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1
Content available remote

Prostaglandins and ulcer healing

100%
Konturek S. J., Konturek P. C., Brzozowski T.
Journal of Physiology and Pharmacology. Supplement
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2005
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tom 56
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nr 5
5-31
Exogenous prostaglandins (PG) applied in small gastroprotective doses fail to affect healing of gastro-duodenal ulcers but accelerate the healing when used in larger gastric inhibitory doses that appear to enhance COX-2 expression and PGE2 generation in the ulcer area. COX-1 and COX-inhibitors delay ulcer healing, particularly when both COX isoforms are suppressed such e.g. by indomethacin. Dexamethasone, that decreases the expression of COX-2 and mucosal generation of PGE2, delays ulcer healing that can be reversed by the addition of small dose of exogenous PGE2. Proton pump inhibitors (PPI) such as omeprazole and PGE analogs, accelerate ulcer healing mainly due to potent inhibition of gastric acid secretion, but they also augment the COX-2 expression and enzyme activity in the ulcerated mucosa. Endogenous PG generated at ulcer margin appear to be involved in ulcer healing promoted by growth factors and gut hormones such as gastrin or CCK and melatonin acting, at least in part, through increase of induction of COX-2 and local release of PGE2 in the ulcer area . The ulcer healing activity of growth factors (e.g. EGF, TGFalpha, HGF) and certain gut hormones (gastrin, CCK) as well as melatonin, can be attenuated by treatment with COX-1 or COX-2 inhibitors which suppress the release of PGE2 but enhance the expression of COX-2. It is concluded that endogenous PG originating mainly from upregulated COX-2 at the ulcer margin play crucial role in ulcer healing by exogenous PG, PPI, growth factors, gut hormones and melatonin, while COX-1 and COX-2 inhibitors delay ulcer healing by suppressing PG generation, and increasing COX-2 expression in the ulcer area.
2
Content available remote

Frequency of Helicobacter pylori infection in children under 4 years of age

100%
Przybyszewska K., Bielanski W., Fyderek K.
Journal of Physiology and Pharmacology. Supplement
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2006
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tom 57
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nr 3
113-122
The work aimed at establishment of frequency of Helicobacter pylori (Hp) infection in children under 4 years of age. One hundred ninety-eight children (6 month to 4 year) were tested using urea breath test (UBT) with the non-radioactive isotope 13C (50 mg of urea). The air was collected before and in the 20th and 30th minute after standard meal. The results of measurements (mass spectrometry IRMS) were given as a quotient 13CO2 /CO2 (), and a positive value was set at >3,5‰. Parents of tested children were asked to fill in a questionnaire on a somatic development, the digestive tract symptoms of a child and family members as well as socioeconomic conditions. The data were analyzed to establish the risk factors in Hp infection in children. Hp infection was found in 18,38% of children. It was not related to child’s sex nor age. The statistical significance was found in the occurrence of Hp infection among children whose family members had infection and among those attending créches or kindergartens. Non-radioactive 13C UBT is very useful and easy method to use in epidemiological studies even in youngest children. The course of infection was asymptomatic and had no impact on their somatic development. Factors increasing the risk of Hp infection were occurrence of Hp among other family members and contact with other children in educational facilities.
3

Helicobacter pylori eradication in duodenal ulcer disease in cost-beneficial: a Belgian model

100%
Deltenre M., Ilunga K. O.
Journal of Physiology and Pharmacology. Supplement
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1997
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tom 48
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nr 4
4

Central stimuli increase duodenal HCO3 secretion by release of mucosal melatonin

100%
Flemstrom G., Sjoblom M.
Journal of Physiology and Pharmacology. Supplement
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2001
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tom 52
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nr 2
5
Content available remote

Central nervous stimuli increase duodenal bicarbonate secretion by release of mucosal melatonin

100%
Sjoblom M., Flemstrom G.
Journal of Physiology and Pharmacology
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2001
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tom 52
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nr 4,1
A number of common diseases in humans, including gastroduodenal ulcer and irritable bowel syndrome, show circadian rhythms in pain and discomfort. The neurohormone melatonin is released from enterochromaffin cells in the intestinal mucosa and from the pineal gland but its role in gastrointestinal function is largely unknown. We have studied the involvement of melatonin in stimulation of the mucosa-protective alkaline secretion by the duodenal mucosa. A 12-mm segment of proximal duodenum with an intact blood supply was cannulated in situ in anesthetized rats and duodenal HCO3– secretion titrated by pH-stat. Duodenal close intra-arterial infusion of melatonin or the full agonist 2-iodo-N-butanoyl- 5-methoxytryptamine significantly increased the secretion and pretreatment with the melatonin (predominantly MT2-receptor specific) antagonist luzindole almost abolished the response. Intracerebroventricular (i.c.v.) infusion of the alpha1-adrenoceptor agonist phenylephrine (12.2 µmol kg-1·h-1 ) caused an up to fivefold increased in the alkaline secretion and the melatonin antagonist luzindole or cutting all peri-carotid nerves abolished the duodenal secretory response to i.c.v. phenylephrine. Peripheral melatonin thus stimulates duodenal mucosal HCO3 – secretion and endogenous melatonin, very likely released from mucosal enterochromaffin cells, is involved in mediating neural stimulation of the secretion.
6
Content available remote

Functional-eicosanoid-test (FET) and disease

80%
Baenkler H.-W.
Journal of Physiology and Pharmacology. Supplement
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2006
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tom 57
|
nr 12
65-72
Eicosanoids are involved in most cellular activities. Measurement of their levels in tissue or blood renders information about the function of activated cells. An extended analysis will improve the conclusions regarding eicosanoid-related diseases. Peripheral white blood cells (WBC) were used for the test. Stimulating or inhibiting substances to influence the generation and the metabolism of eicosanoids were separately added to the samples. Prostaglandins (PG) and leukotrienes (LT) were measured after incubation in culture medium for 20 minutes at room temperature. Healthy controls rendered normal data. Patients with intolerance to acetylsalicylic acid (ASS) showed an elevated output of PG and LT upon stimulation. Addition of ASS shifted from PG to LT. An altered pattern of eicosanoids also was found in patients suffering from gastroduodenal ulcer and in intestinal malignancy. The senstivity regarding the ASS-intolerance is >80% and the specifity in the same group >70%. We concluded that the FET is a suitable test for the demonstration and verification of intolerance to ASS. It also detects an imbalance of the eicosanoids in intestinal malignancy. This makes the FET a helpful tool for diagnosis and for the elucidation of pathogenic mechanisms.
7
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Content available

Gastric secretion and ulcer healing in mouse stomach infected with cytotoxin expressing strain of Helicobacter pylori

80%
Brzozowski T., Konturek P. C., Konturek S. J., Karczewska E., Pajdo R., Stachura J., Ghiara P., Hahn E. G.
Journal of Physiology and Pharmacology
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1998
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tom 49
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nr 3
8
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Content available

Lipopolysaccharide of Helicobacter pylori protects gastric mucosa via generation of nitric oxide

80%
Brzozowski T., Konturek P. C., Sliwowski Z., Drozdowicz D., Pajdo R., Stachura J., Hahn E. G., Konturek S. J.
Journal of Physiology and Pharmacology
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1997
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tom 48
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nr 4
9
Content available remote

Effects of melatonin and tryptophan on healing of gastric and duodenal ulcers with Helicobacter pylori infection in humans

71%
Celinski K., Konturek P. C., Konturek S. J., Slomka M., Cichoz-Lach H., Brzozowski T., Bielanski W.
Journal of Physiology and Pharmacology
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2011
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tom 62
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nr 5
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