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E Toth

Publications and source records attributed to E Toth.

At least 37 records · Page 2Linked to original sources
PubMed1996

Oat bran concentrate bread products improve long-term control of diabetes: a pilot study.

OBJECTIVE: To evaluate the long-term effects oat bran concentrate bread products in the diet of free-living subjects with non-insulin-dependent diabetes (NIDDM) via dietary, clinical, and biochemical methods. DESIGN: A 24-week crossover study consisting of two 12-week periods. SUBJECTS/SETTING: Eight men with NIDDM (mean age = 45 years) who lived in the community. Glucose and insulin profiles were conducted in a clinical investigation unit. INTERVENTION: Palatable, high-fiber, oat bran concentrate (soluble fiber [beta-glucan] content = 22.8%) bread products were developed. Four randomly chosen subjects ate oat bran concentrate breads first; the other subjects ate control white bread first. MAIN OUTCOME MEASURES: Dietary intake (four 48-hour dietary recalls per period) was assessed. Blood glucose and insulin (8-hour profiles) and lipid parameters after fasting were measured (at 0, 12, and 24 weeks). STATISTICAL ANALYSES PERFORMED: Analysis of variance and repeated-measures analysis of variance. RESULTS: Total energy and macronutrient intakes were similar in both periods. Mean total dietary fiber intake was 19 g/day in the white bread period and 34 g/day (9 g soluble fiber per day from oat bran concentrate) in the oat bran concentrate period. Body weight remained stable. Mean glycemic and insulin response areas (area under the curve) were lower (P < or = .05 and not significant, respectively) for the oat bran concentrate period than the white bread period. After breakfast, area under the curve for the oat bran concentrate period was lower for glucose (P < or = .01) and insulin (P < or = .05); insulin peak was reached earlier (P < or = .05) than in the white bread period. Dietary fiber intake was correlated negatively with insulin area under the curve (P < or = .05). Mean total plasma cholesterol and low-density lipoprotein cholesterol levels were lower (P < or = .01) in the oat bran concentrate period than in the white bread period. In the oat bran concentrate period, the mean ratio of low-density lipoprotein cholesterol to high-density lipoprotein cholesterol was reduced by 24% (P < or = .05). CONCLUSIONS: The well-accepted oat bran concentrate bread products improved glycemic, insulinemic, and lipidemic responses.

Adult↗
PubMed1996

Immunochemical and functional properties of biliary alpha-1-antitrypsin.

Alpha-1-antitrypsin (AAT), the archetype of the serpin (serine proteinase inhibitor) superfamily, is synthesized by hepatocytes and excreted to some extent into bile. The role of intact biliary AAT in gallstone pathogenesis is unsettled, but its 36-residue C-terminal peptide was found to promote cholesterol crystallization in a bile model. The present study showed biliary AAT to have specific properties that differ from serum AAT regarding immunoreactivity, heat stability and antiproteolytical activity. Electrophoretical and immunochemical methods were used to characterize biliary AAT. The level of its inhibitory activity was determined spectrophotometrically. In 18 samples from common bile duct and 12 samples from gallbladder bile, AAT was found to be heat-stable and functionally inactive. Added to the untreated, temperature-inactivated or protease inhibitors containing bile, native AAT became functionally inactive, heat-stable and lost its immunoreactivity. In contrast, heat-inactivated AAT, native albumin, transferrin, alpha-1-antichymotrypsin and IgG were unaffected on being added to bile. AAT in human bile manifests specific biochemical properties, such as functional inactivity and heat stability, that may be consistent with a conformational transition of the serpin molecule induced by the hydrophobic environment, and which must be considered when evaluating its role in gallstone pathogenesis.

Adult↗
PubMed1995

Subtype-specificity of the presynaptic alpha 2-adrenoceptors modulating hippocampal norepinephrine release in rat.

