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Biomedical subjects

F Gallyas

Publications and source records attributed to F Gallyas.

At least 19 recordsLinked to original sources
PubMed1992

Delayed degeneration of the optic tract and neurons in the superior colliculus after forebrain ischemia.

Neuronal damage induced by 15-min forebrain ischemia was investigated in adult rats 1-5 days (short-term group) and 1-5 months (long-term group) after the initial ischemic attack. In addition to the vulnerable areas reported previously, we observed that the optic tract was also very susceptible. Degeneration of the optic tract and subsequent transsynaptic cell death in the superior colliculus developed slowly and was observed only in the long-term group. The delayed, progressive neuronal damage in this sensory system may serve as a suitable model to investigate the mechanisms of long-term changes in the injured brain.

Animals↗
PubMed1992

Coexistence of cholinergic, catecholaminergic, serotonergic, and glutamatergic neurotransmitter markers in mouse clonal hybrid neurons derived from the septal region.

Two clonal immortalized neurons designated SN6.1b and SN6.2a were isolated by limiting dilution from a mouse embryonic septal cholinergic neuronal hybrid cell line SN6 (Hammond et al., 1986). In the serum-containing medium without extra differentiating agents, one-third of SN6.1b cells stably exhibited a morphology of differentiated neurons with extensive elaborate neurites, while a majority of SN6.2a cells, along with the parent cell line SN6, were round in shape with poorly branched short processes. Neurochemical studies showed that both clones synthesized choline acetyltransferase (ChAT), dopamine, norepinephrine, serotonin, and glutamate. Immunocytochemically, they expressed a number of neuronal antigens, such as 200-kDa neurofilament protein, neuron-specific enolase, microtubule-associated protein 2, tau protein, tubulin, neural cell adhesion molecule, Thy-1.2, saxitoxin-binding sodium channel protein, ChAT, tyrosine hydroxylase, serotonin, and glutamate. The coexistence of cholinergic, catecholaminergic, serotonergic, and glutamatergic neurotransmitter markers in the clonal hybrid septal neurons that express a variety of immunocytochemical properties of differentiated neurons suggests that embryonic septal cholinergic neurons are potentially multiphenotypic with respect to neurotransmitter synthesis.

Amino Acids↗
PubMed1992

Establishment of mouse-immortalized hybrid clones expressing characteristics of differentiated neurons derived from the cerebellar and brain stem regions.

Two clonal immortalized neurons designated CL8c4.7 and CL8a5.2 were established by somatic cell fusion between a hypoxanthine phosphoribosyltransferase-(HPRT-) deficient neuroblastoma N18TG2 and newborn mouse cerebellar/brain stem neurons. In the serum-containing medium without extra differentiating agents, both clones exhibited a morphology of differentiated neurons. They contained high levels of glutamate but no gamma-aminobutyric acid (GABA). The CL8a5.2 clone synthesized choline acetyltransferase and serotonin. In immunocytochemical studies, both clones expressed 200 kD neurofilament protein, neuron-specific enolase, microtubule-associated protein 2 (MAP2), tau protein, neuronal cell adhesion molecule (N-CAM), HNK-1, Thy-1.2, saxitoxin-binding sodium channel protein, and glutamate. Synaptophysin immunoreactivity was identified in the neuritic terminals of CL8c4.7 cells. Most of these antigens were barely detectable on N18TG2 cells. Electrophysiologically, both clones generated action potentials in response to electrical stimuli. The hybrid clones that express characteristics of differentiated neurons derived from the cerebellar and brain stem regions might be invaluable for the study of the molecular basis of neuronal differentiation and degeneration in these regions.

Amino Acids↗
PubMed1992

Light microscopic response of neuronal somata, dendrites and axons to post-mortem concussive head injury.

Forty anesthetized rats were cooled below 3 degrees C by 30-min transcardial perfusion of chilled physiological saline before a concussive head injury. The animals were then perfusion-fixed with a buffered formaldehyde-glutaraldehyde solution. Another forty rats were fixed by 30-min transcardial perfusion of the same fixative before a similar concussive head injury. In brain sections of both groups of animals a new silver method stained, in a Golgi-like fashion, a number of neurons and long axonal segments scattered among unstained ones. The similarity between these findings and those obtained following in vivo concussive head injuries described in accompanying papers suggests that the formation of traumatically induced argyrophilic neuronal damage is independent of metabolic processes, i.e., it may be a primary morphopathological process.

Animals↗
PubMed1992

Formation of "dark" (argyrophilic) neurons of various origin proceeds with a common mechanism of biophysical nature (a novel hypothesis).

