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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; · 1.37 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; · 1.37 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.
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ABSTRACT: Interaction of genotype and environment results in a specific phenotype of the clinical course of asthma. TGFβ-1 gene belongs to the important group of genes involved in the regulation of proliferation, differentiation, adhesion, and migration of a variety of cell types. TGFβ-1 is inhibitory for B and T cells, as well as IgE production. In particular, it is engaged in inflammation of the bronchi and airway remodeling in asthma, which processes are critical in the pathogenesis of the disease. The aim of this study was to evaluate the correlation between the level of expression of TGFβ-1 and the severity of asthma.
The study included 39 participants (20 healthy subjects and 19 patients with asthma). Each sample was analysed by using real time PCR.
There was statistical associations between the control group and the group of patients (p = 0,00007). It was demonstrated strong correlation between healthy and patients with severe asthma according GINA guidelines (p = 0,017). It was found the strong statistical correlation between healthy and patients with severe corticosteroid dependent asthma (p = 0,013). Correlations were observed between levels of asthma severity according to the ATS guidelines and controls. The influence of the level of TGFβ-1 mRNA expression and the severity of asthma (ATS) in the FEV1 (%) parameter value was found.
It was found that an important role is played by TGFβ-1 in the pathogenesis of asthma.
International journal of biochemistry and molecular biology. 01/2013; 4(1):67-74.
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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.
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ABSTRACT: Bronchial asthma is a disease of multifactorial etiology. The natural variability of the DNA sequence within the h-GR/NR3C1 gene affects both the conformation and the activity of glucocorticoid receptors. There are 2 major types of resistance to glucocorticoids (GCS)-resistant asthma failing to respond to treatment with high doses of inhaled and oral glucocorticoids. Type I GCS-resistant asthma is cytokine-induced or acquired. Type II GCS resistance involves generalized primary cortisol resistance, which affects all tissues and is likely to be associated with a mutation in the glucocorticoid receptor (GCR) gene or in genes that modulate GCR function. There are clear examples of glucocorticoid gene h-GR/NR3C1 polymorphisms that can influence responses and sensitivity to glucocorticosteroids. Among the numerous polymorphisms observed within this gene, N363S and I559N single nucleotide polymorphisms (SNPs) may play an important role in the development of bronchial asthma and in the alteration of sensitivity to GCS in severe bronchial asthma. The aim of this research project was to study the correlation between the N363S and I559N polymorphisms of the h-GR/NR3C1 gene and the occurrence of asthma in a population of Polish asthmatics. Peripheral blood was obtained from 210 healthy volunteers and 234 asthma patients. Structuralized anamnesis, spirometry and allergy skin prick tests were performed in all participants. Genotyping was carried out using the polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) and PCR-HRM methods. In the healthy, non-atopic population, the GG variant of the N363S polymorphism was found with a 5.7% frequency. In asthma patients, GG SNP of N363S occurred with the frequency of 6.4%. In the groups of patients with uncontrolled moderate asthma and uncontrolled severe disease, the genotype distribution for the investigated polymorphisms were as follows: N363S, AA, AG, GG occurring with 0.8750/0.0834/0.0416 frequency and I559N, TT, TA, AA occurring with 1.000/0.000/0.000 frequency. The analysis demonstrated a significantly higher frequency of the A and G variants of the N363S polymorphisms in uncontrolled moderate asthma and uncontrolled severe disease than in the healthy population. No variant-related differences in the frequency of the studied I559N polymorphism were demonstrated in healthy controls and asthma patients. In conclusion, the N363S polymorphism of the h-GR/NR3C1 gene is significantly associated with an increased sensitivity to glucococorticoids in vivo and susceptibility to the development of a moderate to severe form of uncontrolled bronchial asthma in the Polish population. This observation needs to be confirmed in a larger group of subjects.
