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J Piotrowski

Publications and source records attributed to J Piotrowski.

At least 19 recordsLinked to original sources
PubMed2006

The Werner syndrome protein is required for recruitment of chromatin assembly factor 1 following DNA damage.

The Werner syndrome protein (WRN) and chromatin assembly factor 1 (CAF-1) are both involved in the maintenance of genome stability. In response to DNA-damaging signals, both of these proteins relocate to sites where DNA synthesis occurs. However, the interaction between WRN and CAF-1 has not yet been investigated. In this report, we show that WRN interacts physically with the largest subunit of CAF-1, hp150, in vitro and in vivo. Although hp150 does not alter WRN catalytic activities in vitro, and the chromatin assembly activity of CAF-1 is not affected in the absence of WRN in vivo, this interaction may have an important role during the cellular response to DNA replication fork blockage and/or DNA damage signals. In hp150 RNA-mediated interference (RNAi) knockdown cells, WRN partially formed foci following hydroxyurea (HU) treatment. However, in the absence of WRN, hp150 did not relocate to form foci following exposure to HU and ultraviolet light. Thus, our results demonstrate that WRN responds to DNA damage before CAF-1 and suggest that WRN may recruit CAF-1, via interaction with hp150, to DNA damage sites during DNA synthesis.

Blotting, Western↗
PubMed2005

Impact of intraoperative myocardial cellular damage on early hemodynamics after off-pump versus on-pump coronary artery bypass surgery.

BACKGROUND: Due to the surgical trauma a small amount of myocardial cellular damage is inherent during coronary artery bypass grafting (CABG). The purpose of the present study was to assess the degree of myocardial cellular damage after off-pump (OPCAB) and on-pump CABG (ONCAB) as measured by cardiac troponin I (cTnI), creatine kinase (CK), its MB isoenzyme (CK-MB) and myoglobin (Myo) and to examine its impact on early hemodynamics after surgery. METHODS: Ninety-nine consecutive OPCAB patients, operated between 01/1999 and 01/2004, were enrolled in the present study and compared to 99 ONCAB patients operated during the same period of time, who were matched for baseline data and mean number of grafts per patient. Early hemodynamics, cTnI, CK/CK-MB and Myo were measured preoperatively and at 1, 6, 12, 24 and 48 hours (h) postoperatively. Perioperative inotropic support, clinical data and potoperative outcome were recorded prospectively. RESULTS: The two groups were similar concerning preoperative characteristics. The mean number of distal grafts/patient was 2.1 +/- 1.0 in OPCAB and 2.1 +/- 0.8 in ONCAB patients (mean +/- SD). There was no significant difference among the groups regarding early hemodynamics in terms of cardiac index (CI), systemic vascular resistance index (SVRI), and left ventricular stroke work index (LVSWI), and inotropic support. However, cTnI, CK/CK-MB but not Myo levels were significantly lower in OPCAB compared to ONCAB patients at 1, 6, 12, 24, 36 and 48 h postoperatively (P<0.05). CONCLUSIONS: Off-pump surgery results in equal early hemodynamics despite a significantly lower release of cTnI and CK, suggesting a reduced myocardial cell damage as compared to ONCAB surgery.

Aged↗
PubMed2004

Severe left ventricular failure after double lung transplantation: pathophysiology and management.

Patients undergoing bilateral lung transplantation for end-stage pulmonary hypertension may experience various complications. We describe a patient who underwent transplantation for chronic pigeon breeder's disease, who had secondary pulmonary hypertension and deteriorated right heart function, and who developed severe left heart failure during the weaning phase after successful double lung transplantation. The patient was stabilized with catecholamines and an intra-aortic balloon pump. Left heart function increased within 7 days and normalized at Day 18. Otherwise, the post-operative course was uneventful.

Bird Fancier's Lung↗
PubMed2003

Efficacy and safety of single-triple capsules of bismuth biskalcitrate, metronidazole and tetracycline, given with omeprazole, for the eradication of Helicobacter pylori: an international multicentre study.

