Paweł Górski

University of Lodz, Łódź, Łódź Voivodeship, Poland

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Publications (71)81.79 Total impact

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    ABSTRACT: Persistent airways obstruction (PAO) may affect some patients with severe asthma and may significantly worsen the prognosis. This study was designed to detect risk factors associated with persistent airflow limitation in nonsmoking adult patients with severe asthma. A total of 68 adults with severe asthma were recruited and followed prospectively for four to six weeks during the stable phase of disease. For all patients, at every visit spirometry with reversibility test was performed. Based on the results, patients were stratified into group 1 (reversible obstruction) or group 2 (PAO). In both cohorts, associations of postbronchodilatator forced expiratory volume in one second/forced vital capacity ratio (FEV1/FVC) with patients' age, gender, asthma duration, history of atopy and allergy, family history, medications, frequency of previous exacerbations, infections, hospitalizations, and artificial ventilation due to the asthma attack-related respiratory failure were investigated. Using a univariate logistic regression analysis, we have shown that older age, more than six exacerbations per year, artificial ventilation in the past, at least one hospitalization per year, the presence of atopic dermatitis, and exposure to domestic visible mold were all independent risk factors of PAO. Furthermore, multivariate regression analysis demonstrated that especially those with domestic exposure to visible molds, with very frequent exacerbations and with at least one hospitalization throughout the last year, were at risk for developing PAO. Domestic exposure to molds, hospitalization during the last year, and very frequent exacerbations were associated with PAO in patients with severe asthma. These factors may help in predicting fixed airflow limitation in nonsmoking patients with severe asthma.
    Allergy and Asthma Proceedings 10/2014; 35(5). · 2.19 Impact Factor
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    ABSTRACT: INTRODUCTION Sustained inflammation in sarcoidosis may lead to lung fibrosis. The activity of many chemokines responsible for proliferation and activity of T lymphocytes may play crucial role in this process, and may have predictive value. Examples are cytokines induced by interferon-γ, such as CXCL9, 10 and 11 - ligands of chemokine receptor CXCR3. OBJECTIVES The aim was to estimate the role of CXCR3 ligands in the pathogenesis of sarcoidosis and predictive value of BAL (bronchoalveolar lavage) concentrations of these cytokines. PATIENTS AND METHODS BAL CXCL9, 10 and 11 concentrations were measured in BAL fluid by ELISA, in sarcoidosis (n=59) and control (n=34) groups. 46 patients were followed-up for 24 months to compare results in a subgroup of patients with a complete remission and with chronic disease. RESULTS Standardized BAL CXCL11 concentration in stage 2 was higher than in stage 1 (0.95, 0.26-2.39 vs. 0.32, 0.13-0.74 pg/μg protein, P=0.02). CXCL10 in BAL of non-LS was higher than of LS patients (0.69, 0.51-1.05 vs. 0.40, 0.27-0.70 pg/μg protein, P=0.05). None of these markers were predictive for chronicity. BAL CXCL10 correlated with SACE and CXCL11 with HRCT parenchymal score. Only non-standardized BAL CXC11 concentration was higher in sarcoidosis. CONCLUSIONS Our results support the hypothesis, that these molecules may be involved in sustaining the sarcoid inflammation. However, the lack of consistent differences between sarcoidosis and the control group, as well as the lack of relation to the chronic course are the reasons, that these molecules should not be considered as reliable prognostic markers.