In vivo brain microdialysis and high-performance liquid chromatography with electrochemical detection were used to study the effect of different selective alpha 2-antagonists on hippocampal norepinephrine (NE) release in freely moving awake rat. Systemic administration (0.5 mg/kg i.p.) of either the alpha 2AD-antagonist BRL 44408 or the alpha 2BC-antagonist ARC 239 did not significantly change the basal release of NE. At a higher dose (5 mg/kg i.p.) ARC 239 was still ineffective, whereas BRL 4408 caused a significant increase of the extracellular level of NF. Similar results were obtained from in vitro perfusion experiments. Rat hippocampal slices were loaded with [3H]NE and the electrical stimulation-evoked release of [3H]NE was determined. The alpha 2-antagonists were applied in a concentration range of 10(-8) to 10(-6) M, ARC 239 was ineffective, whereas BRL 44408 significantly increased the electrically induced release of [3H]NE. In agreement with the data of microdialysis and perfusion experiments, BRL 44408 displaced [3H]yohimbine from hippocampal and cortical membranes of rat brain with high affinity whereas ARC 239 was less effective. The pKi values of eight different alpha 2-adrenergic compounds showed a very good correlation (r = 0.98, slope = 1.11 P < 0.0001) in hippocampus and frontal cortex have the alpha 2-adrenoceptors have been characterized as alpha 2d-subtype. Our data indicate that hippocampal NE release in rat is regulated by alpha 2D-adrenoceptors, a species variation of the human alpha 2A-subtype.

Animals↗
PubMed1995

Chronic atrophic fundic gastritis diagnosed by a modified Congo red test.

BACKGROUND AND STUDY AIMS: Chronic atrophic fundic gastritis (CAFG) is associated with several diseases, such as gastric cancer, gastric ulcer, pernicious anemia, and bacterial overgrowth. In spite of recent technical improvements, the gastroscopic diagnosis of CAFG remains uncertain. Congo red chromogastroscopy is capable of visualizing acid-producing normal fundic mucosa, but has hitherto not been suitable for routine use. The aim of our study was to establish a reliable endoscopic technique with which to diagnose CAFG. PATIENTS AND METHODS: This prospective study comprises 124 consecutive patients (71 women, 53 min) with a mean age of 65 years (range 36-92). Macroscopic evaluation of the gastric fundic mucosa in routine endoscopy using video techniques was compared with evaluation by means of a modified endoscopic Congo red test (MCRT). In routine gastroscopy, CAFG was recognized by the thin, friable mucosa, with a marked visible vascular pattern and fold atrophy. With MCRT, the diagnosis of CAFG was made within five minutes' observation when no red-to-blue color shift in the fundic mucosa could be induced by 0.2 mu g/kg intravenous pentagastrin. The results were then compared with the histological examination of biopsies from the fundic mucosa. RESULTS: CAFG was confirmed by histology in 40 of 124 cases. The diagnostic sensitivity of MCRT was 1.0 (40/40), with a positive predictive value of 0.90, whereas the values for macroscopic gastroscopic evaluation were 0.25 (10/40) and 0.50, respectively. CONCLUSIONS: We conclude that MCRT is a sensitive, fast, and cost-effective method of identifying patients with CAFG, and well suited for use in routine gastroscopy.

Adolescent↗
PubMed1993

Effect of acetyl-L-carnitine on extracellular amino acid levels in vivo in rat brain regions.