BACKGROUND: The high prevalence of Helicobacter pylori resistance to metronidazole demands treatments more effective than standard bismuth-based triple therapy against these strains. AIM: To evaluate the H. pylori eradication rate in both metronidazole-sensitive and -resistant strains following quadruple therapy using single-triple capsules of bismuth biskalcitrate, metronidazole and tetracycline, given with omeprazole. METHODS: One hundred and seventy valid patients with duodenal ulcer, gastric ulcer or non-ulcer dyspepsia were treated in eight centres located in five countries. H. pylori was confirmed at baseline using 13C-urea breath test, histology and/or culture. Patients received three single-triple capsules q.i.d. and omeprazole, 20 mg b.d., for 10 days. Each capsule contained bismuth biskalcitrate, 140 mg (as 40 mg Bi2O3 equivalent), metronidazole, 125 mg, and tetracycline, 125 mg. 13C-Urea breath test was repeated at least 4 and 8 weeks post-treatment. RESULTS: Overall eradication rates were 93% (158/170) by modified intention-to-treat analysis and 97% (142/146) by per protocol analysis. Eradication rates were 93% (40/43) and 95% (38/40) for strains resistant to metronidazole and 95% (82/86) and 99% (75/76) for strains sensitive to metronidazole by modified intention-to-treat and per protocol analysis, respectively. CONCLUSION: This omeprazole-bismuth biskalcitrate-metronidazole-tetracycline 10-day regimen is a very effective and well-tolerated treatment, which overcomes metronidazole resistance.

Adolescent↗
PubMed2001

Werner syndrome protein interacts with human flap endonuclease 1 and stimulates its cleavage activity.

Werner syndrome (WS) is a human premature aging disorder characterized by chromosomal instability. The cellular defects of WS presumably reflect compromised or aberrant function of a DNA metabolic pathway that under normal circumstances confers stability to the genome. We report a novel interaction of the WRN gene product with the human 5' flap endonuclease/5'-3' exonuclease (FEN-1), a DNA structure-specific nuclease implicated in DNA replication, recombination and repair. WS protein (WRN) dramatically stimulates the rate of FEN-1 cleavage of a 5' flap DNA substrate. The WRN-FEN-1 functional interaction is independent of WRN catalytic function and mediated by a 144 amino acid domain of WRN that shares homology with RecQ DNA helicases. A physical interaction between WRN and FEN-1 is demonstrated by their co-immunoprecipitation from HeLa cell lysate and affinity pull-down experiments using a recombinant C-terminal fragment of WRN. The underlying defect of WS is discussed in light of the evidence for the interaction between WRN and FEN-1.

Adenosine Triphosphatases↗
PubMed2001

A functional interaction of Ku with Werner exonuclease facilitates digestion of damaged DNA.

Werner syndrome (WS) is a premature aging disorder where the affected individuals appear much older than their chronological age. The single gene that is defective in WS encodes a protein (WRN) that has ATPase, helicase and 3'-->5' exonuclease activities. Our laboratory has recently uncovered a physical and functional interaction between WRN and the Ku heterodimer complex that functions in double-strand break repair and V(D)J recombination. Importantly, Ku specifically stimulates the exonuclease activity of WRN. We now report that Ku enables the Werner exonuclease to digest through regions of DNA containing 8-oxoadenine and 8-oxoguanine modifications, lesions that have previously been shown to block the exonuclease activity of WRN alone. These results indicate that Ku significantly alters the exonuclease function of WRN and suggest that the two proteins function concomitantly in a DNA damage processing pathway. In support of this notion we also observed co-localization of WRN and Ku, particularly after DNA damaging treatments.

Adenine↗
PubMed2001

[Surgical treatment of infective endocarditis: the Essen experiences].

BACKGROUND: Instead of immediate diagnosis and effective antibiotic treatment morbidity and mortality in infective endocarditis remains high. If the infection cannot be controlled or the disease progresses irreversible destruction of cardiac structures results. SURGICAL THERAPY: In this case surgical therapy should be considered immediately. The outcome of surgical repair is not depending on the implanted prosthesis, but solely on timing of the operation.

Acute Disease↗
PubMed2001

Up-regulation of gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide by aspirin but not indomethacin.

