Lead and iron contents in parsley being cultivated in the area of Chrzanów geochemical anomaly

Selected research polygon is both a geochemical anomaly and suburban area (Krakow City & Upper Silesia agglomeration). The inhabitants here have detached houses with gardens of one or two acres size, where “home-made”, fresh, low-processed food could be produced. The anomaly is reflected in high values of heavy metals contents, especially cadmium, lead and zinc, in the soils of the region. This is the result of both natural and anthropogenic factors. The purpose of the paper was to evaluate lead and iron contents in roots and leaves of parsley being cultivated in Trzebinia Commune, which is located in the area. Considering , there is a positive geochemical anomaly, the lead contents in soil were low – the average value was 88.67 mg*kg-1 d.m. and only two contents – 218.98 and 119.35 exceeded 100 mg*kg-1d.m. From the other hand the lead contents in parsley roots were high, many times higher than the allowable values. The lead contents in parsley leaves were also high. Phytoaccumulation indices were low, only one had the average value, but at their minimal range (1.02 and 10.3 adequately for leaves and roots). Translocation index of lead was close to one. The iron contents in soils were not high and they fell within the scope of low and average ranges that occur in Polish soils. The iron contents in leaves were high, attractive from nutrition point of view

Cell phenotype determines PAI-1 antiproliferative effect - suppressed proliferation of the lung cancer but not prostate cancer cells

Wstęp: Inhibitor aktywatora plazminogenu typu 1 (PAI-1) jest ważnym regulatorem procesu wzrostu guza i tworzenia przerzutów nowotworowych, działając poprzez bezpośrednie hamowanie urokinazy (mechanizm antyfibrynolityczny) oraz niezależnie od kinaz poprzez powinowactwo z witronektyną. Autorzy pracy w poprzednim badaniu wykazali, że PAI-1 modyfikuje aktywność angiogenną komórek śródbłonka w stopniu zależnym od jego stężenia, jak również fenotypu komórek. Celem niniejszej pracy była ocena wpływu PAI-1 na aktywność proliferacyjną linii komórek nowotworowych - raka płuca (A549) i raka gruczołu krokowego (DU145), a także komórek strukturalnych - śródbłonka naczyniowego (HUVEC). Wyniki: Zmutowana postać PAI-1 (1, 10, 100 &#956;g/ml) charakteryzująca się znacząco przedłużoną aktywnością antyfibrynolityczną (T1/2 ~ 7000 godz.) w stopniu wyraźnie zależnym od dawki (p < 0,001) i czasu (p < 0,001) znamiennie hamowała aktywność proliferacyjną komórek raka płuca A549. Natomiast istotny wpływ PAI-1 na aktywność proliferacyjną komórek raka gruczołu krokowego DU145 wykazano tylko dla najwyższego użytego stężenia (100 &#956;g/ml) i tylko po 72 godzinach zahodowli (p < 0,001). Aktywność proliferacyjna komórek śródbłonka (HUVEC) była hamowana jedynie przez dawkę 100 &#956;g/ml PAI-1 po 24, 48 i 72 godzinach hodowli. Wniosek: Inhibitor aktywatora plazminogenu typu 1 moduluje aktywność proliferacyjną komórek w mechanizmie hamowania urokinazy w stopniu ściśle zależnym od fenotypu komórek, czasu działania i dawki. Pneumonol. Alergol. Pol. 2010; 78, 4: 279-283Introduction: Plasminogen inhibitor activator type 1 (PAI-1) is an important regulator of tumor growth and metastasis formation acting directly via specific urokinase complexing or indirectly due to its affinity to vitronectin. We have shown previously that PAI-1 modifies angiogenic activity of endothelial cells in a dose-dependent manner but also in close relationship to the cell phenotype. Present study aimed on evaluating the PAI-1 effect on the proliferative activity of lung cancer cells (A549), prostate cancer cells (DU145) as well as endothelial cells (HUVEC). Results: Mutated PAI-1 (1, 10, 100 &#956;g/mL) characterized by the prolonged antifibrinolytic activity (T1/2 ~ 7000 h) inhibited proliferation of lung cancer A549 cells in a dose-dependent (p < 0.001) and time-dependent (p < 0.001) manner. No significant effect on the DU145 prostate cancer cells has been observed except of the 72 h cultures with highest PAI-1 concentration (100 &#956;g/ml) (p < 0.001). Proliferative activity of endothelial cells (HUVEC) was affected by 100 &#956;g/ml PAI-1 only, and independent of the culture period (24, 48 and 72 h, p < 0.001). Conclusion: Plasminogen inhibitor activator type 1 modulates cell proliferation via antifibrynolitic mechanizm time- and dose-dependently, however final outcome is strongly affected by the cell phenotype. Pneumonol. Alergol. Pol. 2010; 78, 4: 279-28

