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Biomedical subjects

J Piotrowski

Publications and source records attributed to J Piotrowski.

At least 73 records · Page 4Linked to original sources
PubMed1997

Chronic alcohol ingestion enhances tumor necrosis factor-alpha expression and salivary gland apoptosis.

We investigated the extent of induction in sublingual salivary gland cells apoptosis and tumor necrosis factor-alpha (TNF-alpha) expression with chronic ethanol ingestion. The experiments were conducted on rats pair-fed for 8 weeks with alcohol-containing and control liquid diet. The animals were killed, their sublingual glands dissected, and the glandular tissue used for quantization of TNF-alpha expression and the assays of acinar cells apoptosis employing sandwich enzyme immunoassay for histone-associated DNA fragments. The mean value for TNF-alpha in sublingual gland of the control group was 22.3 pg/mg of protein and showed a 1.6-fold increase in the chronic ethanol diet group to 36.5 pg/mg of protein. In comparison with the controls, the sublingual gland of the chronic ethanol diet group also exhibited a 3.4-fold enhancement in acinar cell apoptosis. These findings suggest that chronic ethanol ingestion causes the enhancement in TNF-alpha expression and leads to the induction in salivary gland acinar cells apoptosis. Thus, the diminished secretion of saliva in alcoholics may be a direct result of increased salivary gland apoptosis.

Alcoholism↗
PubMed1996

Salivary mucins in oral mucosal defense.

1. Salivary mucins are well recognized as an important factor in the preservation of the health of the oral cavity. These large glycoproteins play a major role in the formation of protective coatings covering tooth enamel and oral mucosa, which act as a dynamic functional barrier capable of modulating the untoward effects of oral environment, and are of significance to the processes occurring within the epithelial perimeter of mucosal defense. 2. Based on macromolecular characteristics, the mucins in saliva fall into high (> 1000 kDa) and low (200-300 kDa) molecular weight forms. The two forms, although differ with respect to bacterial clearance ability, display virtually identical carbohydrate chain make-up, ranging in size from 3 to 16 sugar units. 3. Of the two mucin forms, the low molecular weight form more efficient in bacterial aggregation, predominates in saliva and oral mucosal mucus coat of caries-resistant individuals, while the level of the high molecular weight form is higher in caries-susceptible subjects. The saliva of caries-resistant individuals also exhibits greater activity of protease capable of conversion of the high molecular weight mucin to the low molecular weight form. 4. The bacterial aggregating activity of salivary mucins appears to be associated with sulfomucins rather than sialomucins. While the removal of sialic acid causes only partial loss in mucin aggregating capacity, a complete loss in the bacterial aggregating activity occurs following mucin desulfation. 5. The mucins in oral mucosal mucus coat interact with the epithelial surfaces through specific membrane receptors. This interaction apparently involves the carbohydrate moiety of mucin molecule and may be rendered vulnerable to disruption by opportunistic bacteria colonizing the oral mucosa. 6. Salivary sulfo- and sialomucins actively participate in the modulation of the oral mucosal calcium channel activity through the inhibition of EGF-stimulated channel protein tyrosine phosphorylation. This function of salivary mucins is of paramount importance to mucosal calcium homeostasis.

Animals↗
PubMed1996

Helicobacter pylori lipopolysaccharide induces gastric epithelial cells apoptosis.

H. pylori is recognized as a primary etiologic factor in the pathogenesis of gastric disease. Here, we assessed the effect of intragastric administration of H. pylori lipopolysaccharide at 50 and 200 micrograms dose on the epithelial cell apoptosis. Histological examination of the mucosal tissue two days following the treatment revealed that lipopolysaccharide at both doses induced in the rat stomach mucosal inflammatory responses typical of gastritis. The in situ DNA fragmentation assay demonstrated that these changes were associated with a marked increase in gastric epithelial cell apoptosis. The apoptotic index in the controls averaged 0.3%, and increased dramatically to 59% with the lipopolysaccharide at 50 micrograms dose, while at the 200 micrograms dose the apoptotic index of 71.9% was attained. The results point towards cell wall lipopolysaccharide as a virulence factor responsible for the induction of gastric epithelial cell apoptosis by H. pylori.

Animals↗
PubMed1996

Susceptibility of growth factors to degradation by Helicobacter pylori protease: effect of ebrotidine and sucralfate.