Infection with Helicobacter pylori and the use of non-steroidal anti-inflammatory drugs (NSAIDs) are recognized as the two primary factors in the etiology of gastric disease. In this study, we applied the animal model of H. pylori-induced gastritis to assess the influence of NSAIDs on the course of mucosal inflammatory responses to H. pylori. Two days following intragastric application of H. pylori lipopolysaccharide, rats were divided into groups and administered daily for up to 8 days either indomethacin, aspirin or the vehicle, and their gastric mucosal tissue subjected to histological and biochemical assessment. H. pylori lipopolysaccharide elicited within 2 days a pattern of acute mucosal inflammatory responses accompanied by a massive epithelial cell apoptosis, and a marked increase in the expression of membrane-bound and soluble forms of TNF-alpha. The extent of mucosal inflammatory involvement reached a maximum by the 4th day and showed a decline by the 10th day; this was reflected in a 38.1% reduction in apoptosis, a 53.2% decline in membrane-bound TNF-alpha and a 63.8% decrease in soluble TNF-alpha. Compared to the vehicle controls, aspirin caused a 36.2% increase in the severity of the mucosal inflammatory involvement by the second day of administration and a 25.9% increase in the inflammatory involvement occurred by the 8th day; this effect of aspirin was accompanied by a significant (54.5%) induction in apoptosis, a 58.2% decline in membrane-bound TNF-alpha and a 61% increase in soluble TNF-alpha. In contrast, administration of indomethacin evoked only a marginal increase (5-7%) in apoptosis, and caused no discernible changes in the severity of gastric mucosal involvement and the expression of TNF-alpha forms elicited by H. pylori lipopolysaccharide. The findings indicate that aspirin, but not indomethacin, increases the severity of gastric mucosal inflammatory responses to H. pylori. This detrimental influence of aspirin appears to result from up-regulation in the mucosal expression of soluble form of TNF-alpha, which leads to the amplification of apoptotic events that potentiate gastric mucosal inflammatory reaction to H. pylori.

Animals↗
PubMed2000

Suppression of endothelin-converting enzyme-1 during buccal mucosal ulcer healing: effect of chronic alcohol ingestion.

Among the factors affecting the efficiency of soft oral tissue healing is endothelin-1 (ET-1), a potent vasoactive peptide produced from a biologically inactive big ET-1 by the action of endothelin-converting enzyme-1 (ECE-1). We investigated the expression of ECE-1 during buccal mucosal ulcer healing in rats maintained for 5 weeks on alcohol containing or control diet. The mucosal activity of ECE-1, characterized by sensitivity to phosphoramidon, was associated with microsomal fraction and showed an elevated (3.1-fold) level in the alcohol diet group. Moreover, the ulcer onset in the alcohol group was reflected in a 39% greater expression of ECE-1 activity, and was accompanied by a 1.4-fold greater increase in TNF-alpha and a 2.5-fold greater enhancement in epithelial cell apoptosis. While in both groups the ulcer healing was associated with a decrease in buccal mucosal expression of ECE-1, as well as a decline in TNF-alpha and apoptosis, the changes were significantly slower in the alcohol diet group and manifested by a 40% delay in healing. Thus, chronic alcohol ingestion leads to up-regulation of ECE-1 expression, induction of TNF-alpha, and triggering apoptotic events that delay the mucosal repair.

Animals↗
PubMed2000

Up-regulation of endothelin-converting enzyme-1 in gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide.

Endothelin-1 (ET-1) is a vasoactive peptide produced from a biologically inactive big ET-1 by the action of endothelin-converting enzyme-1 (ECE-1). We investigated gastric mucosal expression of ECE-1 during a 10-day course of inflammatory responses associated with acute gastritis elicited by Helicobacter pylori lipopolysaccharide. The ECE-1 activity was associated with microsomal fraction and the level of its expression reflected the extent of mucosal inflammatory involvement. The histologic pattern of inflammation reached a maximum on the 4th day following the lipopolysaccharide and was accompanied by a 4.1-fold enhancement in the expression of ECE-1 activity and a significant elevation in ET-1 (3.1-fold), TNF-alpha (8.8-fold), and apoptosis (11.6-fold). A 41.5% decrease in the severity of mucosal inflammation by the 10th day following the lipopolysaccharide was reflected in a 62.3% reduction in the mucosal expression of ECE-1 and a decline in TNF-alpha, ET-1, and apoptosis. Thus, H. pylori infection causes up-regulation of gastric mucosal ECE-1 expression, which leads to the enhancement of ET-1 production, induction of TNF-alpha, and triggering the apoptotic events that exacerbate the inflammatory process.

Animals↗
PubMed2000

Werner syndrome protein: biochemical properties and functional interactions.

