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Biomedical subjects

C Larsson

Publications and source records attributed to C Larsson.

At least 379 records · Page 21Linked to original sources
PubMed1977

Liver function in asymptomatic adult individuals with severe alpha1-antitrypsin deficiency (Pi Z).

Eleven adult individuals (aged 24 to 66 years) with severe alpha1-antitrypsin deficiency, Pi Z, and with no clinical signs of liver disease, were investigated with a broad spectrum of liver function tests. Except for low alpha1-antitrypsin levels, no evidence of abnormal hepatic protein synthesis was found. Neither could any biochemical signs of liver cell necrosis or increased liver cell regeneration be disclosed. In spite of the well-known pronounced distension of hepatic endoplasmic reticulum (E.R.) by aggregated asialo-alpha1-antitrypsin in this disease, the function of the E.R. tested with the aminopyrine breath test was not found to be impaired.

Adult↗
PubMed1976

The serum sialyltransferase activity in alpha 1-antitrypsin deficiency.

alpha 1-Antitrypsin phenotypes Pi M and Z, purified by the thiol-disulfide exchange procedure, were desialylated by treatment with neuraminidase covalently coupled to Sepharose and used as acceptors of sialic acid in an assay system for serum sialic acid transferase (CMP-N-acetylneuraminate:D-galactosyl-glycoprotein N-acetylneuraminyltransferase, EC 2.4.99.1) activity. Both asialoantitrypsins were equally effective as acceptors in contrast to native Pi Z antitrypsin which did not accept any sialic acid. Serum sialyltransferase activity was determined in 38 adult alpha 1-antitrypsin deficient individuals (Pi Z, MZ, FZ, SZ) with normal liver function and was found to be of the same magnitude as the activity in normal individuals (Pi M). Equal activities were also found in 5 Pi Z patients with cirrhosis of the liver. The results strongly argue against the concept that sialyltransferase deficiency provides the molecular basis for alpha 1-antitrypsin deficiency.

Fasting↗
PubMed1976

Properties of chloroplasts isolated by phase partition.

Chloroplasts from spinach can be separated into at least three different populations by countercurrent distribution using polymer two-phase systems. The chloroplast particles of the three populations differ in protein/chlorophyll ratio, ultrastructure and metabolism. One population, peak I, consists of intact chloroplasts surrounded by the chloroplast envelope; the second population, peak II, consists of chloroplasts, which have lost their envelopes and much of their stromal material; the third population, peak III, consists of particles containing intact chloroplasts surrounded by a membrane-bound cytoplasmic layer including mitochondria and peroxisomes. Rapid batch procedures of peak I chloroplasts incorporated 14C almost entirely into glycolate and intermediates of the Calvin cycle and starch synthesis. Only small amounts were found in sucrose and amino acids. On the other hand preparations of peak III chloroplasts have a much broader spectrum of 14C-labelled products. Sucrose, malate and some amino acids contained about 40% of the 14C incorporated. It is concluded from these experiments that sucrose is formed not within the chloroplast but in the cytoplasm from intermediates exported by the chloroplast. The origin of peak III particles and their use for studying the cooperation between the chloroplast and the surrounding cytoplasm including mitochondria and peroxisomes is discussed.

Carbon Dioxide↗
PubMed1976

Reduction by indomethacin of furosemide effects in the rabbit.

The effects of furosemide on urine flow, sodium and potassium excretion and on plasma renin activity (PRA) were studied in anesthetized rabbits with and without pretreatment with indomethacin 5 mg/kg. Furosemide caused a 10-fold increase in urine flow and in sodium excretion, and a 2-3 fold increase in PRA. Pretreatment with the prostaglandin synthesis inhibitor, indomethacin, reduced the effects of furosemide on diuresis and on electrolyte excretion by over 80% (p less than 0.01) and PRA did not increase over the initial level. The results suggest that the effects of furosemide on PRA and on urinary sodium excretion may be related to the intrarenal activation of the prostaglandin system.

Animals↗
PubMed1976

Effects of stimulation and inhibition of the renal prostaglandin synthetase system on renin release in vivo and in vitro.

