The development of low-emission public urban transport in Poland

The aim of the paper is to identify the main factors and mechanisms behind the development of low-emission public transport vehicles in Polish cities. This innovation is primarily connected with growing environmental requirements for transport, with the EU environmental and transport policies being the key factors. However, strategies of local governments and municipal transport companies as well as the organization of urban transport - which differs significantly between cities - also play an important role. Three basic types of approach towards low-emission buses can be observed in Polish cities: tests of electric and hybrid vehicles, purchases of small quantities of buses in order to implement new solutions, and finally attempts to replace the majority or even the entire transport fleet with low-emission vehicles. It should be emphasised that an important element which affects the development of low emission public urban transport in Poland is the fact that the country has become one of the main bus producers in Europe - a fact which is a result of both large-scale foreign investments and the success of Polish manufacturers

Rapid decrease of CD16 (Fc\gammaRIII) expression on heat-shocked neutrophils and their recognition by macrophages

Accumulation of neutrophils in the site of inflammation is a typical mechanism of innate immunity. The accumulated neutrophils are exposed to stressogenic factors usually associated with inflammation. Here, we studied response of human peripheral blood neutrophils subjected to short, febrile-range heat stress. We show that 90 min heat stress slowed down the spontaneous apoptosis of neutrophils. In the absence of typical markers of apoptosis the heat-shocked neutrophils induced antiinflammatory effect in human monocyte-derived macrophages (hMDMs), yet without being engulfed. Importantly, the expression of Fc\gammaRIII (CD16) was sharply reduced. Surprisingly, concentration of the soluble CD16 did not change in heat-shocked neutrophil supernates indicating that the reduction of the cell surface CD16 was achieved mainly by inhibition of fresh CD16 delivery. Inhibitors of 90 kDa heat shock protein (HSP90), a molecular chaperone found in membrane platforms together with CD16 and CD11b, significantly increased the observed effects caused by heat shock. The presented data suggest a novel systemic aspect of increased temperature which relies on immediate modification by heat of a neutrophil molecular pattern. This effect precedes cell death and may be beneficial in the initial phase of inflammation providing a nonphlogistic signal to macrophages before it comes from apoptotic cells

Cepheids and Long Period Variables in M33

We are conducting a long-term photometric survey of the nearby galaxy M33 to discover Cepheids, eclipsing binaries, and long-period variables. The dataset combines previously-obtained optical images from the DIRECT project with new observations acquired at the WIYN 3.5m telescope. The entire data set spans over 7 years with excellent synoptic coverage which will enable the discovery and characterization of stars displaying variability over a wide range of timescales (days, weeks, months, years). In this preliminary work we show representative light curves of different variables we found so far in two fields, color-magnitude diagrams, and optical Cepheid Period-Luminosity relations for M33. The ultimate goal of the project is to provide an absolute calibration of the Cepheid Period-Luminosity relation, and to study its metallicity dependence at optical wavelengths.Comment: 3 pages, 6 figures. To appear in "Stellar Pulsation: Challenges for Theory and Observation", Eds. J. Guzik and P. Bradle

Mechanisms of oxidative stress in human aortic aneurysms — association with clinical risk factors for atherosclerosis and disease severity

Aortic abdominal aneurysms (AAA) are important causes of cardiovascular morbidity and mortality. Oxidative stress may link multiple mechanisms of AAA including vascular inflammation and increased metalloproteinase activity. However, the mechanisms of vascular free radical production remain unknown. Accordingly, we aimed to determine sources and molecular regulation of vascular superoxide (O2radical dot−) production in human AAA. Methods and results: AAA segments and matched non-dilated aortic samples were obtained from 40 subjects undergoing AAA repair. MDA levels (determined by HPLC/MS) were greater in plasma of AAA subjects (n = 16) than in risk factor matched controls (n = 16). Similarly, superoxide production, measured by lucigenin chemiluminescence and dihydroethidium fluorescence, was increased in aneurysmatic segments compared to non-dilated aortic specimens. NADPH oxidases and iNOS are the primary sources of O2radical dot− in AAA. Xanthine oxidase, mitochondrial oxidases and cyclooxygenase inhibition had minor or no effect. Protein kinase C inhibition had no effect on superoxide production in AAA. NADPH oxidase subunit mRNA levels for p22phox, nox2 and nox5 were significantly increased in AAAs while nox4 mRNA expression was lower. Superoxide production was higher in subjects with increased AAA repair risk Vanzetto score and was significantly associated with smoking, hypercholesterolemia and presence of CAD in AAA cohort. Basal superoxide production and NADPH oxidase activity were correlated to aneurysm size. Conclusions: Increased expression and activity of NADPH oxidases are important mechanisms underlying oxidative stress in human aortic abdominal aneurysm. Uncoupled iNOS may link oxidative stress to inflammation in AAA. Oxidative stress is related to aneurysm size and major clinical risk factors in AAA patients

