Time filter

Source Type

Auckland, New Zealand

Gardiner R.A.,University of Queensland | Gwynne R.A.,Royal Brisbane and Womens Hospital | Roberts S.A.,LabPlus
BJU International | Year: 2011

The clinical condition of perinephric abscess can present dramatically as an acute emergency or insidiously as a chronic condition. The clinical characteristics and contemporary treatment approaches of these different types of perinephric abscess are outlined in this overview of the topic. © 2011 BJU INTERNATIONAL. Source

Tate J.R.,Pathology Queensland | Johnson R.,LabPlus | Barth J.,Clinical Biochemistry | Panteghini M.,University of Milan
Clinica Chimica Acta | Year: 2014

Harmonization in laboratory testing is more far-reaching than merely analytical harmonization. It includes all aspects of the total testing process from the "pre-pre-analytical" phase through analysis to the "post-post-analytical" phase. Harmonizing the pre-analytical phase requires use of standardized operating procedures for correct test selection, sample collection and handling, while standardized test terminology, and units and traceability to ISO standard 17511 are required to ensure equivalency of measurement results. Use of harmonized reference intervals and decision limits for analytes where platforms share allowable bias requirements will reduce inaccurate clinical interpretation and unnecessary laboratory testing. In the post-analytical phase, harmonized procedures for the management of critical laboratory test results are required to improve service quality and ensure patient safety. Monitoring of the outcomes of harmonization activities is through surveillance by external quality assessment schemes that use commutable materials and auditing of the "pre-pre-analytical" and "post-post-analytical" phases. Successful implementation of harmonization in laboratory testing requires input by all stakeholders, including the clinical laboratory community, diagnostics industry, clinicians, professional societies, IT providers, consumer advocate groups and governmental bodies. © 2013. Source

Jansson D.,University of Auckland | Rustenhoven J.,University of Auckland | Feng S.,University of Auckland | Hurley D.,University of Auckland | And 5 more authors.
Journal of Neuroinflammation | Year: 2014

Background: Brain inflammation plays a key role in neurological disease. Although much research has been conducted investigating inflammatory events in animal models, potential differences in human brain versus rodent models makes it imperative that we also study these phenomena in human cells and tissue.Methods: Primary human brain cell cultures were generated from biopsy tissue of patients undergoing surgery for drug-resistant epilepsy. Cells were treated with pro-inflammatory compounds IFNγ, TNFα, IL-1β, and LPS, and chemokines IP-10 and MCP-1 were measured by immunocytochemistry, western blot, and qRT-PCR. Microarray analysis was also performed on late passage cultures treated with vehicle or IFNγ and IL-1β.Results: Early passage human brain cell cultures were a mixture of microglia, astrocytes, fibroblasts and pericytes. Later passage cultures contained proliferating fibroblasts and pericytes only. Under basal culture conditions all cell types showed cytoplasmic NFκB indicating that they were in a non-activated state. Expression of IP-10 and MCP-1 were significantly increased in response to pro-inflammatory stimuli. The two chemokines were expressed in mixed cultures as well as cultures of fibroblasts and pericytes only. The expression of IP-10 and MCP-1 were regulated at the mRNA and protein level, and both were secreted into cell culture media. NFκB nuclear translocation was also detected in response to pro-inflammatory cues (except IFNγ) in all cell types. Microarray analysis of brain pericytes also revealed widespread changes in gene expression in response to the combination of IFNγ and IL-1β treatment including interleukins, chemokines, cellular adhesion molecules and much more.Conclusions: Adult human brain cells are sensitive to cytokine challenge. As expected 'classical' brain immune cells, such as microglia and astrocytes, responded to cytokine challenge but of even more interest, brain pericytes also responded to such challenge with a rich repertoire of gene expression. Immune activation of brain pericytes may play an important role in communicating inflammatory signals to and within the brain interior and may also be involved in blood brain barrier (BBB) disruption . Targeting brain pericytes, as well as microglia and astrocytes, may provide novel opportunities for reducing brain inflammation and maintaining BBB function and brain homeostasis in human brain disease. © 2014 Jansson et al.; licensee BioMed Central Ltd. Source

