal pregnancy, enzymuria increased progressively to levels 3-4 times above normal in the third trimester. In diabetic mothers, enzyme excretion followed a similar pattern, but was generally higher than in uncomplicated pregnancies. Also in preeclampsia, enzymuria tended to be higher than in normal pregnancy. Enzyme excretion normalized about a year after normal pregnancies, but remained elevated in diabetic subjects and in patients who had developed preeclampsia. This latter finding indicates that marginal persistent renal damage may occur during preeclampsia.

Acetylglucosaminidase↗

Enzymuria in workers exposed to inorganic mercury.

Urinary excretion of beta-hexosaminidase (NAG = N-acetyl-beta-glucosaminidase) and albumin was examined in 41 chlor-alkali workers exposed to inorganic mercury and 41 age-matched controls. Either U-HG or B-Hg levels for these workers were available dating from the 1960s to the present. Increased U-NAG was seen in workers with a U-Hg today of more than 4 micrograms/mmol creat (about 50 micrograms/l: 35 ug/g creat). Multiple linear regression analysis showed that U-NAG was correlated to U-Hg and integrated dose but not to the present B-Hg level. No albuminuria (detection limit 12.5 mg/l) was found in any of the subjects. In a longitudinal study, no decrease in U-NAG levels was seen in 15 chlor-alkali workers after their vacation (means = 20d). In five workers followed for ten months after a short exposure period, no definite time trend could be seen. The results show that there is a slight effect on renal tubules even at rather low levels of exposure to mercury vapour. The clinical significance of the enzymuria levels found here is, however, debatable.

Acetylglucosaminidase↗

Higher total plasma homocysteine in vitamin B12 deficiency than in heterozygosity for homocystinuria due to cystathionine beta-synthase deficiency.

Homocysteine is an amino acid considered to cause vascular injury, arteriosclerosis, and thromboembolism. Total plasma homocysteine (free and protein-bound) was found to be twice as high in asymptomatic vitamin B12-deficient subjects (23.8 +/- 3.8 mumol/L, means +/- SEM, n = 20) as in controls (11.5 +/- 0.9 mumol/L, P less than .0001, n = 21), and higher than in heterozygotes for homocystinuria due to cystathionine beta-synthase deficiency (13.8 +/- 1.6 mumol/L, P less than .01, n = 14), who were recently shown to be much more common among patients with premature vascular disease than expected. Eight (40%) vitamin B12-deficient and two (14%) heterozygote subjects had significant homocysteinemia (greater than mean +2 SD for controls). After administration of hydroxycobalamin to vitamin B12-deficient subjects, homocysteine levels decreased to normal (-49%, 12.2 +/- 1.5 mumol/L, P less than .0001, n = 20). Thus, if homocysteine does cause vascular injury, theoretically vitamin B12-deficiency might be associated with an increased frequency of vascular disease.

Cystathionine beta-Synthase↗

Lysosomal enzymes in pregnant and steroid treated rats.

The contents of three lysosomal enzymes (beta-hexosaminidase, beta-glucuronidase and alpha-fucosidase) were studied in plasma and different tissues of pregnant and steroid treated rats. All these enzymes were found to be increased in plasma from pregnant rats in analogy with the findings in pregnant women. In liver tissue only beta-hexosaminidase and alpha-fucosidase were significantly increased. In rats with diethylstilbestrol (DES) and a combination of DES and progesterone, there was an increase of alpha-fucosidase in plasma and liver. No significant changes were observed for the other two enzymes. Thus, steroid treatment did not fully reproduce the enzyme changes seen in pregnancy, which may indicate that these are not solely due to a hormone effect.

Alkaline Phosphatase↗

The effect of porta-caval shunt, ammonia infusion and alcohol administration on rat plasma beta-hexosaminidase.

The activity of the lysosomal enzyme, beta-hexosaminidase, is increased in plasma of patients with various forms of liver disease as well as in plasma from rats with experimental cholestasis or cirrhosis. In this experimental study in the rat, the effect of porta-caval shunt, ammonia infusion and ethanol feeding on plasma beta-hexosaminidase activity was studied. Porta-caval shunted animals had significantly increased plasma beta-hexosaminidase activity compared to sham-operated animals. Ammonia infusion in porta-caval shunted rats resulted in a further increase of plasma enzyme activity. Ethanol feeding for different periods of time (1 day to 4 weeks) did not have any influence on plasma beta-hexosaminidase activity.

Ammonia↗

Source of increased serum beta-hexosaminidase in rat liver cirrhosis.