    Polskie Archiwum Medycyny Wewnetrznej. 05/2014;
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    ABSTRACT: The purpose of this study is to evaluate the relationship between the concentration of interleukin-8 (IL-8) in exhaled breath condensate (EBC) and bronchoalveolar lavage fluid (BALF) with the disease activity score and pulmonary function of systemic lupus erythematosus (SLE) patients with and without pulmonary fibrosis. Thirty-four SLE patients and 31 healthy controls were enrolled and evaluated using high-resolution computed tomography (HRCT), pulmonary function tests, systemic lupus activity measure (SLAM), assessing BALF and EBC. IL-8 levels in BALF and EBC samples were measured with an enzyme-immunosorbent assay kit. The mean (±SEM) IL-8 concentrations in BALF and EBC were higher in SLE patients compared to healthy controls (34.84 ± 95.0 vs. 7.65 ± 21.22 pg/ml, p < 0.001; 3.82 ± 0.52 pg/m vs. 1.7 ± 1.7 pg/ml, p < 0.001, respectively). SLE patients had increased percentage of neutrophils in BALF when compared with control group (1.00 ± 5.99 vs. 0.00 ± 0.56 %, p = 0.0003). Pulmonary fibrosis in HRCT was found in 50 % of SLE patients. The disease activity scored by SLAM was significantly higher and total lung capacity was significantly lower in SLE patients with pulmonary fibrosis (8.00 ± 3.17 vs. 6.00 ± 2.31, p = 0.01; 88.00 ± 28.29 vs. 112.00 ± 21.08 % predicted, p = 0.01, respectively). In SLE patients with pulmonary fibrosis, correlations were found between SLAM and IL-8 concentration in BALF, forced expiratory volume in 1 s and forced vital capacity (r = 0.65, p = 0.006; r = -0.53, p = 0.035; r = -0.67, p = 0.006, respectively). Our results indicate that IL-8 plays an important role in the pathogenesis of SLE. An increased concentration of IL-8 according to BALF could be considered as a useful biomarker of SLE activity and pulmonary fibrosis in SLE.
    Archivum Immunologiae et Therapiae Experimentalis 02/2014; · 2.38 Impact Factor
  • Pneumonologia i alergologia polska: organ Polskiego Towarzystwa Ftyzjopneumonologicznego, Polskiego Towarzystwa Alergologicznego, i Instytutu Gruzlicy i Chorob Pluc 01/2014; 82(3):194-7.
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    ABSTRACT: Pulmonary veno-occlusive disease (PVOD) is a rare cause of severe pulmonary hypertension characterised by poor prognosis. We report the case of a 24-year-old male patient with increasing dyspnea and exercise intolerance treated with calcium channel blockers and glucocorticosteroids, due to suspicion of pulmonary hypertension and interstitial lung disease, until lung biopsy was performed and a diagnosis of PVOD was established on the basis of the histological analysis of the lung biopsy sample. This case highlights that pulmonary veno-occlusive disease is a disorder that is difficult to diagnose and resistant to medical treatment, which is particularly poor prognostic factor. Due to poor response to medical therapy and high mortality in patients with PVOD, understanding the pathogenesis, differentiation with pulmonary arterial hypertension and the search for a new methods of treatment should be the key challenges for modern medicine.
    Pneumonologia i alergologia polska: organ Polskiego Towarzystwa Ftyzjopneumonologicznego, Polskiego Towarzystwa Alergologicznego, i Instytutu Gruzlicy i Chorob Pluc 01/2014; 82(3):271-5.
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    ABSTRACT: Patient: Male, 26 Final Diagnosis: Sarcoidosis Symptoms: Disseminated lung parenchymal changes Medication: - Clinical Procedure: - Specialty: Pulmonology.
    The American journal of case reports. 01/2014; 15:216-20.
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    ABSTRACT: Signal transducers and activators of transcription (STATs), their inhibitors and cyclooxygenase-2 (COX-2) participate in transformations of many various types of cancers. The aim of the present study was to evaluate the relationship between STAT5A/B, COX-2, and PIAS3 mRNA expression and tumor staging, metastasis status, and histopathological subtype in 71 patients with confirmed non-small cell lung cancer (NSCLC) diagnosis. Total RNA was isolated from NSCLC tissue samples and the expression of the studied genes was assessed using TaqMan probes in real-time PCR assay. The expression levels of STAT5A, STAT5B, and COX-2 genes were increased in 69%, 79%, and 71% NSCLC samples respectively, while PIAS3 expression was decreased in the majority (69%) of the studied tissues. Statistically significant differences were observed between STAT5 isoforms (P = 0.0008), with higher expression of STAT5B. We found statistically significant positive correlation between STAT5B and COX-2 (rho = 0.045), and significant negative correlation between STAT5B and PIAS3 (rho = -0.049). The negative correlation between STAT5B and PIAS3 (rho = -0.43) was also observed in T2a+T2b tumor group. Additionally, STAT5B and COX-2 expression levels were significantly different between T1a+T1b and T2a+T2b tumors (P = 0.002 and P = 0.041, respectively), with higher expression of both genes in T2 tumor stage. PIAS3 expression was significantly lower in NSCC subtype as compared with SCC subtype (P = 0.017). Also, STAT5A and STAT5B immunoexpression was assessed, and the results indicated significantly higher protein levels in NSCLC patients as compared with controls (P = 0.048 and P = 0.034, respectively). High STAT5B immunoexpression was positively correlated with STAT5B gene expression in tumors (rho = 0.755). STAT5B protein level was also significantly higher in T2a+T2b tumors, reflecting high STAT5B gene expression in this group. There was no statistically significant association between mRNA and protein expression levels of the studied genes and patients' characteristics: age, gender, smoking. The obtained results highlight the importance of the genes STAT5B and COX-2 in lung cancer progression.