Werner syndrome is a premature aging syndrome displaying numerous signs and symptoms found in normal aging. The disease is associated with a mutation in the WRN gene. We have purified the Werner protein (WRN) and studied its biochemical activities and its protein interactions. WRN is a helicase and an exonuclease and also has an associated ATPase activity. WRN interacts physically and functionally with replication protein A (RPA), which stimulates its helicase activity. We have studied the WRN exonuclease activity and found that it can be blocked by certain DNA lesions and not by others. Thus, while WRN does not bind to DNA damage, it may have properties that allow it to sense the presence of damage in DNA. More recently we have found other protein interactions that involve physical and functional interactions with WRN, which could suggest a role for WRN in DNA repair.

Antigens, Nuclear↗
PubMed2000

Disruption of the silver and non-silver coated sewing cuff of a new generation bileaflet valve prosthesis during aortic valve replacement: report on four cases.

OBJECTIVES: New generation bileaflet valve prostheses with a silver-coated sewing cuff like the St Jude Medical (SJM((R)) Regent) model are designed to offer a larger valvular orifice as well as a better resistance to postoperative prosthetic endocarditis, at the expense of a smaller sewing cuff. METHODS AND RESULTS: We report on four cases of aortic valve replacement where during the implantation procedure the fixation cuff disrupted, leading to the exchange of all four valve prostheses. This happened three times with silver- coated sewing cuffs and after withdrawal of the silver- coated cuff prostheses from the market, once with a non silver- coated sewing cuff. This was due to the arbitrary cutting of the cuff fixation suture at the ventricular side of the prosthesis, although the implantation was performed according to the recommendations of the company. This problem didn't occur previously, using other models of the same manufacturer, although the sewing cuff had been fixed in the same technique. CONCLUSION: Fixation of smaller sewing cuffs of mechanical valve prostheses with a critically exposed fixation suture at the ventricular side of the prosthesis represents a significant risk for disruption during the implantation process through cut off by chance. We recommend meticulous inspection of the sewing cuff for signs of disruption before seating the valve into position. During follow-up particular attention should be paid to valve dislodgement and leakage. The company was informed and advised by us to modify the fixation of the prosthetic annulus of the SJM((R)) Regent valve, which has led to an alternative cuff design, called the SJM Flex cuff.

Aortic Valve↗
PubMed2000

Role of interleukin-4 in down-regulation of endothelin-1 during gastric ulcer healing: effect of sucralfate.

BACKGROUND: The course of events associaed with healing gastric mucosal injury involves an orderly interplay between the array of signaling molecules that exert their influence on the processes leading to the restoration of the mucosal integrity. In this study, we investigated the effect of antiulcer agent, sucralfate, on the mucosal apoptotic processes during gastric ulcer healing by analyzing the expression of interleukin-4 (IL:4), endothelin-1 (ET-1), tumor necrosis factor-alpha (TNF-alpha), and the mucosal activity of capase-3, and constitutive (cNOS) and inducible nitric oxide synthase (NOS-2). METHODS: Rats with experimentally induced chronic gastric ulcers were administered twice daily for 14 days either sucralfate at 100 mg/kg or vehicle, and at different stages of treatment their stomachs were used for macroscopic and biochemical assessments. RESULTS: The ulcer onset was characterized by a massive epithelial apoptosis associated with a 33-fold increase in caspase-3 activity, 5.7-fold increase in TNF-alpha, 17.5-fold increase in NOS-2 and a 3.9-fold increase in ET-1, while the mucosal expression of cNOS activity showed a 7.6-fold drop and IL-4 expression fell by 37.2%. The healing was reflected in a rapid recovery in IL-4, and a decrease in apoptosis, caspase-3, TNF-alpha, ET-1 and NOS-2, and a slow recovery in cNOS activity, and the process was accelerated in the sucralfate-treated group. While in the absence of sucralfate the expression of IL-4 returned to that of the normal mucosa by the 7th day of healing and that of ET-1 and TNF-alpha by the 14th day, an accelerated ulcer healing with sucralfate treatment was associated with IL-4 recovery by the 4th day and that of ET-1 and TNF-alpha by the 10th day when the ulcer heated, while recovery in cNOS activity required 14 days. Yet, in both groups of animals the apoptotic DNA fragmentation rate, caspase-3 and the expression of NOS-2 activity remained significantly elevated even after the ulcer healed. CONCLUSIONS: The results suggest that a decrease in the mucosal expression of the regulatory cytokine IL-4 at the ulcer onset may well be a key factor causing dysregulation of ET-1 production, induction of TNF-alpha, and triggering the apoptotic events that affect the efficiency of mucosal repair process. We also show that accelerated ulcer healing by sucralfate may be the result of a rapid mucosal IL-4 generation that leads to the suppression of the mucosal apoptotic events.

