Survival rates associated with in vitro low-temperature storage of kutum (Rutilus kutum) eggs

To study the effects of post-stripping oocyte ageing at low temperatures on the viability of kutum (Rutilus kutum) oocytes, unfertilised eggs of five females were stored in ovarian fluid at temperatures of 4 and 7 degrees centigrade for 24 hours post stripping (HPS). The stored ova of five female kutum were separately fertilised at 0 (i.e., control eggs fertilised prior to storage), 4, 8, 12, 16, 20, and 24 HPS. The eyeing and hatching rates were recorded as indices of the egg quality. The results indicated that the maximum eyeing and hatching rates of the eggs (92% and 74%, respectively) were observed at 0 HPS, whereas the storage of the eggs at 4 °C for 24 HPS decreased the eyeing and hatching rates to 36% and 28%, respectively. The use of the higher storage temperature resulted in a more rapid decrease in the egg viability: eyeing and hatching rates of 9% and 2%, respectively, were obtained after storage at 7 °C for 24 HPS. The present study demonstrated that stripped kutum eggs that are stored in ovarian fluid at 4 and 7 degrees centigrade should be fertilised within 12 and 8 HPS, respectively, to obtain viability rates higher than 50%

The Dynamics of Morphotactic Change in Sango

Proceedings of the Twentieth Annual Meeting of the Berkeley Linguistics Society: Special Session on Historical Issues in African Linguistics (1994

Characterisation of metakaolin-based geopolymers using beam-based and conventional PALS.

The nano-porosity of metakaolin-based geopolymers and the effect of heat-treatment on porosity have been studied with conventional and beam-based positron annihilation lifetime spectroscopy (PALS). Conventional PALS found significant nano-porosity in the geopolymers, as indicated by the presence in the PALS spectrum of two long lifetime components, τ3 = 1.58 ns and τ4 = 47 ns, associated with pore diameters of approximately 0.5 and 3 nm respectively. The lifetime of the shorter component was found to decrease monotonically with successive heat treatments of 300°C and 600°C. Beam-based PALS, conducted at 5 keV, also indicated two long lifetime components, τ3 = 4.84 ns and τ4 = 54.6 ns. These are significantly longer than those observed by conventional PALS and the monotonic decrease of τ3 with successive heat treatments was not observed. As the beam-based PALS probed only the near-surface region, with an average implantation depth of about 350 nm, these results suggest that the near-surface structure may vary significantly from that of the bulk. This could be an inherent property of the samples or an artefact caused by surface effects or sample outgassing.ARC Centre for Antimatter-Matter Studies; Australian National University (ANU); Flinders University; James Cook University (JCU); The Institute of Physics; Australian Government Department of Innovation, Industry, Science and Researc

Cell type-specific regulation of CCN2 protein expression by PI3K–AKT–FoxO signaling

The biological activity of connective tissue growth factor (CTGF, CCN2) is regulated at the level of intracellular signaling leading to gene expression, and by its extracellular interaction partners which determine the functional outcome of CCN2 action. In this overview, we summarize the data which provide evidence that one of the major signaling pathways, phosphatidylinositol-3 kinase (PI3K)–AKT signaling, shows a remarkable cell type-dependence in terms of regulation of CCN2 expression. In smooth muscle cells, fibroblasts, and epithelial cells, inhibition of this pathway either reduced CCN2 expression or was not involved in CCN2 gene expression depending on the stimulus used. In microvascular endothelial cells by contrast, activation of PI3K–AKT signaling was inversely related to CCN2 expression. Upregulation of CCN2 upon inhibition of PI3K–AKT was also observed in primary cultures of human endothelial cells (HUVEC) exposed to laminar flow in an in vitro flow-through system. In different types of endothelial cells, FoxO transcription factors, which are negatively regulated by AKT, were identified as potent activators of CCN2 gene expression. In HUVEC, we observed a correlation between enhanced nuclear localization of FoxO1 and increased synthesis of CCN2 protein in areas of non-uniform shear stress. These data indicate that FoxO proteins are key regulators of CCN2 gene expression which determine the effect of PI3K–AKT activation in terms of CCN2 regulation. Short summary Phosphatidylinositol-3 kinase (PI3K)–AKT signaling shows a remarkable cell type-dependence in terms of regulation of CCN2 expression. In endothelial cells activation of PI3K - AKT signaling was inversely related to CCN2 expression. FoxO transcription factors, which are negatively regulated by AKT, were identified as potent activators of CCN2 gene expression

Experimental Evidence of Radiation Reaction in the Collision of a High-Intensity Laser Pulse with a Laser-Wakefield Accelerated Electron Beam

The dynamics of energetic particles in strong electromagnetic fields can be heavily influenced by the energy loss arising from the emission of radiation during acceleration, known as radiation reaction. When interacting with a high-energy electron beam, today's lasers are sufficiently intense to explore the transition between the classical and quantum radiation reaction regimes. We present evidence of radiation reaction in the collision of an ultrarelativistic electron beam generated by laser-wakefield acceleration (μ 500 MeV) with an intense laser pulse (a0>10). We measure an energy loss in the postcollision electron spectrum that is correlated with the detected signal of hard photons (γ rays), consistent with a quantum description of radiation reaction. The generated γ rays have the highest energies yet reported from an all-optical inverse Compton scattering scheme, with critical energy >30 MeV

Protein kinase C activation disrupts epithelial apical junctions via ROCK-II dependent stimulation of actomyosin contractility

<p>Abstract</p> <p>Background</p> <p>Disruption of epithelial cell-cell adhesions represents an early and important stage in tumor metastasis. This process can be modeled <it>in vitro </it>by exposing cells to chemical tumor promoters, phorbol esters and octylindolactam-V (OI-V), known to activate protein kinase C (PKC). However, molecular events mediating PKC-dependent disruption of epithelial cell-cell contact remain poorly understood. In the present study we investigate mechanisms by which PKC activation induces disassembly of tight junctions (TJs) and adherens junctions (AJs) in a model pancreatic epithelium.</p> <p>Results</p> <p>Exposure of HPAF-II human pancreatic adenocarcinoma cell monolayers to either OI-V or 12-O-tetradecanoylphorbol-13-acetate caused rapid disruption and internalization of AJs and TJs. Activity of classical PKC isoenzymes was responsible for the loss of cell-cell contacts which was accompanied by cell rounding, phosphorylation and relocalization of the F-actin motor nonmuscle myosin (NM) II. The OI-V-induced disruption of AJs and TJs was prevented by either pharmacological inhibition of NM II with blebbistatin or by siRNA-mediated downregulation of NM IIA. Furthermore, AJ/TJ disassembly was attenuated by inhibition of Rho-associated kinase (ROCK) II, but was insensitive to blockage of MLCK, calmodulin, ERK1/2, caspases and RhoA GTPase.</p> <p>Conclusion</p> <p>Our data suggest that stimulation of PKC disrupts epithelial apical junctions via ROCK-II dependent activation of NM II, which increases contractility of perijunctional actin filaments. This mechanism is likely to be important for cancer cell dissociation and tumor metastasis.</p