Based on recent findings described in accompanying reports as well as on relevant observations in the literature we hypothesize that: (1) the fundamental elements in the mechanism of the formation of "dark" (argyrophilic) neurons are independent of the causative conditions including post-mortem or in vivo mechanical injuries and various in vivo pathometabolic processes such as blood recirculation following ischemia; (2) the causative conditions, each in its own mechanical or metabolic way, induce the same morphopathological damage at one point only within each affected neuron; (3) this damage spreads throughout the respective somato-dendritic or axonal domain and entails type III argyrophilia; (4) the intraneuronal spread of the morphopathological damage consumes mechanical energy stored by the neurofilaments in the form of a metastable inner structure, and (5) is propagated by a process working, in certain structural and energetical respects, on the domino principle; and (6) the primary neuronal damage caused in the above manner might be secondarily modified in different directions by different postcausation conditions.

Animals↗
PubMed1992

An immediate light microscopic response of neuronal somata, dendrites and axons to non-contusing concussive head injury in the rat.

Sixteen rats were killed by transcardial perfusion fixation 1 min after a non-contusing concussive head injury, and seven rats 1 day later. In each of the "1-min" animals Golgi-like neurons and long axonal segments scattered in various proportions among unstained neurons and axons were demonstrated by a new silver method both near to and far from the impact site in a parenchymal environment unaffected by contusion. The silver-stained neurons, dendrites and axons were considered to have been damaged by the trauma because they were consistently absent from control brains. In the "1-day" brains silver-stained dendrites and axons had a beaded appearance, indicating an advanced stage of morphopathological damage. From details of these findings the following conclusions were drawn: (1) trauma can directly induce some kind of morphopathological damage in neurons which manifests itself in shrinkage of the soma and tortuosity of appendages as well as in type III argyrophilia; (2) different vulnerability of various brain areas is likely due to the inhomogeneity of the trauma-induced pressure wave propagating through the brain; and (3) the somato-dendritic and axonal domains of the neuron are selectively vulnerable to different values of the parameters of the intracranial pressure wave.

Animals↗
PubMed1992

An immediate light microscopic response of neuronal somata, dendrites and axons to contusing concussive head injury in the rat.

Thirty-four rats were killed by transcardial perfusion fixation 1 min after a contusing concussive head injury, and 17 rats 1 day later. From the results obtained with a new silver method demonstrating traumatically damaged neuronal somata, dendrites and axons the following conclusions were drawn: (1) outside the contused territories all features of traumatically induced neuronal argyrophilia are similar to those found in non-contusing concussive head injury, as reported in an accompanying paper; (2) within contused territories the neuronal argyrophilia is abolished by some substance released either from damaged blood vessels or damage parenchymal cells, while the neuronal damage otherwise underlying the induction of argyrophilia is present; (3) different phenotypes of neurons are vulnerable to different values of the parameters of the intracranial pressure wave generated by the trauma; (4) some of the neurons may recover from the traumatically induced argyrophilic damage; (5) traumatically induced inundation of neurons with extracellular tracers, as reported by other authors, and somato-dendritic argyrophilia may be different manifestations of one and the same phenomenon; and (6) diffuse primary traumatic axonal injury in human neuropathology may be closely correlated to axonal argyrophilia.

Animals↗
PubMed1979

Simultaneous determination of the amounts of metallic and "reducible" silver in histologic specimens.

Acids and weak complexing agents (pK less than 8) are not able to remove, without leaving a residue, silver bound to biological tissues by ionic or complex bonds ("reducible" silver), whereas, strong complexing agents (pK greater than 8) can also partially or completely dissolve metallic silver formed under the influence of reducing groups in the tissue. For this reason, the chemical nature of the silver contained in tissue sections, be it metallic or reducible, must not be determined on the basis of solubility tests; moreover, the amount of neither of the two above fractions can be determined by removing the other with any kind of washing. Using radioactive impregnating baths, radioactive silver bound to the tissue as reducible silver can be replaced in a quantitative manner with inactive silver ions by means of a one-hour incubation in 1% inactive silver nitrate dissolved in 10% acetic acid, but the radioactive silver existing in reduced (atomic) state will be left unaffected. Consequently, radioactivity remaining in the tissue after the above treatment represents metallic silver. The amount of reducible silver can be calculated by subtracting that of the metallic silver from the total silver content of the sections.

Histocytochemistry↗
PubMed1979

Kinetics of formation of metallic silver and binding of silver ions by tissue components.

The effect of time on the formation of metallic silver by tissue reducing groups follows a curve which can be divided into three main parts. In the first, which may last for several hours, the reaction is very slow, and only an undetectably small amount of metallic silver is produced. In the second period the speed of the reaction first increases in a progressive manner and then begins to decrease gradually; during the third period the speed approaches zero asymptotically. Binding of the silver ions by the tissue commences initially at its fastest rate; the level then decreases steadily to zero within about a quarter of an hour. There is no direct relationship between the amount of silver ion bound to the tissue and the formation of metallic silver. The latter cannot take place by way of direct (non-catalysed) reaction. The following mechanism is proposed for the process: Transfer of electrons from the reducing molecules to the silver ions is mediated at first by certain tissue sites (catalytic points) and then also by the steadily increasing total surface area of the metallic silver grains (autocatalysis). On the basis of this mechanism, several anomalies of both the argentaffin and argyrophil reactions are explained.