    PLoS ONE 01/2014; 9(8):e104265. · 3.73 Impact Factor
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    ABSTRACT: Background: Both histamine H1- and H2-receptors (H2R) were found on regulatory T (Treg) cells; however, there is a paucity of information regarding the role of H2R in Treg function. This study aimed to investigate the effects of natural allergen stimulation and specific immunotherapy (SIT) on H2R expression in Treg cells in patients with allergic rhinitis (AR). Methods: In this prospective, double-blind, placebo-controlled study 41 patients with AR were screened for 1 year and treated with SIT (n = 21) or placebo (n = 20) for the next 2 years. Fifteen healthy subjects were included as a control. Subsets of Treg cells that expressed H2R were assessed annually in the blood by flow cytometry: before, at the height of the pollen season, and after, at the end of the pollen season. In addition, total nasal symptom score, the use of rescue medication, and nasal eosinophilia were evaluated. Results: Treg cells of AR patients slightly up-regulate H2R out of the pollen season. Natural allergen stimulation results in prompt up-regulation of H2R within these cells. SIT significantly decreased the number of Treg cells with increased expression of H2R in the blood exclusively at the height of pollen season, which, however, had no impact on the expression of H2R in Treg cells. SIT improved significantly the symptom score, rescue medication use, and decreased nasal eosinophilia. Conclusion: Natural pollen exposure results in up-regulation of H2R in Treg cells. Immunotherapy might transiently decrease the number of Treg-H2R+ cells in the blood, which may be associated with their migration to the peripheral tissues.This study was part of the clinical trial registered in www.clinicaltrials.gov
    American journal of rhinology & allergy 01/2014; 28(3). · 1.74 Impact Factor
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    ABSTRACT: The STAT3 gene functions as both the oncogene and the regulator of immunity. Despite its important role in cancer development and regulation of the immune cells, studies of single nucleotide polymorphisms (SNPs) of the STAT3 gene and the associated risk of lung cancer are sparse. In the present study, we evaluated the association of SNPs (rs744 166 [AG] and rs3 816 769 [CT]) with predisposition to nonsmall cell lung cancer (NSCLC) development and their potential effect on STAT3 expression. DNA and RNA, isolated from lung tissue samples, were obtained from patients with diagnosed NSCLC (n = 71) and those without NSCLC, included in a control group (n = 104). STAT3 SNP genotyping and relative expression were performed using TaqMan® probes. STAT3 CC (rs3 816 769) and AA genotypes (rs744 166) were associated with lower lung cancer risk, whereas TT (rs3 816 769) and GG genotypes (rs744 166) were found to be associated with significantly elevated lung cancer risk. In the NSCLC group, odds ratio analysis showed that allele A was rare and might be linked with decreased while allele G with increased lung cancer risk. We demonstrated that overexpression of STAT3 positively correlated with TT genotype (rs3 816 769) in NSCLC patients (P = 0.0464). Moreover, the differences in STAT3 gene expression between squamous cell carcinoma and large cell carcinoma histopathological subtypes were observed. It has been shown that rs3816769 STAT3 gene polymorphisms are associated with NSCLC susceptibility and might be regarded as having a significant functional and diagnostic value.