Orde M.M.,Sydney South West Area Health Service | Orde M.M.,University of Sydney | Puranik R.,University of Sydney | Morrow P.L.,LabPlus | And 2 more authors.
Heart | Year: 2011

Objective: To assess the nature of necroinflammatory changes identified in postmortem histological sections of the right ventricular myocardium in cases of fatal pulmonary thromboembolism (PTE). Design/setting: A retrospective study examining coronial autopsy cases (n=28, age 58±21 years, 9 men/19 women) of PTE in which isolated right ventricular myocardial pathology was encountered. Detailed immunohistological analysis was undertaken on sections of myocardium, and comparison was made to age- and sex-matched controls (n=28, age 57±21 years, 9 men/19 women) without significant cardiorespiratory disease. Results: The PTE was considered extensive in 86% of cases, and histological features of organisation were observed in 68%. PTE cases had similar body mass indices to controls (32±2 kg/m2 vs 28±2 kg/m2, p=0.13) but greater heart weights (414±17 g vs 358±18 g, p=0.02) and, where documented, thicker right ventricular walls (4.8±0.3 mm (n=18) vs 3.4±0.2 mm (n=15), p=0.0008). The inflammatory infiltrate in PTE cases comprised predominantly macrophages and T cells, though neutrophilic inflammation was a frequent accompaniment. Myocyte necrosis was identified in association with the inflammatory foci in 64%. There was a 6.6-fold greater amount of diffuse macrophage recruitment within the right ventricle in cases of PTE compared to controls (p<0.0001), and there was a 6.1-fold increase in right ventricular fibrosis (p=0.01). Right ventricular fatty replacement was similar between the two groups (p=0.46). Conclusions: We conclude that PTE may result in right ventricular myocardial inflammation and necrosis, distinct from that seen in typical myocardial infarction due to atherosclerotic coronary artery disease, or myocarditis. This observation may be explained, in part, by local stretch and strain of the right ventricle due to increased afterload, possibly compounded by diminished diastolic blood flow to the right ventricular myocardium and the effects of global myocardial hypoxia. Source

Logan P.C.,University of Auckland | Ponnampalam A.P.,University of Auckland | Rahnama F.,LabPlus | Lobie P.E.,University of Auckland | And 2 more authors.
Human Reproduction | Year: 2010

Background Decidualization, the differentiation of endometrial stromal cells is a crucial step for successful implantation of an embryo, development of the placenta and completion of pregnancy to term. Epigenetic mechanisms are thought to be strongly involved in the regulation of processes controlling implantation, placentation, organ formation and foetal growth. Recent studies suggest that decreased DNA methylation facilitates a receptive endometrium. Hence, the aim of this project was to compare the transcriptional profile changes induced by the inhibitor of DNA methylation, 5-Aza-2′- deoxycytidine (AZA) to the transcriptional changes that happen during decidualization. Methods AND RESULTSWhen DNA methylation was inhibited in a human endometrial stromal cell (HESC) line with AZA, it resulted in the fibroblast-like stromal cells being transformed into decidual-like morphology after 9 days. Expression of both prolactin and insulin-like growth factor binding protein-1, the two established decidualization marker genes, were minimally up-regulated by AZA after 10 days of treatment. In a microarray of a three-way experiment between AZA-treated and oestradiol/progestin/cAMP-treated [medroxy-progesterone acetate (MPA)-mix] HESC and the untreated controls, we detected more than 1000 common genes that had a significant difference of expression compared with the controls. AZA-treated cells in the microarray significantly expressed 76 genes in common with the MPA-mix treated cells, and AZA treatment also differentially regulated 148 genes independently to that of MPA-mix treatment. The MPA-mix regulated at least 36 genes in the cell adhesion, extracellular matrix remodelling and RhoGTPase cytoskeletal reorganization pathway; AZA regulated 19 of these genes in common and 15 other RhoGTPase pathway genes. Conclusionaza induced some decidualization-like responses of endometrial stromal cells independently of progestins or cAMP, possibly via the cytoskeletal reorganization pathway of the RhoGTPase family. © 2010 The Author. Source

Discover hidden collaborations