[en] Due to their high ionic conductivity, solid polymer electrolyte (SPE) systems have attracted wide spread attention as the most appropriate choice to fabricate all-solid-state electrochemical devices, namely batteries, sensors and fuel cells. In this work, ion conductive polymer electrolyte membranes have been prepared for battery fabrication. However, fractals were found to grow in these polymer electrolyte membranes weeks after they were prepared. It was believed that the formation of fractal aggregates in these membranes were due to ionic movement. The discovery of fractal growth pattern can be used to understand the effects of such phenomenon in the polymer electrolyte membranes. Digital images of the fractal growth patterns were taken and a simulation model was developed based on the Brownian motion theory and a fractal dialect known as L-system. A computer coding has been designed to simulate and visualize the fractal growth. (author)

No abstract available

[en] Transforming growth factor beta (TGFβ) markedly inhibited growth of canine tracheal epithelial (CTE) cells. Reduced responsiveness to TGFβ-induced growth inhibition accompanied neoplastic progression of these cells from primary to transformed to neoplastic. This was similar to the relationship between neoplastic progression and increased resistance to TGFβ-induced growth inhibition seen for rat tracheal epithelial (RTE) cells. The canine cells were more sensitive than rat cells to TGFβ-induced growth inhibition at all stages in the neoplastic process. (author)

[en] Background and purpose: The epidermal growth factor receptor (EGFR) is overexpressed, amplified or mutated in various human epithelial tumors, and is associated with tumor aggressiveness and therapy resistance. Autophagy activation provides a survival advantage for cells in the tumor microenvironment. In the current study, we assessed the potential of autophagy inhibition (using chloroquine (CQ)) in treatment of EGFR expressing tumors. Material and methods: Quantitative PCR, immunohistochemistry, clonogenic survival, proliferation assays and in vivo tumor growth were used to assess this potential. Results: We show that EGFR overexpressing xenografts are sensitive to CQ treatment and are sensitized to irradiation by autophagy inhibition. In HNSSC xenografts, a correlation between EGFR and expression of the autophagy marker LC3b is observed, suggesting a role for autophagy in EGFR expressing tumors. This observation was substantiated in cell lines, showing high EGFR expressing cells to be more sensitive to CQ addition as reflected by decreased proliferation and survival. Surprisingly high EGFR expressing cells display a lower autophagic flux. Conclusions: The EGFR high expressing cells and tumors investigated in this study are highly dependent on autophagy for growth and survival. Inhibition of autophagy may therefore provide a novel treatment opportunity for EGFR overexpressing tumors

[en] Urothelial cancers have an environmental etiological component, and previous studies from our laboratory have shown that arsenite (As⁺³) can cause the malignant transformation of the immortalized urothelial cells (UROtsa), leading to the expression of keratin 6 (KRT6). The expression of KRT6 in the parent UROtsa cells can be induced by the addition of epidermal growth factor (EGF). Tumors formed by these transformed cells have focal areas of squamous differentiation that express KRT6. The goal of this study was to investigate the mechanism involved in the upregulation of KRT6 in urothelial cancers and to validate that the As⁺³-transformed UROtsa cells are a model of urothelial cancer. The results obtained showed that the parent and the As⁺³-transformed UROtsa cells express EGFR which is phosphorylated with the addition of epidermal growth factor (EGF) resulting in an increased expression of KRT6. Inhibition of the extracellular-signal regulated kinases (ERK1/2) pathway by the addition of the mitogen-activated protein kinase kinase 1 (MEK1) and MEK2 kinase inhibitor U0126 resulted in a decrease in the phosphorylation of ERK1/2 and a reduced expression of KRT6. Immuno-histochemical analysis of the tumors generated by the As⁺³-transformed isolates expressed EGFR and tumors formed by two of the transformed isolates expressed the phosphorylated form of EGFR. These results show that the expression of KRT6 is regulated at least in part by the ERK1/2 pathway and that the As⁺³-transformed human urothelial cells have the potential to serve as a valid model to study urothelial carcinomas. - Highlights: • Keratin 6 is induced in As⁺³-transformed transformed UROtsa cells by EGF. • The ERK1/2 signaling pathway regulates the expression of KRT6. • As⁺³-transformed human urothelial cells can serve as a model to study urothelial carcinomas.

