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Biomedical subjects

A Czajkowski

Publications and source records attributed to A Czajkowski.

33 records · Page 2Linked to original sources
PubMed1993

Enhancement in gastric mucosal laminin receptor expression with ulcer healing.

The expression of gastric mucosal laminin receptor with chronic ulcer healing was investigated. The receptor protein was isolated from gastric epithelial cell membrane of rats at various stages of ulcer healing and following radioiodination incorporated into vesicles which exhibited specific affinity towards laminin-coated surface. The binding assays revealed that the ulcer healing was accompanied by an increase in laminin receptor expression. A significant increase (2.5-fold) in the receptor expression occurred by the third day following the development of ulcer, reached a maximum of 8.6-fold increase by the 14th day when the ulcer was virtually healed, and its high level remained for at least 20 days. The results demonstrate the importance of laminin receptor as an indice of gastric mucosal repair in ulcer healing.

Acetates↗
PubMed1993

Characterization of gastric mucosal mucin receptor.

Mucin receptor was isolated from gastric epithelial cell membrane by a procedure involving membrane solubilization with octylglucoside followed by affinity chromatography on Sepharose-bound wheat germ agglutinin. The receptor protein yielded on SDS-PAGE a single 97kDa band and displayed specific affinity, in a concentration-dependent manner, towards the mucin-coated surface. The receptor showed requirement for carbohydrate chains in mucin for binding, as their removal caused a marked (87%) reduction in binding capacity. Scatchard analysis revealed a linear plot with a single class of high affinity binding (Kd = 43.8 nM; Bmax = 140 pmol/mg protein) sites. The results demonstrate for the first time the presence in gastric mucosa of a specific receptor for mucin.

Animals↗
PubMed1993

Inhibition of Helicobacter pylori colonization by an antiulcer agent, sulglycotide.

Sulglycotide, a potent antiulcer agent derived from duodenal mucus glycopeptide through sulfation of the carbohydrate moieties, was evaluated with respect to its ability to interfere with H. pylori mucosal attachment. H. pylori cells were incubated with sulglycotide or human gastric mucin and then examined for their inhibitory capacity of H. pylori attachment to erythrocytes. Titration data revealed that the mucin inhibitory activity was confined to its sulfomucin fraction, the titer of which was found to be 16-fold higher than that of intact mucin. The data with sulglycotide showed that the inhibitory titer of this agent against H. pylori attachment was at least 30-fold higher than that of the sulfated gastric mucin fraction. The results point towards the involvement of sulfomucins in the protection of gastric mucosa from H. pylori colonization and demonstrate that sulglycotide, because of structural similarities, is ideally suited to augment the inherent mucosal defenses against this pathogen.

Anti-Ulcer Agents↗
PubMed1992

Identification of human salivary protease activity toward mucin: differences with caries.

A protease activity directed toward high molecular weight salivary mucus glycoprotein was identified in the secretion of human submandibular salivary gland. The protease exhibited maximum activity at pH 7.0-7.4, and following ammonium sulfate fractionation yielded an active enzyme at 60% saturation which on SDS-PAGE gave 48 and 53kDa protein bands. The enzyme exhibited serine-protease properties by showing susceptibility to phenyl methyl sulfonyl fluoride, alpha 1-antitrypsin, and egg white and soybean inhibitors. The protease activity in submandibular saliva of caries-resistant subjects was found to be 3.8-fold greater than that in saliva of caries-susceptible individuals, thus suggesting that the enzyme expression may be linked to the resistance to caries.

Adult↗
PubMed1992

Expression of salivary mucin bacterial aggregating activity: difference with caries.

The low and high molecular weight mucin forms were isolated from saliva of individuals with different caries status and assessed for their bacterial aggregating potential towards S. mutans and S. sanguis. The high molecular weight mucin from both groups exhibited similar protein and carbohydrate content, but the level of covalently bound fatty acids was lower in the caries-resistant group. The mucin from caries-resistant group showed only a weak inhibitory potential, while no inhibitory activity was observed with the mucin of caries-susceptible group. The low molecular weight mucins from both groups, while displaying compositional similarities, showed a marked variation in the bacterial aggregating activity, and the titer of the mucin from caries-resistant group was at least 128-fold greater than that of caries-susceptible group. The results demonstrate that the bacterial aggregating epitope of salivary mucins is expressed to a greater extent in caries-resistant individuals, and that this epitope is apparently more accessible to bacteria in the low molecular weight mucin form.

Dental Caries↗
PubMed1992

Effect of Helicobacter pylori lipopolysaccharide on the synthesis of sulfated gastric mucin.

