ORCID Profile
0000-0001-8165-6893
Current Organisation
Deakin University
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Publisher: EURORAD
Date: 2014
Publisher: AME Publishing Company
Date: 11-2019
Publisher: Public Library of Science (PLoS)
Date: 27-10-2021
DOI: 10.1371/JOURNAL.PONE.0259211
Abstract: Although neutrophil elastase (NE) may play a role in lung fibrosis and liver fibrosis, NE involvement in the development of nephrogenic systemic fibrosis has been unclear. We investigated the involvement of NE in the development of nephrogenic systemic fibrosis-like skin lesions post-injections of linear gadolinium-based contrast agents in renal failure mouse models. Renal failure mouse models were randomly ided into three groups: control group (saline), gadodiamide group, and gadopentetate group. Each solution was intravenously administered three times per week for three weeks. The mice were observed daily for skin lesions. Quantification of skin lesions, infiltrating inflammatory cells, and profibrotic cytokines in the affected skin was performed by immunostaining and reverse-transcription polymerase chain reaction (RT-PCR). Blood s les were collected from the facial vein to quantify NE enzymatic activity. The 158 Gd concentrations in each s le were quantified using inductively coupled plasma mass spectrometry (ICP-MS). In the gadodiamide group, the mRNA expression of fibrotic markers was increased in the skin lesions compared to the control group. In the gadopentetate group, only collagen 1α and TGF-β mRNA expression were higher than in the control group. The expression of CD3+, CD68+, NE cells and the NE activity in the blood serum were significantly higher in the gadodiamide and gadopentetate groups compared to the control group. Gadolinium concentration in the skin of the gadodiamide group was significantly higher than the gadopentetate group, while almost no traces of gadolinium were found in the control group. Although gadopentetate and gadodiamide affected the fibrotic markers in the skin differently, NE may be involved in the development of fibrosis linked to the GBCAs injections in renal failure mouse models.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 10-2016
Publisher: British Institute of Radiology
Date: 07-2019
DOI: 10.1259/BJR.20190062
Abstract: To investigate the role of transporter proteins in gadolinium (Gd) distribution and retention in the brain after one high-dose injection of Gd-based contrast agent (GBCA). 30 ddY mice were randomly ided into three treatment groups to be intravenously injected with either Gadodiamide (linear GBCA), Gadobutrol (macrocyclic GBCA), or Gadoterate (macrocyclic GBCA) at a dose of 5 mmol/kg, while five mice in the control group received 250 µL saline. Five minutes (5 min) and ten days (10d) post-injection, the cerebrospinal fluid (CSF), choroid plexus (CP), and meninges and associated vasculature (MAV) were collected. The brain was then dissected to obtain the olfactory bulb, cerebral cortex, hippoc us, cerebellum, and brainstem. Proteins were extracted and separated by a size-exclusion high-performance liquid chromatography (SEC) system, and Gd concentrations were quantified by inductively coupled plasma mass spectrometry (ICP-MS). 5 m post-injection, the Gadodiamide group had the highest Gd concentration, while Gadoterate had the lowest Gd concentration in all parts of the brain (p .05). Gd concentration was highest in the cerebrospinal fluid (CSF) of the Gadodiamide group (578.4 ± 135.3 nmol), while Gd concentration was highest in MAV in the Gadobutrol group (379.7 ± 75.4 nmol) at 5 min post-injection. At 10d, in spite of the significant decrease of Gd from all GBCAs ( p 0.01), retained Gd from Gadodiamide was detected all over the brain in several molecules that varied in size. Gd from Gadobutrol detected in the olfactory bulb (8.7 ± 4.5 nmol) was significantly higher than in other parts of the brain. Although most Gd from Gadobutrol was found in molecules similar in size to Gadobutrol, it was also found in several protein molecules of molecular size larger than the contrast agents. Only a small amount of Gd from Gadoterate was found in the brain. GBCAs may be able to pass through intact brain barriers, and the chemical structures of GBCAs may affect the penetration capability of Gd into the brain. Retained Gd in the brain tissue from Gadodiamide and Gadobutrol may be bound to some organic molecules, including proteins. Intact GBCA are able to penetrate a series of brain barrier immediately after administration regardless the type of the chelate. Gd may be bound with macromolecules that may cause Gd retention in the brain.