Lysosomal enzymes were studied by histo- and biochemical methods in cirrhotic rat livers in order to explain the serum increase of lysosomal enzymes in cirrhosis. Biochemically, the most evident increase was found in isolated hepatocytes. Histochemically, the lysosomal enzymes were increased mainly in rows of macrophages and necrotic or atrophic hepatocytes adjacent to strands of connective tissue at the periphery of the cirrhotic nodules. The results were compared to similar studies in cholestatic rats. It is concluded that most of the increased serum activities of the lysosomal enzymes derive from the hepatocytes.

Animals↗

Treatment of septicaemia in immunocompromised patients with ceftazidime or with tobramycin and cefuroxime, with special reference to renal effects.

Fifty-two immunocompromised patients with suspected septicaemia were randomized on 61 occasions to treatment with ceftazidime or with tobramycin and cefuroxime. Most (90%) of the patients had haematological malignancies and were neutropenic (granulocytes less than 1 X 10(9)/1 in 40 of the 61 episodes). Blood cultures were positive in 22 (39%) febrile episodes and in four other instances positive cultures were obtained from other sources. Clinical cure or improvement was noted in 10 of 12 culture verified infections in the tobramycin and cefuroxime group and 11 of 14 episodes in the ceftazidime-group. The effect on the kidney of the two antibiotic regimens was studied by following the serum levels of creatinine, urea and beta 2-microglobulin and the urinary excretion of alanine aminopeptidase, N-acetyl-beta-D-glucosaminidase (beta-NAG) and beta 2-microglobulin. No clinically important renal side effects were observed. However, an increase in the urinary excretion of AAP was seen in both groups with significantly greater elevation in the tobramycin and cefuroxime group. Urinary beta-NAG increased only in the tobramycin and cefuroxime group.

Adult↗

Early biochemical and histological changes in rats exposed to a single injection of thioacetamide.

Liver injury was induced by one subcutaneous administration of thioacetamide (200 mg/kg b.wt.) and studied 24 and 48 hrs later. Levels of aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) increased after 24 and 48 hrs. The lysosomal enzymes beta-hexosaminidase (beta-NAG) and beta-glucuronidase (beta-GLU) increased significantly after 24 hrs, while the level of beta-GLU returned to normal after 48 hrs, but the activity of beta-NAG remained significantly high even after 48 hrs. Histopathological examination showed necrotic hepatocytes around the central vein with infiltration of macrophages, neutrophils and eosinophils. The plasma zinc level decreased after 24 hrs and returned to normal after 48 hrs. Liver zinc content increased simultaneously at 24 hrs, returning to normal after 48 hrs. No alterations of plasma copper were observed after 24 and 48 hrs. Copper content of the liver increased significantly after 24 and 48 hrs. The present study thus shows that one dose of thioacetamide results in profound liver injury and supplementation of zinc prior to and simultaneously with thioacetamide normalized plasma zinc, increased liver zinc content and reduced the increase of beta-NAG, but did not influence the histological changes.

Acetamides↗

Serum proteins in liver cirrhosis: effects of shunt surgery.

The serum protein patterns of 38 patients with alcoholic liver cirrhosis were studied and compared with those of 15 patients with cryptogenic cirrhosis and of 18 normal volunteers. Serum prealbumin and albumin were significantly lowered in alcoholic liver cirrhosis in comparison with the normals. In liver cirrhosis, the four acute phase reactants, alpha 1-antiproteinase, orosomucoid, and haptoglobin and caeruloplasmin, showed a pattern in serum, in which alpha 1-antiproteinase was increased, orosomucoid and haptoglobin were decreased, and caeruloplasmin was normal. Immunoglobulins G, A and M were significantly elevated. IgA was significantly more elevated in patients with alcoholic disease than in patients with cryptogenic cirrhosis. The construction of a surgical portal-systemic shunt resulted in a significant decrease in serum concentrations of the acute phase reactants, while prealbumin, albumin and immunoglobulins were unaffected.

Acute-Phase Proteins↗

beta-Hexosaminidase in plasma and liver after partial hepatectomy in normal and cirrhotic rats.

The liver and plasma level of the lysosomal enzyme beta-hexosaminidase was analyzed in partially (about 70%) hepatectomized rats with normal liver or carbon tetrachloride (CCl4)-induced cirrhosis. The enzyme level of the liver did not show marked changes after partial hepatectomy in either normal or cirrhotic rats. In contrast, the plasma basal level was significantly higher in cirrhotic rats and increased to a peak at 6 h, followed by a decrease to a minimum level 24 h after operation. The enzyme returned to its high plasma basal level at 36 h after partial hepatectomy, when the liver had recovered to 70% of its initial weight. In rats with normal liver the plasma beta-hexosaminidase showed another pattern, with a rapid increase at 6 h and thereafter gradually reaching a peak at 36 h after hepatectomy. We conclude that the cells responsible for increased plasma beta-hexosaminidase in cirrhotic rats are situated in the liver.

Alanine Transaminase↗