ORCID Profile
0000-0003-2154-5950
Current Organisation
University of Adelaide
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Biomedical Instrumentation | Optical Properties of Materials | Nanobiotechnology | Animal Developmental and Reproductive Biology | Medical Biotechnology | Other Physical Sciences | Biochemistry and Cell Biology | Nanotechnology | Biologically Active Molecules | Crop and Pasture Biochemistry and Physiology | Synchrotrons; Accelerators; Instruments and Techniques | Medical Biotechnology Diagnostics (incl. Biosensors) | Nanophotonics | Biochemistry and Cell Biology not elsewhere classified | Optical Physics not elsewhere classified
Expanding Knowledge in the Biological Sciences | Expanding Knowledge in Technology | Expanding Knowledge in the Chemical Sciences | Expanding Knowledge in the Physical Sciences | Expanding Knowledge in the Medical and Health Sciences | Scientific Instruments | Expanding Knowledge in the Agricultural and Veterinary Sciences |
Publisher: American Chemical Society (ACS)
Date: 10-09-2018
Abstract: Cytokine sensing is challenging due to their typically low abundances in physiological conditions. Nanomaterial fabricated interfaces demonstrated unique advantages in ultrasensitive sensing. Here, we demonstrate an erometric sensing device based on graphene oxide (GO) and structure-switching aptamers for long-term detection of cytokines in a living organism. The device incorporates a single layer of GO acting as a signal lifier on glassy carbon electrodes. The hairpin aptamers specific to interferon-γ (IFN-γ), which were loaded with redox probes, are covalently attached to GO to serve as biorecognition moieties. IFN-γ was able to trigger the configuration change of aptamers while releasing the trapped redox probes to introduce the electrochemical signal. This in vivo device was capable of quantitatively and dynamically detecting IFN-γ down to 1.3 pg mL
Publisher: Elsevier
Date: 2018
Publisher: Wiley
Date: 12-09-2021
DOI: 10.1002/JNR.24959
Abstract: Cancer patients may experience symptom clusters, including chemotherapy‐induced (CI) gut toxicity (CIGT) and cognitive impairment. Analgesic selection for pain associated with CIGT is difficult as opioids induce glial reactivity and unwanted side effects. This study quantified central glial reactivity and proinflammatory effects in rats with CIGT using three mechanistically different analgesics. Regional adaptations were indicative of immune‐to‐brain signaling routes. Utilizing a 5‐fluorouracil‐induced GT (5IGT) rat model and analgesic intervention (carprofen (CAR), buprenorphine (BUP), and tramadol (TRAM)), spinal and brain neuroimmune modulation was examined via microglial, astrocyte, and proinflammatory (cluster of differentiation molecule 11b CD11b, glial fibrillary associated protein GFAP, and interleukin‐1 beta IL1β) reactivity marker expression changes by western blot analysis. 5IGT significantly increased thoracic GFAP ( p 0.05) and IL‐1β ( p 0.0001) expression, CAR and BUP ameliorated these effects. BUP and TRAM with 5‐FU synergistically increased hippoc al GFAP expression. CAR administered with 5IGT significantly elevated hippoc al and thoracic CD11b expression levels ( p 0.05). The neuroimmune responses observed in this study suggest activation of peripheral‐to‐central immune signaling pathways. We speculate that the opioid‐induced hippoc al changes inferred a humorally mediated mechanism, whereas thoracic neuroimmune modifications indicated activation of an indirect neural route. Although TRAM ameliorated 5IGT‐intestinal inflammation, this opioid presents complications relating to bodyweight and regional glial dysregulation (neuroinflammation) and may not be optimal in the management of pain associated with 5IGT. The chemotherapy‐induced gut‐derived neuroimmune consequences observed suggest a potential mechanistic contribution to central components of the cancer symptom cluster experience, while the opioid‐related glial changes have implications for optimal pain management in this setting warranting further investigation.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 11-2009
Publisher: Elsevier BV
Date: 08-2011
Publisher: Informa UK Limited
Date: 09-07-2018
Publisher: Wiley
Date: 14-09-2015
DOI: 10.1111/HEAD.12655
