Cryptic speciation in the cosmopolitan <Emphasis Type="Italic">Epiphanes senta</Emphasis> complex (Monogononta,Rotifera) with the description of new species

The phytoplankton species composition and seasonal succession were examined in Lake Kastoria during the period November 1998–October 1999. A total of 67 species and 19 functional groups were identified. Only 4 out of the 67 species, all Cyanobacteria, were dominant (Limnothrix redekei, Microcystis aeruginosa, Cylindrospermopsis raciborskii and Aphanizomenon gracile). Diatoms were rare, not only in terms of species number, but also in terms of biomass (contributing <5% to the total phytoplankton biomass) in relation to the rather low silicon concentrations throughout the year. The functional groups S1, S_N, M and H1 were found dominant in the lake. The species A. gracile (functional group H1) behaved like the species Cylindrospermopsis raciborskii (functional group S_N) which is tolerant to mixing and poor light conditions. The phytoplankton seasonal succession showed similar patterns in all six sampling stations, both at the surface and the bottom water layer, with minor differences during Microcystis aeruginosa dominance. Two steady-state phases were identified within a year lasting for 4 months under relatively stable physical conditions. In these steady-states, the Limnothrix redekei persistent dominance under low light availability and low inorganic nitrogen has been explained by its specific ability such as buoyancy regulation to exploit resources in the water column. Moreover, high population densities over the winter and before the development of daphnids may contribute to the steady-state dominance of Limnothrix. Different niches separated vertically in the water column is one of the explanations for the Limnothrix–Microcystis steady-state when a replacement between the two species was observed in different water layers and areas of the lake. Long lasting steady-states of Cyanobacteria observed in Lake Kastoria and in other Mediterranean and tropical freshwaters may indicate influence of warm climate properties on phytoplankton dynamics. Electronic Supplementary Material Supplementary material is available to authorized users in the online version of this article at http://dx.doi.org/10.1007/s10750-006-0360-4 Handling editor: K. Martens     

Oxidative stress delays development and alters gene expression in the agricultural pest moth,Helicoverpa armigera

Stress is a widespread phenomenon that all organisms must endure. Common in nature is oxidative stress, which can interrupt cell homeostasis to cause cell damage and may be derived from respiration or from environmental exposure through diet. As a result of the routine exposure from respiration, many organisms can mitigate the effects of oxidative stress, but less is known about responses to oxidative stress from other sources. Helicoverpa armigera is a major agricultural pest moth that causes significant damage to crops worldwide. Here, we examined the effects of oxidative stress on H. armigera by chronically exposing individuals to paraquat—a free radical producer—and measuring changes in development (weight, developmental rate, lifespan), and gene expression. We found that oxidative stress strongly affected development in H. armigera, with stressed samples spending more time as caterpillars than control samples (>24 vs. ~15 days, respectively) and therefore living longer overall. We found 1,618 up‐ and 761 down‐regulated genes, respectively, in stressed versus control samples. In the up‐regulated gene set, was an over‐representation of biological processes related to cuticle and chitin development, glycine metabolism, and oxidation–reduction. Oxidative stress clearly impacts physiology and biochemistry in H. armigera and the interesting finding of an extended lifespan in stressed individuals could demonstrate hormesis, the phenomenon whereby toxic compounds can actually be beneficial at low doses. Collectively, our findings provide new insights into physiological and gene expression responses to oxidative stress in invertebrates.     

A role for the apoptosis inhibitory factor AIM/Spalpha/Api6 in atherosclerosis development

Macrophages play a central role in the development of atherosclerosis through the accumulation of oxidized LDL (oxLDL). AIM (Spα/Api6) has previously been shown to promote macrophage survival; however, its function in atherogenesis is unknown. Here we identify AIM as a critical factor that protects macrophages from the apoptotic effects of oxidized lipids. AIM protein is induced in response to oxLDL loading and is highly expressed in foam cells within atherosclerotic lesions. Interestingly, both expression of AIM in lesions and its induction by oxidized lipids require the action of LXR/RXR heterodimers. AIM^−/− macrophages are highly susceptible to oxLDL-induced apoptosis in vitro and undergo accelerated apoptosis in atherosclerotic lesions in vivo. Moreover, early atherosclerotic lesions in AIM^−/−LDLR^−/− double knockout mice are dramatically reduced when compared to AIM^+/+LDLR^−/− controls. We conclude that AIM production facilitates macrophage survival within atherosclerotic lesions and that loss of AIM decreases early lesion development by increasing macrophage apoptosis.     

