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1

Brytyjski rynek spozywczy

100%
Dembinski M.
Przemysł Spożywczy
|
2007
|
tom 61
|
nr 01
28-29
2
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Wpływ poziomów nawożenia azotowego na plony trzech odmian rzepaku ozimego w warunkach suszy w 1992 roku

63%
Walkowiak T., Dembinski M.
Postępy Nauk Rolniczych
|
1993
|
tom 40
|
nr 6
3

Eksploatacja nowego typu fundamentu traka

51%
Dembinski M., Lanczak W., Albrecht R.
Przemysł Drzewny
|
1999
|
tom 50
|
nr 11
20-23
4

Ekonomiczna ocena metod zwalczania chwastów jesienią w rzepaku ozimym na tle dwóch sposobów uprawy przedsiewnej

51%
Walkowski T., Dembinski M., Sikora B.
Rośliny Oleiste - Oilseed Crops
|
1994
|
tom 15
|
nr 2
5
Content available remote

Ghrelin accelerates the healing of oral ulcers in non-sialoadenectomized and in sialoadenectomized rats

39%
Warzecha Z., Kownacki P., Ceranowicz P., Dembinski M., Cieszkowski J., Dembinski A.
Journal of Physiology and Pharmacology
|
2013
|
tom 64
|
nr 5
6
Content available remote

Involvement of cyclooxygenase-1 and cyclooxygenase-2 activity in the therapeutic effect of ghrelin in the course of ethanol-induced gastric ulcers in rats

39%
Warzecha Z., Ceranowicz P., Dembinski M., Cieszkowski J., Ginter G., Ptak-Belowska A., Dembinski A.
Journal of Physiology and Pharmacology
|
2014
|
tom 65
|
nr 1
7
Content available remote

Role of sensory nerves in gastroprotective effect of anandamide in rats

39%
Warzecha Z., Dembinski A., Ceranowicz P., Dembinski M., Cieszkowski J., Kownacki P., Konturek P. C.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
nr 2
Previous studies have shown that stimulation of cannabinoid 1 (CB1) receptor protects the gastric mucosa against stress-induced lesion. Aim of the present study was to examine the influence of anandamide on lipid peroxidation and antioxidant defense system in gastric mucosa and the role of sensory nerves in gastroprotective effects of cannabinoids. Studies were performed on rats with intact or ablated sensory nerves (by neurotoxic doses of capsaicin). Gastric lesions were induced by water immersion and restrain stress (WRS). Anandamide was administered at the dose of 0.3, 1.5 or 3.0 µmol/kg, 30 min before exposure to WRS. CB1 receptor antagonist, AM251 (4.0 µmol/kg) was administered 40 min before WRS. WRS induced gastric lesions associated with the decrease in gastric blood flow, mucosal DNA synthesis and mucosal activity of superoxide dismutase (SOD). Serum level of interleukin-1ß (IL-1ß) and mucosal level of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) were increased. Administration of anandamide reduced the ulcers area, generation of MDA+4-HNE and serum level of IL-1ß, and this effect was associated with the reduction in the WRS-induced decrease in gastric mucosal blood flow, mucosal DNA synthesis and SOD activity. Ablation of sensory nerves increased the area of ulcers, serum level of IL-1ß and mucosal content of MDA+4-HNE, whereas mucosal DNA synthesis, SOD activity and blood flow were additionally decreased. In rats with ablation of sensory nerves, administration of anandamide at the high doses (1.5 and 3.0 µmol/kg) partly reduced deleterious effect of WRS on gastric mucosa, but this effect was weaker than in animals with intact sensory nerves. Low dose of anandamide (0.3 µmol/kg) was ineffective in the protection of gastric mucosa against the WRS-induced lesions in rats with ablation of sensory nerves. In rats with intact sensory nerves and exposed to WRS, administration of AM251 exhibited deleterious effect. In rats with ablation of sensory nerves and exposed to WRS, AM251 failed to affect mucosal injury in the stomach. We conclude that anandamide reduces the mucosal oxidative stress and exhibits gastroprotective effect against WRS-induced ulcers. These effects are partly mediated by sensory nerves.
8
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Content available

