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1.
J Physiol Pharmacol ; 60 Suppl 4: 57-62, 2009 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-20083852

RESUMEN

OBJECTIVE: FHIT gene encodes human diadenosine triphosphate hydrolase involved in the regulation of cell cycle and nucleotide metabolism and is a candidate tumor suppressor gene. AIM: To investigate expression of FHIT gene at the mRNA and protein levels in sporadic inflammatory bowel disease (IBD). MATERIALS AND METHODS: FHIT mRNA was quantified by the validated real-time PCR (QPCR) and FHIT protein was detected by immunohistochemistry (IHC) in mucosal biopsies of 139 ulcerative colitis (UC), 19 Crohn's disease (CD) and 37 control patients. RESULTS: Significant FHIT gene overexpression was found in 78% of active UC but not in CD. IHC showed comparable results to QPCR. CONCLUSION: The local up-regulation of FHIT gene and protein expression in active UC may represent an adequate response against inflammatory challenge of epithelial cell homeostasis and protect against DNA damage and cell cycle disturbances.


Asunto(s)
Ácido Anhídrido Hidrolasas/biosíntesis , Enfermedades Inflamatorias del Intestino/metabolismo , Proteínas de Neoplasias/biosíntesis , Ácido Anhídrido Hidrolasas/genética , Adolescente , Adulto , Anciano , Colitis Ulcerosa/genética , Colitis Ulcerosa/metabolismo , Colitis Ulcerosa/patología , Enfermedad de Crohn/genética , Enfermedad de Crohn/metabolismo , Enfermedad de Crohn/patología , Cartilla de ADN , Femenino , Humanos , Inmunohistoquímica , Enfermedades Inflamatorias del Intestino/genética , Mucosa Intestinal/metabolismo , Mucosa Intestinal/patología , Masculino , Persona de Mediana Edad , Proteínas de Neoplasias/genética , Polonia , ARN Mensajero/biosíntesis , ARN Mensajero/genética , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Adulto Joven
2.
Rocz Akad Med Bialymst ; 49: 93-7, 2004.
Artículo en Inglés | MEDLINE | ID: mdl-15631321

RESUMEN

PURPOSE: Assessment of the gastroesophageal reflux disease (GERD) influence on myocardial ischemia and autonomic nervous system (ANS) activity. MATERIAL AND METHODS: In 50 patients with angiographically confirmed ischemic heart disease (IHD) in I-III CCS class, simultaneous 24-hour ECG and esophageal pH-metry monitoring was performed. We assessed: (1) GERD occurrence in patients with IHD, (2) influence of pathological reflux (PR) on myocardial ischemia--number and total duration of ST depression episodes in GERD and non-GERD patients, (3) temporary activity of ANS was determined according to the dynamics of spectral HRV (Heart Rate Variability) analysis components (LF, HF, VLF, LF/HF). RESULTS: 23 patients (46%) fullfilled the GERD criteria. Patients with GERD had significantly higher number of ST depression episodes (4.13 vs 2.85, p = 0.013) as well as longer total duration of ischemia (64.73 vs 35.2 min, p = 0.034). Spectral HRV analysis showed the significant decrease of LF/HF ratio (p < 0.035), which indicates the sympathovagal balance shift towards the parasympathetic system caused by PR. CONCLUSIONS: 1. GERD is frequent condition in patients with angiographically confirmed IHD. Coexistence of GERD may predispose to the myocardial ischemia. 2. Gastroesophageal reflux may cause the shift of sympathovagal balance towards its parasympathetic component. This mechanism may induce esophago-cardiac reflex, leading to diminished myocardial perfusion.