In this study, we investigated the susceptibility of the growth factors (EGF, bFGF, TGF beta and PDGF) to degradation by the protease elaborated by H. pylori and assessed the effect of antiulcer agents, ebrotidine and sucralfate, on this enzymatic action of the bacterium. The colonies of H. pylori were washed with saline, filtered to retain the bacteria, and the filtrate used as an enzyme source. The assays revealed that while EGF and beta FGF showed only marginal (5-7%) susceptibility to H. pylori protease, a 61.7% degradation occurred with PDGF and 62.3% with TGF beta. Introduction of ebrotidine or sucralfate to the assay system led to the reduction in the rate of growth factors degradation, which at 50 micrograms/ml ebrotidine reached the value of 85.1% for PDGF and 88.6% for TGF beta, while with sucralfate the optimal inhibition of PDGF (79.6%) and TGF beta (82.7%) degradation occurred at 200 micrograms/ml. The results demonstrate that PDGF and TGF beta are susceptible to H. pylori degradation and that antiulcer agents, ebrotidine and sucralfate are capable of counteracting this effect.

Benzenesulfonates↗
PubMed1996

Synchronized induction in bFGF and Cdk2 during gastric ulcer healing.

The processes of gastric mucosal repair are regulated by growth factors triggering the signals for cell cycle progression. We examined the expression of gastric mucosal basic fibroblast factor (bFGF) and cyclin dependent kinase (p34Cdk2) at different stages of chronic ulcer healing. The results of assays revealed that ulcer healing was accompanied by an increase in mucosal expression of bFGF and Cdk2. A significant induction in bFGF and Cdk2 occurred by the 2nd day of ulcer healing, reached the respective maximums of 2.3- and 2.2-fold increase by the 4th day of healing, and remained still elevated (20%) on the 14th day when the ulcer was essentially healed. The results demonstrate a synchronized induction in bFGF and cell cycle regulatory kinase, Cdk2, with ulcer healing.

Acetic Acid↗
PubMed1995

The protein kinase C-activated MAP kinase pathway of Saccharomyces cerevisiae mediates a novel aspect of the heat shock response.

The PKC1 gene of budding yeast encodes a homolog of the alpha, beta, and gamma isoforms of mammalian PKC that is proposed to regulate a MAPK-activation pathway. Mutants in this pathway undergo cell lysis resulting from a deficiency in cell wall construction when they attempt to grow at elevated temperatures. We show that the PKC1-regulated pathway is important for induced thermotolerance and that the MPK1 protein kinase (the MAPK of this pathway) is strongly activated by mild heat shock. This activation is sustained during growth at high temperature and is dependent on the function of pathway components proposed to function upstream of MPK1, including PKC1. Expression of genes under the control of known heat shock-inducible promoter elements (HSEs and STREs) was not compromised in PKC1 pathway mutants, indicating that this pathway mediates a novel aspect of the yeast heat shock response. We propose that the heat-induced signal for pathway activation is generated in response to weakness in the cell wall created during growth under thermal stress, perhaps as a result of increased membrane fluidity. Evidence is presented that the mechanism by which the cell detects this weakness is by measuring stretch of the plasma membrane.

Base Sequence↗
PubMed1995

Antagonism of botulinum toxin-induced muscle weakness by 3,4-diaminopyridine in rat phrenic nerve-hemidiaphragm preparations.

The effects of the potassium channel inhibitor and putative botulinum toxin antagonist 3,4-diaminopyridine (3,4-DAP) were investigated in vitro on the contractile properties of rat diaphragm muscle. In the presence of 100 pM botulinum neurotoxin A (BoNT/A), twitches elicited by supramaximal nerve stimulation (0.1 Hz) were reduced to approximately 10% of control in 3 hr at 37 degrees C. Addition of 3,4-DAP led to a rapid reversal of the BoNT/A-induced depression of twitch tension. In the presence of 100 microM 3,4-DAP, antagonism of the BoNT/A-induced blockade began within 30-40 sec and reached 82% of control with a half-time of 6.7 min. The beneficial effect of 3,4-DAP was well maintained and underwent little or no decrement relative to control for at least 8 hr after addition. Application of 1 microM neostigmine 1 hr after 3,4-DAP led to a further potentiation of twitch tension, but this action lasted for < 20 min. Moreover, neostigmine caused tetanic fade during repetitive stimulation. In contrast to the efficacy of the parent compound, the quaternary derivative of 3,4-DAP, 3,4-diamino-1-methyl pyridinium produced little or no twitch potentiation up to a concentration of 1 mM. The potassium channel blocker, tetraethylammonium, generated a transient potentiation followed by a sustained depression of twitch tensions. It is concluded that 3,4-DAP is of benefit in antagonizing the muscle paralysis following exposure to BoNT/A. Co-application of neostigmine or tetraethylammonium with 3,4-DAP, however, appears to confer no additional benefit.

Aminopyridines↗
PubMed1995

Enhancement in gastric mucosal EGF and PDGF receptor expression with ulcer healing by sulglycotide.

