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  1. 16 Journal of Physiology and Pharmacology

  2. 7 Journal of Physiology and Pharmacology. Supplement

  3. 5 Folia Morphologica

  4. 3 Folia Histochemica et Cytobiologica

  5. 3 Weterynaria po Dyplomie

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  1. 17 Dembinski A.

  2. 17 Warzecha Z.

  3. 16 Ceranowicz P.

  4. 16 Konturek S. J.

  5. 10 Stachura J.

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  1. 1 2019

  2. 1 2018

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1

Ultrastructural study of hepatocytes in the experimental model of acute pancreatitis

100%
Romanowska-Sarlej J., Kifer-Wysocka E., Krolikowska-Prasal I., Jodlowska-Jedrych B., Matysiak W.
Folia Histochemica et Cytobiologica
|
1999
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tom 37
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nr 2
2

Evaluation of histopathological changes of the pancreatic tissue in the course of acute experimental pancreatitis

100%
Anasiewicz A., Madej B., Maciejewski R., Miroslaw C., Draus J., Lakowska H., Radzikowska E.
Folia Morphologica
|
1996
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tom 55
|
nr 4
3

Kinetic properties of AMP deaminase in acute experimental pancreatitis

100%
Kossowska E., Purzycka-Preis J., Wozniak M., Zydowo M., Sledzinski Z.
Acta Biochimica Polonica
|
1994
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tom 41
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nr 2
4

Changes of amylase levels in the acute experimental pancreatitis treated with fibrolan

88%
Madej B., Anasiewicz A., Maciejewski R.
Folia Morphologica
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1996
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tom 55
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nr 4
5

The histological chenges of the pancreatic tissue during the course of acute experimental pancreatitis treated with fibrolan

75%
Madej B., Anasiewicz A., Maciejewski R.
Folia Morphologica
|
1996
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tom 55
|
nr 4
6

The role of phospholipases A2 in the pathophysiology of acute pancreatitis. A review

75%
Hietaranta A. J., Kemppainen E. A., Gronroos J. M., Nevalainen T. J.
Journal of Physiology and Pharmacology. Supplement
|
1998
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tom 49
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nr 2
7
Content available remote

Ghrelin attenuates the development of acute pancreatitis in rats

75%
Dembinski A., Warzecha Z., Ceranowicz P., Tomaszewska R., Stachura J., Konturek S. J., Konturek P. C.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
nr 4
Ghrelin, a circulating growth hormone-releasing peptide isolated from human and rat stomach, stimulates growth hormone secretion, food intake and exhibits gastroprotective properties. Ghrelin is predominantly produced by a population of endocrine cells in the gastric mucosa, but its presence in bowel, pancreas, pituitary and hypothalamus has been reported. In human fetal pancreas, ghrelin is expressed in a prominent endocrine cell population. In adult pancreatic islets the population of these cell is reduced. The aim of present study was to investigate the influence of ghrelin administration on the development of acute pancreatitis. Methods: Acute pancreatitis was induced in rat by caerulein injection. Ghrelin was administrated twice (30 min prior to the first caerulein or saline injection and 3 h later) at the doses: 2, 10 or 20 nmol/kg. Immediately after cessation of caerulein or saline injections the following parameters were measured: pancreatic blood flow, plasma lipase activity, plasma interleukin-1ß (IL-1ß) and interleukin 10 (IL-10) concentration, pancreatic DNA synthesis, and morphological signs of pancreatitis. Results: Administration of ghrelin without induction of pancreatitis did not affect significantly any parameter tested. Caerulein led to the development of acute edematous pancreatitis. Treatment with ghrelin at the dose 2 nmol/kg, during induction of pancreatitis, was without effect on pancreatic histology or biochemical and functional parameters. Treatment with ghrelin at the dose 10 and 20 nmol/kg attenuated the development of pancreatitis and the effects of both doses were similar. Administration of ghrelin (10 or 20 nmol/kg) reduced inflammatory infiltration of pancreatic tissue and vacuolization of acinar cells. Also, plasma lipase activity and plasma IL-1ß concentration were reduced, and caerulein-induced fall in pancreatic DNA synthesis was reversed. Administration of ghrelin at the dose 10 and 20 nmol/kg was without effect on caerulein-induced pancreatic edema and pancreatitis-related fall in pancreatic blood flow. Conclusions: (1) Administration of ghrelin attenuates pancreatic damage in caerulein-induced pancreatitis; (2) Protective effect of ghrelin administration seems to be related the inhibition in inflammatory process and the reduction in liberation of pro-inflammatory IL-1ß.
8

Elastase activity and histological changes in lungs and in pancreas due to experimental pancreatitis

