Where trees cannot grow - Particulate matter accumulation by urban meadows.

It has already been proven that trees and shrubs, can efficiently remove particulate matter (PM) from air. However, almost nothing is known about PM accumulation by herbaceous plants (grasses and forbs) found in urban meadows. Meadows, unlike trees and shrubs, can be located close to roads, one of the main sources of PM in cites. The aim of this study was to investigate the tolerance to urban condition and PM accumulation in the immediate roads vicinity of selected plants species in urban meadows. PM accumulation of annual and perennial meadows was compared with that of lawns. Results were interpreted in the context of species composition, biomass production, soil conditions and ambient PM concentrations. Of the species grown in annual meadows, the highest PM accumulation was found in Achillea millefolium L., Chenopodium album L. and Echium vulgare L., while Centaurea scabiosa L., Echium vulgare L. and Convolvulus arvensis L. accumulated the largest amounts of PM in perennial meadows. PM deposition on plants was positively correlated with a feathery leaf shape. For species in the annual meadows, a positive correlation was also found between PM accumulation and the wax content on plants. The presence of hairs on leaves, leaf size and plant growth pattern had no effect on PM deposition on plants. PM accumulation in one square metre of urban meadow was on average greater than that of lawn, regardless of meadow species' composition, age and location. The greatest accumulation of PM was found in a perennial meadow with low biodiversity but the greatest biomass. It would appear that the biomass produced by meadows and canopy structure has a crucial impact on the amount of PM accumulated by meadow plants. The results obtained indicate that meadows could be an important element of nature-based solutions for mitigating air pollution in urbanised areas.

Urban wastelands: On the frontline between air pollution sources and residential areas.

In urban areas, particulate matter (PM) represents an increasing threat to human health. The ability of plants in parks and along roads in cities to accumulate PM has already been demonstrated, but nothing is known about the effect of wasteland vegetation on air quality, despite a significant proportion of greenery in polluted areas being on wastelands. The aim of this study was to document the accumulation of PM and trace elements (TE) by wasteland species (Robinia pseudoacacia L., Populus × canescens (Aiton) Sm., Acer negundo L., Solidago gigantea (Aiton) and Poaceae) growing on Central European urban wastelands with differing levels of air pollution. On average, the largest amounts of PM accumulated on the foliage of R. pseudoacacia and S. gigantea, and the smallest amounts accumulated on P. × canescens leaves. However, accumulation of PM depended more on the distance from the emission source than on species selection, and was higher on the polluted wasteland where the plants' gas exchange was the lowest. The results also suggest that in order to effectively accumulate PM from the air, it is critical to have the correct configuration of plants, with the wasteland vegetation having a layered structure and layers differing in PM retention, as shown in this study using the examples of R. pseudoacacia (a tall tree with low PM retention) and S. gigantea (below-tree vegetation with high PM retention). P. × canescens accumulated the highest concentrations of Cd and Zn, S. gigantea accumulated the highest concentration of Cu, and Poaceae accumulated the highest concentrations of Cr and Ni. These findings have implications for urban vegetation management in areas where there is no organised greenery, and offer proof that vegetation in wasteland areas should be maintained since it is an excellent tool for reducing concentrations of PM at its place of origin.

Impaired kinetics of Bax-GFP and Smac/DIABLO-GFP in caspase-8- and bid-silenced and Bcl-2 overexpressed breast cancer MCF-7 cells exposed to camptothecin.

Smac/DIABLO, a proapoptotic protein released from mitochondrial intermembrane space during apoptosis, promotes caspases activation by IAPs neutralization. The kinetics and molecular mechanism of Smac/DIABLO release from mitochondria has remained obscure. Present study is focused on the role of Bid in the control of Bax-GFP and Smac/DIABLO-GFP kinetics in breast cancer MCF-7 cells stimulated to apoptosis with camptothecin (CPT). Minute kinetics of proteins was examined by homeostatic confocal microscopy. The release of Smac/DIABLO-GFP from mitochondria comprised two phases: initial-rapid, lasting 20-30 min and subsequent 30 min-plateau phase, followed by the decrease of Smac/DIABLO-related fluorescence due to cell destruction. The kinetics of Bax-GFP aggregation on mitochondria coincided in time with Smac/DIABLO-GFP release from these organelles. Bid knock down and Bcl-2 overexpression delayed Bax-GFP aggregation and completely inhibited Smac/DIABLO-GFP release from mitochondria. Knock down of caspase 8 (activator of Bid) delayed both Bax-GFP aggregation and Smac/DIABLO-GFP release in CPT-treated cells. In conclusion, Bid protein is crucial for the control of the release of Smac/DIABLO from mitochondria in breast cancer MCF-7 stimulated to apoptosis with CPT.

Synovial fibronectin fragmentation and domain expressions in relation to rheumatoid arthritis progression.

