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K Fredens

Publications and source records attributed to K Fredens.

At least 37 records · Page 2Linked to original sources

Extracellular deposit of the cationic proteins ECP and EPX in tissue infiltrations of eosinophils related to tissue damage.

In a series of eosinophil inflammatory states affecting various organs (heart, gut, bladder and skin) we performed an immunohistochemical study of the eosinophil cationic proteins ECP and EPX. A strong correlation was noted between the liberation of ECP and EPX and tissue necrosis in all organs. In most cases ECP and EPX were found on the same location. However, one case indicated a possible differential release. Extracellular ECP and EPX were revealed concurrently with the two polyclonal antibodies and the monoclonal EG2 antibody. The latter binds to both ECP and EPX, but only during secretion. Since EG2 does not differentiate between ECP and EPX, but only during secretion. Since EG2 does not differentiate between EXP and EPX, it is for the first time demonstrated that both cationic proteins are correlated to tissue damage. The chymotrypsin-like cationic protein (CCP), related to neutrophils, showed a low correlation with the eosinophil cationic proteins in cases of tissue damage. The hypothesis is put forward that the release of eosinophil granule proteins and especially ECP results in a non-specific tissue damage.

Adult↗

Epithelial injury by human eosinophils.

The human eosinophil is armed with a number of very potent cytotoxic granule proteins that upon extracellular release may produce considerable damage. The toxic effect of the proteins seems to be quite unselective, involving most mammalian and nonmammalian cells including the epithelial cells. The demonstration of a close relation between the deposition of eosinophil granule proteins and areas of epithelial cell destruction in a variety of diseases including asthma and the fact that cytotoxic concentrations of the proteins have been measured in the fluid phase suggest that the eosinophil participates actively in the pathogenesis of airway diseases. The protection towards the adverse actions of the eosinophil, particularly towards their proteins, therefore seems vital. The discovery of alpha-2-macroglobulin as a specific binder of eosinophil cationic protein may be relevant in this regard.

Asthma↗

Localization of cholecystokinin in the dentate commissural-associational system of the mouse and rat.

Cholecystokinin immunoreactivity (CI) was demonstrated in the inner one third of the molecular layer of area dentata in the rat and 3 strains of mice. This part of the molecular layer coincides with the terminal field of the commissural-associational system (C/A-system). In rats there is also CI in the middle third of this layer where the medial perforant path terminates, but there is no CI in this area in any of the 3 strains of mice. Different selective lesions except those involving the hilus, did not change this staining pattern. Electrolytic lesions of the hilus removed the CI in the terminal field of the C/A-system. Similarly, after kainic acid injections, the CI in the C/A-zone is reduced to a degree that is proportional to the amount of damage of the hilus. In the rat these lesions produced virtually no change in the CI of the medial perforant path terminal zone. The predominant type of cell within the hilus is the mossy cell and the cells of this type contain CI. The mossy cells have both commissural and ipsilateral projections that terminate in the inner one third of the molecular layer. Other cell types within the hilus contain CI, such as basket cells, oviform-like and fusiform-like cells. However, there was no evidence that any of these cells had commissural projections. Apart from the mossy cells there are other cells with commissural projections such as those in regio inferior. However, there was no evidence that any of them contained CI or also gave rise to an associational projection to the inner one third of the molecular layer. Moreover, there was a difference in the distribution of commissurally projecting cells that contained CI in the rat as compared to the mouse brain. This difference is the same as that occurring in the distribution of mossy cells where in the rat cells are found throughout the hilus, with most close to, but never inside the granule cell layer as compared to the mouse where virtually all are at a central part of the hilus. Thus these results are consistent with the hypothesis that all mossy cells contain CI and are the sole source of the C/A-system. After X-ray irradiation of the neonatal rat it is known that only part of the infrapyramidal blade of the granule cell layer is formed.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

An immunofluorescent method for a specific demonstration of granulocytes and some of their proteins (ECP and CCP).

Using p-benzoquinone as a fixative the non-specific fluorescence of granulocytes and especially the eosinophils is removed for both FITC and TRITC. In this way we have been able to detect the eosinophil cationic protein (ECP) and the chymotrypsin-like cationic protein (CCP) in human lung tissue and by double immunofluorescent labelling shown that these two proteins very likely are related to eosinophils respectively the neutrophils.

Adult↗

Eosinophils and cellular injury: the Gordon phenomenon as a model.

Three eosinophil proteins, eosinophil cationic protein (ECP), eosinophil protein-X (EPX), and eosinophil-derived neurotoxin (EDN), have neurotoxic properties. EDN and EPX may be identical. ECP is by far the most potent neurotoxic eosinophil-derived protein. The damaging effect of the three proteins have been claimed to be selective. This selectivity can, at least in part, be explained by way of the experimental injections. Several observations are in favour of a selectivity through accumulation. Immunocytochemical localization of intraventricular injected ECP supports this hypothesis and indicates furthermore that ECP has an immediate reactivity towards and possible toxic effect against nervous tissue in general.

Animals↗

Localization of enkephalin and cholecystokinin immunoreactivities in the perforant path terminal fields of the rat hippocampal formation.