International Journal of Molecular Medicine 04/2012; 30(1):142-50. · 1.98 Impact Factor
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ABSTRACT: N363S and ER22/23EK polymorphisms observed within glucocorticoid receptor gene (NR3C1) may play an important role in the development of bronchial asthma. NR3C1 gene is associated with an altered sensitivity to GCs. The aim of the research project was to study the correlation between this NR3C1 gene polymorphisms and occurrence of asthma in the population of Polish asthmatics. Peripheral blood was obtained from 207 healthy volunteers and 221 asthma patients. Genotyping was carried out with PCR-RFLP method. In the groups of patients with uncontrolled moderate asthma and uncontrolled severe disease, the genotype distribution for the investigated polymorphisms was as follows: N363S-AA, AG, GG occurring with 0.881/0.073/0.046 frequency and ER22/23EK-GG, GA, AA occurring with 0.963/0.037/0.000 frequency. Chi-square analysis revealed a significantly different (P < 0.05) distribution between cases and controls for the N363S polymorphisms. The N363S polymorphism of NR3C1 gene is significantly associated with bronchial asthma, susceptibility to the development of moderate to severe form of uncontrolled bronchial asthma.
Molecular Biology Reports 04/2012; 39(4):4749-57. · 2.93 Impact Factor
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ABSTRACT: The teacher's profession is regarded to be susceptible to professional burnout. Its early markers include high neuroticism and tendency to depressive reactions. The aim of the study was to assess the depression intensity and the occurrence of mood disorders in the population of full-time and extramural course students of pedagogy aged 19-30, as well as the difference in intensity of the measured constructs between men and women.
The study was carried out on the group of 223 women and 162 men aged 19-30 studying pedagogy at Piotrków Trybunalski Division of Jan Kochanowski Memorial University in Kielce in the years 2008-2011. The control group consisted of 76 women and 88 men studying economics. Students of full-time and extramural courses were included. All the participants were assessed with Beck Depression Inventory. Depression as a syndrome was diagnosed if the score of 10 of more was obtained.
Among female students of pedagogy, 21 out of 223 obtained Beck Depression Inventory scores equal to, or above 10; whereas among female students of economics 1 out of 76 obtained such a result. The relative risk of developing depression (understood as Beck Depression Inventory result of 10 or more) was found to be significantly higher among female pedagogues (OR 7.797; CI 1.0306 to 58.9856) than among female economists. Among male pedagogy students, 2 out of 162 obtained 10 points, or more. It means that the risk of depression in female pedagogues was as much as over eight-fold higher than in male pedagogues (OR 8.3168; CI 1.9215 - 35.9979). The risk of depression in men studying pedagogy was not higher than in men studying economics, who obtained the Beck Depression Inventory scores of 10 or more in 1 case out of 88 (OR 1.1; CI 0.0983 to 12.3032). Considering all pedagogues irrespectively of gender versus all economists, the risk of depression in the group of pedagogues is over five-fold higher than among economists (OR 5.1464; CI 1.1991 to 22.0885). In the whole group of women, irrespectively of the study profile, the risk of Beck Depression Inventory result equal to, or exceeding was six-fold higher than among men (OR 6.5391; CI 1.9336 to 22.1144). There was no statistically significant correlation between the Beck Depression Inventory scores obtained in the studied group and the subjects' ages. The mean scores obtained in the particular groups are presented in table. The Beck Depression Inventory scores obtained by women studying pedagogy was found to differ with statistical significance from the scores obtained by male pedagogy students (p = 0.001925), female economics students (p = 0.015781) and female economics students (p = 0.000611). The mean intensity of depression in men studying pedagogy did not differ from the mean intensity of depression in women studying economics (p = 0.94128) and in men studying economics (p = 0.330382). No differences in the mean Beck Depression Inventory scores of female and male students of economics were noted, either (p = 0.444554). The mean intensity of depression in women representing both fields of study was 6.094 +/- 3.13, vs 4.97 +/- 2.45 in men; the difference was statistically significant at the significance level of p = 0.00005. The mean intensity of depression in pedagogy students of both sexes was 5.92 +/- 3.024 vs 4.79 +/- 2.39 in students of economics; the difference was statistically significant at the significance level of p = 0,000026.
