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Biomedical subjects

L Persson

Publications and source records attributed to L Persson.

At least 271 records · Page 15Linked to original sources
PubMed1978

Aspects on diamine oxidase activity and its determination.

Homogenate of guinea-pig liver and human placenta, tissues known to be rich in diamine oxidase, were incubated with 14C-putrescine and the metabolites formed were determined. In the incubate of guinea-pig liver, the major metabolites were GABA and some unidentified compound(s); delta1-pyrroline and 14CO2 were also obtained. In both the maternal and fetal parts of human placenta, radioactive GABA and the unidentified compound(s) as well as delta1-pyrroline were found. The results indicate that GABA is an important intermediate in putrescine metabolism. Determination of the amount of delta1-pyrroline is thus not well suited as a measure of the diamine oxidase activity in tissues.

Amine Oxidase (Copper-Containing)↗
PubMed1978

Polyamines and nucleic acids in the mouse kidney induced to growth by testosterone propionate.

Daily injections of testosterone propionate to castrated mice resulted in a striking increase in kidney weight. Renal putrescine rose sharply and the amounts of spermidine were also increased. The activity or ornithine decarboxylase was enhanced to values of more than 1 000 times the control level within a few days of testosterone substitution. A moderate and temporary increase in the activity of the putrescine-activated S-adenosyl-L-methionine decarboxylase was observed. Testosterone injections produced a large increase of renal RNA but only a minor change in DNA. It is apparent that in mice distinct alterations in polyamine metabolism occur during the development of renal hypertrophy induced by testosterone administration.

Adenosylmethionine Decarboxylase↗
PubMed1977

14-3-2 protein in rat brain synapses.

The distribution of the 14-3-2 protein in rat brain synapses was studied by immuno electron microscopy. The protein was localized to the postsynaptic web and to the postsynaptic membrane, but was also prominent both in the presynaptic membrane and in the presynaptic densities. No significant activity was observed in the synaptic vesicles.

Animals↗
PubMed1977

Enhanced blood-brain barrier leakage to evans blue-labelled albumin after air embolism in ethanol-intoxicated rats.

Control and ethanol-intoxicated rats were given a small air embolus in the right common carotid artery after ligation of the external carotid branch. The extravasation of Evans blue-labelled albumin (EBA) was studied. Control rats dispalyed a slight extravasation of EBA through arteries and arterioles at the surface of the right hemisphere with a slight spread into adjacent brain parenchyma. Additionally, ethanol-intoxicated rats showed a great leakage through small blood vessels even deep in the right hemisphere and a blue-staining of most of the embolized hemisphere. Thus it was shown that during embolization, ethanol increases the vascular permeability to macromolecules. It is proposed that this phenomenon mainly is due to injury to the endothelial cells.

Albumins↗
PubMed1977

Increased blood-brain barrier permeability around cerebral stab wounds, aggravated by acute ethanol intoxication.

Control and ethanol-intoxicated rats were injured with a small cerebral stab wound and the extravasation of Evans blue-labelled albumin (EBA) was studied. Control rats displayed an extravasation of EBA in the immediate peri-traumatic area with subsequent uptake of EBA in neurons and glia. Ethanol-intoxicated rats showed a greater leakage of EBA as well as a wider area of leaking blood vessels around the stab wound, both in the peri-traumatic and in the early post-traumatic period. Neuronal uptake of EBA was enhanced and observed in a wider area in intoxicated than control rats. The difference in distribution of EBA among neurons and glia between intoxicated and control rats was partly a consequence of the difference in leakage of EBA in the experimental groups. However, part of the increased neuronal uptake of EBA might be explained by an effect of ethanol on nueronal plasmalemma. The results obtained indicated a more pronounced injury to endothelial and neuronal cells after small cerebral stab wounds in ethanol-intoxicated compared to control rats.

Alcoholic Intoxication↗
PubMed1977

Evidence of decarboxylation of lysine by mammalian ornithine decarboxylase.

