Myxobolus desaequalis n. sp. (Myxozoa,Myxosporea), parasite of the Amazonian freshwater fish,Apteronotus albifrons (Teleostei,Apteronotidae)

Myxobolus desaequalis n. sp. is described from the gill lamellae of the freshwater fish Apteronotus albifrons, collected in the Amazon River, near the city of Salvaterra, Brazil. Large spherical plasmodia filled with disporic pansporoblasts and spores were observed. Ellipsoidal to pyriform spores are 18.3 microm length x 11.2 microm width x 4.4 microm thickness. The anterior end of the spores contain two extremely unequal pyriform polar capsules measuring: (larger): 11.2 microm length, 4.9 microm width, and an isofilar polar filament with 11 to 12 turns obliquely to the longitudinal axis; (smaller): 4.6 microm length, 2.8 microm width, and an isofilar polar filament with 4 to 5 turns, obliquely to the longitudinal axis.     

Release of NO by a nitrosyl complex upon activation by the mitochondrial reducing power

The reaction of trans-[Ru(NH(3))(4)P(OEt)(3)NO](3+) and mitochondria was investigated through differential pulse polarography and fluorimetry. The nitrosyl complex undergoes one-electron reduction centered on the NO ligand site. The reaction between the mitochondrial reductor and trans-[Ru(NH(3))(4)P(OEt)(3)NO](3+) exhibits a second order specific rate constant calculated as k=2 x 10(1) M(-1) s(-1). The reduced species, trans-[Ru(NH(3))(4)P(OEt)(3)NO](2+), quickly releases NO, yielding trans-[Ru(NH(3))(4)P(OEt)(3)H(2)O](2+). The low toxicities of both trans-[Ru(NH(3))(4)P(OEt)(3)(NO)](2+) and trans-[Ru(NH(3))(4)P(OEt)(3)H(2)O](2+) and its ability to release NO after reductive activation in a biological medium make the nitrosyl compound a useful model of a hypotensive drug.     

Steady-state luminescence investigation of the binding of Eu(III) and Tb(III) ions with synthetic peptides derived from plant thionins

This work reports Eu(III) and Tb(III) luminescence titrations in which the lanthanide ions were used as spectroscopic probes for Ca(II) ions to determine the metal binding ability of Ac-NESVKEEGGW-NH(2) and Ac-NESVKEDGGW-NH(2). These decapeptides correspond to the putative calcium binding region of the plant antifungal proteins SI-alpha1 from Sorghum bicolor and of Zeathionin from Zea mays, respectively. The luminescence spectra for the Eu(III)-decapeptide system (red emission) with the excitation at the Trp band at 280 nm showed an enhancement of the intensities of the 5D(0)-->7F(J) transitions (where J=0-4) with increments of Eu(III) ion concentration. The photoluminescence titration data of the terbium ion (green emission) in the decapeptide solutions showed intensification of the 5D(4)-->7F(J) transitions (J=0-6), similar to that observed for the Eu(III) ion. Thus, energy transfer from Ac-NESVKEEGGW-NH(2) and Ac-NESVKEDGGW-NH(2) to the trivalent lanthanide ions revealed that these peptides are capable of binding to these metal ions with association constants of the order of 10(5) M(-1). The amino acid derivative Ac-Trp-OEt also transferred energy to Tb(III) and Eu(III) ions as judged from the quenching of tryptophan luminescence. However, the energy transfers were significantly lower. Taken together the luminescence titration data indicated that Ac-NESVKEEGGW-NH(2) and Ac-NESVKEDGGW-NH(2) bind efficiently to both trivalent lanthanide ions and that these ions may be used as probes to distinguish an anionic peptide from a neutral amino acid derivative.     

Sharp borders from fuzzy gradients

Critical boundaries in the early Drosophila embryo are set by morphogenetic gradients. A new quantitative study shows that the placement of one such boundary is more accurate than the gradient thought to set it. Genetic analysis of the accuracy of the process implicates a gene not previously thought to be involved.     

TGFbeta1 -mediated epithelial to mesenchymal transition is accompanied by invasion in the SiHa cell line

It has recently been suggested by several investigators that the epithelial-mesenchymal transition-inducing capacity of TGFbetas contributes to invasive transition of tumors at later stages of carcinogenesis. In the present study, we examined the possibility of TGFbeta1-stimulated epithelial-mesenchymal transition in SiHa cell line, detailed molecular events in the process, and its possible contribution to the invasive transition of tumors. TGFbeta1-induced epithelial-mesenchymal transition of SiHa cells was based on morphological and biochemical criteria; actin stress fiber formation, focal translocalization of integrin alphav, talin, and vinculin, fibronectin-based matrix assembly at the cell periphery, and translocalization and down-regulation of E-cadherin. TGFbeta1 also stimulated surface expression of integrin alphavbeta3 and FAK activation. Focal translocalization of integrin alphav preceded actin reorganization and fibronectin matrix assembly, and functional blocking of the integrin suppressed actin stress fiber formation. Furthermore, induction of actin reorganization and fibronectin matrix assembly by TGFbeta1 were shown to be mutually independent events. These changes were irreversible because 5 minutes pulse exposure to TGFbeta1 was sufficient to stimulate progress of actin reorganization and fibronectin matrix assembly. In further studies with raft culture, TGFbeta1 was found to stimulate invasion of SiHa cells into a type I collagen gel matrix. In conclusion, TGFbeta1 stimulated epithelial-mesenchymal transition of SiHa cells, indicating a positive role in the invasive transition of tumors.     

Parathyroid hormone effects on signaling pathways in endothelial cells vary with peptide concentration

We have previously reported that parathyroid hormone (PTH) has specific effects on a human umbilical vein endothelial cell line. Further studies were performed to characterize the signaling cascades initiated by PTH. We report that PTH induced the appearance of voltage sensitive calcium channels. Furthermore, PTH increased ceramide but not diacylglycerol content. Since elevations in [Ca(2+)](i) and phospholipid turnover are signals for the activation of protein kinase C (PKC), the cells were screened for PKC isoforms. PTH induced a redistribution of the PKCepsilon to the particulate fractions of cell homogenates. In summary, PTH induced PKC translocation through a calcium-phospholipid pathway in an endothelial cell line.     

Laminin affects polymerization,depolymerization and neurotoxicity of Abeta peptide

Amyloid deposition in Alzheimer fibrils forms neurotoxic senile plaques in a process that may be modulated by associated proteins. In this work we demonstrate the ability of laminin-1 and laminin-2 to inhibit fibril formation and toxicity on cultured rat hippocampal neurons. We confirm that the laminin-1-derived peptide YFQRYLI inhibits efficiently both fibril formation and neurotoxicity and show that the IKVAV peptide inhibits amyloid neurotoxicity despite its slight inhibition of fibril formation. On other hand, laminin-1 induces disaggregation of preformed fibrils in vitro, characterized as a progressive disassembly of fibrils into protofibrils and further clearance of these latter species, leading to a continual inhibition of amyloid neurotoxicity.