https://ogma.newcastle.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:50942 Wed 28 Feb 2024 16:05:34 AEDT ]]> 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:23403 Wed 11 Apr 2018 15:33:10 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:13480 Wed 11 Apr 2018 15:24:54 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:16813 Wed 11 Apr 2018 14:42:05 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:22344 Wed 11 Apr 2018 10:22:35 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:24375 Wed 10 Nov 2021 15:05:57 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:31502 Tue 02 Apr 2019 14:06:11 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:19491 Thu 12 Apr 2018 13:50:57 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:12743 Sat 24 Mar 2018 08:16:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:10479 Sat 24 Mar 2018 08:09:15 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:19930 Sat 24 Mar 2018 07:58:37 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:17878 Sat 24 Mar 2018 07:56:13 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:19229 9/L. The blood eosinophil/lymphocyte ratio (ELR) and eosinophil/neutrophil ratio (ENR) were increased in eosinophilic asthma, and the neutrophil/lymphocyte ratio (NLR) was increased in neutrophilic asthma. Neutrophilic asthma could also be detected by blood neutrophil percentages and NLR, but with less accuracy. Conclusions and Clinical Relevance: Blood eosinophil counts and derived ratios (ELR and ENR) can accurately predict eosinophilic asthma in patients with persistent uncontrolled asthma despite treatment. Blood neutrophil parameters are poor surrogates for the proportion of sputum neutrophils. Blood counts may be a useful aid in the monitoring of uncontrolled asthma.]]> Sat 24 Mar 2018 07:54:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:5567 Sat 24 Mar 2018 07:49:11 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:396 Sat 24 Mar 2018 07:42:32 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:300 Sat 24 Mar 2018 07:42:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:27825 Sat 24 Mar 2018 07:41:14 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:29078 Sat 24 Mar 2018 07:39:58 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:25812 postmortem brain tissue, and later in studies of peripheral blood. The collective body of schizophrenia microarray literature contains apparent inconsistencies between studies, with failures to replicate top hits, in part due to small sample sizes, cohort-specific effects, differences in array types, and other confounders. In an attempt to summarize existing studies of schizophrenia cases and non-related comparison subjects, we performed two mega-analyses of a combined set of microarray data from postmortem prefrontal cortices (n = 315) and from ex-vivo blood tissues (n = 578). We adjusted regression models per gene to remove non-significant covariates, providing best-estimates of transcripts dysregulated in schizophrenia. We also examined dysregulation of functionally related gene sets and gene co-expression modules, and assessed enrichment of cell types and genetic risk factors. The identities of the most significantly dysregulated genes were largely distinct for each tissue, but the findings indicated common emergent biological functions (e.g. immunity) and regulatory factors (e.g., predicted targets of transcription factors and miRNA species across tissues). Our network-based analyses converged upon similar patterns of heightened innate immune gene expression in both brain and blood in schizophrenia. We also constructed generalizable machine-learning classifiers using the blood-based microarray data. Our study provides an informative atlas for future pathophysiologic and biomarker studies of schizophrenia.]]> Sat 24 Mar 2018 07:34:35 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:24376 Sat 24 Mar 2018 07:16:18 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:24991 Sat 24 Mar 2018 07:09:56 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:38481 2) on haemoglobin concentrations and the prevalence of anaemia, respectively, among 10,611 older Chinese adults enrolled in World Health Organization (WHO) Study on global AGEing and adult health (SAGE) China. The average community exposure to ambient air pollutants (PM with an aerodynamic diameter of 10 μm or less (PM₁₀), 2.5 μm or less (PM_2.5), 1 μm or less (PM₁) and nitrogen dioxide (NO₂)) for each participant was estimated using a satellite-based spatial statistical model. Haemoglobin levels were measured for participants from dried blood spots. The models were controlled for confounders. Results: All the studied pollutants were significantly associated with increased anaemia prevalence in single pollutant model (e.g., the prevalence ratios associated with an increase in inter quartile range in three years moving average PM₁₀ (1.05; 95% CI: 1.02–1.09), PM_2.5 (1.11; 95% CI: 1.06–1.16), PM₁ (1.13; 95% CI: 1.06–1.20) and NO₂(1.42; 95% CI: 1.34–1.49), respectively. These air pollutants were also associated with lower concentrations of haemoglobin: PM₁₀ (−0.53; 95% CI: −0.67, −0.38); PM_2.5 (−0.52; 95% CI: −0.71, −0.33); PM₁ (−0.55; 95% CI: −0.69, −0.41); NO₂ (−1.71; 95% CI: −1.85, −1.57) respectively. Conclusions: Air pollution exposure was significantly associated with increased prevalence of anaemia and decreased haemoglobin levels in a cohort of older Chinese adults.]]> Mon 29 Jan 2024 18:02:14 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:47575 Mon 23 Jan 2023 14:00:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:45440 Fri 28 Oct 2022 12:58:16 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:46094 1 and FVC. Trends towards similar clinical associations with elevated MCs were observed in a paucigranulocytic subpopulation (n = 15) lacking airway eosinophilia or neutrophilia. Receiver operator characteristic (ROC) analysis showed peripheral blood eosinophil (PBE) count predicted elevated sputum eosinophils and basophils, but not MCs. Conclusions and Clinical Relevance: Sputum MCs are elevated in asthma, and their measurement may be useful as they relate to key clinical features of asthma (spirometry, asthma control, AHR). PBE count did not predict airway MC status, suggesting direct measurement of airway MCs by sensitive methods such as flow cytometry should be further developed.]]> Fri 11 Nov 2022 11:01:15 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:30274 Streptococcus pneumoniae and vaccination are inversely associated with asthma. Studies in animal models demonstrate that airway administration of S. pneumoniae (live or killed), or its vaccines or components, suppresses the characteristic features of asthma in mouse models of allergic airway disease (AAD). These components could be developed into immunoregulatory therapies. S. pneumoniae components are recognized by Toll-like receptors (TLR) 2 and TLR4, and both induce inflammatory cell responses through the adaptor protein myeloid differentiation primary response gene 88 (MyD88). The involvement of TLR2, TLR4 and MyD88 in the pathogenesis of AAD and asthma is incompletely understood, and has not been studied in S. pneumoniae-mediated suppression of AAD. We investigated the role of TLR2, TLR4 and MyD88 in the development of AAD and S. pneumoniae-mediated suppression of AAD. Methods and Findings: OVA-induced AAD and killed S. pneumoniae-mediated suppression of AAD were assessed in wild-type, TLR2 ^-/-, TLR4 ^-/-, TLR2/4 ^-/- and MyD88 ^-/- BALB/c mice. During OVA-induced AAD, TLR2, TLR4 and MyD88 were variously involved in promoting eosinophil accumulation in bronchoalveolar lavage fluid and blood, and T-helper type (Th)2 cytokine release from mediastinal lymph node T cells and splenocytes. However, all were required for the induction of airways hyperresponsiveness (AHR). In S. pneumoniae-mediated suppression of AAD, TLR2, TLR4 and MyD88 were variously involved in the suppression of eosinophilic and splenocyte Th2 responses but all were required for the reduction in AHR. Conclusions: These results highlight important but complex roles for TLR2, TLR4 and MyD88 in promoting the development of OVA-induced AAD, but conversely in the S. pneumoniae-mediated suppression of AAD, with consistent and major contributions in both the induction and suppression of AHR. Thus, TLR signaling is likely required for both the development of asthma and the suppression of asthma by S. pneumoniae, and potentially other immunoregulatory therapies.]]> Fri 01 Apr 2022 09:28:59 AEDT ]]>