    Polskie archiwum medycyny wewnȩtrznej 12/2013; 123(12):672-9. · 2.05 Impact Factor
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    ABSTRACT: The role of monokine induced by interferon-γ (IFN-γ, MIG/CXCL9), IFN-γ-inducible protein (IP-10/CXCL10), and IFN-inducible T cell α chemoattractant (I-TAC/CXCL11) in allergic inflammation has not been explored in detail in vivo. The aim of the study was to examine the changes in concentrations of MIG/CXCL9, IP-10/CXCL10 and I-TAC/CXCL11 in nasal lavages collected from healthy and allergic subjects during nasal allergen challenge. Subjects allergic to grass pollen and healthy controls were included. Nasal allergen challenge preceded by placebo administration was performed outside the pollen season. Nasal lavages were collected before and 30 min after application of the placebo and 30 min after allergen administration. Concentrations of chemokines were determined using ELISA. We observed significantly higher concentrations of IP-10/CXCL10 in allergic patients compared to the healthy subjects before (354.49 ±329.24 vs. 164.62 ±175.94 pg/ml; p = 0.036), 30 min after placebo (420.3 ±421.28 vs. 246.88 ±353.24 pg/ml; p = 0.021) and 30 min after allergen administration (403.28 ±359.29 vs. 162.68 ±148.69 pg/ml; p = 0.025). IP-10/CXCL10 levels did not change 30 min after allergen provocation. In contrast, MIG/CXCL9 levels were similar in both groups before and after placebo. However, a significant rise in MIG/CXCL9 concentration was noted in allergic patients 30 min after the allergen (138.88 ±109.59 vs. 395.8 ±301.2 pg/ml; p = 0.00026). I-TAC/CXCL11 concentrations increased after placebo as well as the allergen in both groups. IP-10/CXCL10 concentrations are elevated in nasal lavages from allergic patients and this chemokine may play a role in chronic allergic inflammation. MIG/CXCL9 levels increase rapidly after allergen application, which may suggest its role in the early allergic response. Results on I-TAC/CXCL11 concentrations remain inconclusive.
    Archives of Medical Science 10/2013; 9(5):849-853. · 1.89 Impact Factor
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    ABSTRACT: In lung cancer pathogenesis, genetic instability, i.e., loss of heterozygosity (LOH) and microsatellite instability (MSI) is a frequent molecular event, occurring at an early stage of cancerogenesis. The presence of LOH/MSI in non-small cell lung carcinoma (NSCLC) was found in many chromosomal regions, but exclusive of 3p their diagnostic value remains controversial. In this study we focused on other than 3p regions-1p31.2, 7q32.2, 9p21.3, 11p15.5, 12q23.2 and 16q22-the loci of many oncogenes and tumour suppressor genes. To analyze the potential role of LOH/MSI involved in NSCLC pathogenesis we allelotyped a panel of 13 microsatellite markers in a group of 56 cancer specimens. Our data demonstrate the presence of allelic loss for all (13) analyzed markers. Total LOH/MSI frequency in NSCLC was the highest for chromosomal region 11p15.5 (25.84 %), followed by 9p21.3 and 1p31.2 (19.87 and 16.67 % respectively). A statistically significant increase of total LOH/MSI frequency was detected for the 11p15.5 region (p = 0.0301; χ(2) test). The associations of total LOH/MSI frequency: 1) increase in 11p15.5 region (p = 0.047; χ(2) test) and 2) decrease in 7q32.2 region (p = 0.037; χ(2) test) have been statistically significant in AJCC III (American Joint Committee on Cancer Staging). In Fractional Allele Loss (FAL) index analysis, the correlation with cigarette addiction has been statistically significant. The increased amount of cigarettes smoked (pack years) in a lifetime correlates with increasing FAL (p = 0.024; Kruskal-Wallis test). These results demonstrate that LOH/MSI alternation in studied chromosomal regions is strongly influenced by tobacco smoking but do not seem to be pivotal NSCLC diagnostic marker with prognostic impact. http://link.springer.com/article/10.1007%2Fs11033-013-2782-1/fulltext.html
    Molecular Biology Reports 10/2013; · 2.51 Impact Factor
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    ABSTRACT: The aim of the study was to investigate the influence of allelic imbalance (AI) in several loci of tumor suppressor genes in 3p region on the non-small cell lung cancer (NSCLC) development. We evaluated the frequency of loss of heterozygosity and/or microsatellite imbalance (LOH/MSI) and assessed their association with patients' characteristics (age, gender, tobacco addiction) and NSCLC classification according to TNM/AJCC staging. To analyze the potential role of AI involved in NSCLC pathogenesis, we allelotyped a group of 74 NSCLC patients using 7 microsatellite markers. The highest frequency of LOH/MSI, however, not statistically significant, was observed in RARβ and MLH1 (p = 0.104 and p = 0.216, respectively) loci. The association between high LOH/MSI frequency in 3p region with male gender (p = 0.041) as well as with age (especially >60 years) for RARβ and MLH1 genes (p = 0.0001 and p = 0.020, respectively) was documented. Statistically significant increased frequency of MLH1 allelic loss in squamous cell carcinoma (SCC) versus non-squamous cell carcinoma (non-SCC) was observed (p = 0.01). Significant increase in LOH/MSI frequency in 3p region (mainly in FHIT and MLH1 loci) in correlation with cigarette addiction in a lifetime (≥40 years and ≥40 Pack Years) was also documented (p < 0.05). The highest LOH/MSI was revealed in RARβ locus in IA tumors (p = 0.0001), while the similarly high allelic loss of MLH1 correlated with III A/B tumors (p = 0.0002), according to AJCC staging. The obtained results demonstrate that AI is influenced by tobacco smoking and seems to be vital in the molecular diagnosis of NSCLC, especially of SCC subtype.