Abstract: Medication overuse headache (MOH) is a condition bordering between a chronic pain condition and a substance dependence disorder. Activation of immunocompetent glial cells in the central nervous system has been linked to both pathological pain and drug addiction/reward. Preclinically, ibudilast attenuates glial activation and is able to reduce neuropathic pain and markers of substance dependence. We therefore hypothesized ibudilast would reduce headache burden and opioid analgesic requirements in patients with opioid overuse headache. To determine if treatment with ibudilast provides a greater reduction in headache index than placebo in MOH patients consuming opioids. Participants with MOH who were using opioids were randomized via computer-generated code to ibudilast 40 mg or placebo twice daily for 8 weeks in a double-blind, parallel groups study. Before randomization participants completed a 4-week baseline headache diary. During treatment, headache diary data collection continued and participants attended 4 study visits during which quantitative sensory testing was performed. Blood s les for immune biomarker analyses were collected before and after treatment in a subgroup of participants. Thirty-four participants were randomized, 13 of 15 randomized to ibudilast and 17 of 19 randomized to placebo completed treatment. Ibudilast was generally well-tolerated with mild, transient nausea reported as the most common adverse event (66.7% vs 10.5% in placebo group). Results are shown as mean (SD). At the end of treatment no differences in the primary outcome average daily headache index (placebo 62 [44] vs ibudilast 77 [72] groups, difference -15, CI -65 to 35 h × numerical rating scale), or secondary outcomes headache frequency (placebo 23 [8.1] vs ibudilast 24.5 [6.2], difference -1.5, CI -7.7 to 4.8 days/month) and opioid intake (placebo 20.6 [43] vs ibudilast 19 [24.3], difference 1.6, CI -31.5 to 34.8 mg morphine equivalent) were observed between placebo and ibudilast groups. Using the current dosing regimen, ibudilast does not improve headache or reduce opioid use in patients with MOH without mandated opioid withdrawal. However, it would be of interest to determine in future trials if ibudilast is able to improve ease of withdrawal during a forced opioid down-titration when incorporated into an MOH detoxification program.
Publisher: Wiley
Date: 03-02-2004
DOI: 10.1046/J.1365-2125.2003.02002.X
Abstract: To determine the Michaelis-Menten kinetics of hydrocodone metabolism to its O- and N-demethylated products, hydromorphone and norhydrocodone, to determine the in idual cytochrome p450 enzymes involved, and to predict the in vivo hepatic intrinsic clearance of hydrocodone via these pathways. Liver microsomes from six CYP2D6 extensive metabolizers (EM) and one CYP2D6 poor metabolizer (PM) were used to determine the kinetics of hydromorphone and norhydrocodone formation. Chemical and antibody inhibitors were used to identify the cytochrome p450 isoforms catalyzing these pathways. Expressed recombinant cytochrome p450 enzymes were used to characterize further the metabolism of hydrocodone. Hydromorphone formation in liver microsomes from CYP2D6 EMs was dependent on a high affinity enzyme (Km = 26 microm) contributing 95%, and to a lesser degree a low affinity enzyme (Km = 3.4 mm). In contrast, only a low affinity enzyme (Km = 8.5 mm) formed this metabolite in the liver from the CYP2D6 PM, with significantly decreased hydromorphone formation compared with the livers from the EMs. Norhydrocodone was formed by a single low affinity enzyme (Km = 5.1 mm) in livers from both CYP2D6 EM and PM. Recombinant CYP2D6 and CYP3A4 formed only hydromorphone and only norhydrocodone, respectively. Hydromorphone formation was inhibited by quinidine (a selective inhibitor of CYP2D6 activity), and monoclonal antibodies specific to CYP2D6. Troleandomycin, ketoconazole (both CYP3A4 inhibitors) and monoclonal antibodies specific for CYP3A4 inhibited norhydrocodone formation. Extrapolation of in vitro to in vivo data resulted in a predicted total hepatic clearance of 227 ml x h-1 x kg-1 and 124 ml x h-1 x kg-1 for CYP2D6 EM and PM, respectively. The O-demethylation of hydrocodone is predominantly catalyzed by CYP2D6 and to a lesser extent by an unknown low affinity cytochrome p450 enzyme. Norhydrocodone formation was attributed to CYP3A4. Comparison of recalculated published clearance data for hydrocodone, with those predicted in the present work, indicate that about 40% of the clearance of hydrocodone is via non-CYP pathways. Our data also suggest that the genetic polymorphisms of CYP2D6 may influence hydrocodone metabolism and its therapeutic efficacy.