Women studying pedagogy demonstrate higher depression intensity than men studying pedagogy, as well as male and female students of economics. Students of pedagogy demonstrate higher depression intensity than students of economics. On the overall, women in the whole studied population have higher depression intensity than men; however, no such gender-related differences were observed among students of economics.
Polski merkuriusz lekarski: organ Polskiego Towarzystwa Lekarskiego 03/2012; 32(189):163-6.
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ABSTRACT: Increased activity of metalloproteinases may play a role in the initiation and propagation of inflammation in sarcoidosis, and may also be one of the factors responsible for the development of lung fibrosis. The aim of this study was to verify whether polymorphisms of MMP2 C-735T, MMP7 A-181G, MMP9 T-1702A and tissue inhibitor of metalloproteinase (TIMP)2 G-418C predispose to sarcoidosis.
The study included 139 patients with sarcoidosis and 100 healthy subjects. MMPs and TIMP2 mRNA were measured in peripheral blood lysate using real-time RT-PCR. DNA for genetic polymorphism was extracted from peripheral blood by GTC method. Protein concentrations in peripheral blood lysates were measured by ELISA, and MMP2 and 9 activities in BAL fluid were estimated by gel zymography.
TT genotype in MMP9 T-1702A was more frequent in sarcoidosis (p<0.0001, OR = 13.71, 95% CI 7.02-26.80) and resulted in higher expression of MMP9 mRNA (p<0.0001). No differences were found between TT and AT/AA patients in terms of radiological stage, lung function test parameters, activity markers and the presence/absence of Löfgren syndrome. There were no differences in the distribution of MMP2, MMP7 and TIMP2 polymorphisms. Messenger RNAs, as well as protein concentrations of MMP2, 7, 9, and TIMP2 were elevated in patients with sarcoidosis (p<0.0001 for each).
The TT homozygotes of MMP9 T-1702A genotype may be predisposed to sarcoidosis. Elevated MMP2, 7, 9, and TIMP2 mRNAs suggest their inducibility.
Medical science monitor: international medical journal of experimental and clinical research 10/2011; 17(10):CR598-607. · 1.70 Impact Factor
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ABSTRACT: Cyclooxygenase two (COX-2) is an important enzyme metabolizing arachidonic acid. In contrast to constitutive cyclooxygenase one (COX-1), COX-2 is induced by proinflammatory factors. Polymorphism -765 G/C in COX-2-encoding gene promoter is associated with development of Alzheimer's disease, depression, carcinoma of the pancreas in smokers, breast cancer and rheumatoid arthritis. It is interesting whether the -765 G/C polymorphism in COX-2-encoding gene promoter can be associated with COPD, a disease which is inflammatory in character. It is highly probable as the breast and pancreas cancers, whose associations with the analyzed polymorphism have been studied, are smoking-dependent tumors. Additionally, tobacco smoke has been demonstrated to induce COX-2 in the lungs. The study group consisted of 122 COPD patients (48 females, 74 males). The control group consisted of 149 healthy nonsmoking subjects (83 females, 66 males). Polymerase chain reaction/restriction fragment length polymorphism was used for genotyping. A statistically significant difference in genotype distribution was observed as a result of the comparison between healthy subjects and patients with COPD. The distribution of alleles in both groups conformed with Hardy-Weinberg equilibrium. In the group of COPD patients, GG allele was found in 79 subjects, GC in 36, and CC in 7 subjects (F = 0.094, P = 0.296927); in the control group, 73 subjects had GG allele, 68--GC and 8--CC (F = 0.12728, P = 0.120265). The allele frequency revealed differences between those groups, attaining the level of statistical significance (χ(2) = 29.043, df = 2, P = 0.0000. The carriers of -765 G allele are at 1.53-fold higher risk of developing COPD. The presence of GG genotype does not increase significantly the risk of the disease. It is also noteworthy that the carriers of CC or GC genotypes are at significantly lower risk of developing COPD than the group of subjects with GG genotype.
