Jerzy A. Polański
Medical University of Warsaw
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Featured researches published by Jerzy A. Polański.
PLOS Neglected Tropical Diseases | 2013
Wacław Nahorski; Józef Piotr Knap; Z. Pawlowski; Marek Krawczyk; Jerzy A. Polański; Jerzy Stefaniak; Waldemar Patkowski; Beata Szostakowska; Halina Pietkiewicz; Anna Grzeszczuk; Iwona Felczak-Korzybska; Elżbieta Gołąb; Natalia Wnukowska; Małgorzata Paul; Elżbieta Kacprzak; Elżbieta Sokolewicz-Bobrowska; Aleksandra Czyrznikowska; Lidia Chomicz; Danuta Cielecka; Przemysław Myjak
Background Alveolar echinococcosis (AE) caused by Echinococcus multilocularis infections is a dangerous old disease in the Northern Hemisphere. The aim of the paper was to collect and analyze data on human AE in Poland in the last two decades. Methodology/Principal Findings The sources of data were both the cases officially registered and detected by an active field and laboratory surveillance. The cases were verified by clinical, epidemiological, and laboratory criteria. Altogether 121 human cases of AE were detected. Among these 83 (68,6%) cases were classified as confirmed, 16 as probable and 22 as possible. During the two decades a continuous increase in detection rate was noticed. The cases were 6–82 years old at the time of diagnosis (mean - 47.7 years). Sex ratio M/F was 0.86/1.0. The AE was fatal in 23 (19%) patients (mean age at death - 54.1 years). Family agglomeration of AE was found in 4 foci, involving 9 patients. Seventy six of the cases were diagnosed in an advanced stage of disease. In all cases the liver was the primary location of AE. In 30 (24.8%) patients a spread to other organs was observed. Ninety four of the patients were treated with albendazole. In 73 (60%) patients a surgical operation was performed, including 15 liver transplantations. Conclusions/Significance The studies confirmed that AE is an emerging disease in Poland, which is the fourth country in Europe with over 120 cases detected. The results also indicate the need of a wider national programme for implementation of screening in the highest AE risk areas (north-eastern Poland) with an effort to increase the public awareness of the possibility of contracting E. multilocularis, and above all, training of the primary care physicians in the recognition of the risk of AE to allow for an early detection of this dangerous disease.
Transplantation Proceedings | 2003
Lidia Chomicz; A Szubert; P Fiedor; J Stefaniak; P Myjak; J Żbrowska; Jerzy A. Polański
The human cystic and alveolar echinococcoses are zoonotic diseases caused by larval stages of the tapeworms Echinococcus granulosus and E multilocularis. In man the liver form of the diseases develops most frequently. Recent epidemiological data indicate that the distribution of E multilocularis in the central Europe is wider than was previously anticipated; more cases of human alveococcosis during the last years have also been noted in Poland. In the present paper we analyzed several cases of human echinococcoses from Poland with respect to diagnosis and treatment as well as the indications for liver transplantation.
Comparative Hepatology | 2004
Barbara Lukomska; Joanna Dłużniewska; Jerzy A. Polański; Leszek Zajac
Liver has a remarkable ability to replace lost cell mass. Surgical resection of hepatic lobes triggers hepatocyte replication. Normally hepatocytes have a quiescent, highly differentiated phenotype and rarely divide in adult humans [1,2]. However, their capacity to replicate is readily activated after liver resection or after toxic injury. A number of studies have demonstrated the involvement of specific cytokines and growth factors in liver regeneration. The intact liver is relatively unresponsive to exogenous factors but partial hepatectomy provides some critical element that makes hepatocytes competent to fully respond to these substances [3,4]. Many growth factors play important roles in liver regeneration, most notably hepatocyte growth factor (HGF) and transforming growth factor a (TGF-alpha) [5,6]. HGF is an important multifunctional cytokine involved in liver repair after an injury. It acts as a motogen, a morphogen and a mitogen. Mesenchymal cells are responsible for the production of HGF whereas epithelial cells of various organs and tissues including the liver normally express HGF receptor cMET. In the liver HGF is produced by nonparenchymal cells especially perisinusoidal cells (PC), Kupffer cells (KC) and endothelial cells (EC). The expression of HGF mRNA during liver regeneration is also seen in mesenchymal cells in the lung and spleen and level of HGF increases in the blood after partial hepatectomy [7-9]. In contrast to HGF, which stimulates hepatocyte replication by a paracrine mechanism, TGF-alpha is an autocrine growth factor that is produced by hepatocytes and acts on these cells through binding the epidermal growth factor receptor (EGF-R) [10]. It is not known whether HGF and TGF-alpha have identical or complementary functions in hepatocyte replication. Human liver regeneration is known to be influenced by the size of resection and also by the condition of the liver. Vascular complications and ischemic injury in hepatectomized patients could result in adequate regeneration, leading to hepatic insufficiency [11]. Moreover, regeneration of human liver is influenced by coexisting liver diseases. Clinical experience has shown that resection of diseased liver sometimes results in postoperative liver failure due to limited hepatic functional reserve. While considerable interest has been focused on the tumor recurrence in liver cancer patients who underwent partial hepatectomy (PH) no data have been reported regarding the regenerating process after PH in liver tumor-bearing patients. The growth factors released by cancer cells may possibly regulate the growth of other cells in paracrine manner. The aim of the present study was initiated to determine the hepatocyte proliferation in relation to the expression of HGF and TGF-alpha in blood and liver tissue of patients with benign and malignant liver tumors after liver resection.
