Chromosomal disorders and male infertility

Infertility in humans is surprisingly common occurring in approximately 15% of the population wishing to start a family. Despite this, the molecular and genetic factors underlying the cause of infertility remain largely undiscovered. Nevertheless, more and more genetic factors associated with infertility are being identified. This review will focus on our current understanding of the chromosomal basis of male infertility specifically: chromosomal aneuploidy, structural and numerical karyotype abnormalities and Y chromosomal microdeletions. Chromosomal aneuploidy is the leading cause of pregnancy loss and developmental disabilities in humans. Aneuploidy is predominantly maternal in origin, but concerns have been raised regarding the safety of intracytoplasmic sperm injection as infertile men have significantly higher levels of sperm aneuploidy compared to their fertile counterparts. Males with numerical or structural karyotype abnormalities are also at an increased risk of producing aneuploid sperm. Our current understanding of how sperm aneuploidy translates to embryo aneuploidy will be reviewed, as well as the application of preimplantation genetic diagnosis (PGD) in such cases. Clinical recommendations where possible will be made, as well as discussion of the use of emerging array technology in PGD and its potential applications in male infertility

Left-Right Symmetry and Supersymmetric Unification

The existence of an SU(3) X SU(2)_L X SU(2)_R X U(1) gauge symmetry with g_L = g_R at the TeV energy scale is shown to be consistent with supersymmetric SO(10) grand unification at around 1O^{16} GeV if certain new particles are assumed. The additional imposition of a discrete Z_2 symmetry leads to a generalized definition of R parity as well as highly suppressed Majorana neutrino masses. Another model based on SO(10) X SO(10) is also discussed.Comment: 11 pages, 2 figures not included, UCRHEP-T124, Apr 199

Centaurus A at Ultra-High Energies

We review the importance of Centaurus A in high energy astrophysics as a nearby object with many of the properties expected of a major source of very high energy cosmic rays and gamma-rays. We examine observational techniques and the results so far obtained in the energy range from 200 GeV to above 100 EeV and attempt to fit those data with expectations of Centaurus A as an astrophysical source from VHE to UHE energies.Comment: 11 pages, 4 figures, accepted for publication in PAS

Bounds on g5Zg_5^Z from Precision LEP Measurements

The parity violating but CP conserving anomalous three-gauge-boson coupling $g_5^Z$ induces a universal contribution to the left-handed coupling of the $Z$ boson to fermions. We find that the LEP measurements of the partial $Z$ widths and lepton forward-backward asymmetries are sufficiently precise to place a bound of order $|g_5^Z|$ less than $\sim~10\%$. This bound is significantly better than what can be obtained at present from rare $K$ and $B$ meson decays.Comment: Phys. Lett. B333 (1994) 207. A few minor errors in the table are corrected and updated experimental and theoretical numbers are used. The conclusions are unchanged. These changes will appear in an erratum to the published pape

VHMPID: a new detector for the ALICE experiment at LHC

This article presents the basic idea of VHMPID, an upgrade detector for the ALICE experiment at LHC, CERN. The main goal of this detector is to extend the particle identification capabilities of ALICE to give more insight into the evolution of the hot and dense matter created in Pb-Pb collisions. Starting from the physics motivations and working principles the challenges and current status of development is detailed.Comment: 4 pages, 6 figures. To be published in EPJ Web of Conference

Downregulation of CIITA Function by Protein Kinase A (PKA)-Mediated Phosphorylation: Mechanism of Prostaglandin E, Cyclic AMP, and PKA Inhibition of Class II Major Histocompatibility Complex Expression in Monocytic Lines

Prostaglandins, pleiotropic immune modulators that induce protein kinase A (PKA), inhibit gamma interferon induction of class II major histocompatibility complex (MHC) genes. We show that phosphorylation of CIITA by PKA accounts for this inhibition. Treatment with prostaglandin E or 8-bromo-cyclic AMP or transfection with PKA inhibits the activity of CIITA in both mouse and human monocytic cell lines. This inhibition is independent of other transcription factors for the class II MHC promoter. These same treatments also greatly reduced the induction of class II MHC mRNA by CIITA. PKA phosphorylation sites were identified using site-directed mutagenesis and phosphoamino acid analysis. Phosphorylation at CIITA serines 834 and 1050 accounts for the inhibitory effects of PKA on CIITA-driven class II MHC transcription. This is the first demonstration that the posttranslational modification of CIITA mediates inhibition of class II MHC transcription