|2014||Dyson RM, Palliser HK, Latter JL, Chwatko G, Glowacki R, Wright IMR, 'A Role for H2S in the microcirculation of newborns: The major metabolite of H2S (thiosulphate) is increased in preterm infants', PLoS ONE, 9 (2014) [C1]|
Excessive vasodilatation during the perinatal period is associated with cardiorespiratory instability in preterm neonates. Little evidence of the mechanisms controlling microvascular tone during circulatory transition exists. We hypothesised that hydrogen sulphide (H2S), an important regulator of microvascular reactivity and central cardiac function in adults and animal models, may contribute to the vasodilatation observed in preterm newborns. Term and preterm neonates (24-43 weeks gestational age) were studied. Peripheral microvascular blood flow was assessed by laser Doppler. Thiosulphate, a urinary metabolite of H2S, was determined by high performance liquid chromatography as a measure of 24 hr total body H2S turnover for the first 3 days of postnatal life. H2S turnover was greatest in very preterm infants and decreased with increasing gestational age (p = 0.0001). H2S turnover was stable across the first 72 hrs of life in older neonates. In very preterm neonates, H2S turnover increased significantly from day 1 to 3 (p = 0.0001); and males had higher H2S turnover than females (p = 0.04). A significant relationship between microvascular blood flow and H2S turnover was observed on day 2 of postnatal life (p = 0.0004). H2S may play a role in maintaining microvascular tone in the perinatal period. Neonates at the greatest risk of microvascular dysfunction characterised by inappropriate peripheral vasodilatation - very preterm male neonates - are also the neonates with highest levels of total body H2S turnover suggesting that overproduction of this gasotransmitter may contribute to microvascular dysfunction in preterms. Potentially, H2S is a target to selectively control microvascular tone in the circulation of newborns. © 2014 Dyson et al.
|2014||Dyson RM, Palliser HK, Lakkundi A, de Waal K, Latter JL, Clifton VL, Wright IM, 'Early microvascular changes in the preterm neonate: a comparative study of the human and guinea pig.', Physiol Rep, 2 (2014) [C1]|
|2014||Johnson NA, Kypri K, Latter J, McElduff P, Saunders JB, Saitz R, et al., 'Prevalence of unhealthy alcohol use in hospital outpatients', Drug and Alcohol Dependence, 144 270-273 (2014)|
|2014||Johnson NA, Kypri K, Latter J, McElduff P, Saunders JB, Saitz R, et al., 'Prevalence of unhealthy alcohol use in hospital outpatients', Drug and Alcohol Dependence, 144 270-273 (2014) [C1]|
Background: Few studies have examined the prevalence of unhealthy alcohol use in the hospital outpatient setting. Our aim was to estimate the prevalence of unhealthy alcohol use among patients attending a broad range of outpatient clinics at a large public hospital in Australia. Methods: Adult hospital outpatients were invited to complete the Alcohol Use Disorders Identification Test Consumption questions (AUDIT-C) using an iPad as part of a randomised trial testing the efficacy of alcohol electronic screening and brief intervention. Unhealthy alcohol use was defined as an AUDIT-C score =5 among men and =4 among women. Results: Sixty percent (3616/6070) of invited hospital outpatients consented, of whom 89% (3206/3616) provided information on their alcohol consumption (either reported they had not consumed any alcohol in the last 12 months or completed the AUDIT-C). The prevalence of unhealthy alcohol use was 34.7% (95% confidence interval [CI]: 33.0-36.3%). The prevalence among men aged 18-24 years, 25-39 years, 40-59 years and 60 years and older, was 74.4% (95% CI: 68.4-80.4%), 54.3% (95% CI: 48.7-59.8%), 44.1% (95% CI: 39.9-48.3%), and 27.0% (95% CI: 23.6-30.4%), respectively (43.1% overall; 95% CI: 40.8-45.5%). The prevalence among women aged 18-24 years, 25-39 years, 40-59 years, and 60 years and older, was 48.6% (95% CI: 39.2-58.1%), 36.9% (95% CI: 31.2-42.6%), 25.2% (95% CI: 21.5-29.0%) and 14.5% (95% CI: 11.7-17.3%), respectively (24.9% overall; 95% CI: 22.7-27.1%). Conclusion: A large number of hospital outpatients who are not currently seeking treatment for their drinking could benefit from effective intervention in this setting.
|2014||Wan C, Latter JL, Amirshahi A, Symonds I, Finnie J, Bowden N, et al., 'Progesterone Activates Multiple Innate Immune Pathways in Chlamydia trachomatis-Infected Endocervical Cells', American Journal of Reproductive Immunology, 71 165-177 (2014) [C1]|
Problem: Susceptibility to Chlamydia trachomatis infection is increased by oral contraceptives and modulated by sex hormones. We therefore sought to determine the effects of female sex hormones on the innate immune response to C. trachomatis infection. Method of study: ECC-1 endometrial cells, pre-treated with oestradiol or progesterone, were infected with C. trachomatis and the host transcriptome analysed by Illumina Sentrix HumanRef-8 microarray. Primary endocervical epithelial cells, prepared at either the proliferative or secretory phase of the menstrual cycle, were infected with C. trachomatis and cytokine gene expression determined by quantitative RT-PCR analysis. Results: Chlamydia trachomatis yield from progesterone-primed ECC-1 cells was significantly reduced compared with oestradiol-treated cells. Genes upregulated in progesterone-treated and Chlamydia-infected cells only included multiple CC and CXC chemokines, IL-17C, IL-29, IL-32, TNF-a, DEFB4B, LCN2, S100A7-9, ITGAM, NOD2, JAK1, IL-6ST, type I and II interferon receptors, numerous interferon-stimulated genes and STAT6. CXCL10, CXCL11, CX3CL1 and IL-17C, which were also upregulated in infected secretory-stage primary cells, and there was a trend towards higher levels of immune mediators in infected secretory-phase compared with proliferative-phase cells. Conclusion: Progesterone treatment primes multiple innate immune pathways in hormone-responsive epithelial cells that could potentially increase resistance to chlamydial infection. © 2013 John Wiley & Sons Ltd.
|2011||Amirshahi A, Wan C, Beagley K, Latter JL, Symonds IM, Timms P, 'Modulation of the Chlamydia trachomatis In vitro transcriptome response by the sex hormones estradiol and progesterone', BMC Microbiology, 11 150 (2011) [C1]|| |
|2007||Wark PA, Bucchieri F, Johnston SL, Gibson PG, Hamilton L, Mimica J, et al., 'IFN-gamma-induced protein 10 is a novel biomarker of rhinovirus-induced asthma exacerbations', Journal of Allergy and Clinical Immunology, 120 586-593 (2007) [C1]|