Asunto(s)
Sistema Nervioso Autónomo/fisiopatología , Reflujo Gastroesofágico/complicaciones , Sistema de Conducción Cardíaco/fisiopatología , Isquemia Miocárdica/complicaciones , Isquemia Miocárdica/fisiopatología , Adulto , Anciano , Electrocardiografía Ambulatoria , Femenino , Determinación de la Acidez Gástrica , Reflujo Gastroesofágico/metabolismo , Reflujo Gastroesofágico/fisiopatología , Frecuencia Cardíaca , Humanos , Concentración de Iones de Hidrógeno , Masculino , Persona de Mediana Edad , Isquemia Miocárdica/metabolismo
3.
Biochem Mol Biol Int ; 42(2): 247-54, 1997 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-9238522

RESUMEN

In this study, we investigated gastric epithelial cells' apoptosis and tumor necrosis factor-alpha (TNF-alpha) expression with ethanol-induced mucosal injury, and the effect of antiulcer agents on this process. Rats received intragastric pretreatment with the agent or vehicle followed 1h later by ethanol, and after 30 min the gastric mucosa was assessed for TNF-alpha and apoptosis. In the absence of antiulcer agents, ethanol caused extensive mucosal lesions accompanied by a 9.5-fold enhancement in apoptosis and a 2.5-fold increase in TNF-alpha. Pretreatment with omeprazole evoked a 54% reduction in TNF-alpha, but had no effect on ethanol-induced mucosal damage or apoptosis, the sucralfate reduced the extent of mucosal damage by 95%, apoptosis by 39% and TNF-alpha by 52%, while ebrotidine not only prevented mucosal injury and rise in TNF-alpha, but also caused a 70% reduction in epithelial cells' apoptosis. The results demonstrate that ethanol-induced gastric epithelial cells apoptosis triggered by the enhancement in mucosal TNF-alpha is efficiently counteracted by ebrotidine.


Asunto(s)
Antiulcerosos/farmacología , Apoptosis/efectos de los fármacos , Etanol/toxicidad , Mucosa Gástrica/efectos de los fármacos , Animales , Bencenosulfonatos/farmacología , Mucosa Gástrica/metabolismo , Mucosa Gástrica/patología , Antagonistas de los Receptores H2 de la Histamina/farmacología , Omeprazol/farmacología , Inhibidores de la Bomba de Protones , Ratas , Ratas Sprague-Dawley , Sucralfato/farmacología , Tiazoles/farmacología , Factor de Necrosis Tumoral alfa/efectos de los fármacos , Factor de Necrosis Tumoral alfa/metabolismo
4.
Gen Pharmacol ; 28(5): 705-8, 1997 May.
Artículo en Inglés | MEDLINE | ID: mdl-9184806

RESUMEN

1. Among the consequences of H. pylori infection is an increase in gastric acid secretion due to the impairement in feedback inhibition by somatostatin. Here, we show that lipopolysaccharide from H. pylori inhibits the binding of somatostatin to gastric mucosal receptor, and that antiulcer agents, ebrotidine and sulglycotide, are capable of countering this effect. 2. The somatostatin receptor was prepared from the solubilized gastric mucosal epithelial cell membranes by affinity chromatography on Affi-Gel-bound [D-Tryp8] SRIF-14 and used in the binding assays for 125I-labeled somatostatin in the presence of H. pylori lipopolysaccharide and antiulcer agents. 3. The assays revealed a dose-dependent inhibition in the receptor-somatostatin binding by the lipopolysaccharide which reached a maximum of 94.1%. The effect of H. pylori lipopolysaccharide was countered by ebrotidine and sulglycotide, which at their optimal doses produced 94.9% and 84% restoration in somatostatin-receptor binding, respectively. 4. The results demonstrate that the antiulcer agents, ebrotidine and sulglycotide, possess the ability to counteract the H. pylori interference with somatostatin regulatory effect on gastric acid secretion.


