K0-Sigma+ Photoproduction with SAPHIR

Preliminary results of the analysis of the reaction p(gamma,K0)Sigma+ are presented. We show the first measurement of the differential cross section and much improved data for the total cross section than previous data. The data are compared with model predictions from different isobar and quark models that give a good description of p(gamma,K+)Lambda and p(gamma,K+)Sigma0 data in the same energy range. Results of ChPT describe the data adequately at threshold while isobar models that include hadronic form factors reproduce the data at intermediate energies.Comment: 4 pages, Latex2e, 4 postscript figures. Talk given at the International Conference on Hypernuclear and Strange Particle Physics (HYP97), Brookhaven National Laboratory, USA, October 13-18, 1997. To be published in Nucl. Phys. A. Revised version due to changes in experimental dat

Aufbau und Test einer MWPC als Strahlprofilmonitor und Vetozaehler fuer den SAPHIR-Detektor

This report describes a two plane Multiwire Proportional Chamber which is developed for the measurement of the photon beam profile at SAPHIR. For the photon flux normalisation it is essential that the entire tagged photonbeam crosses the SAPHIR target. This can be monitored with this MWPC. Additionally the chamber will be used as a fast veto detector for charged particles coming from the beamline. (orig.)SIGLEAvailable from TIB Hannover: RN 4852(93-25) / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekDEGerman

Immunocytochemical and ultrastructural evidence of glial cells and hyalocytes in internal limiting membrane specimens of idiopathic macular holes.

PURPOSE: To provide new information on epiretinal cell proliferation and the cells' origin in idiopathic macular holes and to overcome the effects of embedding and sectioning preparation procedures on cell-distribution patterns. METHODS: Interference and phase-contrast microscopy, immunocytochemistry, and scanning and transmission electron microscopy were performed on surgically excised whole-mounted internal limiting membrane (ILM) specimens removed from 60 eyes with idiopathic macular holes. Cell distribution and cell morphology were correlated with immunocytochemical staining characteristics. Twelve cell type-specific antibodies were used to detect glial cells, hyalocytes, retinal pigment epithelial cells, retinal ganglion cells, and immune cells. Cell viability was analyzed. RESULTS: Epiretinal cell proliferation was found in all ILM specimens, irrespective of the stage of the macular hole. Cell density showed a broad variety. Immunocytochemistry frequently revealed simultaneous expression of GFAP/CD45, GFAP/CD64, GFAP/CD68, GFAP/CRALBP, and GFAP/CD90. Some cells presented with intracellular contractile filaments (anti-αSMA); others were not immunoreactive to any antibody examined. The percentage of viable cells showed a broad variety with a mean of 73% (SD 29%). Electron microscopy demonstrated glial cells, hyalocytes, and myofibroblast-like cells. CONCLUSIONS: The presence of epiretinal cells at the ILM in all macular hole stages strongly suggests a substantial involvement of cell migration and proliferation in the course of macular hole development. Glial cells and hyalocytes play the predominant role in epiretinal cell proliferation. Given the co-expression of glial cell and hyalocyte markers, transdifferentiation of epiretinal cells needs further elucidation, especially with respect to αSMA-positive cells leading to traction at the vitreoretinal interface

Mitochondrial glutathione peroxidase 4 disruption causes male infertility

none16Glutathione peroxidase 4 (GPx4), first described as an antioxidant enzyme, is the predominant selenoenzyme in testis and has been suspected of being vital for spermatogenesis. Cytosolic, mitochondrial, and nuclear isoforms are all encoded by the same gene. While disruption of entire GPx4 causes early embryonic le- thality in mice, inactivation of nuclear GPx4 does not impair embryonic development or fertility. Here, we show that deletion of mitochondrial GPx4 (mGPx4) allows both normal embryogenesis and postnatal devel- opment, but causes male infertility. Infertility was associ- ated with impaired sperm quality and severe structural abnormalities in the midpiece of spermatozoa. Knockout sperm display higher protein thiol content and recapitu- late features typical of severe selenodeficiency. Interest- ingly, male infertility induced by mGPx4 depletion could be bypassed by intracytoplasmic sperm injection. We also show for the first time that mGPx4 is the prevailing GPx4 product in male germ cells and that mGPx4 disruption has no effect on proliferation or apoptosis of germinal or somatic tissue. Our study finally establishes that mito- chondrial GPx4 confers the vital role of selenium in mammalian male fertility and identifies cytosolic GPx4 as the only GPx4 isoform being essential for embryonic development and apoptosis regulationmixedSchneider, M.; Forster, H.; Boersma, A.; Seiler, A.; Wehnes, H.; Sinowatz, F.; Neumuller, C.; Deutsch, M. J.; Walch, A.; DE ANGELIS, M. H.; Wurst, W.; Ursini, Fulvio; Roveri, Antonella; Maleszewski, M.; Maiorino, Matilde; Conrad, M.M., Schneider; H., Forster; A., Boersma; A., Seiler; H., Wehnes; F., Sinowatz; C., Neumuller; Deutsch, M. J.; A., Walch; DE ANGELIS, M. H.; W., Wurst; Ursini, Fulvio; Roveri, Antonella; M., Maleszewski; Maiorino, Matilde; M., Conra

Mitochondrial glutathione peroxidase 4 disruption causes male infertility.

Selenium is linked to male fertility. Glutathione peroxidase 4 (GPx4), first described as an antioxidant enzyme, is the predominant selenoenzyme in testis and has been suspected of being vital for spermatogenesis. Cytosolic, mitochondrial, and nuclear isoforms are all encoded by the same gene. While disruption of entire GPx4 causes early embryonic lethality in mice, inactivation of nuclear GPx4 does not impair embryonic development or fertility. Here, we show that deletion of mitochondrial GPx4 (mGPx4) allows both normal embryogenesis and postnatal development, but causes male infertility. Infertility was associated with impaired sperm quality and severe structural abnormalities in the midpiece of spermatozoa. Knockout sperm display higher protein thiol content and recapitulate features typical of severe selenodeficiency. Interestingly, male infertility induced by mGPx4 depletion could be bypassed by intracytoplasmic sperm injection. We also show for the first time that mGPx4 is the prevailing GPx4 product in male germ cells and that mGPx4 disruption has no effect on proliferation or apoptosis of germinal or somatic tissue. Our study finally establishes that mitochondrial GPx4 confers the vital role of selenium in mammalian male fertility and identifies cytosolic GPx4 as the only GPx4 isoform being essential for embryonic development and apoptosis regulation