OBJECTIVE: To determine whether the expression of some fibronectin (FN) domains and a degree of FN degradation are associated with the progression of rheumatoid arthritis (RA). METHODS: Based on the radiographs of the hands of RA patients, three groups of synovial fluid and plasma samples were distinguished: (i) those with early radiological changes, (ii) established and (iii) late progressive radiological changes. The expressions of FN domains were determined by ELISA using appropriate domain-specific monoclonal antibodies. FN fragmentation was analysed by immunoblotting. RESULTS: In the early RA group, synovial FN was found to be totally degraded to a mixture of FN fragments. In the established group, it consisted of a portion of intact FN molecules and a smaller part of FN fragments, whereas in the late group the synovial FN immunoblotting pattern was similar to that of intact FN. The FN fragmentation was accompanied by decreases in FN immune reactivity with monoclonal antibodies specific to the collagen, fibrin and C-terminal FN domains. In the blood plasma of all studied groups of RA patients, the FN immunopattern was analogous to that in normal plasma. However, the expressions of the plasma FN domains were higher than those of healthy individuals. CONCLUSIONS: Profound degradation of FN and low collagen, fibrin and C-terminal domain expressions in FN were only associated with early destructive changes observed in radiographs of the RA patients' hands.

Apoptosis and autophagy in mammary gland remodeling and breast cancer chemotherapy.

Apoptosis - programmed cell death (PCD) type I is physiological process responsible for cell loss during mammary gland involution after natural weaning or litter removal in rodents, after weaning in sow and during drying off in goat and cow. The regulation of mammary epithelial cell (MEC) apoptosis in bovine mammary gland occurs at three levels. The first level comprises intracellular regulatory proteins, e.g. Bcl-2 family death promoters and inhibitors. The second level is represented by intramammary inductors of apoptosis, e.g. FIL, IGFBPs, Fas ligand, TGF-betas. The expression and activity of these auto/paracrine inductors of apoptosis is controlled and modulated by the third level factors, e.g. systemic galactopoetic hormones, nutrition, reproductive status and milking management. Our recent study proved that apoptosis in involuting bovine mammary gland is accompanied by increased intensity of autophagy, regarded as a cytoprotective process but in advanced stage as a PCD type II. Moreover, we have reported for the first time the ability of TGF-beta(1) to induce both apoptosis and autophagy in bovine BME-UV1 MEC. Much more pronounced heterogeneity of PCD was observed when breast cancer cells were exposed to anticancer drugs. The primary responses of breast cancer MCF-7 cells to camptothecin (CPT) are apoptosis and autophagy (as a cytoprotective process). In this case autophagy occurs in cells which are resistant to apoptosis as a tool of cancer cell survival. The fail-safe responses of breast cancer cells to persisting CPT-induced stress are apoptosis accompanied by morphological and biochemical features of autophagy or type II PCD with advanced subcellular degradation. The threshold between autophagy as a cytoprotective process (reversible) or PCD (irreversible) is difficult to establish and probably depends on the extent of degradation of cellular components. Proapoptotic protein Bid may serve as a molecular switch between apoptosis and autophagy. Bid knock down in MCF-7 cells exposed to CPT leads to a shift of cell death from apoptosis to autophagy. Since bid and other proapoptotic genes undergo mutations in malignant cells, the ability of cancer cells commitment to autophagy may have important therapeutic implications.

Cathepsins and BID are involved in the molecular switch between apoptosis and autophagy in breast cancer MCF-7 cells exposed to camptothecin.

The details of molecular switching points between apoptosis and autophagy in tumor cells have still not been fully elucidated. This study focused on the role of cathepsin B and its substrate, BID as molecular links between apoptosis and autophagy in human breast cancer MCF-7 cells exposed to camptothecin. Apoptosis occurred rapidly with a peak in 60 min after drug administration, whereas autophagy developed at a much slower rate with continuous progression during 24 h of cell exposure to the drug. CPT induced very rapid activation of cathepsin B. Inhibition of cathepsins by E64d prevented CPT-induced BAX and BID aggregation on mitochondria and reduced significantly reduced apoptotic cell number. The above effects were accompanied by an increase in autophagosome formation, measured by expression of MAP I LC3. BID knock down resulted in strong suppression of CPT-induced apoptosis and a shift of cell death towards autophagy, manifesting with an increase of Beclin 1 and MAP I LC3 cellular content.

[Multifunction of fibronectin]. / Wielofunkcyjnosc fibronektyny.

Fibronectin is an extracellular matrix component which appears in different isoforms, due to alternative mRNA splicing of the ED-A, ED-B and III-CS regions and subsequent post-translational modification. It is composed of multiple homologous repeats and contains many functional domains. Because of its ability to interact with many ligands including cells, heparin, fibrin, collagen, DNA, immunoglobulin, fibronectin can play the role in variety of biological processes.

The melatonin generating system in the rat retina and pineal gland: effect of single and repeated electroconvulsive shock (ECS).

N-Acetyltransferase (NAT), a rate-limiting enzyme in the melatonin synthesis which converts serotonin to N-acetylserotonin, shows a distinct circadian rhythm in the rat pineal gland and retina, with low activities during the light phase and peak activities during the dark phase. Hydroxyindole-O-methyltransferase (HIOMT), an enzyme which methylates N-acetylserotonin to melatonin, did not show any significant diurnal variations in both analyzed tissues. Isoproterenol, a selective beta-adrenoceptor agonist, when administered during morning hours of the light phase, markedly increased NAT activity in the pineal gland, but not in the retina. Electroconvulsive shock (ECS), especially when applied repeatedly (ECS x 10, once daily) significantly increased NAT activity in the retina and tended to decrease the enzyme activity in the pineal gland in isoproterenol-treated rats. ECS x 10 slightly increased and decreased the nocturnally-stimulated NAT activity in the rat retina and pineal gland, respectively.