Histamine in stress ulcer prophylaxis in rats

39%
Warzecha Z., Dembinski A., Brzozowski T., Ceranowicz P., Dembinski M., Stachura J., Konturek S. J.
Journal of Physiology and Pharmacology
|
2001
|
tom 52
|
nr 3
9
Content available remote

Pretreatment with obestatin inhibits the development of cerulein-induced pancreatitis

33%
Ceranowicz P., Warzecha Z., Dembinski A., Cieszkowski J., Dembinski M., Sendur R., Kusnierz-Cabala B., Tomaszewska R., Kuwahara A., Kato I.
Journal of Physiology and Pharmacology
|
2009
|
tom 60
|
nr 3
95-101
Obestatin is a peptide derived from the proghrelin, a common prohormone for ghrelin and obestatin. Obestatin, like the ghrelin has been originally extracted from rat stomach, and the stomach seems to be a major source of circulating obestatin. Previous studies have shown that administration of ghrelin exhibits protective effect in the pancreas, inhibiting the development of acute pancreatitis. Recent study has shown that obestatin promotes survival of ß-cells and pancreatic islets. Aim of the present study was to investigate the influence of obestatin administration on the development of cerulein-induced pancreatitis. Studies were performed on male Wistar rats. Acute pancreatitis was induced by cerulein given intraperitoneally 5 times at a dose of 50 µg/kg/dose with 1-h intervals. Obestatin was injected twice intraperitoneally at the dose of 4, 8 or 16 nmol/kg/dose. In control saline-treated rats, obestatin was without effect on pancreatic morphology, serum activity of pancreatic enzymes, serum level of pro-inflammatory interleukin-1b or pancreatic cells proliferation. In animals with induction of acute pancreatitis, morphological examination showed that administration of obestatin decreased pancreatic leukocyte infiltration and vacuolization of acinar cells. These effects were accompanied by reduction in the pancreatitis-evoked increase in serum level of pancreatic digestive enzymes, lipase amylase and poly-C ribonuclease. Obestatin administered at the highest dose of 16 nmo/kg/dose reduced serum activity of these enzymes by 33, 42 and 44%, respectively. Also serum concentration of pro-inflammatory interleukin-1ß was decreased by obestatin in rats with acute pancreatitis; whereas the pancreatitis-evoked decrease in pancreatic blood flow and pancreatic DNA synthesis was partially reversed. Administration of obestatin reduces the severity of cerulein-induced acute pancreatitis. This effect is related, at least in part, to the improvement of pancreatic blood flow and reduction in pro-inflammatory interleukin-1ß release.
10
Content available remote

Protective and therapeutic effect of heparin in acute pancreatitis

33%
Ceranowicz P., Dembinski A., Warzecha Z., Dembinski M., Cieszkowski J., Rembiasz K., Konturek S. J., Kusnierz-Cabala B., Tomaszewska R., Pawlik W. W.
Journal of Physiology and Pharmacology. Supplement
|
2008
|
tom 59
|
nr 4
103-125
11
Content available remote

Pretreatment with low doses of acenocoumarol inhibits the development of acute ischemia/reperfusion-induced pancreatitis

33%
Warzecha Z., Sendur P., Ceranowicz P., Dembinski M., Cieszkowski J., Kusnierz-Cabala B., Tomaszewska R., Dembinski A.
Journal of Physiology and Pharmacology
|
2015
|
tom 66
|
nr 5
12
Content available remote