The effect of H. pylori lipopolysaccharide on the synthesis and secretion of sulfated mucus glycoprotein in gastric mucosa was investigated. The lipopolysaccharide, while showing no discernible effect on the apomucin synthesis, exerted a profound inhibitory effect on the process of mucus glycoprotein glycosylation and sulfation, and evoked a rapid (within 15 min) inhibition (65%) in both mucin glycosylation and sulfation at its optimal concentration of 100 micrograms/ml. The data on mucin secretory responses indicated that the added lipopolysaccharide caused a 57% stimulation in sulfated mucin secretion within 15 min followed thereafter by inhibition, which reached a maximum of 32% by 45 min. The high molecular weight mucin form predominated in the initial secretion, while prolonged exposure to the lipopolysaccharide caused a significant increase in the low molecular weight mucin form. The results suggest that H. pylori lipopolysaccharide exerts detrimental effect on mucus glycoprotein sulfation and assembly.

Animals↗
PubMed1988

Feedback regulation of stimulated pancreatic enzyme secretion during intraduodenal perfusion of trypsin in man.

The pancreatic enzyme secretion in several species is controlled by a negative feedback mechanism induced by the presence of active proteases in the duodenum. The existence of this mechanism in man is controversial. The purpose of the present study was to evaluate the effect of tryptic activity in the duodenum on phenylalanine-stimulated pancreatic enzyme secretion in healthy volunteers. A double-balloon, multi-lumen tube was used for the collection of duodenal juice containing pancreatic enzymes. The continuous infusion of phenylalanine (100 mM) into the duodenum evoked an almost constant secretion of trypsin, amylase and lipase for 160 min. The infusion of trypsin (150 mg h-1; 1.25 g l-1) caused a reduction of phenylalanine-stimulated amylase and lipase output by 25%. The subsequent infusion of aprotinin at a dose of 1.5 X 10(6) KIU for 30 min led to an almost complete inhibition of trypsin. Simultaneously, the amylase and lipase output returned to the values seen before trypsin perfusion. Infusion of a higher dose of trypsin (300 mg h-1; 2.5 g l-1) caused a more pronounced decrease in phenylalanine-stimulated amylase and lipase output by 45%. These data indicate that active trypsin in the duodenum is responsible for the inhibition of phenylalanine-stimulated pancreatic enzyme secretion in man in a dose-dependent fashion, thus confirming the existence of a feedback control of pancreatic secretion regulated by the amount of proteases in the gut.

Adolescent↗
PubMed1987

Changes in some hemostatic parameters in patients with infections treated with ceftazidime and latamoxef.

In comparative studies made in patients with pneumonia we have treated 14 cases with Latamoxef and 16 cases with Ceftazidime. We have concentrated our attention on the side effects of these drugs on hemostasis. In 8 patients treated with Latamoxef we have found a prolongation bleeding time, moderate hypoprothrombinemia, thrombocytopenia and nearly no normalization of APTT and plasma euglobulin fibrinolysis. In one patient treated with Ceftazidime only slight effect of this drug on hemostasis was observed. Crucial reason for coagulopathy is probably due to impaired synthesis of vitamin K by diminished gut flora conditioned by antibiotics treatment. In the case of Ceftazidime mentioned there seem to be minimal side effects.

Bacterial Infections↗
PubMedDate not supplied

Does feedback regulation of pancreatic enzyme secretion by duodenal trypsin exist in cholecystectomized patients?

Recent studies have supported the existence of a feedback regulation of pancreatic enzyme secretion in man. The aim of present study was to evaluate whether a feedback regulation of pancreatic enzyme secretion exists in cholecystectomized patients. The study was carried out in 12 healthy volunteers and in 6 cholecystectomized patients, 7-14 years (mean 9 years) after the operation. Pancreatic secretion was stimulated by intraduodenal infusion of L-phenylalanine (100 mmo 1.1-1). The calculated outputs of pancreatic alpha-amylase and lipase were estimated. The feedback phenomenon was studied using consecutive intraduodenal infusion of trypsin (300 mg/h) and aprotinin (1.5 x 10(6) KIU/30 min). In 6 healthy persons, the infusion of trypsin caused a significant decrease (35-45%) in phenylalaninestimulated alpha-amylase and lipase outputs (p less than 0.05). This effect was completely reversed by intraduodenal aprotinin infusion. In contrast, the increase or the inhibition of tryptic activity in the duodenum was without any effect on pancreatic secretion in cholecystectomized patients. A feedback control of pancreatic secretion could not be demonstrated in patients 6-14 years after cholecystectomy.

Adolescent↗
PubMedDate not supplied

Effect of duodenal trypsin on pancreatic secretion in men.

The effect of tryptic activity in duodenum on L-phenylalanine (100 mmol.1-1 intraduodenally) stimulated pancreatic secretion in 18 healthy volunteers has been evaluated. Intraduodenal infusion of trypsin (150 mg) during 1 h caused the reduction of alpha-amylase and lipase output by ca 30%. The infusion of aprotinin at the dose of 0.5.10(6) KIU during 30 min caused return of the alpha-amylase and lipase output to the pretryptic values. The infusion of trypsin in higher dose (300 mg) caused more pronounced decrease of amylase and lipase output (ca 45%). Our data indicate that active trypsin in duodenum is responsible for the inhibition of L-phenylalanine stimulated pancreatic enzyme secretion in man. These results corroborate the existence of feedback regulation of stimulated pancreatic secretion by intraduodenal trypsin in man.

Adolescent↗