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Biomedical subjects

Z Fekete

Publications and source records attributed to Z Fekete.

33 records · Page 2Linked to original sources
PubMed1993

Activation of gastric mucosal calcium channels by epidermal growth factor.

1. Gastric mucosal calcium channel complex was isolated from the solubilized epithelial cell membranes by affinity chromatography on wheat germ agglutinin. 2. The complex following labeling with [3H]PN200-110 was reconstituted into phosphatidylcholine vesicles which exhibited active 45Ca2+ uptake into intravesicular space as evidenced by La3+ displacement and osmolarity measurements. The 45Ca2+ uptake was independent of sodium and potassium gradients indicating the electroneutral nature of the process. 3. The gastric mucosal channels on epidermal growth factor binding in the presence of ATP responded by an increase in protein tyrosine phosphorylation of 55 and 170 kDa subunits of calcium channel. 4. The phosphorylated channels following reconstitution into vesicles displayed at 48% greater 45Ca2+ uptake, thus indicating the tyrosine kinase involvement in EGF dependent activation of calcium channel. 5. The results point towards the importance of epidermal growth factor in the maintenance of gastric mucosal calcium homeostasis.

Animals↗
PubMed1993

Modulation of buccal mucosal calcium channel activity by salivary mucins.

The effect salivary mucus glycoproteins on the activity of calcium channel isolated from buccal mucosal cell membranes was investigated. The channel complex following reconstitution into phospholipid vesicles exhibited an active 45Ca2+ uptake and responded to calcium channel activator, BAY K8644, and the antagonist, PN200-110. The uptake of 45Ca2+, while only moderately (15%) affected by the intact mucus glycoprotein was significantly inhibited (60-64%) by the acidic mucus glycoprotein fractions. This effect was associated with the sialic acid and sulfate ester groups of the carbohydrate chains. The channel complex in the presence of epidermal growth factor (EGF) and ATP responded by an increase in protein tyrosine phosphorylation of 55 and 170kDa proteins, and the vesicles containing the phosphorylated channels showed a 46% increase in 45Ca2+ uptake. The phosphorylation and the calcium uptake were susceptible to inhibition by a specific tyrosine kinase inhibitor, genistein. The binding of EGF to buccal mucosal calcium channel receptor protein was also inhibited (36-41%) by acidic mucus glycoprotein. The reduction in binding was dependent upon the presence of sulfate ester and sialic acid groups, as evidenced by the loss of the glycoprotein inhibitory capacity following removal of these groups. The results for the first time demonstrate that salivary mucins actively participate in the modulation of the buccal mucosal calcium channel activity, a process of importance to the preservation of soft oral integrity.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1993

Salivary mucin modulation of buccal mucosal calcium channel activity.

The effect of the low and high molecular weight salivary mucins on the activity of calcium channel isolated from buccal epithelial cell membranes was investigated. The 45Ca2+ uptake into the vesicle-reconstituted channels, while only moderately (15%) affected by the intact mucin forms, was significantly inhibited (60%) by the acidic mucin fractions. This effect was associated with the sialic acid and sulfate ester groups of the glycoproteins. The channel complex in the presence of epidermal growth factor (EGF) and ATP responded by an increase in protein tyrosine phosphorylation, and the vesicles containing the phosphorylated channels showed a 46% increase in 45Ca2+ uptake. The phosphorylation process was inhibited by the acidic mucins, which also interfered with the binding of EGF to the channel protein. The inhibitory effect was dependent upon the presence of sulfate ester and sialic acid groups, and the loss of the inhibitory capacity occurred following their removal. The results demonstrate the salivary mucins actively participate in the modulation of buccal mucosal calcium channel activity.

Adenosine Triphosphate↗
PubMed1993

Salivary and plasma insulin levels in man.

Changes in plasma and salivary immunoreactive insulin were studied in saliva and blood of 9 healthy subjects following either oral glucose or a test meal ingestion at 30 min intervals for up to 3h. The levels of plasma immunoreactive insulin reached maximum at 60 min with a value of 62.77 +/- 6.52 microU/ml after the glucose load and 62.62 +/- 6.52 microU/ml after the test meal. In the case of salivary immunoreactive insulin levels, the maximum was attained at 90 min with a value of 18.47 +/- 2.68 microU/min after the glucose load and 22.40 +/- 2.01 microU/min after the test meal. Positive linear correlation (r = 0.74) was found between the salivary and plasma immunoreactive insulin levels.

Administration, Oral↗
PubMed1992

Activation of dihydropyridine-sensitive parotid salivary gland calcium channels by epidermal growth factor.