Role of immune system in the pathomechanism of obstructive sleep apnea

Układ odpornościowy odgrywa znaczącą rolę w patomechanizmie zespołu obturacyjnego bezdechu sennego (OBS), współuczestniczy w procesach prowadzących do rozwoju powikłań, głównie ze strony układu sercowo-naczyniowego. Charakterystyczne dla OBS zaburzenia struktury snu i częste epizody przerywanego niedotlenienia z szybką reoksygenacją są główną przyczyną wzmożonej immunoreaktywności i rozwoju przewlekłego stanu zapalnego, zarówno systemowego, jak i miejscowego, w górnych drogach oddechowych. W pracy opisano podstawowe mechanizmy z udziałem komórek odpornościowych i mediatorów prozapalnych prowadzące do powstania tych zaburzeń.Immune system plays an essential role in the pathomechanism of obstructive sleep apnea syndrome (OSA), in the development of certain OSA complications, like the increased risk of cardiovascular diseases. Indeed, it is the sleep fragmentation and chronic intermittent hypoxia/reoxygenation, that stimulates increased immunoreactivity and chronic inflammatory response, both systemic and local in the upper airways. This review summarizes current evidence on the most important regulatory mechanisms involving immune cells and mediators

Molecular and clinical characterization of new patient with 1,08 Mb deletion in 10p15.3 region

Abstract Background Three distinct contiguous gene deletion syndromes are located at 10p chromosomal region. The deletion, involving 10p15.3 region, has been characterized by (DeScipio et al., Am J Med Genet A 158A:2152-61, 2012). However, because of the variation in size of the described deletions and lack of knowledge about the involved genes, the correlation between genotypes and patients’ phenotypes remains unknown. Case presentation We describe female patient with de novo 1,08 Mb deletion in 10p15.3 region, similar to the patient nr seven reported by (DeScipio et al., Am J Med Genet A 158A:2152-61, 2012) but with more severe clinical features. Our patient demonstrated speech and motor delay, dysmorphic features, brain abnormalities and Tetralogy of Fallot with pulmonary atresia. Conclusions This case shows the importance of collection of more patients with deletion in order to obtain a more precise physical map of 10p region

Cell Phenotype Determines PAI-1 Antiproliferative Effect—Suppressed Proliferation of the Lung Cancer but Not Prostate Cancer Cells

Introduction: Plasminogen inhibitor activator type 1 (PAI-1) is an important regulator of tumor growth and metastasis formation acting directly via specific urokinase complexing or indirectly due to its affinity to vitronectin. We have shown previously that PAI-1 modifies angiogenic activity of endothelial cells in a dose-dependent manner but also in close relationship to the cell phenotype. Present study aimed on evaluating the PAI-1 effect on the proliferative activity of lung cancer cells (A549), prostate cancer cells (DU145) as well as endothelial cells (HUVEC). Results: Mutated PAI-1 (1, 10, 100 μg/ml) characterized by the prolonged antifibrinolytic activity (T1/2~7000 h) inhibited proliferation of lung cancer A549 cells in a dose-dependent (p &lt; 0.001) and time-dependent (p &lt; 0.001) manner. No significant effect on the DU145 prostate cancer cells has been observed except of the 72 h cultures with highest PAI-1 concentration (100 μg/ml) (p &lt; 0.001). Proliferative activity of endothelial cells (HUVEC) was affected by 100 μg/ml PAI-1 only, and independent of the culture period (24, 48 and 72 h, p &lt; 0.001). Conclusion: Plasminogen inhibitor activator type 1 modulates cell proliferation via antifibrynolitic mechanizm time- and dose-dependently, however final outcome is strongly affected by the cell phenotype

