Shape-memory effects in biopolymer networks with collagen-like transient nodes

In this article we study shape-memory behavior of hydrogels, formed by biodegradable and biocompatible recombinant telechelic polypeptides, with collagen-like end blocks and a random coil-like middle block. The programmed shape of these hydrogels was achieved by chemical cross-linking of lysine residues present in the random coil. This led to soft networks, which can be stretched up to 200% and "pinned" in a temporary shape by lowering the temperature and allowing the collagen-like end blocks to assemble into physical nodes. The deformed shape of the hydrogel can be maintained, at room temperature, for several days, or relaxed within a few minutes upon heating to 50 °C or higher. The presented hydrogels could return to their programmed shape even after several thermomechanical cycles, indicating that they remember the programmed shape. The kinetics of shape recovery at different temperatures was studied in more detail and analyzed using a mechanical model composed of two springs and a dashpot.     

Comparison of Macromolecular Oxidation by Reactive Oxygen Species in Three Bacterial Genera Exposed to Different Antibiotics

Proteins and lipids maybe important targets of oxidation and this may alter their functions. We evaluated whether ceftazidima (CAZ), piperacillin (PIP), chloramphenicol (CMP), and ciprofloxacin (CIP) could oxidize the macromolecules in the three bacterial genera Staphylococcus aureus, Escherichia coli, and Pseudomonas aeruginosa. There was an increase in lipid peroxidation observed in these three species. However, this was lower in the Gram negative bacteria than in S. aureus. A reduction of the carbonyl residue in S. aureus with ciprofloxacin was observed whereas in Gram negative bacteria the antibiotics increased the carbonyl residue with respect to the control. Although the strains suffered a rise in advanced oxidation protein products (AOPP) in the presence of ciprofloxacin, the S. aureus strain had a smaller increase of AOPP than the other strains. The results described in this article provide data about the susceptibility of the three bacterial genera to the oxidative stress induced by the antibiotics studied.     

Xanthophyll cycle--a mechanism protecting plants against oxidative stress

Six different xanthophyll cycles have been described in photosynthetic organisms. All of them protect the photosynthetic apparatus from photodamage caused by light-induced oxidative stress. Overexcitation conditions lead, in the chloroplast, to the over-reduction of the NADP pool and production of superoxide, which can subsequently be metabolized to hydrogen peroxide or a hydroxyl radical, other reactive oxygen species (ROS). On the other hand, overexcitation of photosystems leads to an increased lifetime of the chlorophyll excited state, increasing the probability of chlorophyll triplet formation which reacts with triplet oxygen forming single oxygen, another ROS. The products of the light-dependent phase of xanthophyll cycles play an important role in the protection against oxidative stress generated not only by an excess of light but also by other ROS-generating factors such as drought, chilling, heat, senescence, or salinity stress. Four, mainly hypothetical, mechanisms explaining the protective role of xanthophyll cycles in oxidative stress are presented. One of them is the direct quenching of overexcitation by products of the light phase of xanthophyll cycles and three others are based on the indirect participation of xanthophyll cycle carotenoids in the process of photoprotection. They include: (1) indirect quenching of overexcitation by aggregation-dependent light-harvesting complexes (LHCII) quenching; (2) light-driven mechanisms in LHCII; and (3) a model based on charge transfer quenching between Chl a and Zx. Moreover, results of the studies on the antioxidant properties of xanthophyll cycle pigments in model systems are also presented.     

Ground beetle (Coleoptera, Carabidae) assemblages inhabiting Scots pine stands of Puszcza Piska Forest: six-year responses to a tornado impact

Ground beetle assemblages were studied during 2003-08 in the Pisz Forest by comparing stands disturbed by a tornado to undisturbed control stands. The following exploratory questions were put forward. (1) How do the carabid assemblages change during six years following the tornado impact? (2) Does the carabid assemblage recovery begin during the six first post-tornado years? To assess the state of carabid assemblages we used two indices: the MIB (Mean Individual Biomass) and the SPC (Sum of Progressive Characteristics). Carabid assemblages in the disturbed and in the control stands, as expressed by these two indices, were compared using the length of a regression distance (sample distance in a MIB:SPC coordinate system). A cluster analysis revealed that the assemblages of the disturbed and the control stands were different. The tornado-impacted stands produced lower carabid catch rates, but species richness was significantly higher there than in the control stands. They hosted lower proportions of individuals of European species, of large zoophages, and of forest and brachypterous species, than the control stands. The observed reduction in SPC and MIB, and an increase in the regression distances may indicate that the carabid assemblages had not started to recover from the tornado-caused disturbance. Carabid assemblages apparently responded to the tornado in two steps. Firstly, the first three years were characterized by moderate decreases of index values. Secondly, from the fourth to the sixth year after the tornado, many observed changes became magnified. We did not observe clear signals of the recovery of forest carabid assemblages during the six follow-up years.     