Publisher: Springer Science and Business Media LLC
Date: 22-01-2018
DOI: 10.1007/S12282-018-0834-Z
Abstract: We evaluated the potential of diffusion-weighted MRI (DW-MRI) and Cisplatin-treated TNBC tumor-bearing mice were categorized as responders or non-responders based on the tumor growth rate. DW-MRI and Both the day 3 and day 7 ratios of ADC The ratios of ADC
Publisher: MDPI AG
Date: 08-12-2021
DOI: 10.3390/DIAGNOSTICS11122310
Abstract: Gadolinium deposition in the brain has been observed in areas rich in iron, such as the dentate nucleus of the cerebellum. We investigated the role of Fe2+ in the effect of gadolinium-based contrast agents (GBCA) on thyroid hormone-mediated Purkinje cell dendritogenesis in a cerebellar primary culture. The study comprises the control group, Fe2+ group, GBCA groups (gadopentetate group or gadobutrol group), and GBCA+Fe2+ groups. Immunocytochemistry was performed with an anti-calbindin-28K (anti-CaBP28k) antibody, and the nucleus was stained with 4′,6-diamidino-2-phenylindole (DAPI). The number of Purkinje cells and their arborization were evaluated with an analysis of variance with a post-hoc test. The number of Purkinje cells was similar to the control groups among all treated groups. There were no significant differences in dendrite arborization between the Fe2+ group and the control groups. The dendrite arborization was augmented in the gadopentetate and the gadobutrol groups when compared to the control group (p 0.01, respectively). Fe2+ significantly increased the effect of gadopentetate on dendrite arborization (p 0.01) but did not increase the effect of gadobutrol. These findings suggested that the chelate thermodynamic stability and Fe2+ may play important roles in attenuating the effect of GBCAs on the thyroid hormone-mediated dendritogenesis of Purkinje cells in in vitro settings.
Publisher: Springer Science and Business Media LLC
Date: 24-10-2019
DOI: 10.1186/S12885-019-6238-4
Abstract: Overexpression of epidermal growth factor receptor (EGFR) has been established as a valid therapeutic target of non-small cell lung cancer (NSCLC). However, the clinical benefit of cetuximab as an EGFR-targeting drug is still controversial, partially due to the lack of effective means to identify suitable patients. This study aimed to investigate the potential of radiolabeled cetuximab as a non-invasive tool to predict cetuximab accumulation in NSCLC tumor xenografts with varying EGFR expression levels. The NSCLC tumors in model mice were subjected to in vivo biodistribution study and positron emission tomography (PET) imaging 48 h after injection of either 111 In- or 64 Cu-labeled cetuximab. The EGFR expression levels of NSCLC tumors were determined by ex vivo immunoblotting. We found that tumors with high EGFR expression had significantly higher [ 111 In]In-DOTA-cetuximab accumulation than tumors with moderate to low EGFR expression ( P 0.05). Strong correlations were found between [ 111 In]In-DOTA-cetuximab tumor uptake and EGFR expression level ( r = 0.893), and between [ 64 Cu]Cu-DOTA-cetuximab tumor uptake with EGFR expression level ( r = 0.915). PET imaging with [ 64 Cu]Cu-DOTA-cetuximab allowed clear visualization of tumors. Our findings suggest that this immuno-PET imaging can be clinically translated as a tool to predict cetuximab accumulation in NSCLC cancer patients prior to cetuximab therapy.
Publisher: Informa UK Limited
Date: 06-10-2021
DOI: 10.1080/15226514.2021.1984388
Abstract: Many studies have demonstrated the
Publisher: British Institute of Radiology
Date: 10-2016
DOI: 10.1259/BJR.20160509
Start Date: 2019
End Date: 2021
Funder: Japan Society for the Promotion of Science
View Funded ActivityStart Date: 2022
End Date: 2024
Funder: Japan Society for the Promotion of Science
View Funded Activity