Acetyl-L-carnitine (ALCAR) was found to have beneficial effects in senile patients. In recent years many of its effects on the nervous system have been examined, but its mechanism(s) of action remains to be elucidated. We previously reported that it causes release of dopamine in the striatum. In the present paper we report that ALCAR, when administered at intracerebral sites via microdialysis, stimulates the release of amino acids in a concentration-dependent and regionally heterogeneous manner. The effect was strong in the striatum and cerebellum, less so in the frontal cortex, and weak in the thalamus. Seven amino acids were measured: the increase in the level of aspartate, glutamate, and taurine was substantial, and the increase in the level of glycine, serine, threonine, alanine, and glutamine in the microdialysate was minor. The stimulatory effect of ALCAR on the release of amino acids in the striatum was inhibited by the muscarinic antagonist atropine, but was not inhibited by the nicotinic antagonist mecamylamine. The effect of ALCAR on the levels of most of the amino acids tested was independent of the presence of Ca2+ in the perfusate. These results indicate that ALCAR, when administered intracerebrally at fairly high concentrations, can affect the level and the release not only of such neurotransmitters as acetylcholine and dopamine, but also of amino acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcarnitine↗
PubMed1993

Effect of nicotine on levels of extracellular amino acids in regions of the rat brain in vivo.

The local effect of nicotine on the extracellular levels of amino acids was examined in the striatum and frontal cortex of rats using microdialysis in vivo. The perfusion of 1 mM nicotine in Ringer's solution increased the extracellular levels of aspartic and glutamic acids by 40-50% in the striatum and had no effect on the levels of serine, glycine, glutamine, taurine or threonine. This effect of nicotine was dose- and Ca-dependent. At a 5 mM concentration, nicotine produced a more than 200% increase in the levels of aspartate, glutamate and taurine in the striatum; levels of glycine and threonine were also increased. Nicotine also increased the levels of these amino acids in the microdialysate from the frontal cortex. The effect of nicotine, tested in the striatum, was not influenced by mecamylamine or tetraethyl-ammonium chloride or haloperidol, but it was blocked by atropine. This indicated that muscarinic, cholinergic receptors participated in this effect of nicotine.

Amino Acids↗
PubMed1993

[Prothrombin fragment 1+2 (F1+2), thrombin-antithrombin III complex(TAT) and thrombophilia parameters in orally anticoagulated patients with inferior vena cava filters].

Prothrombin fragment 1 + 2 (F1 + 2) and thrombin-antithrombin-III-complex (TAT) levels were compared in 31 orally anticoagulated patients with inferior vena caval filters and a control group of 31 orally anticoagulated patients without caval filters and the incidence of markers of thrombophilia (deficiency of antithrombin-III, protein C, protein S and factor XII, presence of lupus anticoagulants) was determined. 8 of 31 patients (26%) from the group of caval filter carriers showed markers of thrombophilia (3 protein S deficiencies, 1 protein C deficiency, 2 factor XII deficiencies and 2 patients with lupus anticoagulants). In all orally anticoagulated patients a significant interdependence (p < 0.05) between F1 + 2- and TAT-levels and intensity (INR) of the oral anticoagulation could be observed. Comparison of F1 + 2- and TAT-levels of caval filter carriers and controls revealed no significant difference which leads to the conclusion that inferior vena caval filters do not induce detectable systemic activation of prothrombin under adequate oral anticoagulation therapy.

Administration, Oral↗
PubMed1993

[Preoperative monitoring of blood coagulation in urologic operations: diagnosis of familial factor XI deficiency within the scope of preoperative blood coagulation studies].

Presurgical coagulation diagnosis should--apart from coagulation monitoring in the laboratory based on a stepwise diagnosis for detection of coagulations disorders, starting with global tests (NT/APTT) followed by appropriate specific investigation in case of pathological findings--consist of an adequate hemostaseological anamnesis and physical checkup of the patient. This would allow detection of important signs of hemostaseological impairment during the pre-analytical phase already and permit subsequent initiation of more specific coagulation tests. The casuistics of a patient with factor XI-deficiency ("Minor Form"), a condition which is extremely infrequent in our country, demonstrates the coagulation diagnostic procedure which led to detection of his inherited factor XI-deficiency. In addition the pre-, peri- and postsurgical therapeutical management of this particular patient using an antifibrinolytic drug (tranexamic acid) is presented.

