Dr Richard Yu
School of Environmental and Life Sciences (Environmental Science and Management)
- Phone:(02) 4921 6990
I received my PhD from City University of Hong Kong in 2002. After my postdoctoral training with Prof. Rudolf Wu, I continued to work in the same institution as a Lecturer until joining the University of Newcastle in 2009. I am now an academic in the Discipline of Environmental Science and Management in the School of Environmental & Life Sciences (SELS).
My primary research interests are in the Molecular Toxicology of Environmental Stressors and Chemicals.
In particular, I am interested in (1) understanding the molecular mechanisms of endocrine disruption caused by hypoxia and environmental chemicals and (2) developing cell- and animal-based assays for the screening and detection of endocrine-disrupting chemicals (EDCs). Overall, my research covers both basic science aimed at understanding the fundamental mechanisms of environmental toxicity and applied science concerned with the development of diagnostic tools for assessing and monitoring environmental toxicity. Outlined below is a summary of my recent research activities and findings:
1. Environmental Obesogens
The prevalence of obesity has been dramatically increasing worldwide during the last several decades. In recent years, there is growing epidemiological evidence indicating a positive correlation between the exposure of human population to EDCs and body weight, suggesting a possible role of EDCs in increasing obesity rates. The "obesogen hypothesis" is an emerging view proposing that exposure to a subset of these chemicals (obesogens) disrupts the weight-control mechanisms and ultimately increases obesity. To date, most of the known obesogens are those directly increasing adipogenesis and lipid accumulation, while the ones that contribute to diet-induced obesity (DIO) are understudied.
Leptin is an adipocyte-derived hormone that represses appetite and increases energy expenditure. Leptin inhibits appetite by decreasing the activity of the orexigenic NPY/AgRP/GABA neurons and increasing the activity of the anorexigenic POMC/CART neurons in the hypothalamus. Leptin action is exerted through its binding to the leptin receptor (OB-R) expressed on the surface of these neurons. Recent research showed that the disruption of OB-R activation (after treatment with leptin antagonists) during early development can lead to adult leptin resistance. Leptin resistance is a medical condition in which individuals are weakly responsive or unresponsive to high circulating levels of leptin and regarded as an important predisposing factor for DIO. Based on this existing knowledge, we hypothesise that early-life exposure to environmental chemicals that act as leptin antagonists can enhance the development of leptin-resistance and DIO in adults.
In collaboration with my co-worker Dr Richard Kong at City University of Hong Kong, a pilot screening program was recently initiated to identify environmental chemicals that act as leptin antagonists using biophysical and cell-based assays. Further effort will be made to assess the ability of the identified candidates to induce the developmental programming of adult leptin resistance and DIO using zebrafish (an important human disease model). This project is anticipated to provide important information regarding the contribution of developmental programming to the obesity epidemic, through assessing the role of early-life exposure of environmental chemicals in the development of adult leptin resistance and obesity. Since the rising prevalence of obesity has been recently noticed in livestock, pets, and wild animals, the knowledge about the mechanism of action of environmental obesogens and the technologies developed in this research could also be applied to a much broader range of biota beyond humans. Eventually, the outcome of this research may aid in devising new regulations on the safety of animal feed and the release of obesogenic chemicals to the environment.
2. Estrogen-mediated Vitellogenesis in Oysters
Oysters respond to EDC mixtures with the induction of the female egg yolk protein, vitellogenin (Vtg), availing a biomarker which indicates the presence of estrogenic contaminants in sewage effluent receiving waters. Despite this, the precise mechanism through which estrogens exert their action to induce vitellogenesis is unknown. Estrogen receptors (ERs) with homology to vertebrate ERs have been identified in selected molluscan taxa, yet those found to date do not bind or are unresponsive to estrogen. We hypothesise that estrogens may bind to receptors yet to be identified in Mollusca, with lower structural similarity to vertebrate-like ERs, and such receptors act as estrogen-dependent transcriptional regulators of vitellogenin expression. In an effort to investigate this possibility, Dr Geoff MacFarlane (UoN) and I initiated a project to isolate and characterise novel “functional” ERs from the native Sydney rock oyster (Saccostrea glomerata). Our recent progress indicated that an invertebrate-like ER isolated from the Sydney rock oyster ovarian tissues shares a similar ligand (estrogen) binding pocket with that of the human ER and is expressed in response to estrogenic compounds. Further effort will be directed at clarifying its functional roles in mediating vitellogenesis and gonadal development and its epigenetic regulation in response to the exposure to estrogenic compounds. At the application level, this research will provide important information (an ER pathway specific to invertebrates) for the development of bioassays for screening xenoestrogens with ecotoxicological relevance to molluscs.