Cell Phenotype Determines PAI1 Antiproliferative Effect—Suppressed Proliferation of the Lung Cancer but Not Prostate Cancer Cells

Introduction: Plasminogen inhibitor activator type 1 (PAI-1) is an important regulator of tumor growth and metastasis formation acting directly via specific urokinase complexing or indirectly due to its affinity to vitronectin. We have shown previously that PAI-1 modifies angiogenic activity of endothelial cells in a dose-dependent manner but also in close relation- ship to the cell phenotype. Present study aimed on evaluating the PAI-1 effect on the proliferative activity of lung cancer cells (A549), prostate cancer cells (DU145) as well as endothelial cells (HUVEC). Results: Mutated PAI-1 (1, 10, 100 μg/mL) characterized by the prolonged antifibrinolytic activity (T1/2 ~ 7000 h) inhibited proliferation of lung cancer A549 cells in a dose-dependent (p &lt; 0.001) and time-dependent (p &lt; 0.001) manner. No significant effect on the DU145 prostate cancer cells has been observed except of the 72 h cultures with highest PAI-1 concentration (100 μg/mL) (p &lt; 0.001). Proliferative activity of endothelial cells (HUVEC) was affected by 100 μg/mL PAI-1 only, and independent of the culture period (24, 48 and 72 h, p &lt; 0.001). Conclusion: Plasminogen inhibitor activator type 1 modulates cell proliferation via antifibrynolitic mechanizm time- and dose-dependently, however final outcome is strongly affected by the cell phenotype

Prenatal Diagnosis by Array Comparative Genomic Hybridization in Fetuses with Cardiac Abnormalities

Congenital heart defects (CHDs) appear in 8–10 out of 1000 live born newborns and are one of the most common causes of deaths. In fetuses, the congenital heart defects are found even 3–5 times more often. Currently, microarray comparative genomic hybridization (array CGH) is recommended by worldwide scientific organizations as a first-line test in the prenatal diagnosis of fetuses with sonographic abnormalities, especially cardiac defects. We present the results of the application of array CGH in 484 cases with prenatally diagnosed congenital heart diseases by fetal ultrasound scanning (256 isolated CHD and 228 CHD coexisting with other malformations). We identified pathogenic aberrations and likely pathogenic genetic loci for CHD in 165 fetuses and 9 copy number variants (CNVs) of unknown clinical significance. Prenatal array-CGH is a useful method allowing the identification of all unbalanced aberrations (number and structure) with a much higher resolution than the currently applied traditional assessment techniques karyotype. Due to this ability, we identified the etiology of heart defects in 37% of cases

Comparative Genomic Hybridization to Microarrays in Fetuses with High-Risk Prenatal Indications: Polish Experience with 7400 Pregnancies

The aim of this study was to determine the suitability of the comparative genomic hybridization to microarray (aCGH) technique for prenatal diagnosis, but also to assess the frequency of chromosomal aberrations that may lead to fetal malformations but are not included in the diagnostic report. We present the results of the aCGH in a cohort of 7400 prenatal cases, indicated for invasive testing due to ultrasound abnormalities, high-risk for serum screening, thickened nuchal translucency, family history of genetic abnormalities or congenital abnormalities, and advanced maternal age (AMA). The overall chromosomal aberration detection rate was 27.2% (2010/7400), including 71.2% (1431/2010) of numerical aberrations and 28.8% (579/2010) of structural aberrations. Additionally, the detection rate of clinically significant copy number variants (CNVs) was 6.8% (505/7400) and 0.7% (57/7400) for variants of unknown clinical significance. The detection rate of clinically significant submicroscopic CNVs was 7.9% (334/4204) for fetuses with structural anomalies, 5.4% (18/336) in AMA, 3.1% (22/713) in the group of abnormal serum screening and 6.1% (131/2147) in other indications. Using the aCGH method, it was possible to assess the frequency of pathogenic chromosomal aberrations, of likely pathogenic and of uncertain clinical significance, in the groups of cases with different indications for an invasive test