The calcium channel complex of the parotid was isolated from solubilized acinar-cell membranes by affinity chromatography on wheatgerm agglutinin. The channel, after labelling the calcium antagonist-receptor site with [3H]-PN200-100, was reconstituted into phosphatidylcholine vesicles that exhibited active 45Ca2+ uptake. This uptake was independent of sodium and potassium gradients, indicating its electroneutrality. The channels responded in a dose-dependent manner to the dihydropyridine calcium antagonist, PN200-110, which at 0.4 microM exerted a maximal inhibitory effect of 75% on 45Ca2+ uptake; a 46% enhancement in 45Ca2+ uptake occurred with a specific calcium-channel activator, BAY K8644. On epidermal growth-factor (EGF) binding in the presence of ATP, there was an increase in tyrosine phosphorylation of 55 and 170 kDa calcium-channel proteins. Such phosphorylated channels, after reconstitution into vesicles, displayed a 61% greater 45Ca2+ uptake, indicating the involvement of tyrosine kinase in EGF-dependent activation of the calcium channel. The results point towards the importance of EGF in the regulation of calcium homeostasis in salivary gland.

Animals↗
PubMed1992

Modulation of dihydropyridine-sensitive gastric mucosal calcium channels by GM1-ganglioside.

1. A dihydropyridine-sensitive calcium channel complex was solubilized from gastric mucosal cell membranes and purified by affinity chromatography on wheat germ agglutinin. 2. The calcium channel complex labeled with [3H]PN200-110, when reconstituted into phosphatidylcholine vesicles, exhibited active 45Ca2+ uptake into intravesicular space as evidenced by La3+ displacement and osmolarity studies. The channel complex responded in a dose-dependent manner to dihydropyridine calcium antagonist, PN200-110, which at 0.5 microM exerted maximal inhibitory effect of 66% in 45Ca2+ uptake. 3. The uptake of 45Ca2+ into vesicle-reconstituted gastric mucosal calcium channel complex was inhibited by GM1-ganglioside. Maximum inhibitory effect was achieved at 10-15 nM GM1, at which point a 74% decrease in 45Ca2+ uptake occurred. Furthermore, GM1 also inhibited dihydropyridine binding to gastric mucosal membranes, indicating the extracellular orientation of calcium channel domains for GM1. 4. The ability of GM1 to modulate the intracellular calcium levels may be an important feature in gastric mucosal protection by this ganglioside.

Animals↗
PubMed1992

Modulation of gastric mucosal calcium channels activity by platelet-derived growth factor.

A dihydropyridine-sensitive gastric mucosal calcium channels were isolated from the solubilized epithelial cell membranes by affinity chromatography on wheat germ agglutinin. The channels following labeling the calcium antagonist receptor site with [3H]PN200-100 were reconstituted into phospholipid vesicles which exhibited active 45Ca2+ uptake as evidenced by La3+ displacement assays. The uptake of calcium was independent of sodium and potassium gradients indicating the electroneutral nature of the process. The channels responded in a dose dependent manner to dihydropyridine calcium antagonist, PN200-110, which at 0.5 microns exerted maximal inhibitory affect of 66% on 45Ca2+ uptake, while a 52% enhacement in 45Ca2+ uptake occurred with a specific calcium channel activator, BAY K8644. On platelet-derived growth factor (PDGF) binding in the presence of ATP, channel protein showed an increase in tyrosine phosphorylation of 55 and 170 kDa calcium channel proteins. Such phosphorylated channels following reconstitution into vesicles displayed a 78% greater 45Ca2+ uptake. The results demonstrate the importance of PDGF in the regulation of gastric mucosal calcium uptake.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Role of sulphation in post-translational processing of rat salivary mucins.

Segments of rat submandibular salivary gland were incubated in MEM supplemented with 10-800 microM sulphate in the presence of [3H]-glucosamine, [3H]-proline and [35S]-Na2SO4, with 0-8 mM chlorate, an inhibitor of 3'-phosphoadenosine-5'-phosphosulphate formation. Incorporation of glucosamine and sulphate depended upon the sulphate content of the medium and reached a maximum at 400 microM sulphate. The introduction of chlorate into the medium, while having no effect on the protein synthesis as shown by [3H]-proline incorporation, caused, at its optimal concentration of 4 mM, a 90% decrease in mucin sulphation and a 29% drop in mucin glycosylation. At low sulphate content in the medium and in the presence of chlorate the incorporation of sulphate and glucosamine was mainly into the low molecular-weight form of mucin. An increase in sulphate in the medium caused an increase in the high molecular-weight form of mucin and in the extent of sulphation in its carbohydrate chain. This effect of sulphate was, however, inhibited by chlorate. The results suggest that sulphation takes place at an early stage of mucin assembly and that sulphate availability is essential for the formation of the high molecular-weight mucin.

Animals↗
PubMed1991

Adrenergic and cholinergic regulation of phospholipid release in sublingual salivary gland in vitro.