75%
Maciejewski R., Madej B., Draus J., Jedrzejewska E., Juskiewicz W.
Folia Histochemica et Cytobiologica
|
1999
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tom 37
|
nr 2
9
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Content available

Platelet activating factor [PAF] inhibitor [TCV-309] reduces caerulein - and PAF-induced pancreatitis. A morphologic and functional study in the rat

75%
Tomaszewska R., Dembinski A., Warzecha Z., Banas M., Konturek S. J., Stachura J.
Journal of Physiology and Pharmacology
|
1992
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tom 43
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nr 4
Caerulein-induced acute pancreatitis was studied in rats. Consistent with this type of acute pancreatitis morphological (edema, leukocytic infiltration and acinar cell vaculization) and biochemical (increase in pancreatic protein content, PAF release and serum amylase) changes developed 5 hours after caerulein administration. In addition increase in pancreatic weight and decrease in pancreatic blood flow were noticed. PAF administration caused pancreatic damage similar in some parameters to caerulein-induced pancreatitis, along with reduction of pancreatic blood flow, increase in pancreatic protein content, and serum amylase. TCV-309, a selective PAF antagonist, administered prior to caerulein and/or PAF, reduced caerulein-induced pancreatitis and prevented PAF-induced pancreatitis. Results of our present studies indicate the crucial role of PAF in pathogenesis of experimental acute pancreatitis.
10
Content available remote

IGF-1 stimulates production of interleukin-10 and inhibits development of caerulein-induced pancreatitis

75%
Warzecha Z., Dembinski A., Ceranowicz P., Konturek S. J., Tomaszewska R., Stachura J., Konturek P. C.
Journal of Physiology and Pharmacology
|
2003
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tom 54
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nr 4
Insulin-like growth factor-1 (IGF-1) and other growth factors overexpression was reported in acute pancreatitis. Previous studies have shown the protective effect of epidermal growth factor (EGF), Hepatocyte Growth Factor (HGF) and Fibroblast Growth Factor (FGF) in the course of experimental acute pancreatitis. The aim of our studies was to determine the effect of IGF-1 administration on the development of caerulein-induced pancreatitis. Methods: Acute pancreatitis was induced by infusion of caerulein (10 µg/kg/h) for 5 h. IGF-1 was administrated twice at the doses: 2, 10, 50, or 100 µg/kg s.c. Results: Administration of IGF-1 without induction of pancreatitis increased plasma interleukin-10 (IL-10). Infusion of caerulein led to development of acute edematous pancreatitis. Histological examination showed pancreatic edema, leukocyte infiltration and vacuolization of acinar cells. Also, acute pancreatitis led to an increase in plasma lipase and interleukin 1ß (IL-1ß) level, whereas pancreatic DNA synthesis and pancreatic blood flow were decreased. Treatment with IGF-1, during induction of pancreatitis, increased plasma IL-10 and attenuated the pancreatic damage, what was manifested by histological improvement of pancreatic integrity, the partial reversion of the drop in pancreatic DNA synthesis and pancreatic blood flow, and the reduction in pancreatitis-evoked increase in plasma amylase, lipase and IL-1ß level. Protective effect of IGF-1 administration was dose-dependent. Similar strong protective effect was observed after IGF-1 at the dose 2 x 50 and 2 x 100 µg/kg. Conclusions: (1) Administration of IGF-1 attenuates pancreatic damage in caerulein-induced pancreatitis; (2) This effect is related, at least in part, to the increase in IL-10 production, the reduction in liberation of IL-1ß and the improvement of pancreatic blood flow.
11

The secretory compartment of exocrine pancreas in taurocholate pancreatitis in rats. Ultrastructural and biochemical aspects

75%
Andrzejewska A., Dlugosz J., Szynaka B.
Folia Histochemica et Cytobiologica. Supplement
|
1996
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tom 34
|
nr 1
12
Content available remote

