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Biomedical subjects

P Kása

Publications and source records attributed to P Kása.

At least 19 recordsLinked to original sources
PubMed1998

[Spherical crystallization in pharmaceutical technology].

Physical properties of crystals, such as size, crystal size distribution and morphology, may predetermine the usefulness of crystalline materials in many pharmaceutical application. The above properties can be regulated with the crystallization process. The spherical crystals are suitable for direct tablet-making because of their better flowability and compressibility properties. These crystals can be used in the filling of the capsule. In this work, the spherical crystals such as "single crystal", "poly-crystals" and agglomerates with other excipients are collected from the literature and the experimental results of the authors. A close cooperation between chemists and the pharmaceutical technologists can help for doing steps in this field.

Chemistry, Physical↗
PubMed1997

Experimental immune-mediated damage of septal cholinergic neurons.

Degeneration of cholinergic neurons in the medial septum and the diagonal band of Broca is a frequent neuropathological feature of Alzheimer's disease. To determine whether an immune process can injure these basal forebrain cholinergic neurons, we serially immunized guinea pigs with septal cholinergic hybrid cells (SN-56). Following immunization, a relatively selective damage of septal cholinergic neurons, reduction in septal choline acetyltransferase (ChAT) activity and decrease in acetylcholine release in hippocampus were detected. Serum IgG from guinea pigs immunized with SN-56 cells and stereotactically injected into the medial septal region of rats produced a loss of ChAT activity in the medial septum, frontal cortex and hippocampus, together with impairment of learning and long term spatial memory. These data suggest that relatively selective damage to septal cholinergic neurons can be caused by an immune-mediated process in experimental animals.

Alzheimer Disease↗
PubMed1997

The cholinergic system in Alzheimer's disease.

The past decade has witnessed an enormous increase in our knowledge of the variety and complexity of neuropathological and neurochemical changes in Alzheimer's disease. Although the disease is characterized by multiple deficits of neurotransmitters in the brain, this overview emphasizes the structural and neurochemical localization of the elements of the acetylcholine system (choline acetyltransferase, acetylcholinesterase, and muscarinic and nicotinic acetylcholine receptors) in the non-demented brain and in Alzheimer's disease brain samples. The results demonstrate a great variation in the distribution of acetylcholinesterase, choline acetyltransferase, and the nicotinic and muscarinic acetylcholine receptors in the different brain areas, nuclei and subnuclei. When stratification is present in certain brain regions (olfactory bulb, cortex, hippocampus, etc.), differences can be detected as regards the laminar distribution of the elements of the acetylcholine system. Alzheimer's disease involves a substantial loss of the elements of the cholinergic system. There is evidence that the most affected areas include the cortex, the entorhinal area, the hippocampus, the ventral striatum and the basal part of the forebrain. Other brain areas are less affected. The fact that the acetylcholine system, which plays a significant role in the memory function, is seriously impaired in Alzheimer's disease has accelerated work on the development of new drugs for treatment of the disease of the 20th century.

Acetylcholinesterase↗
PubMed1996

Chronic aluminum treatment results in aluminum deposits and affects Ml muscarinic receptors in rat brain.

The effects of chronic aluminum (Al) administration on the deposition of the metal and on the receptor binding characteristics of the Ml muscarinic acetylcholine receptors (MlAChR) were studied in selected rat brain areas. Animals were injected intraperitoneally with an AlCl3 solution of 1.0 mg/ml/100 g of body weight for 5 weeks, 5 days a week. Al accumulation was detected by solochrome azurine histochemistry in the brain, where the metal could be visualized in capillaries, endothelial cells and surrounding brain tissues. Changes in the binding properties of the MlAChR after chronic Al treatment were determined with the use of selective and nonselective muscarinic antagonists. Significantly decreased number of maximal MlAChR binding sites (Bmax) as measured by the equilibrium binding of [3H]pirenzepine, were detected in all of the brain areas examined. While the nonselective antagonist [3H] (-)QNB displayed a generally decreased Bmax, value, it reached the level of significance only in the striatum. These results provide a further indication that chronic Al treatment results in the accumulation of Al in the brain and consequently affects the cholinergic neurotransmission.

Aluminum Chloride↗
PubMed1995

[D-Pen2,D-Pen5]enkephalin, a delta opioid agonist reduces endogenous aluminum content in the rat central nervous system.