Heat shock protein and heat shock factor I expression and localization in vaccinia virus infected human monocyte derived macrophages

BACKGROUND: Viruses remain one of the inducers of the stress response in the infected cells. Heat shock response induced by vaccinia virus (VV) infection was studied in vitro in human blood monocyte derived macrophages (MDMs) as blood cells usually constitute the primary site of the infection. METHODS: Human blood monocytes were cultured for 12 – 14 days. The transcripts of heat shock factor 1 (HSF1), heat shock protein 70 (HSP70), heat shock protein 90 (HSP90) and two viral genes (E3L and F17R) were assayed by reverse transcriptase-polymerase chain reaction (RT-PCR), and the corresponding proteins measured by Western blot. Heat shock factor 1 DNA binding activities were estimated by electrophoretic mobility shift assay (EMSA) and its subcellular localization analyzed by immunocytofluorescence. RESULTS: It appeared that infection with vaccinia virus leads to activation of the heat shock factor 1. Activation of HSF1 causes increased synthesis of an inducible form of the HSP70 both at the mRNA and the protein level. Although HSP90 mRNA was enhanced in vaccinia virus infected cells, the HSP90 protein content remained unchanged. At the time of maximum vaccinia virus gene expression, an inhibitory effect of the infection on the heat shock protein and the heat shock factor 1 was most pronounced. Moreover, at the early phase of the infection translocation of HSP70 and HSP90 from the cytoplasm to the nucleus of the infected cells was observed. CONCLUSION: Preferential nuclear accumulation of HSP70, the major stress-inducible chaperone protein, suggests that VV employs this particular mechanism of cytoprotection to protect the infected cell rather than to help viral replication. The results taken together with our previuos data on monocytes or MDMs infected with VV or S. aureus strongly argue that VV employs multiple cellular antiapoptotic/cytoprotective mechanisms to prolong viability and proinflammatory activity of the cells of monocytic-macrophage lineage

Przezskórna angioplastyka Y-pomostu żylnego u pacjenta z niestabilną dławicą piersiową : czy zwężenie bifurkacji Y-pomostu żylnego jest nadal wyzwaniem?