Pancreas; pancreatitis - Polish accomplishments

63%
Dzieniszewski J., Gabryelewicz A.
Journal of Physiology and Pharmacology. Supplement
|
2003
|
tom 54
|
nr 3
155-166
Polish accomplishments in clinical and experimental pancreatology concern acute (AP) and chronic (CP) pancreatitis. Special notice was drawn in Polish studies on hemostasis disorders in acute experimental pancreatitis (AEP), and resulting clinical implications (possibility of thrombotic-embolic complications leading to hemorrhagic defects associated with coagulation factors consumption). Studies on lysosomal hydrolases role in AEP pathogenesis were discussed. In those studies notice was drawn to initiating role of zymogen activation by lysosomal hydrolases, especially ß-glucuronidase, with smaller activity of acid phosphatase and cathepsin in this process. It was stated, that also lysosomal enzymes are released from macrophages obtained from bronchoalveolar lavage fluid in AEP. It was revealed that prostacyclin (PGI2) shows stabilizing effect on lysosomes in liver and kidneys in AEP. Platelets activating factor antagonist inhibits pulmonary lysosomal hydrolases activity in such conditions. Polish studies concerning reactive forms of oxygen role in AEP pathogenesis are one of the first in Europe. Oxidative-antioxidative balance was disturbed in acute pancreatitis course and associated multiorgan changes both under experimental conditions and in humans. Oxidative stress as an early prognostic symptom in AP in humans was also emphasized, showing correlation of oxidative stress indicators with phospholipase A serum activity and polymorphonuclear elastase in plasma of patients with different degree of this disease. In a range of clinical studies special attention should be given to studies concerning lipid disorders as an AP etiological factor in humans. Clear decrease in lipoprotein lipase activity in AP in humans was determined. Polish studies concerning importance of sphincterectomy in acute gallstone derivative pancreatitis (AGP) were presented. Polish researchers accomplishments in chronic alcoholic pancreatitis (CAP) etiopathogenesis were discussed.
13
Content available remote

Exocrine pancreas; molecular basis for intracellular signaling, damage and protection - Polish experience

63%
Dabrowski A.
Journal of Physiology and Pharmacology. Supplement
|
2003
|
tom 54
|
nr 3
167-181
Polish experience in molecular pancreatology mostly involves experimental work on intracellular signal transduction mechanisms in pancreatic acinar cells. It was found that stimulation with cholecystokinin (CCK) or exposure of pancreatic acini to reactive oxygen species induces three separate signaling cascades leading to activation of ERKs, JNK/SAPKs and p38 MAPK. In pancreatic acini, ERK cascade is also activated by epidermal growth factor (EGF). However, CCK and EGF activate this cascade by different mechanisms. EGF activates the cascade in a classical Ras-dependent manner, while CCK-induced activation of the ERK cascade is Ras-independent. Furthermore, stimulation with CCK leads to a rapid activation of PKC, which in turn may directly activate Raf family of kinases. Freshly isolated pancreatic acini contain pancreatic stellate cells which respond to EGF by activation of ERK cascade. It is possible that stimulation with CCK and EGF induces a cross-talk between acinar and stellate cells. Isolated pancreatic acinar cells irradiated with UV-B die predominantly by apoptosis while necrosis predominates among the cells subjected to supraphysiological concentrations of CCK. In pancreatic acini subjected to stressful stimuli the regulation of apoptosis may involve interaction between ERK and p38 MAPK signaling pathways. Acute pancreatitis in rats and in humans is associated with a marked increase in the plasma level of leptin which is caused by increased production of this peptide in the inflamed pancreas. It is possible that exogenous leptin protects the pancreas against development of acute pancreatitis by the activation of nitric oxide pathway.
14

Stimulation of sensory nerves and CGRP administration attenuates development pancreatitis evoked by ischemia-reperfusion

63%
Warzecha Z., Dembinski A., Ceranowicz P., Sendur R., Pawlik W. W., Konturek S. J.
Journal of Physiology and Pharmacology. Supplement
|
2001
|
tom 52
|
nr 2
15

Microcirculatory disturbances in caerulein-induced acute pancreatitis in rats with reference to nitric oxide, heparin and procaine treatment

63%
Dobosz M., Hac S., Wajda Z., Rzepko R., Roszkiewicz A., Zawrocka-Wrzolek T.
Journal of Physiology and Pharmacology. Supplement
|
1998
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tom 49
|
nr 2
16

The morphology of acinar cells during acute pancreatitis in rats induced by intraductal infusion of peracetate

63%
Jankowski K., Kubasik-Juraniec J., Sledzinski Z., Spodnik J. H., Wozniak M.
Folia Morphologica
|
2004
|
tom 63
|
nr 2
Many experimental models have been created to explain the pathophysiology of acute pancreatitis (AP). Investigations have been undertaken in this laboratory into the influence of strong oxidants introduced into the pancreas retrogradely through the bile-pancreatic duct. In these experiments a potentially toxic metabolite of ethanol-peracetic acid was used to induce AP. Wistar rats were treated with 1 mM and 40 mM peracetate and with a solvent as a control for 1 and 3 hours respectively. After a period of observation the samples of pancreata were examined in a light and electron microscope together with the content of sulphydryl groups as a marker of intracellular oxidative stress. The morphological examination showed profound changes in the histology of the pancreas and also in its subcellular structures, especially in groups 3 and 4 (with a higher concentration of peracetate). The changes included parenchymal haemorrhage and widespread acinar cell necrosis. The level of the sulphydryl groups decreased in the rats treated with peracetate. This suggests that the severity of the disease strongly depends on the intensity of the oxidative stress. The results confirmed the axial role of oxygen-derived free radicals in the pathogenesis of AP.
17