1. The prostaglandin precursor arachidonic acid (C20:4) increases plasma renin activity in the rabbit and rat when it is infused into the renal arteries. 2. The increase in plasma renin activity after C20:4 in rats is not changed by volume expansion. 3. The inhibitor of prostaglandin synthesis indomethacin decreases plasma renin activity in the rabbit. 4. The increase plasma in renin activity after total renal ischaemia is abolished by pretreatment with indomethacin. 5. C20:4 increases dose- and time-dependent renin release from slices of rabbit kidney cortex. 6. Indomethacin or 5,8,11,14-eicosatetraynoic acid pretreatment in vivo, and addition to the incubation medium, reduces basal as well as C20:4-stimulated renin release in vitro. 7. The stimulating effect of C20:4 on renin release is assumed to be caused directly by formation of prostaglandin endoperoxides in the kidney cortex and not by prostaglandins since in vitro a natural prostaglandin endoperoxide (PGG2) and two stable synthetic prostaglandin endoperoxide analogues (EPA I and EPA II) do increase the release of renin, but PGE2 has no effect and PGF2alpha inhibits renin release.

Animals↗
PubMed1976

Stimulation of renin release from rabbit renal cortex by arachidonic acid and prostaglandin endoperoxides.

The mechanism by which renal prostaglandins stimulate renin secretion in vivo is unknown. In this in vitro study we measured the effects of activation of the prostaglandin (PG) system on renin release from slices of rabbit renal cortex. The PG precursor arachidonic acid (C20:4), a natural PG endoperoxide (PGG2), two stable synthetic PG endoperoxide analogues (EPA I and II), PGE2, PGF2alpha, and two different PG synthesis inhibitors [indomethacin and 5,8,11,14-eicosatetraynoic acid (ETA)] were used to evaluate the possibility of a direct action of the cortical PG system on renin secretion. Renin release increased significantly with time after addition of C20:4, PGG2, EPA I, and EPA II to the incubation medium. Stimulation of renin release was se-related for C20:4 in concentrations of 0.6 to 4.5 X 10(-6) M, for EPA I in concentrations of 0.7 to 2.8 X 10(-6) M, and for EPA II in concentrations of 1.4 to 14.0 X 10(-6) M. Indomethacin (10(-4) M) and ETA (10(-4) M) significantly decreased basal renin release as well as the renin release stimulated by C20:4 and EPA I. PGE2(10(-12) to 10(-6) M) had no effect on renin release, whereas PGF2alpha (10(-12) to 10(-6) M) decreased renin release in a dose-dependent manner. These data raise the possibility of a direct action of the renal cortical PG system on renin secretion. The results further indicate that stimulation of renin release by C20:4 may depend more specifically on the action of PG endoperoxides than on the primary prostaglandins.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1976

Stimulation and inhibition of renal PG biosynthesis: effects on renal blood flow and on plasma renin activity.

In the present investigation prostaglandins (PGs) were determined in the renal cortex and the functional effects of the renal PGs on renal hemodynamics and on the renin-angiotensin system were evaluated. The levels of PGs, determined by mass fragmentography, were in the medulla: PGE2 4.36 +/- 1.04 mug/g and PGF2 alpha 1.6 +/- 0.50 mug/g and in the cortex: PGE2 0.19 +/- 0.04 mug/g and PGF2 alpha 0.21 +/- 0.07 mug/g. The unequivocal demonstration of PGs in the renal cortex forms a biochemical basis for a role of PGs in the regulation of renal hemodynamics and of the renin-angiotensin system.

Angiotensin II↗
PubMed1976

Lung function studies in asymptomatic individuals with moderately (Pi SZ) and severely (Pi Z) reduced levels of alpha1-antitrypsin.

Extensive physiological evaluation of lung function were conducted in two groups of asymptomatic individuals with deficiencies of alpha1-antitrypsin: seven subjects with phenotype Pi SZ and six subjects with phenotype Pi Z. Four symptomatic individuals of Pi Z type were also investigated. The asymptomatic individuals of both SZ and Z phenotypes revealed reduction of elastic recoil, hypoventilation and hypoperfusion of the lung bases with increased closing and nitogen wash-out volumes. No signs of bronchial obstruction were observed. The asymptomatic Pi SZ subjects revealed as many signs of subclinical disease as did the asymptomatic Pi Z subjects. These data suggest that Pi SZ subjects are at increased risk of emphysema similar to Pi Z subjects.