Molecular Biology Reports 06/2011; 39(3):2163-7. · 2.93 Impact Factor
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ABSTRACT: Nicotinism is the most common addiction in Poland. Nicotine dependence is the cause of numerous behavioral diseases, including ischemic heart disease, neoplasms and chronic obstructive pulmonary disease. A question arises whether a tendency to anxiety and depressive reactions, as well as the strategies of coping with stressful situations, is involved in the clinical presentation of this addiction.
The study was conducted in a group of 88 nicotine addicts without serious systemic comorbidities and in 84 healthy subjects. All the participants were assessed with Beck Depression Inventory (BDI), Spielberger State-Trait Anxiety Inventory (STAI) and the Coping Inventory for Stressful Situations (CISS).
The mean intensity of anxiety as a trait and anxiety as a state, as well as its level, were found to differ between the groups (Sten 6.28±1.52 and 4.86±1.05, p=0,0000 for the trait, and 6.09±1.25 and 4.92±1.29, p=0.0000, for the state, respectively). Similarly, depression was demonstrated to be more intensive in nicotine addicts than in healthy subjects (12.76 points ±4.77 vs. 10.76±4.83, p=0.007). Among the 5 scales assessed by CISS, smokers demonstrated higher prevalence of emotion-oriented coping than controls (standard 9 6.27±1.70 in smokers vs. 5.67±1.57, p=0.019) and involvement in distracting activities (5.84±1.48 vs. 5.28±1.46, p=0.014).
The obtained results indicate that anxiety and depression, as well as differences in coping with stress situations, distinguish nicotine addicts from non-smokers.
Medical science monitor: international medical journal of experimental and clinical research 05/2011; 17(5):CR272-6. · 1.70 Impact Factor
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ABSTRACT: It is estimated, that symptoms of obstructive sleep apnea syndrome (OSAS) affect 2 to 4% of the middle-aged population and their prevalence increases with age (over 50% people aged 65 and older suffer from OSAS). Among risk factors of OSAS we can distinguish: the male sex, race, overweight and obesity, thyroid hypofunction, age and alcohol abuse. Obstructive sleep apnea results in the absence (apnea) or reduction (hypopnea) of airflow lasting at least 10 s despite normal respiratory exertion. The apnea and hypopnea result in decreased oxygen saturation levels in the blood (hypoxemia). A number of consequences of OSAS can appear including: disruption of the sleep cycle, fragmentation of the sleep cycle, sleepiness, fatigue, headaches, cognitive impairments, irritability and mood disturbance, the higher risk of accidents at work and car accidents, the decrease of the quality of life and the higher risk of cardiovascular diseases. Besides various psychiatric and psychological complications presented in this review can occur in obstructive sleep apnea syndrome.
Pneumonologia i alergologia polska: organ Polskiego Towarzystwa Ftyzjopneumonologicznego, Polskiego Towarzystwa Alergologicznego, i Instytutu Gruzlicy i Chorob Pluc 01/2011; 79(1):26-31.
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ABSTRACT: Bcl I in the promoter polymorphism observed within h-GR/NR3C1 gene may play an important role in the development of bronchial asthma and resistance to GCs in the severe bronchial asthma. The aim of the investigation was to study the correlation between this h-GR/NR3C1 gene polymorphism and occurrence of asthma in the population of Polish asthmatics. Peripheral blood was obtained from 70 healthy volunteers and 59 asthma patients. Structuralized anamnesis, spirometry and allergy skin prick tests were performed in all participants. Genotyping was carried out with PCR-RFLP method. In healthy, non-atopic population variants of Bcl I: GG, GC, CC were found with frequency 0.129/0.471/0.400, respectively. In asthma patients Bcl I: GG, GC, CC occurred with respective frequencies of 0.410/0.462/0.128. Chi-square analysis revealed a significantly different (P<0.05) distribution between cases and controls for the Bcl I polymorphism. The Bcl I polymorphism of h-GR/NR3C1 gene is significantly associated with bronchial asthma, susceptibility to the development of severe form and resistance to GCs in Polish population.