1. The effect of an antiulcer agent, sulglycotide, on mucosal expression of EGF and PDGF receptors with chronic ulcer healing was investigated. 2. Rats with experimentally-induced gastric ulcers were treated twice daily for 14 consecutive days, either with sulglycotide at 200 mg/kg or vehicle, and at different stages of treatment used for quantitation of gastric mucosal EGF and PDGF receptors. 3. The ulcer healing was accompanied by an increase in mucosal expression of both types of receptors. A 1.8-fold increase in EGF and 3.1-fold increase in PDGF receptors occurred by the 4th day following the development of ulcer and reached a maximum of 2.4-3.9-fold increase by the 10-14th day. 4. Treatment with sulglycotide caused accelerated ulcer healing accompanied by a significant enhancement in the receptors expression. A 2.3- and 3.6-fold increase in EGF and PDGF receptor expression occurred by the 4th day of sulglycotide treatment, reaching a 5.5- and 5.6-fold respective increase by the 10th day when the ulcer essentially healed. 5. The results attest to the ability of sulglycotide to stimulate the gastric mucosal proliferative activities associated with ulcer healing.

Acetates↗
PubMed1995

Enhancement in the protective qualities of gastric mucus by ebrotidine during duodenal ulcer healing.

1. Gastric mucus from duodenal ulcer patients before and following therapy with a new antiulcer agent, ebrotidine, at 400, 600 and 800 mg dose was examined for changes in the physicochemical qualities and anti-H. pylori activity. 2. The results of physical measurements revealed that successful therapy with ebrotidine was accompanied by a 25% increase in gastric mucus viscosity, and a 20% increase in H+ retardation capacity, while its hydrophobicity increased by 11%. 3. The enhancement in the physical properties of mucus with ebrotidine therapy were also reflected in a marked (2.6-2.9-fold) increase in the proportion of the high molecular weight form of mucin. Furthermore, following therapy with ebrotidine, the gastric mucins showed a 36% higher content of sulfate as compared to that before the therapy. 4. Assays on the H. pylori aggregating titer of gastric mucin revealed that ebrotidine therapy at all three doses evoked a 4-fold increase in mucin anti-H. pylori activity. 5. The data demonstrate that duodenal ulcer therapy with ebrotidine leads to a marked improvement in the protective qualities of gastric mucus essential for the maintenance of mucosal integrity and enhances the inherent mucosal defense against H. pylori infection.

Adult↗
PubMed1995

Inhibition of gastric mucosal mucin receptor by H. pylori lipopolysaccharide: effect of ebrotidine.

1. H. pylori infection causes the loss of mucus coat continuity and its patchy appearance. Here, we present evidence that the bacterium, through its cell wall lipopolysaccharide, disrupts the interaction between mucin and its mucosal receptor, and that ebrotidine is capable of counteracting this process. 2. The receptor for mucin, isolated from the solubilized gastric epithelial cell membrane by affinity chromatography on Sepharose-bound wheat germ agglutinin, displayed a molecular weight of 97 kDa and exhibited specific affinity towards mucin-coated surface. 3. The mucin binding to the receptor was susceptible to the inhibitin by H. pylori lipopolysaccharide and reached a maximum of 91%. This effect of the lipopolysaccharide was counteracted by ebrotidine, which caused a dose-dependent relief of the lipopolysaccharide inhibitory effect with maximum restoration in mucin-receptor binding of 51% at 60 microliters/ml ebrotidine. 4. The results show that H. pylori, through its lipopolysaccharide, is capable of disrupting the integrity of mucus perimeter of gastric mucosal defense and that antiulcer agent, ebrotidine, counteracts this untoward effect.

Animals↗
PubMed1995

Calculated measures of performance in electrical impedance tomography using a finite-element model.

A two-dimensional finite-element model of an electrical impedance tomographic phantom has been investigated. It is perceived that an understanding of the basic measurement system will enable the design of improved data collection hardware, e.g. the number and size of the electrodes. The presented model has sixteen electrodes spaced equidistantly on the perimeter and a centrally placed anomaly. The system is excited using the adjacent-electrode constant-current drive scheme. The size and conductivity of the anomaly are varied in order to investigate how the measurement system will behave to changes in input. Measures of the system's sensitivities to these variations in the anomaly are defined. The four measures derived from the calculated boundary voltages are contrast sensitivity, spatial or radial sensitivity, visibility and rms voltage difference. Results are presented for the four measures, showing how they vary with the parameters of the anomaly. In particular, these results show that there is a clear and distinct difference between spatial and contrast sensitivity. The relationship between the calculated visibility values and the conductivity contrast of the anomaly differs from that predicted theoretically, but is in agreement with the measured relationship. It can also be seen that the presented model is more than twice as sensitive to changes in an anomaly that is more resistive as compared to one that is more conductive than the background or surrounding material.

Body Composition↗
PubMed1995

Helicobacter pylori lipopolysaccharide inhibition of gastric mucosal somatostatin receptor.