Pacjenta w wieku 71 lat po przebytej operacji pomostowania aortalno-wieńcowego przyjęto do Kliniki Kardiologii Interwencyjnej Krakowskiego Szpitala Specjalistycznego im. Jana Pawła II z powodu ostrego zespołu wieńcowego - niestabilnej dławicy piersiowej. W angiografii wieńcowej wykazano obecność istotnego zwężenia rozwidlonego żylnego pomostu wieńcowego jako ostatniego funkcjonującego naczynia. Po kwalifikacji przez lokalny zespół sercowy u pacjenta wykonano angioplastykę rozwidlonego pomostu żylnego z implantacją samorozprężalnego stentu uwalniającego sirolimus (Stentys). W opisie przypadku jest mowa o technicznych aspektach, takich jak wykorzystanie urządzeń do wspomagania funkcji lewej komory, dodatkowych metod obrazowania wieńcowego, rodzaju dostępu zabiegowego, rodzaju stentu i dystalnej protekcji naczynia. Pacjent z licznymi obciążeniami i istotnie obniżoną frakcją wyrzutową lewej komory jest raczej kandydatem do przezskórnej rewaskularyzacji niż do klasycznej operacji. Osiem miesięcy po zabiegu pacjentowi implantowano automatyczny kardiowerter-defibrylator w ramach prewencji pierwotnej nagłej śmierci sercowej w związku z objawową przewlekłą niewydolnością serca. W dyskusji omówiono problem długoterminowego efektu leczenia przezskórnego w tej grupie chorych. Rewaskularyzacja wieńcowa pacjenta z silnymi objawami ze zwężeniem ostatniego funkcjonującego naczynia wieńcowego powinna być obowiązkowa, choć liczne choroby współtowarzyszące zwiększają ryzyko zarówno operacji klasycznej, jak i przezskórnej angioplastyki. Zasadnicze pytanie brzmi: leczyć zabiegowo czy zachowawczo?A 71 year-old patient with a history of coronary artery bypass grafting was admitted to the Department of Interventional Cardiology, John Paul II Hospital, Krakow with acute coronary syndrome - unstable angina. Coronary angiography revealed significant narrowing of a bifurcated venous bypass graft as the last remaining vessel. After consultation from the Heart Team, he underwent percutaneous coronary angioplasty of the venous bypass with implantation of a selfapposing sirolimus-eluting stent (Stentys). The technical aspects of this procedure, such as the use of a left ventricle assist device, additional imaging (intravascular ultrasound), the type of approach and stent, and the protection of the vessel are discussed in this article. A patient with numerous co-morbidities and severely decreased function of the left ventricle was in fact a candidate for percutaneous revascularisation. Eight months later, the patient had a cardioverter- -defibrillator implanted in primary prevention of sudden cardiac death due to symptomatic chronic heart failure with reduced ejection fraction. This discussion raises the topic of the long-term effectiveness of angioplasty in this group of patients. Myocardial revascularisation in a patient with severe symptoms and a diseased last remaining vessel should be obligatory. However, multiple comorbidities increase the risk of cardiac surgery as well as of percutaneous angioplasty. The critical question here is: should the treatment be invasive or would the better option be optimal medical treatment

Przezskórna angioplastyka Y-pomostu żylnego u pacjenta z niestabilną dławicą piersiową. Czy zwężenie bifurkacji Y-pomostu żylnego jest nadal wyzwaniem?

71 years-old patient with history of CABG was admitted to Department of Interventional Cardiology, John Paul II Hospital, Cracow with acute coronary syndrome – unstable angina. The coronary angiography revealed significant narrowing of bifurcated venous bypass graft as the last remaining vessel. After qualification by the Heart Team he underwent percutaneous coronary angioplasty of venous bypass with implantation of self-apposing sirolimus-eluting stent (Stentys). Technical aspects of procedure such as usage of left ventricle assist device, additional imaging (IVUS), type of approach, stent and protection of vessel were considered in this manuscript. Patient with numerous co-morbidities and severely decreased function of left ventricle was rather candidate for percutaneous revascularization. 8 months later patient had implanted implantable cardioverter-defibrillator in primary prevention of sudden cardiac death due to symptomatic chronic heart failure with reduced ejection fraction. Discussion raises the topic of long-term effectiveness of angioplasty in these group of patients. Myocardial revascularization in patient with severe symptoms and diseased last remaining vessel should be obligatory, however multiple comorbidities increases the risk of cardiac surgery as well as percutaneous angioplasty. Critical question is: to treat invasively or with optimal medical treatment?Pacjenta w wieku 71 lat po przebytej operacji pomostowania aortalno-wieńcowego przyjęto do Kliniki Kardiologii Interwencyjnej Krakowskiego Szpitala Specjalistycznego im. Jana Pawła II z powodu ostrego zespołu wieńcowego — niestabilnej dławicy piersiowej. W angiografii wieńcowej wykazano obecność istotnego zwężenia rozwidlonego żylnego pomostu wieńcowego jako ostatniego funkcjonującego naczynia. Po kwalifikacji przez lokalny zespół sercowy u pacjenta wykonano angioplastykę rozwidlonego pomostu żylnego z implantacją samorozprężalnego stentu uwalniającego sirolimus (Stentys). W opisie przypadku jest mowa o technicznych aspektach, takich jak wykorzystanie urządzeń do wspomagania funkcji lewej komory, dodatkowych metod obrazowania wieńcowego, rodzaju dostępu zabiegowego, rodzaju stentu i dystalnej protekcji naczynia. Pacjent z licznymi obciążeniami i istotnie obniżoną frakcją wyrzutową lewej komory jest raczej kandydatem do przezskórnej rewaskularyzacji niż do klasycznej operacji. Osiem miesięcy po zabiegu pacjentowi implantowano automatyczny kardiowerter-defibrylator w ramach prewencji pierwotnej nagłej śmierci sercowej w związku z objawową przewlekłą niewydolnością serca. W dyskusji omówiono problem długoterminowego efektu leczenia przezskórnego w tej grupie chorych. Rewaskularyzacja wieńcowa pacjenta z silnymi objawami ze zwężeniem ostatniego funkcjonującego naczynia wieńcowego powinna być obowiązkowa, choć liczne choroby współtowarzyszące zwiększają ryzyko zarówno operacji klasycznej, jak i przezskórnej angioplastyki. Zasadnicze pytanie brzmi: leczyć zabiegowo czy zachowawczo