Diagnostic Pathology | 2012
Joanna Giebułtowicz; Małgorzata Polańska-Płachta; Piotr Wroczyński; Piotr Zaborowski; Jerzy A. Polański
BackgroundAn increasing number of publications are suggesting that galectin-3 (Gal-3) and soluble cadherin fragments, such as E-cadherin (sE-CAD) and N-cadherin (sN-CAD), may be considered as cancer markers. Despite the promising results of the studies, there are no data concerning their levels in the plasma of echinococcosis patients. In most cases, echinoccocosis affects the liver, and its symptoms and disease course are very similar to those of liver cancer. The aim of the present study was to observe whether echinococcosis affects the concentration of soluble sN-CAD, sE-CAD fragments and Gal-3 in plasma and to determine which of them could be considered reliable liver cancer markers for further research.MethodsThe concentrations of sN-CAD, sE-CAD and Gal-3 in the EDTA plasma of patients suffering from echinococcosis (N = 20), liver cancers (N = 10) and healthy subjects (N = 20) were measured using the ELISA method.ResultsThe plasma concentration of sE-CAD was lower (p = 0.0381), and that of Gal-3 higher (p = 0.0288), in echinococcosis than in the healthy group. However, only the concentration of sE-CAD differed significantly among the three analysed groups. In echinococcosis there was a correlation between the sE-CAD and CRP levels (rs = 0.79; p = 0.0066) as well as a correlation between the sE-CAD level and the number of leukocytes (rs = 0.65; p = 0.0210) in the blood.ConclusionsEchinococcosis affects the concentration of soluble sE-CAD fragments and Gal-3 in plasma. sE-CAD can be considered as a marker for differentiation between liver cancer and echinoccocossis, a parasitic liver disease similar in symptoms. Further study is required to confirm these preliminary results.Virtual SlidesThe virtual slide(s) for this article can be found here:http://www.diagnosticpathology.diagnomx.eu/vs/2115657402650448.
Phytomedicine | 2017
Agnieszka Filipek; Monika E. Czerwińska; Anna K. Kiss; Jerzy A. Polański; Marek Naruszewicz
BACKGROUND In patients with hypertension the haemorrhage into carotid atherosclerotic plaque increases risk of plaque destabilization and rupture. Our previous study showed that oleacein, a secoiridoid present in extra virgin olive oil, enhanced uptake of haemoglobin-haptoglobin complex and change macrophage phenotype from pro-inflammatory M1 to anti-inflammatory M2. PURPOSE The aim this study was to investigate a potential role of oleacein in attenuation of carotid plaque destabilisation ex vivo. METHODS Samples of atherosclerotic plaque were harvested from 20 patients with hypertension /11 women and 9 men/, who underwent carotid endarterectomy after transient ischemic attacks. Matching pieces of each plaque were incubated with increased concentration of pure oleacein /range 0-20 µM/ for 24 h. HMGB1, MMP-9, MMP-9/NGAL, TF and IL-10, as well as HO-1 secretion from plaque was measured by enzyme-linked immunosorbent assay /ELISA/. Statistical significance was set at P < 0.05 and P < 0.001. RESULTS Oleacein at the concentrations of 10 and 20 µM significantly (P < 0.001) decreased secretion of HMGB1 (up 90%), MMP-9 (up to 80%), MMP-9/NGAL complex (up to 80%) and TF (more than 90%) from the treated plaque, as compared to control. At the same time IL-10 and HO-1 release increased by more than 80% (P < 0.001). CONCLUSION Our results indicate that oleacein possess ability to attenuate the destabilization of carotid plaque and could be potentially useful in the reduction of ischemic stroke risk.
Medical Science Monitor | 2002
Joanna Dłużniewska; Dorota Zolich; Jerzy A. Polański; Leszek Zajac; Dariusz Sitkiewicz; Barbara Łukomska
Medical Science Monitor | 2003
E. Skarżyńska; B. Łukomska; J. Dłużniewska; Jerzy A. Polański; L. Zając; R. Proczka; J. Pachecka
Acta Angiologica | 2003
Robert M. Proczka; Jerzy A. Polański; Maciej Małecki; Krzysztof Wikieł
Archive | 2009
Robert M. Proczka; Joanna Chorostowska-Wynimko; Gorzata Polañska; Marta Kędzior; Jerzy A. Polański
Medical Science Monitor | 2001
Szubert A; Zajac L; Walski M; Faryna M; Biejat Z; Jerzy A. Polański