Animals↗
PubMed2000

Up-regulation of endothelin-1 in gastric mucosal inflammatory responses to Helicobacter pylori Lipopolysaccharide: effect of omeprazole and sucralfate.

BACKGROUND: Helicobacter pylori is recognized as a primary etiologic factor in the development of gastric disease and the product of particular significance to the virulent action of the bacterium is its cell wall lipopolysaccharide. We applied the animal model of H. pylori lipopolysaccharide-induced acute gastritis to study the effect of antiulcer agents, omeprazole and sucralfate, on the course of mucosal inflammatory responses by analyzing the interplay between the extent of epithelial cell apoptosis and the mucosal expression of endothelin-1 (ET-1), tumor necrosis factor-alpha (TNF-alpha), and the activity of constitutive (cNOS) and inducible (NOS-2) nitric oxide synthase. METHODS: Rats pretreated twice daily for 3 consecutive days with omeprazole at 40 mg/kg, sucralfate at 100 mg/kg or the vehicle, were subjected to intragastric application of H. pylori lipopolysaccharide at 50 microg/animal, and after 2, 4, and 10 additional days on the antiulcer drug or vehicle regimen their mucosal tissue used for histologic and biochemical assessment. RESULTS: In the absence of antiulcer agents, H. pylori lipopolysaccharide elicited within 2 days a pattern of acute mucosal inflammatory responses accompanied by a massive epithelial cell apoptosis, a 2.9-fold increase in the mucosal expression of ET-1, an 11.7-fold enhancement in TNF-alpha, and a 9.3-fold increase in NOS-2, while cNOS activity showed a 5.5-fold decrease. The extent of mucosal inflammatory involvement reached a maximum by the 4th day and showed a decline by the 10th day. This was reflected in a marked reduction in epithelial cell apoptosis, decrease in the mucosal expression of ET-1, TNF-alpha and NOS-2, and the recovery in cNOS activity. Comparing to the vehicle controls, treatment with proton pump inhibitor, omeprazole, led at the end of a 10 day period to a 48.3% reduction in the extent of mucosal inflammatory involvement elicited by H. pylori lipopolysaccharide, while a 74.2% reduction in the mucosal inflammatory involvement was achieved with gastroprotective agent, sucralfate. Moreover, this advantage of sucralfate over omeprazole in countering the lipopolysaccharide-induced changes was reflected at the end of 10 day treatment period in a 20.4% greater decrease in apoptosis, a 47.5% greater reduction in TNF-alpha and a 50.7% greater reduction in ET-1. However, both agents exerted similar influence on the restoration of gastric mucosal cNOS activity and showed a comparable effect at the end of a 10 day treatment in countering the lipopolysaccharide-induced increase in the expression of NOS-2. CONCLUSIONS: The findings suggest that an increase in the mucosal ET-1 level elicited by H. pylori lipopolysaccharide, combined with a decline in cNOS may be responsible for the induction of TNF-alpha and triggering the inflammatory process. We also show that sucralfate exhibits greater efficacy than omeprazole in suppressing the H. pylori-induced mucosal inflammatory responses. This property of sucralfate may well be due to its ability to suppress the mucosal rise in ET-1.

Acute Disease↗
PubMed2000

Omeprazole fails to suppress up-regulation of gastric mucosal endothelin-converting enzyme-1 by Helicobacter pylori lipopolysaccharide.