Asunto(s)
Antiulcerosos/farmacología , Mucosa Gástrica/efectos de los fármacos , Helicobacter pylori , Lipopolisacáridos/farmacología , Receptores de Somatostatina/antagonistas & inhibidores , Animales , Bencenosulfonatos/farmacología , Membrana Celular/efectos de los fármacos , Membrana Celular/metabolismo , Mucosa Gástrica/citología , Mucosa Gástrica/metabolismo , Ratas , Receptores de Somatostatina/metabolismo , Sialoglicoproteínas/farmacología , Somatostatina/metabolismo , Tiazoles/farmacología
5.
Alcohol Clin Exp Res ; 21(3): 417-23, 1997 05.
Artículo en Inglés | MEDLINE | ID: mdl-9161600

RESUMEN

The effect of ethanol on mucus glycoprotein synthesis, intracellular modification, transport, glycosylation, and secretion was studied in rat gastric mucous cells. Preincubation of the in vitro translation mixture containing gastric mucous cells mRNA for 60 min with 0 to 120 mM ethanol caused a decrease in the synthesis of mucus glycoprotein apopeptide by up to 40%. The reduction in translation was time- and ethanol concentration-dependent. After 60 min, translation in the presence of 30, 60, and 120 mM ethanol decreased to 83.3 +/- 2.3%, 75.5 +/- 0.4%, and 63.6 +/- 2.6%, respectively. The experiments conducted with endoplasmic reticulum microsomes, preincubated with ethanol, and used in the studies of cotranslational translocation of the apomucin showed a 20% decrease in the transfer of mucus glycoprotein apopeptide to the lumen of endoplasmic reticulum microsomes. In the presence of ethanol, processing of mucus glycoprotein apopeptide in Golgi was also inhibited. During the initial 30 min of incubation with 0 to 120 mM ethanol, glycosylation seemed to proceed at the same rate in the samples with and without ethanol. However, during consecutive 30 min of incubation, glycosylation in the presence of 60 mM ethanol decreased by 30 to 35%, and with 120 mM ethanol was completely inhibited. Measurements of the effect of ethanol on the discharge of mucus glycoprotein from the intracellular stores revealed that, on average, the secretory output of the rat gastric mucosa exposed to ethanol liquid diet for 8 weeks decreased by 77% or more, and adherence of the glycoprotein to the gastric epithelium was weakened. Results indicate that ethanol inhibits synthesis, transport, and processing of gastric mucus glycoprotein, and that the processes taking place in different intracellular compartments contribute in the additive fashion and, are reflected in a dramatic decrease in the delivery of mucus glycoprotein to the gastric epithelial surfaces.


Asunto(s)
Etanol/toxicidad , Mucosa Gástrica/efectos de los fármacos , Glicoproteínas/genética , Translocación Genética/efectos de los fármacos , Animales , Células Cultivadas , Relación Dosis-Respuesta a Droga , Retículo Endoplásmico/efectos de los fármacos , Retículo Endoplásmico/genética , Retículo Endoplásmico/metabolismo , Glicoproteínas/metabolismo , Glicosilación/efectos de los fármacos , Microsomas/efectos de los fármacos , Microsomas/metabolismo , Biosíntesis de Proteínas/efectos de los fármacos , Biosíntesis de Proteínas/genética , ARN Mensajero/genética , Ratas , Translocación Genética/genética
6.
Arzneimittelforschung ; 47(4A): 545-50, 1997 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-9205762

RESUMEN

Ebrotidine (N-[(E)-[[2-[[[2-[(diaminomethylene)amino]-4 -thiazoly]methyl]thio]ethyl]amino]methylene]-4-bromo-benzenesulfon amide, CAS 100981-43-9, FI-3542) is a new H2-receptor antagonist characterized by its high receptor affinity and gastroprotective effect. This Phase II study has been undertaken to establish the efficacy and safety of ebrotidine, administered in four dosages as a single evening dose versus placebo in the treatment of duodenal ulcer. A total of 110 duodenal ulcer patients were studied in a randomized, double-blind, placebo-controlled, multicentre clinical trial. The patients were assigned to 5 groups: placebo, 200 mg, 400 mg, 600 mg and 800 mg of ebrotidine once daily. Controls were performed at baseline and every two weeks at four follow-up visits unless ulcer healed before. Endoscopic examination was the main parameter for the assessment of treatment efficacy and ulcer healing rate. Vital signs and blood/ urine analysis were used to establish safety. The three groups treated with higher dosages (400 to 800 mg of ebrotidine daily) showed an endoscopic ulcer healing rate of 90-95%, significantly higher than 55% achieved with placebo (p < 0.05), whilst the differences between these three dosages of ebrotidine were not statistically significant. Healing rate in the group treated with 200 mg of ebrotidine daily was not significantly different from that in the placebo group. The development of symptoms, number of episodes of ulcer-related pain, total ulcerated surface area or subjective ratings by the patients and investigators also differed significantly between ebrotidine (400, 600 and 800 mg daily) and placebo, and again, no marked differences were found between these three doses of ebrotidine. As far as tolerance is concerned, no clinically or statistically significant changes were observed in vital signs and analytical parameters. The incidence of side effects was less than that presented by the placebo group, possibly due to a greater consumption of antacids in this group. Results showed that a daily dose of 400 mg ebrotidine is effective and safe in the treatment of duodenal ulcers.