Publisher: Frontiers Media SA
Date: 22-05-2018
Publisher: AIP Publishing
Date: 10-09-2018
DOI: 10.1063/1.5040861
Abstract: The probing of physiological processes in living organisms is a grand challenge that requires bespoke analytical tools. Optical fiber probes offer a minimally invasive approach to report physiological signals from specific locations inside the body. This perspective article discusses a wide range of such fiber probes developed at the Australian Research Council Centre of Excellence for Nanoscale BioPhotonics. Our fiber platforms use a range of sensing modalities, including embedded nanodiamonds for magnetometry, interferometric fiber cavities for refractive index sensing, and tailored metal coatings for surface plasmon resonance sensing. Other fiber probes exploit molecularly sensitive Raman scattering or fluorescence where optical fibers have been combined with chemical and immunosensors. Fiber imaging probes based on interferometry and computational imaging are also discussed as emerging in vivo diagnostic devices. We provide ex les to illustrate how the convergence of multiple scientific disciplines generates opportunities for the fiber probes to address key challenges in real-time in vivo diagnostics. These future fiber probes will enable the asking and answering of scientific questions that were never possible before.
Publisher: Informa UK Limited
Date: 03-2020
DOI: 10.2147/JPR.S219684
Publisher: Elsevier BV
Date: 05-2020
Publisher: Hindawi Limited
Date: 2013
DOI: 10.1155/2013/796161
Abstract: BACKGROUND: Tension-type headache is the most common form of headache and its chronic form, chronic tension-type headache (CTTH), is one of the most difficult to treat. The etiology of CTTH is not well understood, but is believed to be multifactorial and to vary among in iduals. In the present study, the authors sought to identify common mechanisms of CTTH pathology. Empirical studies have implicated various immunomodulatory cytokines as mediators of chronic pain disorders, including CTTH. OBJECTIVES: To determine the role of peripheral cytokines and genetic factors in the development of CTTH. METHODS: A panel of cytokines hypothesized to play a role in the pathogenesis of CTTH was measured using cytometric bead arrays and ELISAs in 56 in iduals with CTTH and 42 healthy control participants between 18 and 65 years of age. RESULTS: Levels of interleukin (IL)-1β were significantly elevated in participants diagnosed with CTTH relative to healthy controls, while IL-18 levels were found to be significantly elevated in men with CTTH. Because the levels of these immune mediators were increased in the apparent absence of injury or infection, the authors sought to determine whether genetic changes were responsible for fluctuations in cytokine levels. Polymerase chain reaction and restriction fragment length polymorphism analyses were used to determine in idual genotypes at key single nucleotide polymorphism positions in the IL-1B gene. No association was observed between CTTH and single nucleotide polymorphisms in the IL-1β gene. CONCLUSIONS: These findings suggest that increases in key proinflammatory cytokine levels are associated with CTTH and the pathology of the disorder involves sterile neurovascular inflammation.
Publisher: SPIE-Intl Soc Optical Eng
Date: 30-10-2018
Publisher: Cambridge University Press
Date: 07-11-2011
Publisher: Elsevier BV
Date: 08-2020
Publisher: Wiley
Date: 06-2015
DOI: 10.1111/BCP.12614
Publisher: SAGE Publications
Date: 09-11-2012
Abstract: Patients with chronic headache who consume large amounts of analgesics are often encountered in clinical practice. Excessive intake of analgesics is now considered to be a cause, rather than simply a consequence, of frequent headaches, and as such the diagnosis “medication-overuse headache” (MOH) has been formulated. Despite the prevalence and clinical impact of MOH, the pathophysiology behind this disorder remains unclear and specific mechanism-based treatment options are lacking. Although most acute headache treatments have been alleged to cause MOH, here we conclude from the literature that opioids are a particularly problematic drug class consistently associated with worsening headache. MOH may not be a single entity, as each class of drug implicated may cause MOH via a different mechanism. Recent evidence indicates that chronic opioid administration may exacerbate pain in the long term by activating toll-like receptor-4 on glial cells, resulting in a pro-inflammatory state that manifests clinically as increased pain. Thus, from the available evidence it seems opioid-overuse headache is a phenomenon similar to opioid-induced hyperalgesia, which derives from a cumulative interaction between central sensitisation, due to repeated activation of nociceptive pathways by recurrent headaches, and pain facilitation due to glial activation. Treatment strategies directed at inhibiting glial activation may be of benefit alongside medication withdrawal in the management of MOH.