In enzymic preparations from mouse kidney stimulated with the anabolic steroid Durabolin (nandrolone phenpropionate) lysine and ornithine were shown to inhibit the decarboxylation of each other competitively. The Michaelis constants for the decarboxylations were approximately equal to the inhibition constants of the two amino acids. The pH optima of the decarboxylation of lysine and ornithine were found to be identical. Chromatographic studies of the enzyme preparation on a Sephadex G-150 Superfine column did not bring about a separation of the two enzyme activities. The ratio of the decarboxylating activities was practically the same during the elution. Lysine decarboxylating activity was also shown to be present in growth hormone stimulated rat liver. The results are in agreement with the assumption that the decarboxylation of lysine and ornithine is carried out by the same enzyme.

Animals↗
PubMed1976

Cellular reactions to small cerebral stab wounds in the rat frontal lobe. An ultrastructural study.

Small stab wounds were made in the frontal lobe of adult rats by the insertion of a glass capillary or a steel needle with a diameter of 50 mum. Macroscopically, there was a minute lesion filled with red blood cells. Ultrastructurally, there was a prominent edema with 200 mum from the wound during the first 3 days. There was an invasion of neutrophilic leukocytes, monocytes, and pericytes during the first postoperative week and a subsequent phagocytosis of necrotic devris during the first 2 weeks. Neurons within 150-200 mum from the wound degenerated and became phagocytized by macrophages. Astrocytes showed a transitional swelling, later followed by an accumulation of glycogen and filaments. Oligodendrocytes as well as astrocytes took part in phagocytosis. The most prominent early reaction of oligodendrocytes was the formation of multiple vacuoles and, in less injured cells, pinocytotic vesicles. Many cells with a morphology intermediate between the usual appearances of astrocytes and oligodendrocytes were seen. Some of these cells were similar to "third type of neuroglial cells." It was concluded that the healing of this type of small stab wounds occurred in a very regular way. Morpholocially, very little necrosis was seen, but there was a profound reactivity both in invading hematogeneous phagocytes, i.e., neutrophilic leukocytes and monocytes, and in neuroglial cells. Thus, the present type of trauma might be considered a useful model for studying events in healing of brain injuries.

Animals↗
PubMed1976

The brain-specific S 100 protein in small cerebral stab wounds in the rat: a quantitative study.

A quantitative study of the changes in water-soluble proteins and water-soluble S 100 was made in stab-wounded rat frontal cortex as compared to unoperated controls. No great changes occurred until 30 days after the injury. At that time there was no change in the amount of water-soluble S 100 protein/g wet weight, but a large decrease in the amount of water-soluble proteins/g wet weight and thus a proportionate increase in the amount of water-soluble S 100 protein/mg of water-soluble proteins. The significance of the results is discussed.

Animals↗
PubMed1976

Reversible blood-brain barrier dysfunction to peroxidase after a small stab wound in the rat cerebral cortex.

Small stab wounds were made in the rat frontal lobe. The animals were injected with horseradish peroxidase intravenously at different times after the injury in order to study the extravasation of this tracer. There was a leakage of peroxidase into the brain during the first 3 days after the injury. The route of passage from the vessel lumen into the brain was through disrupted blood vessels in the injured region. Endothelial pinocytosis and formation of thin, trans-endothelial channel-like structures with or without a content of peroxidase were two other possible routes of passage across the blood vessels. Occasionally, badly damaged endothelial cells displayed a diffuse cytoplasmic distribution of peroxidase, indication a diffusion into and possibly across these injured cells. No widened tight junctions were seen. Thus, this study indicated four possible routes of passage of horseradish peroxidase across the endothelial cells: cellular gross damage with disrupture of the cells, diffusion across badly injured endothelial cells, possibly pinocytosis and formation of trans-endothelial channel-like structures. The cellular uptake of the tracer was vesicular in most neurons, astrocytes, oligodendrocytes and hematogeneous phagocytes. However, a diffuse distribution of the tracer was seen in some "dark" neurons near leaking vessels in the vicinity of the stab wound.

Animals↗
PubMed1976

Intoxication--suicide or not?

It is often impossible to decide whether a death due to poisoning with drugs and/or alcohol is accidental or intentional. In 1965 WHO introduced the category "uncertain cases of death" in the official statistics. The number of cases in this category has increased and constitutes at present in Sweden between 30 and 70 per cent of the total number of suicides. In Malmö (1972-1973) most of these deaths were due to lethal poisoning with drugs and/or alcohol. When discussing suicidal rates it is important to include those cases.

