Comprehensive Investigation of Stoichiometry-Structure-Performance Relationships in Flexible Polyurethane Foams.

Polyurethane (PU) foams are versatile materials with a broad application range. Their performance is driven by the stoichiometry of polymerization reaction, which has been investigated in several works. However, the analysis was often limited only to selected properties and compared samples differing in apparent density, significantly influencing their performance. In the bigger picture, there is still a lack of comprehensive studies dealing with the stoichiometry impact on PU foams' performance. Herein, flexible PU foams with a similar apparent density but differing in the isocyanate index (IIso) (from 0.80 to 1.20) were prepared. The stoichiometry-structure-performance relationships were investigated considering cellular and chemical structure, as well as the static and dynamic mechanical properties, thermal stability, thermal insulation, and acoustic performance. For IIso of 1.00, the biggest cell diameters of 274 µm were noted, which was 21-25% higher compared to 0.80 and 1.20 values. Increasing IIso reduced open cell content from 83.1 to 22.4%, which, combined with stiffening of structure (rise of modulus from 63 to 2787 kPa) resulting from crosslinking, limited the sound suppression ability around five times. On the other hand, it significantly strengthened the material, increasing tensile and compressive strength 4 and 13 times, respectively. Changes in the foams' performance were also induced by the glass transition temperature shift from 6.1 to 31.7 °C, resulting from a greater extent of urethane groups' generation and additional isocyanate reactions. Generally, the presented work provides important insights into preparing flexible PU foams and could be very useful for the future development of these materials.

Insights into Stoichiometry Adjustments Governing the Performance of Flexible Foamed Polyurethane/Ground Tire Rubber Composites.

Polyurethanes (PU) are widely applied in the industry due to their tunable performance adjusted by changes in the isocyanate index-stoichiometric balance between isocyanate and hydroxyl groups. This balance is affected by the incorporation of modifiers of fillers into the PU matrix and is especially crucial for PU foams due to the additional role of isocyanates-foaming of the material. Despite the awareness of the issue underlined in research works, the contribution of additives into formulations is often omitted, adversely impacting foams' performance. Herein, flexible foamed PU/ground tire rubber (GTR) composites containing 12 different types of modified GTR particles differing by hydroxyl value (LOH) (from 45.05 to 88.49 mg KOH/g) were prepared. The impact of GTR functionalities on the mechanical, thermomechanical, and thermal performance of composites prepared with and without considering the LOH of fillers was assessed. Formulation adjustments induced changes in tensile strength (92-218% of the initial value), elongation at break (78-100%), tensile toughness (100-185%), compressive strength (156-343%), and compressive toughness (166-310%) proportional to the shift of glass transition temperatures (3.4-12.3 °C) caused by the additional isocyanates' reactions yielding structure stiffening. On the other hand, formulation adjustments reduced composites' thermal degradation onset due to the inferior thermal stability of hard segments compared to soft segments. Generally, changes in the composites' performance resulting from formulation adjustments were proportional to the hydroxyl values of GTR, justifying the applied approach.

Comprehensive Enhancement of Prepolymer-Based Flexible Polyurethane Foams' Performance by Introduction of Cost-Effective Waste-Based Ground Tire Rubber Particles.

Material innovations in polyurethane (PU) foams should ideally combine performance enhancement, environmental impact limitation, and cost reduction. These goals can be achieved by applying recycled or waste-based materials without broader industrial applications, implicating their low price. Herein, from 5 to 20 parts by weight of ground tire rubber (GTR) particles originated from the recycling of postconsumer car tires were incorporated into a flexible foamed PU matrix as a cost-effective waste-based filler. A two-step prepolymer method of foams manufacturing was applied to maximize the potential of applied formulation changes. The impact of the GTR content on the foams' processing, chemical, and cellular structure, as well as static and dynamic mechanical properties, thermal stability, sound suppression ability, and thermal insulation performance, was investigated. The introduction of GTR caused a beneficial reduction in the average cell diameter, from 263.1 µm to 144.8-188.5 µm, implicating a 1.0-4.3% decrease in the thermal conductivity coefficient. Moreover, due to the excellent mechanical performance of the car tires-the primary application of GTR-the tensile performance of the foams was enhanced despite the disruption of the cellular structure resulting from the competitiveness between the hydroxyl groups of the applied polyols and on the surface of the GTR particles. The tensile strength and elongation at break were increased by 10 and 8% for 20 parts by weight GTR addition. Generally, the presented work indicates that GTR can be efficiently applied as a filler for flexible PU foams, which could simultaneously enhance their performance, reduce costs, and limit environmental impacts due to the application of waste-based material.

Cytoskeletal reorganization and cell death in mitoxantrone-treated lung cancer cells.

The aim of this study was to investigate the cytotoxic effect of mitoxantrone on two human non-small cell lung cancer cell lines, A549 (p53+) and H1299 (p53-). To our knowledge, this is the first study to evaluate the impact of MXT on the organization of cytoskeletal proteins. Analyses were performed using fluorescence and transmission electron microscopy, spectrophotometric techniques, flow cytometry and Western blotting. It was shown that H1299 cells are significantly more sensitive to mitoxantrone than the A549 cell line, and that the growth-inhibitory effect of the drug is dose-dependent only after longer incubation. The observed presence of ring-like microtubule structures and mitochondria surrounding the nuclei of H1299 cells could be a manifestation of increased tubulin polymerization requiring large amounts of energy, whereas the loss of actin stress fibers was presumably not the cause but rather the consequence of cell death induction. Treatment with mitoxantrone also led to the appearance of structures resembling agresomes in H1299 cells and to nucleolar segregation in both cell lines. It was demonstrated that cells arrested in the S phase were most susceptible to cell death induction, and that triggered intracellular changes led mainly to apoptosis. High concentrations induced necrosis and some H1299 cells exhibited morphological features of mitotic catastrophe.