Publisher: Informa UK Limited
Date: 03-2021
DOI: 10.2147/JPR.S279253
Publisher: BMJ
Date: 06-2022
DOI: 10.1136/BMJOPEN-2021-059723
Abstract: Many people with HIV report both distress and pain. The relationship between distress and pain is bidirectional, but the mechanisms by which distress exacerbates pain are unclear. The inflammatory response to challenge (inflammatory reactivity, IR) may be a partial mediator, given that neuroimmune interactions provide a substrate for IR to also influence neurological reactivity and, thus, pain-related neural signalling. This prospective, observational, case–control study will characterise the relationships between distress, IR, pain-related signalling as captured by induced secondary hyperalgesia (SH), and pain, in people with HIV who report persistent pain (PP) (cases) or no pain (controls). One hundred people with suppressed HIV, reporting either PP or no pain, will be assessed two or four times over 6 months. The primary outcomes are distress (Hopkins 25-item symptom checklist), IR (multiplex assay after LPS challenge), and PP (Brief Pain Inventory), assessed at the baseline timepoint, although each will also be assessed at follow-up time points. Induced SH will be assessed in a subs le of 60 participants (baseline timepoint only). To test the hypothesis that IR partly mediates the relationship between distress and pain, mediation analysis will use the baseline data from the PP group to estimate direct and indirect contributions of distress and IR to pain. To test the hypothesis that IR is positively associated with SH, data from the subs le will be analysed with generalised mixed effects models to estimate the association between IR and group membership, with SH as the dependent variable. Information obtained from this study will be published in peer-reviewed journals and presented at scientific meetings. The study has been approved by the Human Research Ethics Committee of the University of Cape Town (approval number: 764/2019) and the City of Cape Town (ref: 24699). NCT04757987 .
Publisher: Elsevier BV
Date: 07-2018
DOI: 10.1016/J.BBI.2018.04.011
Abstract: Mounting evidence indicates that cytokines secreted by innate immune cells in the brain play a central role in regulating neural circuits that subserve mood, cognition, and sickness responses. A major impediment to the study of neuroimmune signaling in healthy and disease states is the absence of tools for in vivo detection of cytokine release in the brain. Here we describe the design and application of a cytokine detection device capable of serial monitoring of local cytokine release in discrete brain regions. The immunocapture device consisted of a modified optical fiber labeled with a capture antibody specific for the pro-inflammatory cytokine interleukin-1 beta (IL-1β). Using a sandwich immunoassay method, in vitro data demonstrate that the sensing interface of the modified optical fiber has a linear detection range of 3.9 pg mL
Publisher: Springer Science and Business Media LLC
Date: 03-11-2020
DOI: 10.1038/S41467-020-19275-X
Abstract: The capabilities of imaging technologies, fluorescent sensors, and optogenetics tools for cell biology are advancing. In parallel, cellular reprogramming and organoid engineering are expanding the use of human neuronal models in vitro. This creates an increasing need for tissue culture conditions better adapted to live-cell imaging. Here, we identify multiple caveats of traditional media when used for live imaging and functional assays on neuronal cultures (i.e., suboptimal fluorescence signals, phototoxicity, and unphysiological neuronal activity). To overcome these issues, we develop a neuromedium called BrainPhys™ Imaging (BPI) in which we optimize the concentrations of fluorescent and phototoxic compounds. BPI is based on the formulation of the original BrainPhys medium. We benchmark available neuronal media and show that BPI enhances fluorescence signals, reduces phototoxicity and optimally supports the electrical and synaptic activity of neurons in culture. We also show the superior capacity of BPI for optogenetics and calcium imaging of human neurons. Altogether, our study shows that BPI improves the quality of a wide range of fluorescence imaging applications with live neurons in vitro while supporting optimal neuronal viability and function.