Clinical and electrocardiographic covariates of deceleration capacity in patients with ST-segment elevation myocardial infarction

Background: Deceleration capacity (DC) is a novel electrocardiography (ECG) parameter characterizing the overall capacity of slowing down the heart rate. The aim of this study was to evaluate clinical and ECG covariates of DC in patients with the first episode of ST-segment elevation myocardial infarction (STEMI) treated with primary angioplasty. Methods: Deceleration capacity, heart rate variability (HRV) and heart rate turbulence (HRT) were assessed from 24-hour ECG Holter recordings in 70 patients (66 male, mean age 57 years) with STEMI. Deceleration capacity was evaluated as continuous or dichotomized (£ 4.5 vs. > 4.5 ms) variable. Results: The median value of DC was 5.12 ms. Thirty patients (43%) had abnormal DC (£ 4.5 ms). The abnormal DC was more common in female, older and hypertensive patients. Although DC was not associated with either STEMI localization or left ventricular ejection fraction, it was significantly correlated with mean heart rate, standard HRV indices and HRT slope. Multivariate logistic regression showed that hypertension (OR = 3.23, 95% CI = 1.1-9.9, p = 0.039) and mean heart rate > 70 beats/minute (OR = 6.05, 95% CI = 2.0-18.4, p = 0.001) were independently associated with abnormal DC. Conclusions: Deceleration capacity in patients with the first STEMI treated with primary angioplasty is influenced by age, gender, hypertension and heart rate, but not the location of myocardial infarction or left ventricular ejection fraction. Correlation between DC and HRV indices suggests that DC is related to autonomic modulation of heart rate

Oxidized LDLs inhibit TLR-induced IL-10 production by monocytes : a new aspect of pathogen-accelerated atherosclerosis

It is widely accepted that oxidized low-density lipoproteins and local infections or endotoxins in circulation contribute to chronic inflammatory process at all stages of atherosclerosis. The hallmark cells of atherosclerotic lesions—monocytes and macrophages—are able to detect and integrate complex signals derived from lipoproteins and pathogens, and respond with a spectrum of immunoregulatory cytokines. In this study, we show strong inhibitory effect of oxLDLs on anti-inflammatory interleukin-10 production by monocytes responding to TLR2 and TLR4 ligands. In contrast, pro-inflammatory tumor necrosis factor secretion was even slightly increased, when stimulated with lipopolysaccharide from Porphyromonas gingivalis—an oral pathogen associated with atherosclerosis. The oxLDLs modulatory activity may be explained by altered recognition of pathogen-associated molecular patterns, which involves serum proteins, particularly vitronectin. We also suggest an interaction between vitronectin receptor, CD11b, and TLR2. The presented data support a novel pathway for pathogen-accelerated atherosclerosis, which relies on oxidized low-density lipoprotein-mediated modulation of anti-inflammatory response to TLR ligands. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10753-012-9472-3) contains supplementary material, which is available to authorized users