The in vivo effects of [D-Pen2,D-Pen5]enkephalin, a cyclic peptide agonist with high affinity and selectivity for the delta opioid receptors, on the endogenous aluminum content of selected areas of rat brain and spinal cord were studied by means of atomic absorption spectrophotometry. Intracerebroventricular injection of a subanalgesic dose of [D-Pen2,D-Pen5]enkephalin (0.2 microgram/3 microliters) produced a transient, time-dependent reduction of the aluminum content. This effect was statistically significant in the frontal cortex, hippocampus and striatum, but did not reach the level of significance in the medulla and thoracic spinal cord. The partial depleting effect of [D-Pen2,D-Pen5]enkephalin on aluminum content, in the range of 0.2-1.0 micrograms/3 microliters, was dose-dependent and could be reversed by naloxone pretreatment. Serum aluminum levels were unchanged after [D-Pen2,D-Pen5]enkephalin treatment. Chronic (five weeks), systemic AlCl3 treatment increased the endogenous aluminum content in all central nervous system areas examined. Interestingly, [D-Pen2,D-Pen5]enkephalin i.c.v. produced a slight depletion of this elevated metal level in these areas to values not significantly different from those of the respective control values. Chronic in vivo, as well as in vitro, effects of aluminum on opioid receptor binding characteristics were also studied. Neither the specific binding of [3H][D-Pen2,D-Pen5]enkephalin nor [3H]Tyr-D-Ala-Gly-NMePhe-Gly-ol to membranes of frontal or parietal cortices, striatum or hippocampus, prepared from rats chronically treated with AlCl3, were affected.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMed1995

[Preparation and investigation of liposomes].

Vesicles dispersed in an aqueous milieu and containing a phospholipid double-layer are used primarily in cosmetic and dermatological preparations, though experiments are under way to use them as carriers of diagnostics and medicines. Different parenteral and dermatological drug preparations are already in circulation worldwide. Researchers have hopes of using them for the lyophilization of lipophobic pharmacons, to prolong medicinal effects, for the active and passive targeting of drugs etc. The first steps of liposome research started in 1965 and we now know much about liposome technology and their use in therapy, but various questions remain to be answered. On the level of basic research, this paper investigates the preparation of liposomes and characteristics influencing their stability.

Cosmetics↗
PubMed1993

Distribution of GABA-immunoreactive nerve fibers and cells in the cervical and thoracic paravertebral sympathetic trunk of adult rat: evidence for an ascending feed-forward inhibition system.

Neurochemical and immunohistochemical evidence suggests that the superior cervical ganglion (SCG) contains all components of a gamma-aminobutyric acid (GABA)ergic transmission system, which includes GABAergic axons of unknown origin. The number of nerve fibers with and without GABA-like immunoreactivity was determined in interganglionic connectives at all cervical and thoracic levels of the paravertebral sympathetic trunk. In addition, the distribution of GABA-immunoreactive (IR) neurons was established within the ganglion chain and compared with the relative frequency of principal neurons richly innervated by GABA-IR axon terminals. The following results were obtained: 1) the total number of nerve fibers in cross sections did not significantly vary between the cervical levels, but it increased steadily from upper to lower thoracic segments; 2) in contrast, the number of GABA-IR fibers decreased from the cervical sympathetic trunk below the SCG (approximately 300 fibers) down to the seventh to tenth thoracic ganglion, below which no such fiber was seen; 3) GABA-IR nerve fibers originate from a subclass of GABA-IR cells; these are small, bipolar neurons with predominantly ascending, unmyelinated axon-like processes; 4) the number of principal neurons richly innervated by GABA-IR nerve fibers decreased from the SCG to the upper thoracic ganglia, and was very small below; and 5) apart from basket-like innervation, GABA-IR axons also formed diffuse networks around GABA-negative principal neurons predominantly in cervical and upper thoracic ganglia. These data suggest that the GABAergic innervation of paravertebral sympathetic ganglia is more complex than previously suspected. What appears as preganglionic afferents from several spinal segments (C8-Th7) innervate GABAergic neurons in the sympathetic trunk which have ascending axons and focus their inhibitory effects on the cervical sympathetic ganglia, predominantly the SCG. These data suggest that GABAergic small interganglionic neurons form a feed-forward inhibition system, which may be driven by multisegmental spinal input in the paravertebral sympathetic ganglion chain.

Afferent Pathways↗
PubMed1993

Modulation by GABA of neuroplasticity in the central and peripheral nervous system.

Apart from being a prominent (inhibitory) neurotransmitter that is widely distributed in the central and peripheral nervous system, gamma-aminobutyric acid (GABA) has turned out to exert trophic actions. In this manner GABA may modulate the neuroplastic capacity of neurons and neuron-like cells under various conditions in situ and in vitro. In the superior cervical ganglion (SCG) of adult rat, GABA induces the formation of free postsynaptic-like densities on the dendrites of principal neurons and enables implanted foreign (cholinergic) nerves to establish functional synaptic contacts, even while preexisting connections of the preganglionic axons persist. Apart from postsynaptic effects, GABA inhibits acetylcholine release from preganglionic nerve terminals and changes, at least transiently, the neurochemical markers of cholinergic innervation (acetylcholinesterase and nicotinic receptors). In murine neuroblastoma cells in vitro, GABA induces electron microscopic changes, which are similar in principle to those seen in the SCG. Both neuroplastic effects of GABA, in situ and in vitro, could be mimicked by sodium bromide, a hyperpolarizing agent. In addition, evidence is available that GABA via A- and/or B-receptors may exert direct trophic actions. The regulation of both types of trophic actions (direct, receptor-mediated vs. indirect, bioelectric activity dependent) is discussed.

