LD2668 .T4 1954 G9 / Master of Science

Thesis (Ph. D.)--University of Wisconsin--Madison, 1947. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves [i]-IX).

No description available.

No abstract available. / Thesis (Ph.D.)-University of Natal, Durban, 1973.

Thesis (M.Phil.) - University of Queensland, 2005. / Includes bibliography.

M.Tech. (Biomedical Technology) / Despite the introduction of prophylactic treatment for Rh negative females, Rhesus Haemolytic Disease of the Foetus and Newborn (HDN) remains a problem. The serological diagnosis of this disease is mainly by maternal antibody identification and titration and the estimation of the optical density deviation (ODD) at 450 nanometers of the amniotic fluid. The correlation of these two results is not always good. The advent of molecular biology techniques such as the Polymerase Chain Reaction (PCR) and the sequencing of genes heralded the start of prenatal diagnosis of genetically inherited diseases and also enabled the prediction of the Rhesus group of the foetus. It would be advantageous to be able to predict with certainty the RhD status of a foetus suspected of having HDN without subjecting the mother and foetus to the risk of multiple invasive procedures such as Chorionic Villus Sampling (CVS) and Foetal Blood Sampling(FBS). The amniocentesis performed initially on a mother suspected of carrying an affected foetus would provide the sample necessary for the extraction of foetal DNA for prenatal Rh determination. Two PCR assays were used to determine the RhD group of the foetus: one using two primers amplifying a section ofIntron 4 and the other using four primers, two specific for Exon 7 and two specific for Exon 10 of the Rh gene. In 85.7% (18/21 cases) there was complete correlation between the molecular and the serological methods for RhD determination. One White foetus presented a unique profile, that of RhD negative in both molecular assays and RhD positive serologically. In the non-White group there were discrepancies between the two molecular methods as well as between the molecular and the serological methods used. This study shows that great care should be taken in the interpretation of RhD status prenatally using molecular biology techniques especially in the non-Caucasian population of South Africa in which there are many polymorphisrns in the Rhesus blood group system. For the moment, the results should be used in conjunction with serological results and clinical parameters for the diagnosis and treatment of Rh HDN.

No description available.

Thesis (M.P.H.)--University of Michigan, 1945.

Thesis (M.P.H.)--University of Michigan, 1945.

Proteins of the conserved Mep-Amt-Rh superfamily, including mammalian Rhesus factors,<p>mediate ammonium transport. Ammonium is an important nitrogen source for the<p>biosynthesis of amino acids for instance but its accumulation is also known as cytotoxic in<p>animals. Nevertheless, the controlled disposal of ammonium in urine plays a critical role in<p>the regulation of the acid-base homeostasis. Alteration in ammonium transport via human Rh<p>proteins could have clinical outcomes. In this work, we addressed aspects of structurefunction<p>analysis of altered human Rhesus proteins using a heterologous expression system<p>and further characterized aspects of the patho-physiological roles of Rh proteins using<p>knockout mice models available in the laboratory.<p>Using a yeast-based expression assay, we characterized human Rh variants resulting from non<p>synonymous single nucleotide polymorphisms (nsSNPs) with known or unknown clinical<p>phenotypes. The HsRhAG variants (I61R, F65S) associated to overhydrated hereditary<p>stomatocytosis (OHSt), a disease affecting erythrocytes, proved affected in intrinsic<p>bidirectional ammonium transport, suggesting altered ammonium transport as a potential<p>hallmark of the disease. Moreover, these variants showed trans-dominant negative effects on<p>the activity of their native HsRhAG counterpart, suggesting altered cooperation of the<p>subunits in “heteromeric” transport complexes. On the other hand, we revealed that the<p>R202C variant of HsRhCG, the orthologue of mouse Rhcg required for optimal urinary<p>ammonium excretion and blood pH control, shows an impaired inherent ammonium transport<p>activity. HsRhCGR202C may potentially confer susceptibility to disorders leading to metabolic<p>acidosis for instance. <p>MmRhcg has been shown to be expressed in the male mice epididymal tract, its absence<p>leading to a more acidic luminal fluid and to a reduced male fertility. Using mice<p>models, we further investigated the role of Rhcg and Rhbg proteins in the male<p>reproductive function. <p> / Doctorat en Sciences / info:eu-repo/semantics/nonPublished