BACKGROUND: Endothelin-1, a key mediator of inflammatory processes, is produced from its biologically inactive precursor, big ET- by the action of endothelin converting enzyme-1(ECE-1). In this study, we applied the animal model of H. pylori lipopolysaccharide-induced gastritis to assess the effect of three different types of antiulcer agents on the gastric mucosal expression of ECE-1 activity. METHODS: Rats, pretreated twice daily for 3 days with proton pump inhibitor, omeprazole at 40 mg/kg, gastroprotective agent, sulglycotide at 200 mg/kg, H2-receptor antagonist, ebrotidine at 100 mg/kg or the vehicle, were subjected to intragastric application of H. pylori lipopolysaccharide at 50 microg/animal, and after 2, and 4 additional days on the drug or vehicle regimen their mucosal tissue used for histologic and biochemical assessment. RESULTS: In the absence of antiulcer agents, H. pylori lipopolysaccharide elicited a pattern of mucosal inflammatory responses resembling that of acute gastritis which reached a maximum by the 4th day and were accompanied by a 4.1-fold increase in the mucosal expression of ECE-1 activity and an 8.8-fold enhancement in TNF-alpha. Treatment with sulglycotide led to a 56.7% reduction in the extent of mucosal inflammatory involvement, the mucosal expression of ECE-1 activity fell by a 40.5% and the level of TNF-alpha declined by a 69%. Ebrotidine produced a 50.9% decrease in the extent of mucosal inflammatory involvement, a 33.6% decrease in the expression of ECE-1 activity and a 64.1% decline in TNF-alpha, whereas omeprazole elicited a 37.6% reduction in the extent of mucosal inflammatory involvement and a 29.5% decrease in TNF-alpha, but had no effect on the lipoploysaccharide-induced increase in the mucosal expression of ECE-1 activity. CONCLUSIONS: The findings implicate up-regulation of ECE-1 in triggering the induction of TNF-alpha and propagation of gastric mucosal inflammatory responses to H. pylori. We also show that omeprazole, in contrast to sulglycotide and ebrotidine, fails to counter the enhancement in the mucosal expression of ECE-1 caused by H. pylori- lipopolysaccharide.

Animals↗
PubMed2000

Impact of ethanol on innate protection of gastric mucosal epithelial surfaces and the risk of injury.

Earlier investigations on the effect of ethanol on synthesis and posttranlational glycosylation of gastric mucus glycoprotein (mucin) revealed quantitative changes in the apoprotein assembly, glycosylation, and mucin retention on the mucosal surface (Slomiany et al.., Alcoholism: Clin. Exp. Res. 21, 417-423, 1998). To assess whether metabolic consequences of ethanol ingestion, documented in the in vitro system are also occurring in vivo the rats were subjected to 8 weeks of ethanol containing liquid diet. The retention of mucin on the surface of gastric mucosa was quantitated by measuring the binding of gastric mucin to Mucin Binding Protein (MBP) of gastric mucosa. The results were compared with those obtained with the rats subjected to pair-feeding the isocaloric-control diet. Before alcohol administration, and in two weeks' intervals thereafter, the gastric contents from the animals was collected and mucin purified. After 8 weeks of the respective diet, the animals were sacrificed and their gastric mucosa used for MBP preparation. The binding of mucin to MBP before ethanol, and after 2, 4, 6, and 8 weeks of ethanol diet was quantitated with Enzyme Linked Lectin Assay (ELLA). The study with standard mucin revealed that binding of mucin to MBP differs substantially between individual animals. The same variability in binding was observed with the individual mucin preparations collected at the onset of the experiment. However, with the progression of ethanol feeding, the mucin samples besides displaying the variable and animal-specific binding to MBP at the initiation of the experiment, also showed a dramatic decrease in binding. In five animals, after two weeks of ethanol diet, mucin binding to MBP decreased by 50%; in two animals, the drastic decrease in binding was observed in mucin collected after four weeks of alcohol feeding; and in one animal a 20% decrease in binding persisted for six weeks, and then decreased to 50% in the last collection. Also, in two animals, the mucin collected after 8 weeks of ethanol feeding retained only 6-9% of the initial binding capacity. In contrast, in pair-fed controls, the mucin binding to MBP remained the same or increased up to 20%. Results of the studies, performed on mucin of the individual animals and matching preparations of MBP, showed that each animal expresses different degree of mucin binding. Moreover, in chronic ethanol ingestion, the individual variations are accompanied by a decrease in mucin binding to MBP. Since the observed decrease in binding occurred in samples containing the same preparation of MBP, the component affected by alcohol resides on mucin. Thus, considering the in vitro impact of ethanol on generation of carbohydrate chains in Golgi, and the finding on mucin oligosaccharides-dependent mucin-MBP complex formation, we conclude that ethanol impairs the synthesis of mucin oligosaccharide structures required for binding with MBP, and the retention on gastric mucosal surfaces.

Alcohol Drinking↗