Asunto(s)
Bencenosulfonatos/uso terapéutico , Úlcera Duodenal/tratamiento farmacológico , Antagonistas de los Receptores H2 de la Histamina/uso terapéutico , Tiazoles/uso terapéutico , Dolor Abdominal/tratamiento farmacológico , Adulto , Bencenosulfonatos/administración & dosificación , Método Doble Ciego , Femenino , Antagonistas de los Receptores H2 de la Histamina/administración & dosificación , Humanos , Masculino , Persona de Mediana Edad , Tiazoles/administración & dosificación
7.
Scand J Gastroenterol ; 32(3): 203-11, 1997 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-9085455

RESUMEN

BACKGROUND: The preservation of gastric mucosal homeostasis is a complex biologic process, controlled by a dynamic equilibrium of cell loss by apoptosis with that of cellular proliferation, and its abrogation is a prominent feature of Helicobacter pylori-associated gastritis. In this report, we show that H. pylori lipopolysaccharide induces histologic lesions typical of acute gastritis and that these changes are reflected in the increased epithelial cell apoptosis. METHODS: The experiments were conducted with groups of rats subjected to intragastric surface epithelial application of the lipopolysaccharide at 50 and 200 micrograms per animal. The histologic assessment of the mucosal tissue and quantification of apoptotic epithelial cells was performed 2 and 10 days after the lipopolysaccharide treatment. RESULTS: Histologic examination showed that H. pylori lipopolysaccharide at both doses within 2 days induced infiltration of lamina propria with lymphocytes and plasma cells, edema, hyperemia, and hemorrhage extending from the lamina propria to the surface of mucosa, and the effect persisted beyond the 10 days. The in situ DNA fragmentation assay showed that lipopolysaccharide caused a marked increase in epithelial cell apoptosis, with the numerous apoptotic cells present not only in the superficial epithelium but also deeper in the glands. The mean apoptotic index in the mucosa was 59% when assessed 2 days after the administration of the 50-microgram lipopolysaccharide dose and 71.9% after the 200-microgram dose, whereas in the sections assessed 10 days after the lipopolysaccharide treatment the apoptotic index averaged 46% for a 50-microgram dose and 76.8% for a 200-microgram dose. Moreover, the apoptotic index showed positive correlation (r = 0.71) with the grade of the induced inflammatory changes. CONCLUSIONS: Our findings demonstrate that H. pylori lipopolysaccharide can cause gastric mucosal responses typical of acute gastritis and identify the lipopolysaccharide as a virulence factor responsible for the induction of gastric epithelial cell apoptosis by H. pylori.