Phenethyl isothiocyanate-induced cytoskeletal changes and cell death in lung cancer cells.

Isothiocyanates are known for their anticarcinogenic and antitumor potential, however, the exact mechanism of their action has not been fully elucidated. The present study was designed to investigate and compare the effects of phenethyl isothiocyanate on cell morphology, the cytoskeleton and induction of cell death in human non-small cell lung cancer cell lines A549 and H1299 differing in p53 status. Cell viability tests (MTT assay, xCELLigence system) showed that PEITC exhibits lower cytotoxicity to A549 cells containing wild-type p53. The observed growth-inhibitory effect of PEITC was dose-dependent, but time-dependence was observed only at higher concentrations. The results of flow-cytometric and fluorescence-microscopic analyses indicate that PEITC induced disassembly of actin stress fibers and degradation of tubulin which, most likely, contributed to the induction of cell death. Although, 24-h incubation caused G2/M cell cycle arrest, the fraction of G2/M cells decreased in a dose- and time-dependent manner in favor of cells with sub-G1 DNA content. Further experiments (Annexin V staining, electron microscopic observations) confirmed that the apoptosis-inducing potency of PEITC is probably the main factor responsible for cell growth inhibition. However, PEITC treatment also resulted in the appearance of an increased proportion of H1299 cells exhibiting morphological features of mitotic catastrophe.

Actin cytoskeleton reorganization correlates with cofilin nuclear expression and ultrastructural changes in cho aa8 cell line after apoptosis and mitotic catastrophe induction by doxorubicin.

The effect of doxorubicin on the expression of cofilin and actin in CHO AA8 cells was estimated by fluorescence and electron microscopy. The presence of cofilin and actin was observed particularly in the nuclei of cells by different modes after treatment by doxorubicin. Cells undergoing mitotic catastrophe expressed some entirely characteristic features together with overlapping elements of other types of cell death. Additionally, the authors suggest that, as defined here, reorganization of F-actin might be involved in all cell death processes. Changes in the nuclear expression of cofilin are related to F-actin cytoplasm-nuclear translocation and its intranuclear dynamic reorganization.

Cytoskeletal changes during cellular response of the A549 lung cancer cells to continuous cisplatin treatment.

The cytoskeleton is a ubiquitous cellular structure that plays a crucial role in most processes of living cells. There are reports suggesting that this system not only reflects, but also contributes to many different processes, including cell death. In this study, we examined alterations of both MT and MF cytoskeletal systems related to cell death, which was induced in A549 cells by continuous cisplatin treatment. We observed that specific changes in these cytoskeletal proteins accompany cell death, while the others are associated with increased repair and cell survival. It seems that the predominant mode of cell death triggered by cisplatin was an apoptotic-like pathway, but on the other hand, coincidence with some features of necrosis and autophagy was also demonstrated in our conditions.

Taxol-induced polyploidy and cell death in CHO AA8 cells.

The purpose of this study was to assess whether Taxol-induced changes in microtubular dynamics are accompanied by apoptosis. CHO AA8 cells were treated with different Taxol concentrations (0.25microM, 0.5microM, 1microM) for 24h. The effects of Taxol exposure were analyzed using fluorescence microscopy and flow cytometry (TUNEL and annexin V-FITC/propidium iodide assays). 0.25microM Taxol caused the appearance of few multinucleated giant cells exhibiting extensive arrays of fine filaments. Slight increases in the level of polyploidy, phosphatidylserine externalization and in the percentage of TUNEL positive cells were noticed. Concentrations of 0.5 and 1microM resulted in the appearance of a large number of giant cells, which exhibited, depending on the cell, an extensive microtubular network or loose or tightly packed bundles of microtubules. Cells of reduced volume and showing chromatin condensation were also seen. Cell cycle analysis revealed that almost half of the cell population was polyploid. Except in cells exposed to 1microM Taxol, annexin V-FITC/PI labelling did not reveal the loss of plasma membrane integrity or increase in phosphatidylserine externalization; however, TUNEL assay revealed a significant increase in the percentage of cells with DNA fragmentation. These data indicate that CHO AA8 cells treated with Taxol undergo cell death of a type which considerably differs from apoptosis.

[Selected mechanisms of the therapeutic effect of arsenic trioxide in cancer treatment]. / Wybrane mechanizmy terapeutycznego oddzialywania trójtlenku arsenu w leczeniu nowotworów.

The properties of arsenic trioxide (arsenic) have been known for centuries. This compound has been used, among others, in the industrial production of paints and glass and also for the conservation of leather and wood. Although arsenic trioxide is highly toxic, this compound was shown to have a therapeutic potential as early as the fifteenth century. The period between the seventeenth and nineteenth centuries resulted in the development of new arsenic-based drugs which were applied for the treatment of skin diseases and acute promyelocytic leukemia. The mechanism of action of arsenic trioxide is mainly related to the induction of apoptosis (programmed cell death) in cancer cells. In particular it involves effects on the activities of JNK kinases, NF-kB transcription factor, glutathione, caspases, as well as pro- and anti-apoptotic proteins. Experiments investigating the effect of arsenic trioxide on cell lines such as glioma and prostate, breast, stomach, liver, and ovarian cancer are in progress. There are also clinical trials underway aimed at the use of arsenic trioxide with ascorbic acid, retinoid acid, and growth factors in combined therapy.