Survey of Toxoplasma gondii antibodies in meat juice of wild boar (Sus scrofa) in several districts of the Czech Republic

Introduction and objective The aims of the study were: 1) to detect antibodies against Toxoplasma gondii from wild boar meat; 1) establish seroprevalence of toxoplasmosis in the wild boar population; 3) establish risk factors concerned in higher possible seroprevalence; 4) to estimate the usefulness of meat juice for detection of T. gondii antibodies in wild boar. Material and Methods Diaphragm meat juice samples from 656 wild boar (Sus scrofa) were collected during the hunting seasons between September 2008 – October 2010 from 9 districts of the Czech Republic. The samples were stratified per age category into 2 groups: piglets (n = 279) and yearlings together with adults (n = 377). The in-house ELISA test was used for the detection of antibodies against T. gondii from the meat juice samples. Results Antibodies against T. gondii were detected by in-house ELISA in 260 of 656 wild boars (40%) with 26% prevalence in piglets (72/279) and 50% prevalence in yearlings and adults (188/377). The district total seroprevalences ranged between 32% – 59%, with a significantly higher prevalence in the district of Havlíčkův Brod (59%). Statistically significant differences (p-value < 0.05) were found between 2 age categories, and between 9 districts, with a significant variability in the district of Havlíčkův Brod. Seroprevalence correlated positively with farm density, but without any statistical significance. Conclusions The obtained results indicate that consumption of raw or undercooked meat from wild boars can carry an important risk of toxoplasma infection. Post mortem detection of antibodies in meat juice samples using ELISA is a useful alternative to blood serum examination. In addition, a diaphragm sample has been well-proven as a matrix sample for the contemporaneous diagnostics of trichinellosis and toxoplasmosis

First record of chambered hexactinellid sponges from the Palaeozoic

A new chambered hexactinellid sponge, Casearia devonica sp. nov., is described from the Lower Devonian of northern Spain (Cantabrian Mountains). The fossil represents the first evidence of chambered hexactinellid sponges from the Palaeozoic and the oldest representative of the order Hexactinosida. Casearia devonica sp. nov. occurred within small metre-sized mud mounds that developed in deeper water below the storm wave base

Gene Deletion Mutants Reveal a Role for Semaphorin Receptors of the Plexin-B Family in Mechanisms Underlying Corticogenesis ▿

Semaphorins and their receptors, plexins, are emerging as key regulators of various aspects of neural and nonneural development. Semaphorin 4D (Sema4D) and B-type plexins demonstrate distinct expression patterns over critical time windows during the development of the murine neocortex. Here, analysis of mice genetically lacking plexin-B1 or plexin-B2 revealed the significance of Sema4D-plexin-B signaling in cortical development. Deficiency of plexin-B2 resulted in abnormal cortical layering and defective migration and differentiation of several subtypes of cortical neurons, including Cajal-Retzius cells, GABAergic interneurons, and principal cells in vivo. In contrast, a lack of plexin-B1 did not impact on cortical development in vivo. In various ex vivo assays on embryonic forebrain, Sema4D enhanced the radial and tangential migration of developing neurons in a plexin-B2-dependent manner. These results suggest that Sema4D-plexin-B2 interactions regulate mechanisms underlying cell specification, differentiation, and migration during corticogenesis

Gene deletion mutants reveal a role for semaphorin receptors of the plexin-B family in mechanisms underlying corticogenesis

Semaphorins and their receptors, plexins, are emerging as key regulators of various aspects of neural and nonneural development. Semaphorin 4D (Sema4D) and B-type plexins demonstrate distinct expression patterns over critical time windows during the development of the murine neocortex. Here, analysis of mice genetically lacking plexin-B1 or plexin-B2 revealed the significance of Sema4D-plexin-B signaling in cortical development. Deficiency of plexin-B2 resulted in abnormal cortical layering and defective migration and differentiation of several subtypes of cortical neurons, including Cajal-Retzius cells, GABAergic interneurons, and principal cells in vivo. In contrast, a lack of plexin-B1 did not impact on cortical development in vivo. In various ex vivo assays on embryonic forebrain, Sema4D enhanced the radial and tangential migration of developing neurons in a plexin-B2-dependent manner. These results suggest that Sema4D-plexin-B2 interactions regulate mechanisms underlying cell specification, differentiation, and migration during corticogenesis

Plexin-B2, but not Plexin-B1, critically modulates neuronal migration and patterning of the developing nervous system in vivo

Semaphorins and their receptors, plexins, have emerged as important cellular cues regulating key developmental processes. B-type plexins directly regulate the actin cytoskeleton in a variety of cell types. Recently, B-type plexins have been shown to be expressed in striking patterns in the nervous system over critical developmental windows. However, in contrast to the well characterized plexin-A family, the functional role of plexin-B proteins in neural development and organogenesis in vertebrates in vivo is not known. Here, we have elucidated the functional contribution of the two neuronally expressed plexin-B proteins, Plexin-B1 or Plexin-B2, toward the development of the peripheral nervous system and the CNS by generating and analyzing constitutive knock-out mice. The development of the nervous system was found to be normal in mice lacking Plexin-B1, whereas mice lacking Plexin-B2 demonstrated defects in closure of the neural tube and a conspicuous disorganization of the embryonic brain. After analyzing mutant mice, which bypassed neural tube defects, we observed a key requirement for Plexin-B2 in proliferation and migration of granule cell precursors in the developing dentate gyrus, olfactory bulb, and cerebellum. Furthermore, we identified semaphorin 4C as a high-affinity ligand for Plexin-B2 in binding and functional assays. Semaphorin 4C stimulated activation of ErbB-2 and RhoA via Plexin-B2 and enhanced proliferation and migration of granule cell precursors. Semaphorin 4C-induced proliferation of ventricular zone neuroblasts was abrogated in mice lacking Plexin-B2. These genetic and functional analyses reveal a key requirement for Plexin-B2, but not Plexin-B1, in patterning of the vertebrate nervous system in vivo