Histocytochemistry↗
PubMed1979

Factors affecting the formation of metallic silver and the binding of silver ions by tissue components.

The rate of formation of metallic silver has a maximum when plotted as a function of pH. The site of this maximum on a pH scale differs noticeably for various tissue elements. By contrast, the amount of silver ions bound to the tissue is a monotonously increasing function of the pH. A temperature rise decreases the length of the induction period and increases the gradient of the ascending section of the kinetic curve representing the formation of metallic silver. It also increases the maximum amount of silver ions bound to the tissue. An increase in the concentration (activity) of the silver ions in the impregnating bath has the same effect. Chemical composition and concentration of the complexing agent, as well as "special" ions in the impregnating bath to which earlier some definitive role has been attributed in the silver staining methods, proved to be ineffective when both pH and activity of silver ions were kept constant. Illumination of the reaction was also ineffective. The kinetic curves obtained in nonaqueous but polar media (e.g., acetone) exhibited the same qualitative characteristics as those obtained in aqueous solutions. No reaction between silver ions and tissue was observed in apolar solvents.

Histocytochemistry↗
PubMed1979

Silver staining of myelin by means of physical development.

For staining myelin with silver a physical development technique has been devised that can render visible the thinnest fibers in various animal species, including fishes and reptiles, even in the early phase of myelination and may be applied to both frozen and embedded materials. Its principle is as follows: Myelin can form and bind colloidal silver particles in a 0.1% ammoniacal silver nitrate solution of pH 7.5. The production of metallic silver by other tissue elements is suppressed by the sections pretreated with a 2:1 mixture of pyridine and acetic anhydride for 30 min. The colloidal silver particles bound in the myelin are enlarged to microscopic dimensions by a special physical developer.

Animals↗
PubMed1979

Light insensitive physical developers.

Within the pH range 2.5-6.5 tungstic acid (an isopolyacid) prevents the reduction of silver ions by ascorbic or hydroquinone more effectively than either gum acacia or other protective colloids. The colloid state of tungstic acid can be stabilized with nonionic detergents, especially with Triton X-100. For buffering the system a mixture of acetic acid and sodium acetate is optimal. Physical developers constituted on the basis of these observations are, in contrast to those commonly used in histology, light insensitive, and remain clear for about 30 min at room temperature, 2-5 times as long as the time required for development.

Buffers↗
PubMed1979

An improved silver stain for developing nervous tissue.

A reduced silver technique using physical development to stain embryonic nervous tissue is described. Brains are fixed in Bodian's fixative. Paraffin sections are pretreated with 1% chromic acid or 5% formol. They are impregnated with 0.01% silver nitrate dissolved in 0.1 M boric acid/sodium tetraborate buffer of pH 8 or with silver proteinate. Finally they are developed in a special physical developer which contains 0.1% silver nitrate, 0.01-0.1% formol as reducing agent, 2.5% sodium carbonate to buffer the solution at pH 10.3, 0.1% ammonium nitrate to prevent precipitation of silver hydroxide, and 5% tungstosilicic acid as a protective colloid. The development takes several minutes in this solution, thus the intensity of staining can be controlled easily. The method yields uniform, complete and reproducible staining of axons at all developmental stages of the nervous tissue and is easy to handle.

Animals↗
PubMed1977

[Selective and high-contrast staining in nervous tissue (author's transl)].

Using silver as an impregnating medium and controlling the staining process by physical development, a specific and reliable staining of high contrast can be achieved. These properties represent important prerequisites for automatic and quantitative television image analysis. Specificity depends on appropriate pretreatment. Television image analysis cannot only be used for object analysis, but also to quantify reliability and dependency of contrast on developmental conditions, as demonstrated for stained myelin.

Animals↗
PubMed1976

Lactate production during fructose infusion with or without amino acids.

Lactate production from the liver during fructose infusion was decreased when an amino acid infusion was given simultaneously. The most pronounced decrease was observed when the amino acid infusion was started before the simultaneous administration of fructose and amino acids. The explanation of the phenomenon is thought to be a stimulation of gluconeogenesis by amino acids.

Amino Acids↗
PubMed1975

Acute renal failure caused by leptospirosis.

Three patients with severe leptospirosis leading to anuria and treated with haemodialysis are reported. One patient died. The pathomechanism and the underlying pathological and histological changes of the renal failure are discussed. It is stressed that the clinical diagnosis of leptospirosis is often difficult, as other infectious diseases,first of all infectious hepatitis, frequently present the same symptoms.

Acute Kidney Injury↗