Adult↗
PubMed1976

Interactions between the renal prostaglandins and the renin--angiotensin system.

Although the PGs operate mainly in the renal medulla the demonstration of PG biosynthesis in the renal cortex has provided a biochemical basis for a direct relationship between the PGs and the renin-angiotensin system. The formation of PGs is influenced by circulating levels of A I probably by indirect mechanisms. That the release of renin at least under certain experimental conditions is dependent on the PG system is suggested by the following findings: 1. C20:4 increases PRA in the rabbit and rat. 2. Indomethacin decreases PRA in the rabbit. 3. C20:4 stimulates renin release from slices of rabbit kidney cortex. 4. Reduced renal perfusion pressure and ischemia are accompanied by release of both PGs and renin. 5. The release of PG and renin following renal ischemia is blocked by treatment with indomethacin. The actions of the renin-angiotensin system and the renal PGs are, as far as we know them, antagonistic to each other. PGEs are vasodilator, increase renal blood flow, inhibit adrenergic neurotransmission, and cause excretion of electrolytes and water. Conversely, A II is vasoconstrictor, decreases renal blood flow, stimulates adrenergic neurotransmission, and conserves water and electrolytes. Thus, the interaction between the renal PGs and renin seems to be one in which the two hormonal systems stimulate each other's formation or release, but opposes each other's actions. Further studies are necessary to reconcile this apparent contradiction.

Angiotensin II↗
PubMed1975

Characterization of alpha1-antitrypsin in the inclusion bodies from the liver in alpha 1-antitrypsin deficiency.

alpha1-antitrypsin was isolated from periodic acid-Schiff-positive inclusion bodies from the hepatocytes of patients with alpha1-antitrypsin deficiency and further purified to enable more detailed chemical analysis. Amino acid and cyanogen bromide fragmentation studies showed a close similarity between hepatic and serum (PiMM) antitrypsin in contrast to the carbohydrate analysis, which revealed markedly deficient glycosylation of hepatic antitrypsin. A complete lack of sialic acid and a relative deficiency of all other carbohydrate components could fully explain the difference of approximately 6000 daltons in molecular size between the two proteins. The accumulation of hepatic globules is probably related to the physical properties of the defective antitrypsin, which include marked insolubility and tendency toward aggregation. The results strongly suggest an abnormal amino acid sequence in the peptide chain of the deficient antitrypsin. The interference with glycosylation may be related to steric hindrance.

Amino Acid Sequence↗
PubMed1975

Prostaglandin synthesis in membrane fractions from the rabbit renal medulla.

In order to investigate the subcellular location of the prostaglandin synthesizing enzyme complex (prostaglandin synthetase) the distribution of this enzyme was analysed in membrane fractions from the rabbit renal medulla using an improved radioactive assay with arachidonic acid as a substrate. 3 membrane fractions were isolated and the subcellular origin of the membranes was determined by electron microscopy and by their contents of different marker enzymes. Fraction I was a plasma membrane fraction, fraction II was a cytomembrane fraction, mainly derived from the endoplasmic reticulum and fraction III was a mitochondrial fraction. The specific activity of prostaglandin synthetase in the homogenate of rabbit renal medulla was 0-1 nmol arachidonic acid converted/min per mg protein. In fraction II, the cytomembrane fraction, the specific activity was increased 2-4 times over the homogenate, the plasma membrane fraction and the mitochondrial fraction having lower activities. The results suggest that prostaglandin synthetase is located in the endoplasmic reticulum of renal medullary cells.

Animals↗
PubMed1975

A study of DNA from chloroplasts separated by counter-current distribution.

Three types of chloroplasts (Peak I, Peak II, and Peak III chloroplasts) isolated by counter-current distribution in aqueous polymer two-phase systems have been studied with respect to DNA content. (The characterization was performed by studying the buoyant density, the melting profile and the amount of DNA of each type). The DNA was found to differ between the three types of chloroplasts.

Centrifugation, Density Gradient↗