Cannabinoids in acute gastric damage and pancreatitis

33%
Dembinski A., Warzecha Z., Ceranowicz P., Dembinski M., Cieszkowski J., Pawlik W. W., Konturek S. J., Tomaszewska R., Hladki W., Konturek P. C.
Journal of Physiology and Pharmacology. Supplement
|
2006
|
tom 57
|
nr 5
137-154
Recent studies have shown that stimulation of cannabinoid 1 (CB1) receptor reduces the area of ischemic myocardial necrosis and affects activity of the digestive tract. The aim of the present study was to check whether the administration of CB1 receptor agonist or antagonist affects the stress-induced gastric ulceration and development of edematous pancreatitis. Methods: Experiments were performed on rats. Gastric lesions were induced by water immersion and restrain stress (WRS). Acute pancreatitis was induced by cerulein. Prior to WRS or before and during cerulein administration, a natural endogenous ligand for CB1 receptor, anandamide was administered intraperitoneally at the dose of 0.8, 1.5 or 3.0 µmol/kg. A synthetic CB1 receptor antagonist, AM 251 (ALEXIS® Biochemicals) was administrated at the dose of 4 µmol/kg i.p. alone or in combination with anandamide at the dose of 1.5 µmol/kg. Results: Administration of anandamide reduced gastric lesions and this effect was associated with am increase in gastric mucosal blood flow and mucosal DNA synthesis; whereas serum level of pro-inflammatory interleukin-1ß was reduced. Treatment with AM 251 aggravated gastric damage and reversed protective effect of anandamide administration. Opposite effect was observed in the pancreas. Administration of anandamide increased dose-dependently the severity of pancreatitis. In histological examination, we observed an increase in pancreatic edema and inflammatory infiltration. Also, treatment with anandamide augmented the pancreatitis-induced increase in serum level of lipase, amylase, poly-C ribonuclease, and pro-inflammatory interleukin-1ß; whereas pancreatic DNA synthesis was reduced. Treatment with AM 251 reduced histological and biochemical signs of pancreatic damage and reversed deleterious effect of anandamide in cerulein-induced acute pancreatitis. Conclusions: Activation of CB1 receptors evokes opposite effects in the stomach and pancreas: in the stomach, exhibits protective effect against stress-induced gastric mucosal lesions; whereas in the pancreas, increases the severity of cerulein-induced pancreatitis.
13
Content available remote

Heparin inhibits protective effect of ischemic preconditioning in ischemia/reperfusion-induced acute pancreatitis

33%
Warzecha Z., Dembinski A., Ceranowicz P., Dembinski M., Sendur R., Cieszkowski J., Sendur P., Tomaszewska R.
Journal of Physiology and Pharmacology
|
2012
|
tom 63
|
nr 4
14
Content available remote

Immunohistochemical expression of FGF-2, PDGF-A, VEGF and TGFbeta RII in the pancreas in the course of ischemia-reperfusion-induced acute pancreatitis