[en] Simple experiments demonstrate that the development of an organism is both a genetic and a physical process. This statement is so obvious that it is seldom stated explicitly, and yet, there has been little progress toward integrating what should be complementary viewpoints. This paper focuses on the mechanical aspects of morphogenesis—highlighting those areas where mechanics and molecular genetics are converging toward a much-needed synthesis

[en] Transforming Growth Factor β1 (TGF-β1), a well-known neuroprotective and neurotrophic factor in the central nervous system, is also involved in the repair process responses after ischemia-reperfusion injury. Herein, we found that TGF-β1 enhanced Cdk5 expression while decreased Tunel-positive cells compared with the ischemia group, and roscovitine(Cdk5 inhibitor) treatment could blunt these effects. In vitro study, TGF-β1 facilitated Cdk5/p35 complex, the proliferation, neurite growth and differentiation of PC12 cells, effects of which could be blunted by roscovitine and Cdk5 silencing. Moreover, ERK1/2 inhibitor SCH772984 abrogated the effects of TGF- β1 on Cdk5 and Bax levels. Taken together, we conclude that Cdk5 contributes to the neuroprotective function of TGF- β1 via ERK1/2 signaling.

[en] Soil compaction could be either desirable or detrimental to plant growth, depending on the severity of compaction. The compaction treatments applied in this study on a coastal alluvial soil, Bernam series (Typic Endoaquepts) had resulted in significant reduction of oil palm total standing biomass in compacted plots. The oil palm total above-ground standing biomass comprising of fronds and trunk in the control plots was significantly higher than the compacted plots by 12%. Even though there was no significance difference in trunk heights, the palms were taller in 4T plots (tractor with 4 t trailer weight). Palms in compacted plots exhibited a significantly smaller trunk diameter, lower trunk dry weight and reduction in the frond dry weight by about 9%, 8% and 6%, respectively. The total green frond number, total leaf area and leaf area index (LAI) were not significantly different (p less than or equal to 0.05) between the treatments. Total green frond number per palm was 33 to 35 fronds per palm. The LAI averaged more than 5 for all treatments implying compaction did not hinder photosynthesis process. Hence, the changes in soil physical properties such as bulk density, porosity, available water and hydraulic properties were considered not limiting to palm growth as they adapted well to the compaction treatments. (author)

No abstract available

[en] Background: Evodiamine is an alkaloid extracted from Euodia rutaecarpa (Juss.) Benth. There is little information about the mechanisms of evodiamine on the apoptosis of hepatocellular carcinoma (HCC). Materials and methods: A xenograft model and CCK8 assay were used to investigate the anti-HCC effect of evodiamine. The effect of evodiamine on apoptosis was evaluated by DAPI staining and flow cytometry. Western blot analyses and immunohistochemistry were processed to assess the protein expressions of Akt and apoptotic proteins. Results: Evodiamine suppressed tumor growth, improved the expression of cleaved-caspase3 and decreased tumor specific growth factor (TSGF) and alpha fetoprotein (AFP) activities. Furthermore, evodiamine inhibited cell viability and induced cell cycle arrest. DAPI staining revealed nuclear condensation in evodiamine-treated groups. Meanwhile, evodiamine increased the number of apoptotic cells. Furthermore, evodiamine suppressed Akt and regulated apoptotic proteins in HepG2 cells. Evodiamine decreased p-Akt levels activated by SC79, which led to the increase of bax/bcl-2 and cleaved-caspase3. Conclusions: Our findings suggested that evodiamine could exert anti-HCC effect through inducing Akt-mediated apoptosis. Evodiamine has the potential to be a therapeutic medicine for HCCs. - Highlights: • Anti-tumor effect of evodiamine in hepatocellular carcinoma. • Evodiamine induces apoptosis in hepatocellular carcinoma. • The correlation between induction of apoptosis and Akt expression.