Asunto(s)
Apoptosis , Mucosa Gástrica/patología , Gastritis/patología , Helicobacter pylori , Lipopolisacáridos/toxicidad , Animales , Relación Dosis-Respuesta Inmunológica , Epitelio/microbiología , Epitelio/patología , Mucosa Gástrica/microbiología , Gastritis/etiología , Gastritis/microbiología , Helicobacter pylori/inmunología , Helicobacter pylori/patogenicidad , Lipopolisacáridos/administración & dosificación , Ratas , Ratas Sprague-Dawley
8.
Rocz Akad Med Bialymst ; 42(1): 257-66, 1997.
Artículo en Inglés | MEDLINE | ID: mdl-9581490

RESUMEN

The 24 patients with gastric ulcer were treated ranitidine (2 x 150 mg daily) or nocloprost (2 x 200 micrograms daily). The effects of these drugs on the gastric juice components were measured. We evaluated hydrochloric acid, total protein, pepsin and some carbohydrates components secretion. We showed, that ranitidine decreased significantly total protein, fucose, N-acetylneuraminic acid and hexoses contents in the gastric juice in the basal secretion; the same tendency was observed in the pentagastrin-stimulated secretion. The similar direction of the changes, but weakly expressed was confirmed in the patients treated with nocloprost. It has been shown, that ranitidine modified the gastric mucin components content, what can suggest diminished degradation of mucus directly adhering to the gastric mucosa.


Asunto(s)
Antiulcerosos/uso terapéutico , Jugo Gástrico/efectos de los fármacos , Fármacos Gastrointestinales/uso terapéutico , Antagonistas de los Receptores H2 de la Histamina/uso terapéutico , Prostaglandinas F Sintéticas/uso terapéutico , Ranitidina/uso terapéutico , Úlcera Gástrica/tratamiento farmacológico , Femenino , Fucosa/análisis , Ácido Gástrico/química , Ácido Gástrico/metabolismo , Jugo Gástrico/química , Jugo Gástrico/metabolismo , Mucinas Gástricas/química , Mucinas Gástricas/efectos de los fármacos , Mucinas Gástricas/metabolismo , Mucosa Gástrica/efectos de los fármacos , Mucosa Gástrica/metabolismo , Hexosas/análisis , Humanos , Masculino , Ácido N-Acetilneuramínico/análisis , Pentagastrina , Pepsina A/análisis , Pepsina A/efectos de los fármacos , Proteínas/análisis , Proteínas/efectos de los fármacos , Úlcera Gástrica/fisiopatología
9.
Biochem Mol Biol Int ; 40(3): 597-602, 1996 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-8908370

RESUMEN

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.


Asunto(s)
Apoptosis/efectos de los fármacos , Mucosa Gástrica/patología , Helicobacter pylori/química , Lipopolisacáridos/toxicidad , Animales , Apoptosis/genética , Fragmentación del ADN , Relación Dosis-Respuesta a Droga , Células Epiteliales , Epitelio/efectos de los fármacos , Mucosa Gástrica/efectos de los fármacos , Gastritis/patología , Lipopolisacáridos/administración & dosificación , Ratas , Ratas Sprague-Dawley
10.
Pol Arch Med Wewn ; 88(5): 302-9, 1992 Nov.
Artículo en Polaco | MEDLINE | ID: mdl-1300550

RESUMEN

Diagnostic value was assessed of serum testosterone concentration and compared with that of serum assay of CEA and CA 19-9 in the differential diagnosis of pancreatic cancer (PC) and chronic pancreatitis (CP). Thirty-six patients with PC were compared with thirty-two CP patients. The sensitivity of CA 19-9 (76.9%) in detecting PC was greater than that of testosterone and CEA (30.6% and 30.8%, respectively). The specificity of testosterone and CA 19-9 were comparable (93.7% and 96.4%, respectively). The combination of tests did not enhance the sensitivity and specificity of each test when used alone. The serum CA 19-9 concentration in PC patients was significantly higher then in patients with colon cancer, gastric cancer and benign gastrointestinal diseases.


Asunto(s)
Antígenos de Carbohidratos Asociados a Tumores/sangre , Antígeno Carcinoembrionario/sangre , Neoplasias Pancreáticas/diagnóstico , Pancreatitis/diagnóstico , Testosterona/sangre , Enfermedad Crónica , Diagnóstico Diferencial , Femenino , Humanos , Masculino , Neoplasias Pancreáticas/sangre , Pancreatitis/sangre , Sensibilidad y Especificidad
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