Blood Coagulation Tests↗
PubMed1992

Acetyl-L-carnitine releases dopamine in rat corpus striatum: an in vivo microdialysis study.

The effect of acetyl-L-carnitine, a compound reported to be beneficial for senile patients, on the release of dopamine (DA) from the striatum was studied by using in vivo brain dialysis in anesthetized rats coupled with HPLC-electrochemical detection. Striatal infusion of acetyl-L-carnitine increased the efflux of DA with no apparent changes in efflux of DA metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and 4-hydroxy-3-methoxyphenylacetic acid (HVA). The DA-releasing effect of acetyl-L-carnitine was concentration- and Ca(2+)-dependent, and was abolished by omega-conotoxin fraction GVIA and tetrodotoxin, inhibitors of the voltage-dependent Ca2+ and Na+ channels, respectively. Nomifensine, an inhibitor of DA reuptake did not alter the DA-releasing property of acetyl-L-carnitine. DA released from the striatum by acetyl-L-carnitine was decreased by reserpine pretreatment whereas the d-amphetamine-evoked DA outflow was not affected. In contrast to acetyl-L-carnitine, d-amphetamine reduced the extracellular concentrations of DOPAC and HVA. We conclude from the present data that acetyl-L-carnitine evokes DA release from the vesicular pools of the nigrostriatal dopaminergic neurons by a Ca(2+)-dependent, exocytotic process.

Acetylcarnitine↗
PubMed1992

Effect of nicotine on extracellular levels of neurotransmitters assessed by microdialysis in various brain regions: role of glutamic acid.

We studied the effect of local administration of nicotine on the release of monoamines in striatum, substantia nigra, cerebellum, hippocampus, cortex (frontal, cingulate), and pontine nucleus and on the release of glutamic acid in striatum of rats in vivo, using microdialysis for nicotine administration and for measuring extracellular amine and glutamic acid levels. Following nicotine administration the extracellular concentration of dopamine increased in all regions except cerebellum; serotonin increased in cingulate and frontal cortex; and norepinephrine increased in substantia nigra, cingulate cortex, and pontine nucleus. Cotinine, the major nicotine metabolite, had no effect at similar concentrations. The cholinergic antagonists mecamylamine and atropine, the dopaminergic antagonists haloperidol and sulpiride, and the excitatory amino acid antagonist kynurenic acid all inhibited the nicotine-induced increase of extracellular dopamine in the striatum. The fact that kynurenic acid almost completely prevented the effects of nicotine, and nicotine at this concentration produced a 6-fold increase of glutamic acid release, suggests that the effect of nicotine is mainly mediated via glutamic acid release.

Animals↗
PubMed1990

A comparison of the effects of diazepam and scopolamine in two positively reinforced learning tasks.

In a helical maze scopolamine (0.5 and 1 mg/kg) significantly impaired the ability of rats to acquire a spatial learning task using reference memory. In contrast, diazepam (0.5-2 mg/kg) did not impair acquisition of this task and the only effect of diazepam (4 mg/kg) was likely to be secondary to sedative effects. Diazepam (0.5-4 mg/kg) did not impair 8-day retention of the helical maze. In a test of working and reference memory in which spatial processing was minimised, scopolamine (0.5 and 1 mg/kg) significantly impaired acquisition and increased the number of reference memory errors. Diazepam (1 and 4 mg/kg) did not impair acquisition of this task, but when a delay was interposed in the middle of a trial the diazepam-treated rats were slower to complete the task than the controls and made more errors of both working and reference memory. In contrast, when the rats were tested with a change of context, the diazepam-treated rats completed the task more quickly than the controls and made fewer errors of both working and reference memory.

Animals↗
PubMed1989

Maternal adrenalectomy and adult offspring in a conflict situation in the rat.