Publisher: American Chemical Society (ACS)
Date: 29-12-2017
DOI: 10.1021/ACSSENSORS.6B00619
Abstract: We demonstrated a cytokine detection device based on gold nanoparticle modified silica optical fiber for the monitoring of locally variable cytokine interleukin-6 (IL-6) concentrations using a sandwich immunoassay scheme. The fiber is designed to be introduced into an intrathecal catheter with micrometer-sized holes drilled along its length to enable fluid exchange between the outside and inside of the catheter. An exposed optical fiber (diameter 125 μm) modified with a layer of gold nanoparticles was functionalized with the IL-6 capture antibody to form the sensing interface. The immunocapture device was incubated with a cytokine solution to capture the analyte. The device was then exposed to the IL-6 detection antibody which was loaded on the fluorescently labeled magnetic nanoparticles, making it possible to quantify the cytokine concentration based on the intensity of fluorescence. A reliable method for quantifying the fluorescent signal on a 3D structure was developed. This device was applied to the detection of cytokine IL-6 with the low limit of detection of 1 pg mL
Publisher: Elsevier BV
Date: 2023
Publisher: Elsevier BV
Date: 05-2016
DOI: 10.1016/J.BIOS.2016.01.020
Abstract: The detection of cytokines in body fluids, cells, tissues and organisms continues to attract considerable attention due to the importance of these key cell signaling molecules in biology and medicine. In this review, we describe recent advances in cytokine detection in the course of ongoing pursuit of new analytical approaches for these trace analytes with specific focus on immunosensing. We discuss recent elegant designs of sensing interface with improved performance with respect to sensitivity, selectivity, stability, simplicity, and the absence of s le matrix effects. Various immunosensing approaches based on multifunctional nanomaterials open novel opportunities for ultrasensitive detection of cytokines in body fluids in vitro and in vivo. Methodologies such as suspension arrays also known as bead assays together with optical fiber-based sensors, on their own or in combination with microfluidic devices will continue to have an important role to address the grand challenge of real-time in vivo multiplex cytokine detection.
Publisher: Elsevier BV
Date: 04-2016
Publisher: Royal Society of Chemistry (RSC)
Date: 2022
DOI: 10.1039/D2SD00006G
Abstract: Methods for the endogenous detection of nitroxyl (azanone HNO), the reduced and protonated derivative of nitric oxide (NO), are required to define its cardiovascular function and its key role in chronic pain.
Publisher: Royal Society of Chemistry (RSC)
Date: 2017
DOI: 10.1039/C6NR09381G
Abstract: The detection of cytokines in body fluids, cells, tissues and organisms continues to attract considerable attention due to the importance of these key cell signalling molecules in biology and medicine. We report a graphene quantum dot (GQD) based aptasensor able to specifically detect ultra-small amounts of cytokine molecules intracellularly. Graphene quantum dots modified with cytokine aptamers (Ap-GQDs) and epitope modified GQDs (Ep-GQDs) were prepared both are normally fluorescent at sufficient dilution. However, the fluorescence of the conjugates of Ap-GQDs and Ep-GQDs is quenched due to aggregation between Ap-GQDs and Ep-GQDs. After incubation of the cytokine-secreting cells with the conjugates of Ap-GQDs and Ep-GQDs, the cytokines secreted in cells compete for binding with the epitope which is then displaced. The ensuing binding of cytokines with the aptamers results in the disaggregation of Ap-GQDs and Ep-GQDs, and the recovery of fluorescence. The conjugates of Ap-GQDs and Ep-GQDs were used as nanosensors for monitoring intracellular cytokine IFN-γ secretion with very high sensitivity (2 pg mL
Publisher: Springer Berlin Heidelberg
Date: 2015
DOI: 10.1007/978-3-662-46450-2_11
Abstract: Opioids are considered the gold standard for the treatment of moderate to severe pain. However, heterogeneity in analgesic efficacy, poor potency and side effects are associated with opioid use, resulting in dose limitations and suboptimal pain management. Traditionally thought to exhibit their analgesic actions via the activation of the neuronal G-protein-coupled opioid receptors, it is now widely accepted that neuronal activity of opioids cannot fully explain the initiation and maintenance of opioid tolerance, hyperalgesia and allodynia. In this review we will highlight the evidence supporting the role of non-neuronal mechanisms in opioid signalling, paying particular attention to the relationship of opioids and immune signalling.