1. The role of adrenergic and cholinergic mediators in the regulation of salivary phospholipid secretion was investigated using rat sublingual acinar cells maintained in the presence of [3H]choline. 2. The release of [3H]choline containing phospholipids was enhanced by beta-adrenergic agonist, isoproterenol to a greater extent than the cholinergic agonist, pilocarpine. 3. The effect of isoproterenol on phospholipid release was observed even after 5 min and by 30 min a 1.7-fold increase in secretion occurred, whereas pilocarpine evoked 1.2-fold increase by 30 min with no discernible effect in 5 min. The isoproterenol effect was blocked by alprenolol, and an inhibition of pilocarpine effect was observed with atropine. 4. In the absence of mediators, 82% of secreted labeled phospholipids were represented by phosphatidylcholine (PC), 4.3% by lysophosphatidylcholine (LPC) and 12.1% by sphingomyeline (Sph), those secreted in the presence of isoproterenol showed significantly lower (37%) content of LPC, while those secreted in response to pilocarpine were substantially richer in LPC (2.5 times) and Sph (27%), and contained less (17%) PC. 5. The results provide first evidence for the involvement of adrenergic and cholinergic mediators in the regulation of salivary phospholipid secretion.

Alprenolol↗
PubMed1991

Inhibition of Helicobacter pylori colonization by sulfated gastric mucin.

The role of human gastric mucin in mucosal protection against Helicobacter pylori colonization was investigated. H. pylori cells were incubated with purified intact mucin or its acidic fractions and then examined for their inhibitory capacity of H. pylori attachment to erythrocytes. Titration data established that the inhibitory activity of mucin was associated with its acidic component as the fraction enriched in sialic acid and sulfate showed 16-fold higher inhibitory titer than that of the intact mucin. While the inhibitory titer of acidic mucin fraction was not affected by the removal of sialic acid, the desulfation led to a complete loss of its inhibitory activity, thus pointing towards the importance of sulfate ester groups in this process. The results for the first time point towards the involvement of sulfomucins in the protection of gastric mucosa against colonization by H. pylori.

Animals↗
PubMed1989

[Amylase in the mixed saliva of diabetics and nondiabetics on an empty stomach and during the glucose tolerance test].

The catalytic activity of alpha-amylase is significantly elevated in salivary pool from 146 diabetics (2176 +/- 149.3 mu catal.l-1) vs. the salivary pool from 78 nondiabetics (1159 +/- 97.3 mu catal X l-1), the difference in the concentrations of the saliva condensation index (the chloride concentration) in the diabetics and nondiabetics being negligible. Glucose tolerance test has been carried out in 54 subjects. Glucose intake has increased the alpha-amylase catalytic activity and augmented glycosialia in 14 diabetics, in 13 subjects with abnormal glucose tolerance, and in 16 nondiabetics; a negligible rise of glycosialia and a reduction of alpha-amylase catalytic activity have been observed in 11 subjects with a flat glycemia curve. Basing on these data, the authors claim that oral glucose activates amylase and glucose secretion by the salivary glands.

Adult↗
PubMed1978

A comparative study of DNA-induced transformants and spontaneous revertants of inositolless Neurospora crassa.

Inositolless (inl-) Neurospora crassa strains were treated with DNA (allo-DNA) of wild type N. Crassa. Hyphal fragments of a mycelial suspension of the N. Crassa ragged inl- strain used as recipient in our transformation experiments were found to consist of units containing 100--1000 nuclei. In this strain the inositol-independent (inl+) nuclei appearing after DNA treatment or by spontaneous reversion are present in the cytoplasm together with a large number of inl- nuclei. Thus, both transformation and reversion initially must result in heterokaryosis. Under appropriate conditions the inl- nuclei can be detected in the transformed and spontaneous inl+ phenotype revertant strains. Spontaneous revertants are usually characterized by the loss of their inl+ nuclei after transfers on inositol-supplemented medium. On minimal medium, the growth rate of transformed strains is significantly lower than that of spontaneous revertants. The inl+ gene appearing after DNA treatment or by spontaneous reversion is inherited as a trait bound to chromosomes. In crosses with the transformed strains, there is a significant increase in the number of non-Mendelian (6:2 and 5:3) tetrads in the inl locus.

DNA, Fungal↗
PubMedDate not supplied

Pseudoporphyria: an atypical variant resembling toxic epidermal necrolysis.

BACKGROUND: Pseudoporphyria has been attributed to both medication usage and chronic hemodialysis. Histologically, it is identical to porphyria cutanea tarda. It is most commonly seen as localized bullae on sun-exposed skin, often on the dorsum of the hands and fingers. OBJECTIVES: We describe a 31-year-old man with rapidly evolving bullae which became denuded, clinically suggestive of toxic epidermal necrolysis. Pseudoporphyria was proven histologically. However, our patient's eruption was not localized as small bullae but was widespread, with large bullae evolving into large, cutaneous, denuded erosions. CONCLUSIONS: We describe a previously unreported, generalized variant of pseudoporphyria that resembles toxic epidermal necrolysis. We provide a review of pseudoporphyria and compare our variant to toxic epidermal necrolysis and mimicking disorders.

Adult↗