33%
Warzecha Z., Dembinski A., Ceranowicz P., Dembinski M., Kownacki P., Konturek S. J., Tomaszewska R., Stachura J., Hladki W., Pawlik W. W.
Journal of Physiology and Pharmacology
|
2004
|
tom 55
|
nr 4
Acute pancreatitis leads to pancreatic damage followed by subsequent regeneration. The aim of our study was to evaluate the presence of growth factors in the course of spontaneous pancreatic regeneration after ischemia/reperfusion (I/R)-induced pancreatitis. Methods: In rats, I/R was evoked by clamping of splenic artery for 30 min followed by reperfusion. Rats were sacrificed 1, 5, 12 h or 1, 2, 3, 5, 7, 9 or 21 days after removal of vascular clips. Pancreatic blood flow (PBF), plasma lipase, interleukin-1ßb (IL-1ß), interleukin-10, pancreatic cells proliferation and morphological signs of pancreatitis were determined. Pancreatic presence of fibroblast growth factor-2 (FGF-2), vascular endothelial growth factor (VEGF), platelet-derived growth factor-alpha (PDGF-A) and transforming growth factor-ß type II receptor (TGF-ß RII) was detected by immunohistochemisty. Results: Exposure to I/R led to the development of acute necrotizing pancreatitis followed by regeneration. Morphological features showed maximal pancreatic damage between the 1st and 2nd day of reperfusion. It was correlated with a maximal increase in plasma lipase, and pro-inflammatory IL-1ß concentration, as well as, a reduction in PBF and pancreatic DNA synthesis. I/R increased FGF-2 content in pancreatic acinar cells between the 12th and 24th h, and between 5th and 9th day of reperfusion. At the 2nd day the presence of FGF-2 in pancreatic acinar cells was reduced. After I/R PDGF-A appeared in pancreatic vessels from the 12th h to 5th day of reperfusion. PDGF-A was not observed in pancreatic acinar cells in the control or in I/R group. In pancreatic ducts, the presence of PDGF-A was reduced between the 1st and 3rd, and between 7th and 9th day of reperfusion. In acinar cells, VEGF content was increased after I/R at the time between the 1st and 24th h, and between 3rd and 7th day of reperfusion. At the 2nd day of reperfusion, VEGF was not detected in the pancreatic acinar cells. Moreover, VEGF was found in the inflammatory infiltration, in the tubular complexes between the 2nd and 5th day, and in granulation tissue at the 9th day of reperfusion. In pancreatic acinar cells, I/R caused an increase in TGFß RII presence between the 5th and 24th h, and between 7th and 9th day of reperfusion. Between the 2nd and 5th day of reperfusion the acinar presence of TGFß RII was reduced. In the pancreatic ducts, the presence of TGFß RII was increased after I/R from the 1st h to 9th day of observation. Four weeks after induction of acute pancreatitis, the pancreatic regeneration was completed and the presence of growth factors tested returned to control value. Conclusions: The presence of FGF, VEGF, PDGF-A and TGFß RII is modified in the course of I/R-induced acute pancreatitis. Maximal content of FGF, VEGF and TGFß RII has been observed in early stage of pancreatic regeneration suggesting the involvement these factors in pancreatic recovery.
15
Content available remote

Extract of grapefruit-seed reduces acute pancreatitis induced by ischemia-reperfusion in rats; possible implication of tissue antioxidants

33%
Dembinski A., Warzecha Z., Konturek S. J., Ceranowicz P., Dembinski M., Pawlik W. W., Kusnierz-Cabala B., Naskalski J. W.
Journal of Physiology and Pharmacology
|
2004
|
tom 55
|
nr 4
Grapefruit seed extract (GSE) has been shown to exert antibacterial, antifungal and antioxidant activity possibly due to the presence of naringenin, the flavonoid with cytoprotective action on the gastric mucosa. No study so far has been undertaken to determine whether this GSE is also capable of preventing acute pancreatic damage induced by ischemia/reperfusion (I/R), which is known to result from reduction of anti-oxidative capability of pancreatic tissue, and whether its possible preventive effect involves an antioxidative action of this biocomponent. In this study carried out on rats with acute hemorrhagic pancreatitis induced by 30 min partial pancreatic ischemia followed by 6 h of reperfusion, the GSE or vehicle (vegetable glycerin) was applied intragastrically in gradually increasing amounts (50-500 µl) 30 min before I/R. Pretreatment with GSE decreased the extent of pancreatitis with maximal protective effect of GSE at the dose 250 µl. GSE reduced the pancreatitis-evoked increase in serum lipase and poly-C specific ribonuclease activity, and attenuated the marked fall in pancreatic blood flow and pancreatic DNA synthesis. GSE administered alone increased significantly pancreatic tissue content of lipid peroxidation products, malondialdehyde and 4-hydroxyalkens, and when administered before I/R, GSE reduced the pancreatitis-induced lipid peroxidation. We conclude that GSE exerts protective activity against I/R-induced pancreatitis probably due to the activation of antioxidative mechanisms in the pancreas and the improvement of pancreatic blood flow.
16
Content available remote

Influence of central and peripheral administration of pancreatic polypeptide on gastric mucosa growth