Publisher: Informa UK Limited
Date: 03-2012
DOI: 10.1586/ECI.11.99
Publisher: Institution of Engineering and Technology
Date: 2017
DOI: 10.1049/CP.2017.0077
Publisher: Elsevier BV
Date: 10-2023
Publisher: American Chemical Society (ACS)
Date: 16-12-2020
Abstract: IL-1β is a potent pro-inflammatory cytokine critical to multiple pathologies in the central nervous system (CNS). Quantification of IL-1β in vivo is challenging due to pM range of IL-1β released in the spinal cord and also the terminal nature of cerebrospinal fluid (CSF) s ling in rodents. Herein we developed a robust in vivo device on stainless steel suitable for detection of IL-1β in the spinal cord of rats. This approach offers high sensitivity (3.2 pg mL
Publisher: Springer Science and Business Media LLC
Date: 04-12-2017
DOI: 10.1038/S41598-017-17295-0
Abstract: Conventional organic fluorophores lose their ability to fluoresce after repeated exposure to excitation light due to photobleaching. Therefore, research into emerging bright and photostable nanomaterials has become of great interest for a range of applications such as bio-imaging and tracking. Among these emerging fluorophores, metal oxide-based nanomaterials have attracted significant attention as a potential multifunctional material with photocatalytic and angeogenisis abilities in addition to fluorescnce applications. However, most of these applications are highly dependent on size, morphology, and chemo-physical properties of in idual particles. In this manuscript, we present a method to study the intrinsic optical characteristics of in idual copper (I) oxide (Cu 2 O) nanocubes. When excited at 520 nm using only 11 µW excitation power (1.7 W/cm2), in idual nanocubes were observed to emit light with peak wavelengths ~760 nm which is conveniently within the near-infrared 1 (NIR1) biological window where tissue autofluorescence is minimal. Bright and photostable fluorescence was observed with intensities up to 487 K counts/s under constant illumination for at least 2 minutes with a brightness approximately four times higher than the autofluorescence from a fixed cumulus-oocyte complex. With near-IR emission, high fluorescence brightness, and outstanding photostability, Cu 2 O nanocubes are attractive candidates for long-term fluorescent bioimaging applications.
Publisher: Wiley
Date: 13-12-2019
Abstract: A new spiropyran-based stimuli-responsive delivery system is fabricated. It encapsulates and then releases an extraneous compound in response to elevated levels of Zn
Publisher: Elsevier BV
Date: 11-2020
Publisher: Springer Science and Business Media LLC
Date: 11-11-2014
DOI: 10.1038/TP.2014.121
Publisher: Elsevier BV
Date: 10-2019
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 08-2016
DOI: 10.1097/AOG.0000000000001510
Abstract: To synthesize and critically evaluate all available evidence investigating whether localized, provoked vestibulodynia is associated with a specific inflammatory profile at both a local and a systemic level. Comprehensive electronic searches were performed in MEDLINE, EMBASE, Scopus, PubMed, Web of Science, Cumulative Index to Nursing and Allied Health Literature, the Cochrane Collaboration databases, and ClinicalTrials.gov. The search strategy was developed using MeSH terms related to localized, provoked vestibulodynia, and inflammatory markers. Two independent investigators screened titles and abstracts and performed data extraction and risk of bias assessments. Studies were included if they reported at least one baseline inflammatory marker in women with localized, provoked vestibulodynia and compared them with healthy women. Reference lists from published reviews on localized, provoked vestibulodynia were screened for additional studies. There were 1,619 studies identified. Eighteen studies met the inclusion criteria, including 400 women with localized, provoked vestibulodynia and 212 healthy women in a control group. Risk of bias assessment revealed that the methodologic quality was generally low. Fifteen studies investigated local inflammation and three studies investigated systemic inflammation. On a local level, the number of mast cells expressed in vestibular tissues was greater in women with localized, provoked vestibulodynia expressed than in women in the control group. Several studies reported undefined inflammatory infiltrate in vestibular tissues to a greater level in women with localized, provoked vestibulodynia than in women in the control group. Systemically, levels of natural killer cells were lower in women with localized, provoked vestibulodynia than in women in the control group. There were no systemic differences in systemic interferon-α and interferon-ϒ levels between groups. There is limited and contradictory evidence regarding the characteristics of local and systemic inflammation in women with localized, provoked vestibulodynia.
Start Date: 2015
End Date: 2015
Funder: Australian Research Council
View Funded ActivityStart Date: 2012
End Date: 2014
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2018
End Date: 2020
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2014
End Date: 2020
Funder: Australian Research Council
View Funded ActivityStart Date: 2013
End Date: 2013
Funder: Australian Research Council
View Funded ActivityStart Date: 2016
End Date: 2019
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2019
End Date: 2019
Funder: Australian Research Council
View Funded ActivityStart Date: 10-2014
End Date: 12-2020
Amount: $23,000,000.00
Funder: Australian Research Council
View Funded ActivityStart Date: 2015
End Date: 12-2015
Amount: $440,000.00
Funder: Australian Research Council
View Funded ActivityStart Date: 2019
End Date: 12-2019
Amount: $1,480,000.00
Funder: Australian Research Council
View Funded ActivityStart Date: 2021
End Date: 06-2022
Amount: $909,079.00
Funder: Australian Research Council
View Funded Activity