A mathematical model to predict the in vivo pulsatile drag forces acting on bifurcated stent grafts used in endovascular treatment of abdominal aortic aneurysms (AAA)

Endovascular treatment of abdominal aortic aneurysms (AAA) is a promising new alternative to the traditional surgical repair. However, the endovascular approach suffers problems such as stent graft migration, endoleaks and stent mechanism breakage. Fatigue failure is believed to be the major cause of stent graft migration and device breakage. Knowledge of the in vivo forces acting on such devices is a basic requirement for the design of a successful endovascular device. Using a Fourier series trigonometric fit of a typical pressure and flow relationship, a mathematical model, using the control volume method, was developed to predict the pulsatile drag forces acting on various bifurcated stent graft geometries. It was found that for an iliac angle of 30 degrees, a proximal diameter of 24 mm and an iliac diameter of 12 mm, the drag force varied, over the cardiac cycle, between 3.9 and 5.5 N in the axial direction. It was noted that for a specific iliac angle the drag force variation with proximal diameter approximates a quadratic fit, with an increase in proximal diameter producing an increase in drag force. The more compliant the aorta the higher the drag force. Previously published results demonstrated the axial loads (axial drag forces) required for stent graft migration for certain stents types are lower than the drag forces calculated in this study. It is believed that the results of this study can provide guidelines for the quantitative analyses of the in vivo drag forces experienced by stent grafts and could therefore be used as design criteria for such devices.     

Distinct IL-2 receptor signaling pattern in CD4+CD25+ regulatory T cells

Despite expression of the high-affinity IL-2R, CD4(+)CD25(+) regulatory T cells (Tregs) are hypoproliferative upon IL-2R stimulation in vitro. However the mechanisms by which CD4(+)CD25(+) T cells respond to IL-2 signals are undefined. In this report, we examine the cellular and molecular responses of CD4(+)CD25(+) Tregs to IL-2. IL-2R stimulation results in a G(1) cell cycle arrest, cellular enlargement and increased cellular survival of CD4(+)CD25(+) T cells. We find a distinct pattern of IL-2R signaling in which the Janus kinase/STAT pathway remains intact, whereas IL-2 does not activate downstream targets of phosphatidylinositol 3-kinase. Negative regulation of phosphatidylinositol 3-kinase signaling and IL-2-mediated proliferation of CD4(+)CD25(+) T cells is inversely associated with expression of the phosphatase and tensin homologue deleted on chromosome 10, PTEN.     

Validation of the postimplantation rat whole-embryo culture test in the international ECVAM validation study on three in vitro embryotoxicity tests

A detailed report is presented on the performance of the postimplantation rat whole-embryo culture (WEC) test in a European Centre for the Validation of Alternative Methods (ECVAM)-sponsored formal validation study on three in vitro tests for embryotoxicity. Twenty coded test chemicals, classified as non-embryotoxic, weakly embryotoxic or strongly embryotoxic on the basis of their in vivo effects in animals and/or humans, were tested in four laboratories. The outcome showed that the WEC test can be considered to be a scientifically validated test, which is ready for consideration for use in assessing the embryotoxic potentials of chemicals for regulatory purposes.     

Extracellular pressure stimulates colon cancer cell proliferation via a mechanism requiring PKC and tyrosine kinase signals

Pressure in colonic tumours may increase during constipation, obstruction or peri-operatively. Pressure enhances colonocyte adhesion by a c-Src- and actin-cytoskeleton-dependent PKC-independent pathway. We hypothesized that pressure activates mitogenic signals. METHODS: Malignant colonocytes on a collagen I matrix were subjected to 15 mmHg pressure. ERK, p38, c-Src and Akt phosphorylation and PKCalpha redistribution were assessed by western blot after 30 min and PKC activation by ELISA. Cells were counted after 24 h and after inhibition of each signal, tyrosine phosphorylation or actin depolymerization. RESULTS: Pressure time-dependently increased SW620 and HCT-116 cell counts on collagen or fibronectin (P < 0.01). Pressure increased the SW620 S-phase fraction from 28 +/- 1 to 47 +/- 1% (P = 0.0002). Pressure activated p38, ERK, and c-Src (P < 0.05 each) but not Akt/PKB. Pressure decreased cytosolic PKC activity, and translocated PKCalpha to a membrane fraction. Blockade of p38, ERK, c-Src or PI-3-K or actin depolymerization did not inhibit pressure-stimulated proliferation. However, global tyrosine kinase blockade (genistein) and PKC blockade (calphostin C) negated pressure-induced proliferation. CONCLUSIONS: Extracellular pressure stimulates cell proliferation and activates several signals. However, the mitogenic effect of pressure requires only tyrosine kinase and PKCalpha activation. Pressure may modulate colon cancer growth and implantation by two distinct pathways, one stimulating proliferation and the other promoting adhesion.