https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45202 Streptococcus (GBS) and Escherichia coli (E. coli) have dominated as causes of EOS for five decades. Method: An 11-year retrospective cohort study to determine the epidemiology of EOS. Incidence rates were calculated per 1000 live births. Logistic regression with linear temporal trend and covariates for potential effect modifiers were employed. Blood culture utilisation was determined by examining the rate of babies undergoing blood culture within 72 hours of birth. Results: Among 93,584 live born babies, 65 had confirmed EOS (0.69/1000 live births); 22 term, 43 preterm. Across the 4 largest birth units, the proportion of babies having blood culture within 72 hours of birth varied from 1.9–5.1% for term and 21–35% for preterm babies. The annual change in the EOS rate was significant, OR 0.91 (95% CI, 0.84 to 0.99, p = 0.03). Group B Streptococcus was the most common cause of EOS in term neonates at 0.35/1000 live births (95% CI, 0.07–0.63) in 2006 and 0.1/1000 live births (95% CI, 0–0.2) in 2016. Escherichia coli was the most common cause in preterm babies at 3.4/1000 (95% CI, 0.11–6.76) in 2006 reducing significantly to 1.35/1000 live births (95% CI, -0.07–2.78) by 2016. Conclusions: Escherichia coli and GBS were the most common causes of EOS in preterm and term babies respectively. Rates of all cause term and preterm EOS declined significantly as did preterm sepsis due to E. coli. While rate of sepsis due to early-onset GBS declined, this did not reach significance. Given the high proportion of preterm babies undergoing blood culture, it is unlikely that any EOS events were missed.]]> Wed 26 Oct 2022 19:38:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52433 Wed 11 Oct 2023 14:47:33 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35857 Wed 11 Dec 2019 15:19:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26012 Wed 11 Apr 2018 14:44:48 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22606 16 years) were admitted with confirmed influenza to one of 15 of 17 FluCAN sentinel hospitals (excluding 2 paediatric hospitals). Of these, 47% were over 65 years of age, 10% were Indigenous Australians, 3.3% were pregnant and 85% had chronic co-morbidities. The majority of cases were due to influenza A. Influenza B was detected in 7% of patients. There were a large number of hospital admissions detected with confirmed influenza in this national observational surveillance system in 2014. These are estimated to represent a national annual burden of around 15,000 admissions and almost 100,000 bed-days nationally.]]> Wed 11 Apr 2018 10:29:11 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:55012 Wed 03 Apr 2024 10:47:37 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:528 Thu 25 Jul 2013 09:10:32 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:450 Thu 25 Jul 2013 09:09:49 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42205 P=0.06). There was no evidence of heterogeneity between MR estimates produced by different instruments (Q P=0.26). Comparable MR estimates were obtained with weighted median MR (odds ratio, 2.57; 95% CI, 1.05-6.25; P=0.04) and MR pleiotropy residual sum and outlier (odds ratio, 1.81; 95% CI, 0.95-3.46; P=0.08). Conclusions: We found no MR evidence of genetically determined risk of depression affecting ischemic stroke risk but did find consistent MR evidence suggestive of a possible effect on functional outcome after ischemic stroke. Given the widespread prevalence of depression-related morbidity, these findings could have implications for prognostication and personalized rehabilitation after stroke.]]> Thu 25 Aug 2022 11:38:19 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35546 Thu 03 Feb 2022 12:19:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11095 Sat 24 Mar 2018 08:13:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:10462 Sat 24 Mar 2018 08:09:11 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11289 Sat 24 Mar 2018 08:07:45 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16968 Sat 24 Mar 2018 07:55:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25808 Enterococcus faecium is a major nosocomial pathogen causing significant morbidity and mortality worldwide. Assessment of E. faecium using MLST to understand the spread of this organism is an important component of hospital infection control measures. Recent studies, however, suggest that MLST might be inadequate for E. faecium surveillance. Objectives: To use WGS to characterize recently identified vancomycin-resistant E. faecium (VREfm) isolates non-typeable by MLST that appear to be causing a multi-jurisdictional outbreak in Australia. Methods: Illumina NextSeq and Pacific Biosciences SMRT sequencing platforms were used to determine the genome sequences of 66 non-typeable E. faecium (NTEfm) isolates. Phylogenetic and bioinformatics analyses were subsequently performed using a number of in silico tools. Results: Sixty-six E. faecium isolates were identified by WGS from multiple health jurisdictions in Australia that could not be typed by MLST due to a missing pstS allele. SMRT sequencing and complete genome assembly revealed a large chromosomal rearrangement in representative strain DMG1500801, which likely facilitated the deletion of the pstS region. Phylogenomic analysis of this population suggests that deletion of pstS within E. faecium has arisen independently on at least three occasions. Importantly, the majority of these isolates displayed a vancomycin-resistant genotype. Conclusions: We have identified NTEfm isolates that appear to be causing a multi-jurisdictional outbreak in Australia. Identification of these isolates has important implications for MLST-based typing activities designed to monitor the spread of VREfm and provides further evidence supporting the use of WGS for hospital surveillance of E. faecium.]]> Sat 24 Mar 2018 07:34:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26644 Sat 24 Mar 2018 07:26:51 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27055 Sat 24 Mar 2018 07:25:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46291 2+-activated K⁺ channel, K_Ca1.1, and lies within a linkage interval for atrial fibrillation (AF). Insights into the cardiac functions of K_Ca1.1 are limited, and KCNMA1 has not been investigated as an AF candidate gene. Methods; The KCNMA1 gene was sequenced in 118 patients with familial AF. The role of K_Ca1.1 in normal cardiac structure and function was evaluated in humans, mice, zebrafish, and fly. A novel KCNMA1 variant was functionally characterized.Results: A complex KCNMA1 variant was identified in 1 kindred with AF. To evaluate potential disease mechanisms, we first evaluated the distribution of K_Ca1.1 in normal hearts using immunostaining and immunogold electron microscopy. K_Ca1.1 was seen throughout the atria and ventricles in humans and mice, with strong expression in the sinus node. In an ex vivo murine sinoatrial node preparation, addition of the K_Ca1.1 antagonist, paxilline, blunted the increase in beating rate induced by adrenergic receptor stimulation. Knockdown of the K_Ca1.1 ortholog, kcnma1b, in zebrafish embryos resulted in sinus bradycardia with dilatation and reduced contraction of the atrium and ventricle. Genetic inactivation of the Drosophila K_Ca1.1 ortholog, slo, systemically or in adult stages, also slowed the heartbeat and produced fibrillatory cardiac contractions. Electrophysiological characterization of slo-deficient flies revealed bursts of action potentials, reflecting increased events of fibrillatory arrhythmias. Flies with cardiac-specific overexpression of the human KCNMA1 mutant also showed increased heart period and bursts of action potentials, similar to the K_Ca1.1 loss-of-function models. Conclusions: Our data point to a highly conserved role of K_Ca1.1 in sinus node function in humans, mice, zebrafish, and fly and suggest that K_Ca1.1 loss of function may predispose to AF.]]> Mon 14 Nov 2022 16:44:58 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:43034 Mon 12 Sep 2022 11:49:26 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48140 Mon 06 Mar 2023 13:24:13 AEDT ]]>