    Medical Oncology 06/2013; 30(2):532. · 2.14 Impact Factor
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    ABSTRACT: INTRODUCTION Chronic Obstructive Pulmonary Disease (COPD) is most frequent chronic disease in all the world. Increasing severity of inflammatory processes in the respiratory tract is associated with exacerbation of chronic obstructive pulmonary disease. Condition closely connected with the mechanism of cachexia, is very often observed in patients with COPD exacerbations. It is responsible for changes in synthesis of adipohormones, the peptides which play an important role in immunity-related processes. OBJECTIVES The aim of ongoing research is to find more sensitive and specific laboratory markers allowing to diagnose inflammatory processes in COPD patients. PATIENTS AND METHODS The study was carried out in a group of 33 COPD patients (aged 50 - 87 years) and 17 age-matched healthy volunteers. Serum concentrations of adipohormones were measured with using Enzyme-Linked Immunosorbent Assay (ELISA) method. RESULTS In patient with COPD we observed twofold increase of leptin level in comparison with healthy controls (18.8 ± 10.2 vs. 9.06 ± 4.33 ng/ml). Concentration of resistin in patients with COPD was twofold higher than its mean concentration in the control group (8.24 ± 4.18 ng/ml vs 3.58 ± 1.51 ng/ml, respectively). A statistically significant positive correlation between CRP and leptin as well as CRP and resistin levels was observed in COPD (r = 0.75 and r = 0.83, p< 0.05; respectively). However, a statistically significant negative correlation between forced expiratory volume 1-second (FEV1) value and resistin was noted in the group of patients with COPD (r=0.62). The values of FEV1 did not correlate with leptin levels either in patients, or in healthy controls. CONCLUSIONS A significant increase of leptin and resistin levels observed in patients with chronic obstructive pulmonary disease may suggest a role of these adipohormones in the inflammatory process underlying COPD.
    Polskie archiwum medycyny wewnȩtrznej 04/2013; · 2.05 Impact Factor
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    ABSTRACT: INTRODUCTION The inflammatory process in systemic lupus erythematosus (SLE) affects many organs including the lungs. Interleukin-6 and interleukin-10 are suggested to play an important role in the pathogenesis of systemic lupus erythematosus. OBJECTIVES To evaluate the concentrations of IL-6 and IL-10 in exhaled breath condensate (EBC) and bronchoalveolar lavage fluid (BALF) of patients with and without pulmonary involvements of SLE. PATIENTS AND METHODS Thirty-four SLE patients and thirty-one healthy controls were evaluated using high-resolution computed tomography (HRCT), pulmonary function tests, the Systemic Lupus Activity Measure (SLAM), assessing IL-6 and IL-10 level in BALF and EBC (an enzyme-immunosorbent assay kit). RESULTS The mean IL-6 and IL-10 concentrations in the BALF and the IL-10 concentration in EBC were higher in SLE patients compared to healthy controls (4.03±8.3 vs 0.62±1.2 pg/mL, p<0.0001; 5.54±1.85 vs 0.00±1.82 pg/mL, p<0.0001; 8.28±2.7 vs 0.00±1.68 pg/mL, p<0.0001 respectively). The IL-10 level in EBC correlated with SLE activity (r=-0.40, p=0.019). SLAM was significantly higher and TLC (total lung capacity) was significantly lower in the SLE patients with pulmonary manifestation (8.00±3.17 vs 6.00±2.31, p=0.01; 88.00±28.29 vs 112±21.08 pred%, p=0.01 respectively). In SLE patients with pulmonary involvements, correlations were found between IL-10 level in EBC with the percentage of lymphocytes in BALF fluid (r=-0.5, p=0.04). CONCLUSIONS Our results indicate that IL-6 and IL-10 play important roles in the pathogenesis of SLE. These results suggest that IL-10 in EBC may be a useful biomarker for SLE activity. It is likely that IL-10 has a protective role against pulmonary manifestations of SLE.