Molecular Biology Reports 11/2010; 38(6):3953-8. · 2.93 Impact Factor
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ABSTRACT: Polymorphism of the gene encoding the glucocorticoid receptor - h-GR/NR3C1 demonstrates close genetic and biochemical correlation with etiopathogenesis of metabolic, cardiovascular, hematologic, and mental disorders. The natural variability of DNA sequence within the h-GR gene affects both the conformation and the activity of glucocorticoid receptors. Modifications of the amino acid receptor structure give rise to disturbances of the receptor-hormone complex interaction with many genes responsible for normal cellular function. Transactivation, or transrepression, of the genes encoding proteins synthesized within the framework of cellular response to glucocorticosteroids is 1 among many molecular pathways leading to the development of resistance to anti-inflammatory drugs.
A group of 70 healthy participants, with no history of asthma or atopic conditions, qualified for the study. Genotyping was accomplished using PCR-RFLP method.
In healthy, nonatopic population, within the h-GR gene promoter, a polymorphism of Bcl I: GG, GC, and CC occurring with 0.129/0.471/0.40 frequency, were identified. Two polymorphisms were identified in exon 2 at 1220 and 198 position in the h-GR gene: N363S (AA, AG occurring with 0.9/0.1 frequency) and ER22/23EK (GG, GC occurring with 0.843/0.157 frequency).
The frequency of polymorphisms occurring within the h-GR gene has not been assessed to date in the Polish population. The present study is the first attempt of such estimation. The study is an introduction to more-detailed analysis of the correlation between the occurrence of h-GR gene polymorphisms, and the development of severe, steroid-resistant bronchial asthma.
Medical science monitor: international medical journal of experimental and clinical research 10/2010; 16(10):CR475-9. · 1.70 Impact Factor
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ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a severe systemic disease leading to circulatory and respiratory failure. COPD is also a risk factor for the onset of anxiety and mood disturbances. Identification of the correlates of emotional disturbances in the course of COPD can make it possible, on the one hand, to prevent mental and behavioral disorders early in the course of this serious somatic disease, and on the other hand, to institute appropriate treatment. The aim of the study was to determine the correlation between the polymorphism of manganese superoxide dismutase signal peptide and the severity of anxiety and depression in COPD patients.
The study group consisted of 57 patients with grade I, II and III COPD according to GOLD criteria. The control group consisted of 63 healthy nicotine addicts. In all the subjects, the genotype of position 9 of manganese superoxide dismutase signal peptide was determined, depression severity was measured with Beck Depression Scale, and anxiety as a trait and as a state was measured with Spielberg State/Trait Anxiety Inventory (STAI).
Among COPT patients, 16 subjects were found to have Ala/Ala genotype, 23 Val/Ala and 18 Val/Val. In the smokers' group Ala/Ala genotype was found in 29 cases, Val/Ala in 27 and Val/Val in 7. The distribution of genotype frequencies differed between the groups. In COPD patients, the mean depression severity assessed according to Beck Scale amounted to (16.52 +/- 5.63) and was higher than in smokers without COPD (13.85 +/- 4.24, p = 0.003828). The average severity of anxiety as a trait and as a state did not differ significantly in both groups. Among COPD patients, the mean severity of depressive disorders in subjects with Val/ Val genotype was 21.27 +/- 4.32 and was significantly higher than in those with Val/Ala (15.22 +/- 5.29) and Ala/Ala (12.87 +/- 3.72) genotypes. The severity of anxiety as a trait in COPD patients reached 7.72 +/- 1.21 in the subgroup with Val/Val genotype and was also higher than in those with Val/Ala genotype (6.69 +/- 1.48) and with Ala/Ala genotype (5.87 +/- 1.14). A similar correlation was observed for anxiety as a state (subjects with Val/Val genotype 6.78 +/- 1.06, with Val/Ala genotype 6.18 +/- 1.01 and with Ala/ Ala genotype 5.88 +/- 1.41). Among healthy smokers, the mean severities of depression, anxiety as a trait and anxiety as a state did not differ in subjects with different genotypes.