The distribution of enkephalin immunoreactivity (EI) in the molecular layer of the hippocampal formation corresponded to the terminal field of the lateral perforant path and the lateral temporoammonic tract. The distribution of cholecystokinin immunoreactivity (CI) in the molecular layer of the hippocampal formation corresponded to the established terminal field of the medial temporoammonic tract. The exception was a CI band at the deep part of the molecular layer throughout the regio superior. Accordingly, an additional terminal field of the medial temporoammonic tract is suggested. Selective lesion of the entorhinal afferents to the hippocampus and the area dentata resulted in a disappearance of EI throughout the molecular layer with no affection of CI and vice versa. Neonatally X-ray irradiated hippocampi were examined as they appear in the adult animal. These animals are known to possess an altered relation between the granule cells of area dentata and the perforant path zones extending beyond a reduced medial blade into the stratum oriens of the regio inferior. In such animals EI and CI revealed the same pattern of changes by following the perforant path zones into stratum oriens due to neonatal X-ray irradiation. Accordingly, the perforant path may contain EI and CI independent of the granule cell dendrites. Based on a discussion of these observations we conclude that enkephalin immunoreactivity is localized in terminals of the lateral perforant path and the lateral temporoammonic tract and that cholecystokinin immunoreactivity is localized in the terminals of the medial perforant path and the medial temporoammonic tract.

Animals↗

The presence of smooth muscle cells in the rat ovary.

Using a histochemical procedure for the demonstration of glycogen phosphorylase, smooth muscle cells have been demonstrated in the rat ovary around follicles, corpora lutea, atretic follicles and between groups of interstitial cells.

Animals↗

Modulation of cholecystokinin concentrations in the rat hippocampus by chelation of heavy metals.

Previously, we have reported that enkephalins, cholecystokinin, and heavy metals show roughly parallel distributional patterns in the hippocampus. A substantial body of evidence indicates that cholecystokinin-octapeptide (CCK-8) and enkephalins act as neurotransmitters. A CCK-8 degrading enzyme was recently detected in brain synaptosomes. Its activity depended on free thiol groups and the presence of a heavy metal. Since the heavy metal-containing neuropil is closely related to CCK-immunoreactive nerve terminals, we have investigated the effect of metal chelation on CCK components in the rat hippocampus. In vivo treatment of rats with a single dose of the chelating agent diethyldithiocarbamate caused a reversible chelation of heavy metals in the hippocampus. This effect was paralleled by a 3-fold increase in hippocampal content of CCK-8 and a smaller increase in the intermediate forms of CCK (CCK-58, CCK-39, CCK-33). Diethyldithiocarbamate also decreased the spontaneous motility and aggressiveness of the rats. These data show reversible changes of neuronal CCK processing by a drug, and hence they provide additional evidence that CCK is involved in the regulation of neuronal activities.

Animals↗

The Gordon phenomenon induced by the eosinophil cationic protein and eosinophil protein X.

Cerebellar Purkinje cell degeneration after intracerebral injection of eosinophil granulocytes or extracts thereof is known as the Gordon phenomenon. The reaction is said to be highly selective. An eosinophil-derived neurotoxin (EDN) has recently been reported to induce the Gordon phenomenon. However, we report here that two eosinophil-derived proteins, eosinophil cationic protein (ECP) and eosinophil protein X (EPX), may induce the Gordon phenomenon after intraventricular injection. The potency of ECP is far greater than that of EPX and the latter is possibly identical to EDN. The Fink-Heimer staining for degenerating nerve fibers and boutons, however, indicated that the selectivity of the Gordon phenomenon is not as specific as was previously thought, since this method revealed degeneration of all brain areas in proximity to the ventricular system.

Animals↗

Genetic variation in the histoarchitecture of the hippocampal region of mice.

Timm's sulphide-silver method and the histochemical procedures for the demonstration of AChE, MAO and SDH were applied to the brains of three strains of adult mice of either sex: C57/BL/6J, DBA/2J and NMRI. Differences between strains were found 1) in the sulphide-silver pattern of the molecular layer of area dentata, probably reflecting differences in entorhinal, ipsilateral and/or commissural connections, 2) in the distribution of the mossy fibers, 3) in the AChE-staining of a suprapyramidal zone of regio inferior, probably reflecting differences in septal connections, 4) in the AChE-staining of the induseum griseum. The staining patterns for MAO and SDH did not vary, at least not qualitatively, between the strains investigated. Variation in adult age and sex did not influence the results. Since the differences observed seemed to reflect a pattern of genetic differentiation, five more inbred mice (A/J, AKR/A, BALB/c/A, C3H/Tif, St/6Fi) were included to strengthen the hypothesis that different genetic systems are operating at separate septo-temporal levels in the same areas during the development of the hippocampal formation.

Acetylcholinesterase↗

Inhibition of opiate receptor binding by zinc ions: possible physiological importance in the hippocampus.

In the rat and guinea pig hippocampus, the staining pattern for enkephalin (by immunocytochemistry) and for zinc (by the Timm method) is congruent and confined to the mossy fiber system. The stereospecific binding of 3H-enkephalinamide (2-D-Ala-5-L-methionine) to opiate receptors can be totally blocked by zinc ions, both in the hippocampus and in the cerebral cortex, the basal ganglia and the rest of the forebrain. Scatchard analysis of binding isotherms indicates that this inhibitory effect involves a decrease in receptor affinity, whereas the number of binding sites is unaffected. Thiol reductants can reactivate Zn2+-inhibited opiate receptors with a potency correlating to their redox potential (Eo). Thus, our data suggest that zinc ions represent modulators of opiate receptor binding in the hippocampus and that they work through a redox reaction with essential SH-groups of opiate receptors.

Animals↗