33%
Dembinski A., Warzecha Z., Ceranowicz P., Pawlik M., Dembinski M., Kabat K., Konturek S. J., Kownacki P., Hladki W., Pawlik W. W.
Journal of Physiology and Pharmacology
|
2004
|
tom 55
|
nr 1,2
Previous studies have shown that pancreatic polypeptide (PP) inhibits exocrine pancreatic secretion. The aim of present study was to determine the influence of PP administration on gastric growth and blood flow. Methods: Study was performed on regularly fed, fasted or fasted and subsequently refed rats. Rats were treated with saline (intraperitoneally - i.p.), caerulein (0.24 nmol/kg/dose, i.p.), pentagastrin (0.38 µmol/kg/dose, i.p.) or PP (5 nmol/kg/dose, i.p. or 10 pmol/dose intracerebroventricularly - i.c.v.). Saline, caerulein, pentagastrin and PP were administered alone or in combination, 3 times daily during last 48 h of experiment. Results: Treatment with pentagastrin increased gastric mucosa weight, mucosal DNA synthesis and gastric blood flow in all group tested. Intraperitoneal and i.c.v administration of PP alone reduced mucosal DNA synthesis in regularly fed and refed animals, and decreased gastric blood flow in refed animals. Combination of PP i.p. or i.c.v plus pentagastrin significantly reduced the pentagastrin-evoked increase in gastric mucosa weight, gastric DNA synthesis and gastric blood flow in fasted animals, as well as regularly fed animals. In refed animals, influence of PP administration on the pentagastrin-evoked increase in gastric mucosa weight was weak and statistically insignificant, but still i.p or i.c.v administration of PP significantly reduced gastric blood flow and mucosal DNA synthesis in this group of animals. Administration of caerulein caused weak, but significant increase in gastric DNA synthesis, gastric mucosa weight and gastric blood flow in fasted rats. In regularly fed animals, caerulein significantly increased only gastric DNA synthesis and gastric blood flow. In fasted animals with subsequent refeeding, caerulein was without effect on parameters tested in the stomach. Neither i.p. nor i.c.v administration of PP affected the caerulein-evoked effects in the stomach. Conclusions: Peripheral and central administration of PP inhibits food- and pentagastrin-stimulated growth of gastric mucosa. Similar effects of low central doses of PP as the high peripheral doses of PP suggests a crucial role of the central nervous system in the inhibitory effect of PP on gastric mucosa growth.
17
Content available remote

Influence of leptin administration on the course of acute ischemic pancreatitis

33%
Warzecha Z., Dembinski A., Ceranowicz P., Jaworek J., Konturek P. C., Dembinski M., Bilski J., Konturek S. J.
Journal of Physiology and Pharmacology
|
2002
|
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.
18
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Content available

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

33%
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
19
Content available remote

Ischemic preconditioning of the hindlimb or kidney does not attenuate the severity of acute ischemia-reperfusion-induced pancreatitis in rats

33%
Warzecha Z., Dembinski A., Ceranowicz P., Cieszkowski J., Konturek S. J., Dembinski M., Kusnierz-Cabala B., Tomaszewska R., Pawlik W. W.
Journal of Physiology and Pharmacology
|
2008
|
tom 59
|
nr 2
Ischemic preconditioning of several organs, including the pancreas has been shown to protect these organs from injury evoked by subsequent exposure to severe ischemia followed by reperfusion. Moreover, it has been shown that ischemic preconditioning of distant organs such as the kidney, intestine or limb may protect the heart as effectively as cardiac preconditioning itself. This study was designed to determine whether ischemic preconditioning of the kidney or hindlimb protects the pancreas against ischemia/reperfusion-induced pancreatitis. Methods: In male Wistar rats, remote ischemic preconditioning of the pancreas was performed by clamping of right femoral or renal artery twice for 5 min with 5 min interval. Direct ischemic preconditioning was performed by clamping of celiac artery. Thirty min after ischemic preconditioning or sham-operation, acute pancreatitis was induced by clamping of inferior splenic artery for 30 min followed by reperfusion. After 6, 12 h or 1, 2, 3, 5 or 9 days of reperfusion the experiment was ended. Secretory studies were performed 2 h after exposure to direct or remote ischemic preconditioning of the pancreas in conscious rats with chronic pancreatic fistula. Results: Direct ischemic preconditioning of the pancreas applied alone reduced pancreatic exocrine secretion; whereas ischemic preconditioning of the hindlimb or kidney was without effect on pancreatic secretion. Direct ischemic preconditioning of the pancreas attenuated the severity of acute pancreatitis. It was found as a reduction in the pancreatitis-evoked increase in serum activity of lipase and amylase, a decrease in serum concentration of pro-inflammatory interleukin-1ß, diminution of histological signs of pancreatic damage, as well as, an improvement of pancreatic blood flow and DNA synthesis. Remote ischemic preconditioning of the pancreas evoked by short-lasting ischemia of the hindlimb or kidney was without any protective effect in ischemia/reperfusion-induced pancreatitis. Moreover, this procedure led to a significant increase in serum activity of lipase and amylase, and enhanced the morphological signs of pancreatic damage. Conclusion: In contrast to direct ischemic preconditioning, remote ischemic preconditioning of the pancreas is without effect on pancreatic exocrine secretion and does not reduce the severity of ischemia/reperfusion-induced pancreatitis.
20
Content available remote