The study has demonstrated that the severity of depression is higher in COPD patients than in the group of healthy smokers. In the group of patients with COPD, Val/Val genotype at position 9 of MnSOD signal peptide is associated with more severe depression, anxiety as a trait and anxiety as a state in comparison with patients who have Val/Ala and Ala/Ala genotypes. No similar correlations were found in healthy smokers.
Polski merkuriusz lekarski: organ Polskiego Towarzystwa Lekarskiego 09/2010; 29(171):165-8.
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ABSTRACT: Chronic obstructive pulmonary disease (COPD) is associated with the development of respiratory failure, which, in turn, exposes the tissues to oxidative stress, which is both a cause and a result of respiratory insufficiency. The first-line defense against oxidative stress is provided by the mitochondrial enzyme manganese superoxide dismutase (MnSOD), which is a superoxide anion scavenger. It is unknown whether genetic variability of the enzymes protecting against reactive oxygen species (ROS) can influence the development of respiratory failure in COPD patients. The aim of the study was to determine the correlation between polymorphism of MnSOD signal peptide and the occurrence of respiratory failure in the course of COPD.
The study group consisted of 162 COPD patients (113 men and 49 women). The control group consisted of 63 subjects. Respiratory failure was diagnosed in 42 COPD patients. In all the examined subjects, the polymorphism resulting in alanine at residue 9 being replaced by valine and the expression of MnSOD in blood cells were determined.
The Val/Val phenotype was demonstrated to occur in COPD patients more frequently than in the control group, as well as being associated with a lower expression level of MnSOD mRNA. Respiratory failure in the course of COPD also correlates with lower expression of MnSOD mRNA.
The presence of valine at position 9 of the MnSOD signal peptide encoded by exon 2 is a risk factor for the occurrence of respiratory failure in the course of COPD in the Polish population.
Medical science monitor: international medical journal of experimental and clinical research 09/2010; 16(9):CR427-32. · 1.70 Impact Factor
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ABSTRACT: Reactive oxygen species (ROS) may contribute to the pathogenesis of depressive disorder (DD). Functional genetic polymorphisms of manganese superoxide dismutase (MnSOD) are candidates for DD susceptibility. The study examined the relationship between MnSOD gene polymorphisms (Ala-9Val, Ile-58Thr) and DD in the Polish population. The association study was conducted in a case-control design in DD patients (n=149) and healthy controls (CG; n=149) by genotyping. Assessment of Ala-9Val genotype distribution and disease odds ratio demonstrated a statistically significant difference between the compared groups only in the female subgroup. The obtained results suggest a role of the MnSOD polymorphism in the development and course of depression.
Psychiatry Research 08/2010; 179(1):43-6. · 2.52 Impact Factor
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ABSTRACT: A possible role of antioxidants in thyreotoxicosis was investigated. We examined the parameters of lipid peroxidation (LPO): conjugated dienes (CD), malondialdehyde (MDA), Schiff bases (SB) in lung homogenates of male Wistar rats.
Two control groups were created: Group 1 - intact animals and Group 2 - animals injected with 0,9% NaCl. In Experiment I, the animals received L-thyroxin (LT4) i.p. (Groups 3-7). After one week the rats received additionally: Group 4 - melatonin (MEL); Group 5 - propylthiouracil (PTU); Group 6 - Ambroxol (AMB); Group 7 - N-acetylocysteine (NAC). In Experiment II, the animals received only antioxidants.
