The tensile and compressive properties of human glenohumeral cartilage were determined by testing 120 rectangular strips in uniaxial tension and 70 cylindrical plugs in confined compression, obtained from five human glenohumeral joints. Specimens were harvested from five regions across the articular surface of the humeral head and two regions on the glenoid. Tensile strips were obtained along two orientations, parallel and perpendicular to the split-line directions. Two serial slices through the thickness, corresponding to the superficial and middle zones of the cartilage layers, were prepared from each tensile strip and each compressive plug. The equilibrium tensile modulus and compressive aggregate modulus of cartilage were determined from the uniaxial tensile and confined compression tests, respectively. Significant differences in the tensile moduli were found with depth and orientation relative to the local split line direction. Articular cartilage of the humeral head was significantly stiffer in tension than that of the glenoid. There were significant differences in the aggregate compressive moduli of articular cartilage between superficial and middle zones in the humeral head. Furthermore, tensile and compressive stressstrain responses exhibited nonlinearity under finite strain while the tensile modulus differed by up to two orders of magnitude from the compressive aggregate modulus at 0% strain, demonstrating a high degree of tension-compression nonlinearity. The complexity of the mechanical properties of human glenohumeral cartilage was exposed in this study, showing anisotropy, inhomogeneity, and tension-compression nonlinearity within the same joint. The observed differences in the tensile properties of human glenohumeral cartilage suggest that the glenoid may be more susceptible to cartilage degeneration than the humeral head.

The range of hosts exploited by a parasite is determined by several factors, including host availability, infectivity and exploitability. Each of these can be the target of natural selection on both host and parasite, which will determine the local outcome of interactions, and potentially lead to coevolution. However, geographical variation in host use and specificity has rarely been investigated. Maculinea (= Phengaris ) butterflies are brood parasites of Myrmica ants that are patchily distributed across the Palæarctic and have been studied extensively in Europe. Here, we review the published records of ant host use by the European Maculinea species, as well as providing new host ant records for more than 100 sites across Europe. This comprehensive survey demonstrates that while all but one of the Myrmica species found on Maculinea sites have been recorded as hosts, the most common is often disproportionately highly exploited. Host sharing and host switching are both relatively common, but there is evidence of specialization at many sites, which varies among Maculinea species. We show that most Maculinea display the features expected for coevolution to occur in a geographic mosaic, which has probably allowed these rare butterflies to persist in Europe. This article is part of the theme issue ‘The coevolutionary biology of brood parasitism: from mechanism to pattern’.

Colon carcinogenesis is a multistep process where oxygen radicals were found to enhance carcinogenesis at all stages: initiation, promotion, and progression. Since insufficient capacity of protective antioxidant system can result in cancer, the aim of this study was to examine the activity of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) and the levels of reduced glutathione, vitamin C, and vitamin E. The lipid peroxidation products were also determined by measuring malondialdehyde and 4-hydroxynonenal levels in colorectal cancer tissue collected from 55 patients. In these cases the activity of superoxide dismutase, glutathione peroxidase, and glutathione reductase was significantly increased while the activity of catalase was significantly decreased in cancer tissue. However, the level of nonenzymatic antioxidant parameters (glutathione, vitamin C, and vitamin E) was significantly decreased in cancer tissue. Further lipid peroxidation was enhanced during cancer development, manifested by a significant increase in malondialdehyde and 4-hydroxynonenal levels. The obtained results indicate significant changes in antioxidant capacity of colorectal cancer tissues, which lead to enhanced action of oxygen radicals, resulting in lipid peroxidation.

Cyclophosphamide is an inactive cytostatic, which is metabolised into active metabolites mainly in the liver. During bioactivation, reactive oxygen species (ROS) are also formed, which can modify the components of both healthy and neoplastic cells leading to decreased antioxidative capacity. Amifostine is a drug that can inactivate ROS. The aim of the present study was to evaluate the influence of amifostine on the antioxidative system of the liver of rats exposed to cyclophosphamide. Intraperitoneal administration of cyclophosphamide was found to decrease the activity of liver antioxidative enzymes, i.e. superoxide dismutase, glutathione peroxidase and glutathione reductase, and to increase catalase activity. Amifostine slightly influenced antioxidative enzyme activity, causing a significant increase only in superoxide dismutase activity. Co-administration of cyclophosphamide and amifostine nearly prevented changes in activities of superoxide dismutase, glutathione reductase and catalase, as well as to a high degree of glutathione peroxidase. Cyclophosphamide also evoked a decrease in the level of non-enzymatic antioxidants, such as reduced glutathione and vitamins C, E and A, as well as total antioxidant status. Administration of amifostine alone caused a significant increase in non-enzymatic antioxidant level that resulted in an increase in total antioxidant status. Administration of amifostine together with cyclophosphamide to a large extent prevented changes in the evaluated non-enzymatic antioxidative parameters, decreasing values of their concentration to the values of control group. Changes of liver antioxidative abilities during detoxification of cyclophosphamide were accompanied by intensified lipid peroxidation, manifested by an increase in concentration of products such as malondialdehyde and 4-hydroxynonenal. Amifostine caused the inhibition of lipid peroxidation in the liver of both control and cyclophosphamide-treated rats. In conclusion, our results suggest that amifostine significantly protects liver antioxidant properties from changes caused by cyclophosphamide treatment and in consequence prevents oxidative stress and phospholipid peroxidative damage.