Intergenerational and early life influences on the well-being of Australian Aboriginal and Torres Strait Islander children: overview and selected findings from Footprints in Time, the Longitudinal Study of Indigenous Children.

Footprints in Time: The Longitudinal Study of Indigenous Children (LSIC) is a national study of 1759 Australian Aboriginal and Torres Strait Islander children living across urban, regional and remote areas of Australia. The study is in its 11th wave of annual data collection, having collected extensive data on topics including birth and early life influences, parental health and well-being, identity, cultural engagement, language use, housing, racism, school engagement and academic achievement, and social and emotional well-being. The current paper reviews a selection of major findings from Footprints in Time relating to the developmental origins of health and disease for Australian Aboriginal and Torres Strait Islander peoples. Opportunities for new researchers to conduct further research utilizing the LSIC data set are also presented.

A new potexvirus associated with strawberry mild yellow edge disease.

A physical map of cDNA clones prepared from dsRNA associated with the MY-18 source of strawberry mild yellow edge (SMYE) was constructed and 854 nucleotides adjacent to the 3' poly(A) tail were sequenced. The larger open reading frame product of Mr 25714 showed considerable amino acid homology to the coat protein cistrons of six potexviruses and two carlaviruses. A second product of Mr 11216 encoded completely within the coat protein cistron, but in a different frame, has similarities to two potexvirus polypeptides. The Mr 25714 ORF was fused to the Protein A gene in an expression vector and the fusion protein was purified by affinity chromatography and used to immunize a rabbit. The resulting polyclonal antiserum reacted strongly in immunoelectron microscopical tests with filamentous particles resembling those of potexviruses. Such particles were detected in the following SMYE sources: D-74 from Germany, two from the United Kingdom in Fragaria vesca 'Alpine' indicator plants and Oregon MY-18 in Rubus rosifolius. Among 27 potexvirus antisera tested for serological reactions none yielded strong decoration. Examination of ultrathin sections of R. rosifolius and F. vesca tissue infected with SMYE revealed aggregates of filamentous particles in phloem parenchyma cells. dsRNA from nine sources of SMYE collected from around the world reacted with the cDNA clones of this potexvirus in Northern hybridizations. It is concluded that the potexvirus is hitherto undescribed and the name strawberry mild yellow edge-associated potexvirus is proposed.

The effect of SKF-525A and of altered hepatic blood flow on lidocaine clearance in the cat.

Hepatic blood flow and hepatic uptake of lidocaine were determined in cats during constant intravenous infusion of lidocaine. Lidocaine clearance is directly linked to hepatic blood flow with reductions in flow being reflected in equal reductions in hepatic clearance. Altered blood flow did not result in altered rates of lidocaine extraction. Lidocaine extraction ratio was 28%. Hepatic blood flow and lidocaine metabolism were measured before and 60 min after an intramuscular injection of SKF-525A (50 mg/kg). SKF-525A produced a reduction in hepatic clearance of lidocaine to 60% of control values, entirely as a result of a reduction in hepatic extraction ratios. Hepatic blood flow and vascular conductance were not affected by SKF-525A.

Irreversibility of methylandrostenediol-induced hypertension in the rat after suspension of the androgen treatment.

Administration of 10 mg of methylandrostenediol for 10 weeks to uninephrectomized, salt drinking, female Sprague Dawley rats caused severe hypertension with extensive renal and cardiovascular damage. The hypertension was accompanied by increased consumption of sodium, high sodium levels in peripheral plasma, decreased weight of the pituitary, thymus, adrenals and ovaries and decreased content of renal renin. Methylandrostenediol treatment also produced impairment of normal adrenal steroidogenesis, reflected in elevated production in vitro of 11-deoxycorticosterone during incubation of adrenal gland homogenates with (14)C-progesterone. Such increased production of deoxycorticosterone is probably responsible for the development of the hypertensive disease. If the methylandrostenediol-treated animals were kept alive for 12 additional weeks after suspension of the treatment with the androgen, the hypertension, as well as the high sodium consumption, high plasma sodium concentrations and low levels of renal renin, persisted to the end of the experiment. The cardiovascular and renal lesions in these animals, killed 12 weeks after suspension of the androgen administration, were similar to those seen in the rats receiving methylandrostenediol but killed at the tenth week of the treatment. Suspension of methylandrostenediol administration, however, resulted in a return to normal weight of the pituitary, thymus, adrenals and ovaries within 12 weeks. Normal amounts of deoxycorticosterone were formed in vitro by the adrenal glands of these rats and the return to normal structure was also confirmed by a electron microscopic study. Thus, contrary to a previous experiment where methylandrostenediol was given for a shorter period of time and the hypertension was reversible, it was shown in this study that metacorticoid hypertension is induced by methylandrostenediol administration, as it is with treatment with deoxycorticosterone. Since adrenal steroidogenesis returned to normal, some other mechanisms must be involved in maintaining the hypertension. It is very likely that these factors are consequent to the extensive and irreversible renal and cardiovascular damage.