In Experiment I, we noticed a significantly higher MDA and SB level in Group 2, compared to that in Group 1. Moreover, we observed a significantly higher MDA and SB level in Group 3, vs. that in Group 1, but SB level was lower in Group 3 than in Group 2. Melatonin, PTU and NAC reduced CD; PTU, AMB diminished MDA and MEL, AMB lowered SB levels as compared to Group 3. In Experiment II, we observed significantly higher MDA and SB level in Group 2, vs. that in Group 1. Melatonin, AMB and NAC decreased MDA and SB level, when compared to Group 2 but PTU elevated MDA and SB level vs. that in Group 1.
1) L-T4 suppresses LPO, 2) MEL, AMB and NAC protect against LPO, 3) PTU is an antioxidant in thyreotoxicosis, however, when administered alone, it enhances LPO, 4) stress accelerate LPO.
Neuro endocrinology letters 02/2010; 31(1):137-46. · 1.30 Impact Factor
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ABSTRACT: Bronchial asthma is a disease of multi - factored etiology. Current data show that multiple genes may be involved in the pathogenesis of asthma. Corticosteroids (GCS) are the most effective anti-inflammatory therapy for inflammatory disease such as bronchial asthma. There are 2 major types of GCS-resistant asthma to treatment of high doses of inhaled and oral glucocorticoids. Type I GCS-resistant asthma is cytokine-induced or acquired. Type II GCS resistance involves generalized primary cortisol resistance, which affects all tissues and is likely associated with a mutation in the GCR gene or in genes that modulate GCR function. There are clear examples of glucocorticoid gene h-GCR/NR3C1 polymorphisms that can influence responses and sensitivity to glucocorticosteroids. This article may lead to holistic the development analysis of the factors determining the progress of the glucocorticoid resistance in the severe bronchial asthma with special acknowledgement of the influence of polymorphisms of the glucocorticoid receptor gene h-GCR/NR3C1 to formation GCS resistance.
Postepy biochemii 01/2010; 56(4):373-82.
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ABSTRACT: Obstructive disorders (asthma and chronic obstructive pulmonary disease) are associated with considerable emotional burden of the patient, with may result in the development of mood disturbances and anxiety disorders. However, the literature data are contradictory. The aim of the study was to assess the correlation between subjective and objective obstruction symptoms and the intensity of anxiety as a condition, as well as estimation of the intensity of anxiety and depression in patients suffering from obstructive syndromes.
The study enrolled 32 patients diagnosed with obstructive disorders. Structuralized anamnesis was obtained and spirometry was performed in compliance with the standards set by the Polish Society of Lungs Diseases. Disturbances of ventilation and their severity were estimated according to the GINA Report and GOLD Guidelines. All the patients were assessed using Beck Depression Inventory and Spielberg State - Trait Anxiety Inventory (STAI). The subjective dyspnoea levels were estimated with Borg scale. The study was carried out between October 2005 and September 2008 in the Specialist Outpatient Department of the Łódź Medical University Department of Pneumonology and Allergology.
A weak positive correlation was demonstrated between the declared dyspnoea level and the intensity of depression (p < 0.05) as well as the intensity of anxiety as a condition (p < 0.05) and anxiety as a trait (p < 0.05). A weak negative correlation was found to exist between FVC EX and the level of anxiety as condition (p < 0.01) and anxiety as a trait (p < 0.05). No statistically significant correlations between the values of spirometric parameters: FEV1, FEV1%, FEV1%FVC, and the levels of depression, anxiety and reported dyspnoea were found.
A positive correlation between the declared dyspnoea level and the intensity of anxiety and depression as a condition was demonstrated in the studied group of patients with obstructive disorders.
Polski merkuriusz lekarski: organ Polskiego Towarzystwa Lekarskiego 07/2009; 26(156):631-5.