A gastric mucosal somatostatin receptor was isolated from the solubilized epithelial cell membrane by affinity chromatography on a column consisting of covalently coupled [D-Tryp8]SRIF-14 to Affi-Gel 10. The receptor protein displayed a molecular weight of 61kDa and exhibited specific affinity towards 125I-labeled [Tyr11]SRIF-14 with the optimum range of 4-8 micrograms/ml. The binding of somatostatin to its mucosal receptor was inhibited by lipopolysaccharide from H. pylori. The inhibitory effect was proportional to the concentration of lipopolysaccharide up to 50 micrograms/ml and reached a maximum of 94.1% inhibition. The results suggest that H. pylori, through its lipopolysaccharide, is capable of interfering with somatostatin regulatory effect on gastric mucosal G-cell function.

Animals↗
PubMed1995

Susceptibility of Helicobacter pylori to antimicrobial agents: effect of sulglycotide.

H. pylori is regarded as a primary etiologic factor in gastric disease and the therapies now include a combination of antimicrobial agents with antiulcer drugs. Here, the effect of a new gastroprotective agent, sulglycotide, on the in vitro anti-H. pylori activity of metronidazole, erythromycin, tetracycline, and amoxycillin was assessed. The assays in the absence of sulglycotide gave MIC value 0.10mg/L for erythromycin, 0.12mg/L for amoxycillin, 0.15mg/L for tetracycline and 14mg/L for metronidazole, while sulglycotide alone gave MIC value of 20mg/L. The sulglycotide at its optimal dose (5mg/L) evoked a 4-fold enhancement in the MIC of amoxycillin, 5-fold in tetracycline, and 8.3-fold in erythromycin, while the MIC of metronidazole improved 3.5-fold at 10mg/L sulglycotide. The results point towards the advantage of combination therapy of sulglycotide and antibiotics for H. pylori eradication.

Amoxicillin↗
PubMed1995

Sucralfate counteracts the inhibition of gastric mucosal mucin receptor by Helicobacter pylori lipopolysaccharide.

BACKGROUND: Among the disturbances in gastric mucosal defense associated with Helicobacter pylori infection is the loss of mucus coat continuity, which results in a severe disturbance in the ability of mucus coat to maintain its functions as the pre-epithelial element of gastric mucosal defense. Here, we show that H. pylori, through its cell-wall lipopolysaccharide, disrupts the interaction between gastric mucin and its mucosal receptor, and that sucralfate is capable of counteracting this untoward effect of the bacterium. METHODS: The receptor was isolated from octylglucoside-solubilized gastric mucosal epithelial cell membranes by affinity chromatography on Sepharose-bound wheat germ agglutinin and following iodination with 125I, used in the binding assays for mucin in the presence of H. pylori lipopolysaccharide and sucralfate. RESULTS: Preincubation of the receptor protein with H. pylori lipopolysaccharide led to a decrease in mucin binding. The inhibitory effect was proportional to the concentration of lipopolysaccharide and reached a maximum of 91% at 30 micrograms/ml. The effect of H. pylori lipopolysaccharide was countered by sucralfate, which caused a dose-dependent relief of the inhibitory effect. The maximum (75%) restoration in mucin-receptor binding occurred at 60 micrograms/ml sucralfate. CONCLUSIONS: The results provide strong evidence for the effectiveness of sucralfate in preventing the loss of gastric mucus coat continuity caused by H. pylori.

Animals↗
PubMed1995

Sucralfate affects the susceptibility of Helicobacter pylori to antimicrobial agents.

BACKGROUND: Infection with Helicobacter pylori is regarded as a primary factor in the pathogenesis of gastric disease, and successful therapies now include a combination of antiulcer drugs with antimicrobial agents. In this study, we investigated the effect of sucralfate and omeprazole on the vitro anti-H. pylori activity of metronidazole, erythromycin, tetracycline, and amoxycillin. METHODS: Aliquots of H. pylori culture were transferred to the wells containing different concentrations of antibiotics either alone or in the presence of various doses of sucralfate and omeprazole and incubated for 3 days for MIC evaluation. RESULTS: The assays in the absence of sucralfate and omeprazole gave MIC value 0.10 mg/l for erythromycin, 0.12 mg/l for amoxycillin, 0.15 mg/l for tetracycline, and 14 mg/l for metronidazole. Inclusion of sucralfate evoked a 28% enhancement in the MIC of metronidazole, 2.5-fold in tetracycline, 8-fold in erythromycin, and 2-fold in amoxycillin. In the presence of omeprazole, the MIC of erythromycin improved 4-fold, tetracycline 1.6-fold, and amoxycillin, 2-fold. CONCLUSIONS: The results demonstrate that sucralfate enhances the anti-H. pylori activity of antibiotics and that this effect is comparable to that of omeprazole.

Amoxicillin↗