Influence of sensory nerves and CGRP on the course of experimental pancreatitis and pancreatic regeneration

63%
Dembinski A., Warzecha Z., Ceranowicz P., Stachura J., Konturek S. J.
Journal of Physiology and Pharmacology. Supplement
|
2001
|
tom 52
|
nr 2
18
Content available remote

The influence of epidermal growth factor on the course of ischemia-reperfusion induced pancreatitis in rats

63%
Tomaszewska R., Dembinski A., Warzecha Z., Ceranowicz P., Konturek S. J., Stachura J.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 2
Acute pancreatitis is accompanied by the enhanced expression of EGF in the pancreas and the administration of EGF was found to exhibit the beneficial effect on edematous cerulein-induced pancreatitis. Therefore, we decided to determine the influence of EGF on necro-hemorrhagic pancreatitis induced by ischemia and reperfusion (I/R). Acute pancreatitis was induced in rats by restricting the pancreatic blood flow (PBF) in the inferior splenic artery for 30 min using microvascular clips. EGF was administered three times daily (10µg/kg per dose s.c.) starting immediately after the clips removal. Rats were sacrificed on day 1, 3, 5, 10 and 21 following ischemia. PBF was measured using a laser Doppler flowmeter. Morphological signs of pancreatitis, as well as the levels of plasma amylase, lipase, interleukin-1ß and interleukin-10 concentration and pancreatic cell proliferation were examined. Results: Ischemia with reperfusion caused acute necro-hemorrhagic pancreatitis with a histological and biochemical manifestation of pancreatic damage, followed by a spontaneous regeneration. The administration of EGF caused the reduction in the histological signs of pancreatic damage, such as necrosis, edema and leukocyte infiltration, and accelerated the pancreatic repair. Also, EGF treatment significantly attenuated the reduction in pancreatic blood flow and DNA synthesis. The activity of plasma amylase and lipase, as well as plasma interleukin-1ß and interleukin-10 concentrations were decreased in EGF treated animals. Conclusions: EGF exerts beneficial influence on the course of I/R induced pancreatitis and this effect seems to be related to the reduction in the activation of pro-inflammatory interleukin cascade, the improvement of PBF, and the increase in pancreatic cell growth.
19
Content available remote

Influence of leptin administration on the course of acute ischemic pancreatitis

63%
Warzecha Z., Dembinski A., Ceranowicz P., Jaworek J., Konturek P. C., Dembinski M., Bilski J., Konturek S. J.
Journal of Physiology and Pharmacology
|
2002
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tom 53
|
nr 4,2
Leptin is involved in the regulation of food intake and previous studies have shown that leptin affects the inflammatory response in various tissues. The objective of this study was to examine the influence of leptin administration on the development and the course of acute ischemic pancreatitis. Acute pancreatitis was induced by limitation of pancreatic blood flow by clamping of inferior splenic artery for 30 min, followed by reperfusion. Leptin was administered three times daily at the dose 10 or 50 µg/kg. Animals were sacrificed 1, 3, 5, 10 and 21 days after removal of vascular clips. Administration of leptin reduced development of pancreatic damage and accelerated pancreatic regeneration what was manifested by the improvement of pancreatic histology, the decrease in serum lipase and amylase activity, and the reduction in serum interleukin-1ß concentration. Also, treatment with leptin caused the increase in the pancreatic blood flow and pancreatic DNA synthesis. Leptin administration was without effect on serum interleukin-10 concentration. Leptin at the dose 50 µg/kg was more effective than 10 µg/kg. We conclude that leptin reduces the pancreatic damage in the course of ischemic pancreatitis and accelerates the pancreatic tissue repair. The beneficial effects of leptin appear to be dependent on the improvement of pancreatic blood flow, the increase in pancreatic cell growth, and the limitation of pro-inflammatory interleukin-1ß release.
20
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Content available

Pancreatic damage and regeneration in the course of ischemia-reperfusion induced pancreatitis in rats

63%
Dembinski A., Warzecha Z., Ceranowicz P., Stachura J., Tomaszewska R., Konturek S. J., Sendur R., Dembinski M., Pawlik W. W.
Journal of Physiology and Pharmacology
|
2001
|
tom 52
|
nr 2
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