Acetylcholine↗
PubMed1993

Acetylcholine level in the brain and other organs of the bivalve Anodonta cygnea L. and its modification by heavy metals.

Acetylcholine was detected and measured in the ganglia (60-80 nmol/g), in the heart (10-15 nmol/g) and in the adductor muscles (4-5 nmol/g) of the bivalve Anodonta cygnea L. using gas chromatographic determination. Treatment of the animals with low concentration of heavy metals, which cause change in the behaviour, resulted in decrease of the brain acetylcholine level. Within 7 days treatment Cu2+ caused 80 per cent, Cd2+ and Pb2+ 30 per cent reduction with varying types of recovery after wash.

Acetylcholine↗
PubMed1992

The effect of pesticides on carp (Cyprinus carpio L). Acetylcholinesterase and its biochemical characterization.

The activity and molecular forms of acetylcholinesterase (AChE) were characterized in tissues of the carp (Cyprinus carpio). Tissue AChE activity was determined in response to specific inhibitors (ethopropazine, BW 284 C51) or pesticides (CuSO4, paraquat (PQ), methidathion (MD)). The highest AChE activity was found in the serum (878 +/- 100 U/liter), followed by the brain (113 +/- 12 U/liter), heart (89 +/- 6 U/liter), and trunk muscle (35 +/- 5 U/liter). Experiments with specific choline esterase inhibitors revealed a very low amount of pseudocholinesterase in all tissues studied. The ratio of the membrane-bound to the cytoplasmic-free AChE molecular forms was increased in the order of brain, trunk muscle, and heart. In sera of fish treated with MD (2 ppm) there was an 80% inhibition of AChE lasting for 2 weeks. Treatment with CuSO4 or PQ (both 5 ppm) led to a 50% decrease in the serum AChE activity followed by a transient increase over the control level. After 2 weeks of chronic treatment, AChE activity in fish exposed to CuSO4 returned to the control level, whereas in fish treated with PQ an elevated level (130% when compared to the control level) of enzyme activity was found. Our present experimental data indicate that pesticides occurring in natural waters not only inhibit AChE activity in fish but may influence the resynthesis of the enzyme as well.

Acetylcholinesterase↗
PubMed1992

Glial cells in coculture can increase the acetylcholinesterase activity in human brain endothelial cells.

The elements of the cholinergic system (acetylcholinesterase and choline acetyltransferase) and butyrylcholinesterase were studied in human cortical capillary samples, brain-derived endothelial cell cultures and glial cell cultures. It was shown that the elements of the cholinergic system are present in the microvessels, but the choline acetyltransferase activity may be due to contamination with cholinergic nerve terminals since no choline acetyltransferase could be demonstrated in endothelial cell cultures. The present results revealed that the activity of acetylcholinesterase is reduced in the cortical endothelial cell cultures after longer culture times, while butyrylcholinesterase activity is not altered. In a system where endothelial cells were cocultured with embryonic human brain astroglial cells for 12 days in vitro, the acetylcholinesterase activity was increased 2-fold. These results support a glial influence on the enzyme activity of the cerebral endothelium.

Acetylcholinesterase↗
PubMed1991

Regulation of endogenous calcium and magnesium levels by delta opioid receptors in the rat brain.

The effects of the potent agonist (D-Pen2, D-Pen5) enkephalin (DPDPE), a conformationally restricted ligand which is highly selective for delta opioid receptors, were studied on the endogenous levels and regional distributions of selected mono- and divalent cations in rat brain and thoracic spinal cord by means of atomic absorption spectrophotometry. In general, lower Na+, K+, Ca2+, Mg2+ and Mn2+ levels were characteristic of the medulla and spinal cord compared to that of cortices, striatum and hippocampus, while the highest metal ion levels were detected in the olfactory bulb. Sixty minutes after a single dose of 0.2 microgram DPDPE, administered intracerebroventricularly, transient decreases of endogenous Ca2+ and Mg2+ contents in the parietal cortex, hippocampus and striatum were found with no changes observed in the levels of monovalent cations or Mn2+. A time-dependent down-regulation in Ca2+ and Mg2+ content was also demonstrated, with Ca2+ being faster to respond to DPDPE treatment. The action of DPDPE was dose-dependent (0.2-1.0 micrograms) and could be antagonized by a 30 min naloxone pretreatment. Naloxone alone had no effect on the endogenous cation levels. It is concluded that delta opioid receptors may specifically be involved in the regulation of endogenous ion levels and their movements in the central nervous system of rat.

Analgesics↗