    Polskie archiwum medycyny wewnȩtrznej 03/2013; · 2.05 Impact Factor
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    ABSTRACT: The clinical presentation of asthma results from complex gene-gene and gene-environment interactions. The natural variability of the DNA sequence within the NR3C1 gene affects the activity of glucocorticoid receptors (GCRs). The NR3C1 gene is localized on chromosome 5q31-q32. The gene coding for the GCR comprises nine exons. The structural domains of the GCR determine the biological functions of the functional domains. The observed resistance to glucocorticosteroids and the normal metabolic profile of Tth111I single nucleotide polymorphism (SNP) carriers is due to the ER22/23EK polymorphism that is present in them. BclI polymorphism significantly affects the process of alternative NR3C1 gene splicing and within that mechanism increases the sensitivity to glucocorticoids (GCs). A total of 451 subjects were enrolled in the present study, including 235 qualified to the group of bronchial asthma patients. A group of 216 healthy participants with no history of asthma or atopic conditions was qualified for the study. Genotyping was accomplished using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and PCR-high resolution melting (HRM) methods. No statistically significant differences were observed in the frequency of Tth111I, BclI and ER22/23EK polymorphisms of the NR3C1 gene when comparing mild, moderate and severe asthma vs. the control group. Investigative analyses demonstrated statistically significant correlations for alleles and genotypes of Tth111I polymorphism of the NR3C1 gene between healthy subjects and patients with severe asthma characterized by a control profile corresponding to an Asthma Control Test (ACT)™ score ≥20. It was established that only the Tth111I polymorphism of the NR3C1 gene plays an important role in the pathogenesis of chronic bronchitis leading to the development of asthma with both allergic and non-allergic etiology.
    Experimental and therapeutic medicine 02/2013; 5(2):572-580. · 0.34 Impact Factor
  • Pneumonologia i alergologia polska: organ Polskiego Towarzystwa Ftyzjopneumonologicznego, Polskiego Towarzystwa Alergologicznego, i Instytutu Gruzlicy i Chorob Pluc 01/2013; 81(2):162-181.
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    ABSTRACT: Cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) is a potent immunoregulatory molecule that downregulates T-cell activation and thus influences the antitumor immune response. CTLA-4 polymorphisms are associated with various cancers, and CTLA-4 mRNA/protein increased expression is found in several tumor types. However, most of the studies are based on peripheral blood mononuclear cells, and much less is known about the relationship between CTLA-4 expression, especially gene expression, and its polymorphic variants in cancer tissue. In our study we assessed the distribution of CTLA-4 two polymorphisms (+49A/G and -318C/T), using TaqMan probes (rs231775 and rs5742909, resp.), and CTLA-4 gene expression in real-time PCR assay in non-small-cell lung cancer (NSCLC) tissue samples. The increased CTLA-4 expression was observed in the majority of NSCLC patients, and it was significantly correlated with TT genotype (-318C/T) and with tumor size (T2 versus T3 + T4). The presence of G allele and GG genotype in cancer tissue (+49A/G) was significantly associated with the increased NSCLC risk. Additionally, we compared genotype distributions in the corresponding tumor and blood samples and found statistically significant differences. The shift from one genotype in the blood to another in the tumor may confirm the complexity of gene functionality in cancer tissue. http://dx.doi.org/10.1155/2013/576486
    BioMed research international. 01/2013; 2013:576486.
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    ABSTRACT: The aim of this study was to analyze the diagnostic potential of contrast enhanced ultrasound (CEUS) for the recognition of focal lesions of the spleen and liver in patients suffering from sarcoidosis. We analyzed the outcome of diagnostic imaging in a group of 21 patients treated for pulmonary sarcoidosis, searching for the systemic infiltration of the liver and/or spleen. All the participants are patients with inactive disease, who are monitored every 6 months at the Pulmonology Clinic. Apart from the check-up high-resolution computed tomography (HR-CT) - every 2 years, patients underwent an initial ultrasound examination (US) and if there was a suspicion of systemic infiltration, abdominal CT and/or magnetic resonance imaging (MRI) and CEUS were performed. In 18 patients suffering from pulmonary sarcoidosis diagnostic imaging revealed no systemic infiltration. In three patients, the use of CEUS exposed the presence of lesions in the parenchymal organs. In all cases, the images from CEUS were consistent with those from CT/MRI. CEUS has the potential to become a reliable and safe screening tool for systemic infiltration in patients with sarcoidosis. It may also be an important method of monitoring the effects of therapy.