Effect of ischemic preconditioning on pancreatic regeneration and pancreatic expression of vascular endothelial growth factor and platelet-derived growth factor-A in ischemia-reperfusion-induced pancreatitis

33%
Dembinski A., Warzecha Z., Ceranowicz P., Dembinski M., Cieszkowski J., Pawlik W. W., Tomaszewska R., Konturek S. J., Konturek P. C.
Journal of Physiology and Pharmacology
|
2006
|
tom 57
|
nr 1
Ischemic preconditioning has been shown to protect several organs from ischemia/reperfusion-induced injury. In the pancreas, protective effect of ischemic preconditioning has been shown against pancreatitis evoked by ischemia/reperfusion, as well as by caerulein. However, the effect of ischemic preconditioning on the course of acute pancreatic is unclear. The aim of our study was to evaluate the influence of ischemic preconditioning on pancreatic regeneration and pancreatic presence of platelet-derived growth factor-A (PDGF-A) and vascular endothelial growth factor (VEGF) in the course of ischemia/reperfusion-induced pancreatitis. Methods: In male Wistar rats, ischemic preconditioning of the pancreas was performed by short-term clamping of celiac artery (twice for 5 min with 5 min interval). Acute pancreatitis was induced by clamping of inferior splenic artery for 30 min followed by reperfusion. Rats were sacrificed 1, 5, 12 h or 1, 2, 3, 5, 7, 9 and 21 days after the start of reperfusion. Severity of acute pancreatitis and pancreatic regeneration were determined by biochemical and morphological examination, expression of growth factors was determined by immunohistochemical analysis. Results: In ischemia/reperfusion-induced pancreatitis, the pancreatic damage reached the maximal range between the first and second day of reperfusion, and was followed by subsequent pancreatic regeneration. Ischemic preconditioning alone caused mild passing pancreatic damage and an increase in plasma concentration of pro-inflammatory interleukin-1 and anti-inflammatory interleukin-10. Ischemic preconditioning applied before ischemia/reperfusion-induced pancreatitis reduced morphological and biochemical signs of the pancreatitis-evoked pancreatic damage and accelerated pancreatic regeneration. This effect was associated with improvement of pancreatic blood flow. Ischemic preconditioning, ischemia/reperfusion-induced pancreatitis and their combination increased the presence of VEGF in acinar and islet cells, and immunostaining for PDGF-A in blood vessels. This effect was maximally pronounced after combination of ischemic preconditioning plus pancreatitis and occurred earlier than after pancreatitis alone. Conclusions: Ischemic preconditioning reduces pancreatic damage and accelerates pancreatic healing in the course of ischemia/reperfusion-induced pancreatitis. This effect is associated with the increase in plasma concentration of anti-inflammatory interleukin-10, improvement of pancreatic blood flow and alteration of pancreatic immunohistochemical expression of PDGF-A and VEGF.
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