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J Brennand

Publications and source records attributed to J Brennand.

40 records · Page 3Linked to original sources
PubMedDate not supplied

Expression of human HPRT in the central nervous system of transgenic mice.

Severe deficiency of hypoxanthine phosphoribosyltransferase (HPRT) in man results in the Lesch-Nyhan syndrome, an X-linked neurological disorder characterized by mental retardation, choreoathetosis and a compulsive tendency towards self-mutilation. Although the HPRT gene is normally constitutively expressed in all tissues at low levels, expression is elevated approximately fourfold in several regions of the central nervous system, particularly in the basal ganglia. The relationships between HPRT deficiency, tissue-specific alterations of nucleotide metabolism and the neuropathology of the Lesch-Nyhan syndrome remain unclear. Here we have microinjected recombinant molecules containing human HPRT (hHPRT) complementary DNA, the mouse metallothionein-I (MT-I) promoter and the 3'-untranslated portion of the human growth hormone (hGH) gene into mouse embryos to produce transgenic animals that express hHPRT on induction by cadmium. The hHPRT cDNA in these experiments contained 88 base pairs (bp) of 5'-untranslated and 190 bp of 3'-untranslated sequences, and the full-length coding sequence. We studied the in vivo expression of this MT-hHPRT fusion gene and observed preferential hHPRT expression in tissues of the central nervous system (CNS). This study suggests that sequences within the hHPRT transcript (cDNA) influence CNS expression via increased synthesis or stability of messenger RNA.

Animals↗
PubMedDate not supplied

Congenital parvovirus B19 infection: experience of a recent epidemic.

OBJECTIVE: We report the management and outcome of 6 cases of non-immune fetal hydrops secondary to parvovirus B19 infection presenting over a 5-month period. METHODS: The Queen Mothers Hospital is a tertiary referral centre for fetal medicine. All cases were suspected on the basis of ultrasound evidence of hydrops. Two cases were managed conservatively owing to the presence of an active fetus with evidence of resolving hydrops. Fetal blood sampling intra-uterine transfusion and drainage of ascitic fluid were performed in 3 cases. The 6th case unfortunately resulted in an intra-uterine death prior to fetal blood sampling. RESULTS: Maternal parvovirus specific B19 was identified in all cases. Fetal parvovirus B19 IgM was identified in the 3 cases in whom fetal blood sampling was performed. A single intra-uterine transfusion was performed in these 3 cases; fetal hydrops resolved in 2 of these pregnancies progressing to the birth of a healthy baby at term, whereas 1 case was complicated by intra-uterine death. Fetal hydrops resolved in both cases managed conservatively, leading to the birth of a healthy baby at term. CONCLUSIONS: Parvovirus B19 infection should always be suspected in cases of non-immune hydrops. Conservative management will be appropriate in some cases and should involve weekly ultrasonography. The outlook for pregnancies presenting with gross hydrops remains guarded, even if intra-uterine transfusion is performed successfully.

Adult↗