ABSTRACT
The quasi-static penetration properties of hybrid laminates were experimentally investigated. Aramid fabrics, carbon fabrics, and short hemp fibres were applied as the reinforcements of hybrid and non-hybrid composite laminates with polyurethane-polyurea (PUR/PUA) matrix. The laminates were made by hand, in a mould. They were cured at room temperature for 24 h. Hybrid laminates consisted of aramid and carbon layers in two different configurations, i.e., aramid at the innermost layers and outermost layers. Aramid/PUR/PUA and carbon/PUR/PUA composites were fabricated for comparison purposes. Laminates were also prepared via an analogue sequence of laying the reinforcement layers with the addition of 5% by weight of hemp fibres in the PUR/PUA matrix. Quasi-static penetration tests (QSPT) were conducted using a tensile testing machine with a surface-hardened, hemispherical, steel punch (9 mm diameter tip), reflecting the geometry of the Parabellum projectile. A quasi-static puncture test was carried out until the laminate was perforated. The ratio between the support span (Ds) and the punch diameter (Dp) was SPR = Ds/Dp = 5.0. The results showed the influences of laminate hybridisation on the values of absorbed energy, punch shear strength, and damage mechanism in the QSPT test. The addition of hemp fibres to aramid laminates resulted in a positive hybridisation effect. The order of layers of aramid and carbon fabrics in hybrid laminates influenced the results obtained in the QSPT test.
ABSTRACT
Drug resistance in cancer therapy is a multifactorial phenomenon that determines remission or progression. It is known that resistance to used anticancer drugs may be the consequence of drug transport to the cell or intracellular distribution. It may also be the result of its molecular target structural change, apoptosis inhibition or increase in some enzymes activity, e.g. pentose phosphate pathway enzymes. Intrinsic (pre-existed) drug resistance is related to the phenotype of cancer as well as normal cells. Acquired, after partial administration of chemotherapy, type of drug resistance in addition to the starting phenotype is closely linked to the development of new more aggressive clones and adaptive processes. In both, the intrinsic and acquired resistance, role play also mutations. These may be partially spontaneous, but in terms of acquired resistance, they are mostly induced by the exposure to the drugs. The article mentions some traditional mechanisms related to the acquisition of resistance by cancer cells during therapy, through the protein transporters, apoptosis deregulation, angiogenesis and the impact of the tumour microenvironment. We focused however on some more alternative ways of therapy resistance, such as, hypoxia and tumour acidification, cancer stem cells (CSCs), exosomes and radiotherapy resistance. A concise summary of the drug resistance presented in the paper may be an important aspect in studies to increase the effectiveness of cancer therapies.