Alcoholic Intoxication↗
PubMed1976

Extravasation, spread and cellular uptake of Evans blue-labelled albumin around a reproducible small stab-wound in the rat brain.

A small stab wound was made in the frontal lobe of the rat brain in order to study both the acute damage and the restitution of the blood-brain barrier to macromolecules under well-defined experimental conditions. Intravenously administered Evans blue-labelled albumin (EBA) was used as a tracer and the brain sections were observed in a fluorescence microscope. EBA leaked into the neuropil only during the first 3 days after the trauma. The maximal leakage occurred during the first day after the injury. The tracer spread from the area surrounding the stab wound in a reproducible way, initially roughly centrifugally. Nerve and glial cells close to the wound displayed a diffuse fluorescence of their cell bodies 1 to 6 h after the injury, i.e. at times with maximal extravasation of the tracer. A more granular distribution of the tracer was seen in neurons and glial cells at both very short and long times after EBA injection. Thus, the blood-brain barrier lesion induced was reproducible and reversible as judged by the pattern of EBA leakage. Some cells immediately adjacent to the injury had a diffuse cytoplasmic distribution of the tracer complex, in contrast to cells more distant from the injury, having a more granular distribution of the tracer in their cytoplasm. However, the appearance of the fluorescence in neurons and glia was to a large extent dependent upon the time after the injury, at which the cells were exposed to the tracer complex and on the time that had elapsed from the time of injection of the tracer complex to the sacrifice of the animal. Thus, it seems likely that two factors contribute to the appearance of the neuronal EBA distribution: on one hand the location and possibly extent of cellular damage of the cell, and, on the other hand, the time and amount of EBA to which the cells were exposed.

Animals↗
PubMed1976

Cellular and subcellular distribution of the S-100 protein in rabbit and rat central nervous system.

The cellular and subcellular distribution of the S-100 protein in rabbit and rat central nervous system was studied both quantitatively and qualitatively. Microcomplement fixation estimations on bulk-prepared neuronal and glial cells showed at least five to six times higher amounts of water-soluble S-100 in glial cell-enriched fractions as compared to fractions enriched in neuronal perikarya. Nerve cell fractions contained a higher percent of tissue-bound S-100 protein. High levels of S-100 protein were found in mitochondria and soluble protein fractions. Immunoelectron microscope investigations demonstrated S-100 protein in neuronal structures, such as the postsynaptic membrane and part of the plasma membrane. Among glial cells the astrocytic filaments contained high levels of S-100 protein. S-100 was also found in most subcellular membranes of astrocytes and oligodendrocytes.

Animals↗
PubMed1976

Biosynthesis of cadaverine in mice under the influence of an anabolic steroid.

The content of cadaverine (1,5-diaminopentane) in the kidney and urine was investigated in mice treated with the anabolic steroid Durabolin (nondrolone phenpropionate). After administration of this steroid cadaverine was found in the kidneys, whereas this amine could not be detected in the kidney of controls. The urinary excretion of cadaverine was elevated 50 times after Durabolin administration. An enzyme catalyzing the formation of cadaverine from lysine was shown for the first time to be present in mammalian tissue, namely in the kidney of mice after Durabolin administration.

Animals↗
PubMed1976

Immuno-electron microscopic study of the distribution of the S 100 protein in brain glial cells.

The distribution of the brain-specific S 100 protein was studied by an immunohistochemical method at the ultrastructural level. The S 100 protein was localized in the plasma membrane of astrocytes, oligodendrocytes and neurons, but not in that of endothelial cells and pericytes. Astrocytic filaments also possessed S 100 activity. The vascular basement membrane lacked traces of S 100.

Animals↗
PubMed1975

Clinical applications of an automatic data handling system for sexually-transmitted diseases.

An automatic data handling system for the storage and evaluation of data from investigations on sexually-transmitted diseases has been developed. Among the clinical applications are epidemiological investigations, evaluation of diagnostic procedures, and evaluation of treatment regimens. One of the main features of the system is its flexibility, which allows the inclusion of an unlimited number of further evaluation programs. After a running-in period of about 3 years, during which time a number of changes were found to be necessary, the method has been found to satisfy medical and data processing requirements.

Diagnosis, Computer-Assisted↗