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Biomedical subjects

L Tóth

Publications and source records attributed to L Tóth.

At least 73 records · Page 4Linked to original sources
PubMed1987

Neurotoxicity of monosodium-L-glutamate in pregnant and fetal rats.

Monosodium-L-glutamate given subcutaneously to pregnant rats caused acute necrosis of the acetylcholinesterase-positive neurons in the area postrema. The same effect has been observed in the area postrema of fetal rats. The process of neuronal cell death and the elimination of debris by microglia cells proved to be similar in pregnant animals and in their fetuses. However, embryonal neurons were more sensitive to glutamate as judged by the rapidity of the process and the dose-response relationship. These observations raise the possibility of transplacental poisoning in human fetuses after the consumption of glutamate-rich food by the mother.

Acetylcholinesterase↗
PubMed1985

A glutamate-sensitive neuronal system originating from the area postrema terminates in and transports acetylcholinesterase to the nucleus of the solitary tract.

The possible cellular mechanism of action of systemically administered monosodium-L-glutamate and the projections of glutamate-sensitive area postrema neurons have been studied in rats. Parenteral administration of monosodium-L-glutamate induced a selective degeneration of a particular population of AChE-containing area postrema neurons. Electron microscopic cytochemistry and X-ray microanalysis revealed the presence of calcium-containing electron-dense deposits in the mitochondria of degenerating area postrema neurons indicating the possible pathogenetic role of an enhanced intracellular calcium level in the mechanism of monosodium-L-glutamate-induced nerve cell degeneration. Degeneration of area postrema neurons was followed by the appearance of degenerating axon terminals in a well-defined region of the nucleus of the solitary tract, the area subpostrema. Degenerating area postrema neurons and axon terminals were rapidly engulfed by phagocytes predominantly of microglial character. AChE activity, localized to the basal lamina of the capillaries of the area subpostrema under normal conditions, could no longer be detected in rats treated with monosodium-L-glutamate 3-4 weeks previously. These findings provide evidence for the existence of a particular population of glutamate-sensitive, AChE-containing area postrema neurons which project and transport AChE to the nucleus of the solitary tract. This specific neuronal pathway connecting the area postrema with the nucleus of the solitary tract may play an important role in some of the functions attributed to the area postrema. The results also strengthen the hypothesis that brain capillary AChE activity may be of neuronal origin.

Acetylcholinesterase↗
PubMed1985

The humoral leukocyte adherence inhibition test in the investigation of lung cancer treated by surgery and radiotherapy.

17 operable and 13 inoperable lung cancer patients entered the study. In all patients, the humoral leukocyte adherence inhibition (H-LAI) test was positive before treatment. 7-20 days after surgery the H-LAI values decreased to normal levels in 8/8 cases. On radiotherapy, the same decrease was valid in 7/9 patients. Two exceptions in which no H-LAI reduction could be observed were in correlation with tumor progression.

Aged↗
PubMed1985

Acute monosymptomatic aseptic meningitis caused by Toxoplasma gondii.

Acute monosymptomatic aseptic meningitis was observed in a 4 year old male patient. Toxoplasma gondii tachyzoites were detected in Giemsa-stained smears prepared from the CSF. Inoculation of mice gave the same result. The patient was cured after the application of pyrimethamine and sulpha drugs. On basis of the smears, the serological results and data in the literature, a direct infection through the nasal cavity has been assumed.

Acute Disease↗
PubMed1985

Humoral leukocyte adherence inhibition (H-LAI) before and after surgery in human breast cancer.

Eighty-four breast cancer patients were tested by the H-LAI method before and after surgery. In the cancer groups positive H-LAI responses could be stated in 90--100%. In benign breast diseases 94% positivity was also detected. The H-LAI values of the cancer patients did not change significantly at their discharge from hospital and only insignificant reduction in the H-LAI indices were detected even 3--12 months after mastectomy. The benign cases showed, however, a definite declining tendency in H-LAI after surgery.

Adult↗
PubMed1985

[Ultrastructural changes in the supraoptica-neurohypophyseal system after induction of lesions in the pituitary stalk in rats].

Fine structural changes occurring in the supraoptic nucleus and the neural lobe have been studied in rats following the electrolytic lesion of the hypophysial stalk. Supraoptic neurosecretory neurones undergo a typical chromatolytic reaction. In addition, proliferating microglial cells disconnect axosomatic synapses and phagocytose degenerating neurones. Surviving neurones show signs of structural restitution 3 to 4 weeks after surgery. In the neurohypophysis degeneration of secretory nerve endings started with the disintegration of secretory vesicles 3 to 4 d postoperatively. Degenerated axon terminals were engulfed by pituicytes. Signs indicative of axonal regeneration were not observed in the neural lobe up to the end of the 4th postoperative week.

Animals↗
PubMed1985

Intrathoracic vagus nerve tumors: a report of two cases and review of the literature.

We have observed 741 mediastinal tumors during the past 25 years. Among these tumors, two intrathoracic vagal tumors were found; one bilateral neurofibrosarcoma and one neurilemmoma. To date, 49 intrathoracic vagal tumors have been reported in the literature, and the neurofibrosarcoma described here is the fourth malignant vagal tumor reported.

Adult↗
PubMed1984

Neurotoxin induced nerve cell degeneration: possible involvement of calcium.

Neurotoxin induced nerve cell degeneration has been studied in sensory ganglia of newborn and in the area postrema of adult rats following the administration of the selective sensory neurotoxin, capsaicin and the amino acid excitotoxin, glutamic acid, respectively. Light microscopic histochemical, autoradiographic, electroncytochemical and X-ray microanalytical studies revealed that degeneration of certain small-sized, type B primary sensory neurons, induced by capsaicin, was associated with a marked accumulation of calcium predominantly in mitochondria of the damaged ganglion cells. Similarly, monosodium glutamate treatment resulted in the appearance of calcium-containing electron-dense granules in mitochondria of degenerating area postrema neurons. In addition, after a combined administration of 45Ca2+ and capsaicin or monosodium glutamate, significantly higher levels of radioactivity have been detected by liquid scintillation spectroscopy in the Gasserian ganglia and the area postrema, respectively. It is concluded that an enhancement in intracellular calcium level may be intimately involved in the process of neuronal cell death and may represent a common basic mechanism responsible for the development of cellular events leading ultimately to the degeneration of nerve cells.

Animals↗