    Pneumonologia i alergologia polska: organ Polskiego Towarzystwa Ftyzjopneumonologicznego, Polskiego Towarzystwa Alergologicznego, i Instytutu Gruzlicy i Chorob Pluc 01/2013; 81(5):424-8.
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    ABSTRACT: Oxidative stress is a non-specific feature of airway inflammation in asthmatics. 8-Isoprostane (8-IP), a prostaglandin-F(2α) isomer, is a relatively new marker of oxidative stress and may be measured in exhaled breath condensate (EBC) of patients with asthma. This research study aimed to evaluate the usefulness of EBC 8-IP as a marker of severity and control of severe adult asthma. Twenty-seven severe, never-smoking asthmatics were studied. According to positive or negative reversibility testing, this group was subdivided into reversible and irreversible asthma groups. All participants were observed for 8 weeks during which they completed daily diary observations including day and night symptoms, number of awakenings, peak expiratory flow (PEF) variability, daily rescue medication usage and oral steroids consumption. They attended the clinic 3 times and on these occasions spirometry assessments, EBC collection and asthma control tests (ACT) were done. Two control groups were included: 11 healthy never-smokers and 16 newly diagnosed and never-treated, non-smoking mild asthmatics. There were no statistically significant differences between severe asthma and healthy control or never-treated asthma groups in concentrations of EBC 8-IP (median and interquartile range: 4.67; 2.50-27.92 vs. 6.93; 2.5-12.98 vs. 3.80; 2.50-10.73, respectively). No correlations were found between EBC 8-IP and asthma control parameters, such as ACT results, night and day symptoms, consumption of rescue medication, percentage of days free of oral steroids, PEF diurnal variation, lung function test results, forced expiratory volume in the 1 s reversibility, and markers of systemic inflammation. Our study results suggest that EBC 8-IP measurements are not useful for asthma monitoring.
    Archives of medical science : AMS. 07/2012; 8(3):515-20.
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    ABSTRACT: Eicosanoids and oxidants play an important role in inflammation, but their role in chronic obstructive pulmonary disease (COPD) is uncertain. In this study we hypothesized that levels of exhaled leukotrienes, prostaglandins and biomarkers of oxidative stress are increased in infectious exacerbations of COPD and that they decrease after antibiotic therapy. Cysteinyl-leukotrienes (LTs), leukotriene B(4) (LTB(4)), prostaglandin E(4), hydrogen peroxide (H(2)O(2)) and 8-isoprostane were measured in exhaled breath condensate (EBC) in 16 COPD patients with infectious exacerbations (mean age 64 ±12 years, 13 male) on day 1, during antibiotic therapy (days 2-4), 2-4 days after therapy and at a follow-up visit when stable (21-28 days after therapy). There was a significant fall in concentration of cys-LTs, LTB(4) and 8-isoprostane at visit 3 compared to day 1 (cys-LTs: 196.5 ±38.4 pg/ml vs. 50.1 ±8.2 pg/ml, p < 0.002; LTB(4): 153.6 ±25.5 pg/ml vs. 71.9 ±11.3 pg/ml, p < 0.05; 8-isoprostane: 121.4 ±14.6 pg/ml vs. 56.1 ±5.2 pg/ml, p < 0.03, respectively). Exhaled H(2)O(2) was higher on day 1 compared to that at visits 2 and 3 (0.74 ±0.046 µM vs. 0.52 ±0.028 µM and 0.35 ±0.029 µM, p < 0.01 and p < 0.01, respectively). Exhaled PGE(2) levels did not change during exacerbations of COPD. Exhaled eicosanoids and H(2)O(2) in EBC measured at the follow-up visit (stable COPD) were significantly higher compared to those from healthy subjects. We conclude that eicosanoids and oxidants are increased in infectious exacerbations of COPD. They are also elevated in the airways of stable COPD patients compared to healthy subjects.
    Archives of medical science : AMS. 05/2012; 8(2):277-85.