Liver-specific Commd1 knockout mice are susceptible to hepatic copper accumulation

Canine copper toxicosis is an autosomal recessive disorder characterized by hepatic copper accumulation resulting in liver fibrosis and eventually cirrhosis. We have identified COMMD1 as the gene underlying copper toxicosis in Bedlington terriers. Although recent studies suggest that COMMD1 regulates hepatic copper export via an interaction with the Wilson disease protein ATP7B, its importance in hepatic copper homeostasis is ill-defined. In this study, we aimed to assess the effect of Commd1 deficiency on hepatic copper metabolism in mice. Liver-specific Commd1 knockout mice (Commd1(Δhep)) were generated and fed either a standard or a copper-enriched diet. Copper homeostasis and liver function were determined in Commd1(Δhep) mice by biochemical and histological analyses, and compared to wild-type littermates. Commd1(Δhep) mice were viable and did not develop an overt phenotype. At six weeks, the liver copper contents was increased up to a 3-fold upon Commd1 deficiency, but declined with age to concentrations similar to those seen in controls. Interestingly, Commd1(Δhep) mice fed a copper-enriched diet progressively accumulated copper in the liver up to a 20-fold increase compared to controls. These copper levels did not result in significant induction of the copper-responsive genes metallothionein I and II, neither was there evidence of biochemical liver injury nor overt liver pathology. The biosynthesis of ceruloplasmin was clearly augmented with age in Commd1(Δhep) mice. Although COMMD1 expression is associated with changes in ATP7B protein stability, no clear correlation between Atp7b levels and copper accumulation in Commd1(Δhep) mice could be detected. Despite the absence of hepatocellular toxicity in Commd1(Δhep) mice, the changes in liver copper displayed several parallels with copper toxicosis in Bedlington terriers. Thus, these results provide the first genetic evidence for COMMD1 to play an essential role in hepatic copper homeostasis and present a valuable mouse model for further understanding of the molecular mechanisms underlying hepatic copper homeostasis.     

The role of intracellular cAMP in renal gluconeogenesis in view of differential action of various cAMP analogues

Effects of various cAMP analogues on gluconeogenesis in isolated rabbit kidney tubules have been investigated. In contrast to N(6),2'-O-dibutyryladenosine-3',5'-cyclic monophosphate (db-cAMP) and cAMP, which accelerate renal gluconeogenesis, 8-bromoadenosine-3',5'-cyclic monophosphate (Br-cAMP) and 8-(4-chlorophenylthio)-cAMP (pCPT-cAMP) inhibit glucose production. Stimulatory action of cAMP and db-cAMP may be evoked by butyrate and purinergic agonists generated during their extracellular and intracellular metabolism resulting in an increase in flux through fructose-1,6-bisphosphatase and in consequence acceleration of the rate of glucose formation. On the contrary, Br-cAMP is poorly metabolized in renal tubules and induces a fall of flux through glyceraldehyde-3-phosphate dehydrogenase. The contribution of putative extracellular cAMP receptors to the inhibitory Br-cAMP action is doubtful in view of a decline of glucose formation in renal tubules grown in the primary culture supplemented with forskolin. The presented data indicate that in contrast to hepatocytes, in kidney-cortex tubules an increased intracellular cAMP level results in an inhibition of glucose production.     

The inhibitor protein of the F1F0-ATP synthase is associated to the external surface of endothelial cells

The ATPase inhibitor protein (IP) of mitochondria was detected in the plasma membrane of living endothelial cells by flow cytometry, competition assays, and confocal microscopy of cells exposed to IP antibodies. The plasma membranes of endothelial cells also possess beta-subunits of the mitochondrial ATPase. Plasma membranes have the capacity to bind exogenous IP. TNF-alpha decreases the level of beta-subunits and increases the amount of IP, indicating that the ratio of IP to beta-subunit exhibits significant variations. Therefore, it is probable that the function of IP in the plasma membrane of endothelial cells is not limited to regulation of catalysis.