The effects of the absence of maternal adrenals during pregnancy (P), during lactation (L), during pregnancy and lactation (PL) were studied on pain suppressed behavior (punished drinking test) of the adult offspring in comparison with controls (C). The female L offspring showed a lower responsiveness to the anxiogenic stimulus, as demonstrated by increased water intake, decreased percentage of ineffective licks, and decreased time to perform 300 licks compared to C. The male L behavior was not affected. Reduced growth was not responsible for the reduced anxiogenic reactivity because also both male and female PL offspring had lower weight than C, but did not show any significant effect. Pain threshold in the tail flick test was the same in all types of offspring. Thus, absence of maternal adrenals, specifically during lactation, significantly affects behavior of female offspring. It is discussed whether this is due to the lack of a physiological influence of maternal adrenal hormones on brain ontogenesis (hippocampal glucocorticoid receptors), or on the development of the brain-pituitary-adrenal system during neonatal life of the offspring.

Adrenalectomy↗
PubMed1989

Motor effects of intracaudate injection of excitatory amino acids.

In a study of the role of excitatory amino acid receptors in movement disorders, the effect of the injection of glutamate (Glu), aspartate (Asp), N-methyl-D-aspartate (NMDA), quisqualate (Qu), or kainate (K) into the rat striatum was investigated. Rats were microinjected unilaterally through chronically implanted guide cannulas and their motor behavior was recorded. After 10-25 min L-Glu produced reversible periodic choreiform movements lasting 5-10 sec and contraversive rotation lasting 1-2 min. Both episodes were repeated every 2-3 min: the duration of motor effects was 60-80 min. L-Asp had an effect similar to that of L-Glu and in addition produced barrel rolling. The L-isomers of both Glu and Asp were active and the D-isomers were inactive. NMDA, Qu, and K were more potent than Glu or Asp. Each produced effects similar to that of Glu, and in addition NMDA and K produced wet-dog-shakes and masticatory movements. The motor behavior produced by Qu was identical to that of Glu, but it lasted longer. The motor effects of L-Glu were blocked by L-glutamic acid diethyl ester (GDEE) and by a larger sedative dose of 2-amino-5-phosphonopentanoic acid (AP5), but not by haloperidol, GABA, glycine (Gly), or a smaller nonsedative dose of AP5. The results suggest that the motor effects of L-Glu were produced by activation of the Qu-type (glutamatergic) receptors, not involving the dopamine and GABA systems. However, activation of the K-type receptors by L-Glu cannot be ruled out.

Amino Acids↗
PubMed1988

3-Mercaptopropionic acid administration into the caudate-putamen of the rat provokes dyskinesia.

The unilateral administration of 3-mercaptopropionic acid (MPA) through an implanted guide cannula into the caudate-putamen produced dyskinesia in the rat. Striatal GABA and dopamine were decreased and the dopamine metabolites 3,4-dihydroxyphenylacetic and homovanillic acid were increased on the MPA-injected side at 2-10 min after the onset of dyskinesia. The dyskinetic movements were blocked by GABA or alpha-aminooxaloacetic acid but not by glycine or haloperidol.

3-Mercaptopropionic Acid↗
PubMed1987

Cardiac control of salt appetite.

Inflation of a balloon for 2 h at the superior vena caval-right atrial junction of the rat reduced the salt intake of animals that had been sodium and water depleted by peritoneal dialysis with hyperoncotic colloid. After the balloons were deflated, the experimental group drank more than the control group so that the total sodium intake of the two groups was the same. Thus stimulated increased venous return to the heart attenuates salt appetite. Since this phenomenon might be secondary to a reflex reduction in plasma renin activity, the experiment was repeated using a model of salt appetite in which the renin-angiotensin system is known to be suppressed, namely the deoxycorticosterone acetate-treated rat. Salt intake was again significantly reduced by inflation of the right atrial balloon. It is concluded that pathways exist, independent of the renin-angiotensin system, whereby information obtained from the cardiac volume receptors regarding the state of filling of the vasculature may be used to regulate salt intake.

Animals↗