3. Fish Hypoxia
Previously, my co-workers and I have demonstrated for the first time that hypoxia can disrupt sex differentiation via modulation of gene expression for estrogen biosynthesis, leading to a male-biased sex ratio in zebrafish (Shang et al. 2006). This work has highlighted the alarming impacts of aquatic hypoxia on fish reproduction and sustainability, and thus attracted worldwide attention, as exemplified by cover stories written by Science and Nature as well as reports by CNN and ABC. This study has been cited 60 times since its publication in 2006. Later studies also provided scientific evidence that the transcription factor hypoxia-inducible factor-1 (HIF-1) regulates a number of genes involved in fish growth and reproduction in response to hypoxia (Yu et al. 2006a, 2008; Chu et al. 2010). To assess the applicability and specificity of HIF-1-regulated gene expression as biomarkers for monitoring aquatic hypoxia, we also made efforts to decipher the crosstalk between the xenobiotic transformation pathway and the HIF-1 pathway. Intriguingly, we demonstrated that the existence of xenobiotics can enhance HIF-1-mediated gene expression via increasing the cellular levels of reactive oxygen species (ROS), indicating that the presence of environmental xenobiotics must be considered when interpreting HIF-1-based hypoxia biomarker results (Yu et al. 2008). In 2012, my co-workers (Kong & Wu) and I obtained a seed fund ($US 115,384) from the State Key Laboratory in Marine Pollution, China to study the interactive effects of climate change and hypoxia on fish sex determination.
4. Fish Leptin
The study of obesity and appetite control in fish models is an emerging field of research. In the last few years, my co-workers and I highlighted striking similarities in the function and regulation of leptin between fish and mammals. Our recent work suggests that leptin elevation under hypoxic conditions is a pathophysiological response common to both zebrafish and mammalian models (Chu et al. 2010). In another prior study, we reported for the first time the characterization of a fish long-form leptin receptor that contains all the signature motifs and domains found in the mammalian leptin receptors (Wong, Yu et al. 2007), implying the function of leptin receptor is conserved in both fish and mammals. Recently, using gain-or-loss gene function techniques, we demonstrated that leptin is the molecular link between hypoxia and endocrine disruption, leading to the suppression of the aromatase gene (cyp19a) and hence estrogen production in fish (Yu et al. 2012). Taken together, these findings provide novel insights into the molecular mechanism of endocrine disruption under hypoxia. This research successfully attracted $US 108,974 funding from Hong Kong General Research Fund (GRF) in 2011.
5. In-vitro bioassays for EDCs
For years, I have been collaborating with Prof. John Giesy (Canada Research Chair in Environmental Toxicology, University of Saskatchewan) on the development and validation of a H295R cell line screening test to evaluate toxicant-induced effects on steroid biosynthesis (steroidogenesis)—the H295R Steroidogenesis Assay (Gracia et al. 2004; Zhang et al. 2005; Gracia et al. 2006; Xu et al. 2006; Gracia et al. 2007; He et al. 2008; Song et al. 2008). This assay has been successfully used to assess the endocrine-disrupting potential and the mechanisms of action of various chemicals and environmental samples. This assay is currently being developed as part of Tier 1 of the US EPA Endocrine Disruptor Screening Program and an Organization for Economic Cooperation and Development (OECD) test method validation program.
6. In-vivo bioassays for EDCs
We recently demonstrated that induction of hepatic choriogenin H (ChgH, a fish egg-shell protein precursor) mRNA expression in male marine medaka can serve as a highly sensitive biomarker for environmental estrogens (its sensitivity is even better than vitellogenin) (Yu et al. 2006b; Cheng et al. 2008). This novel discovery led us to develop a ChgH-GFP transgenic marine medaka for monitoring environmental estrogens in marine water. Our recent progress indicated that this sentinel fish can detect 17β-estradiol (E2) at nominal concentrations as low as 1 μg/L. To make quantification of in vivo GFP expressed in developing fish embryos feasible, we previously developed an automatic 4D (3D plus time) acquisition system and the imaging processes of deconvolution and thresholding (Yu et al. 2006c). This 4D imaging system provides a simple but powerful means to quantify in vivo gene expression in a developmental toxicology context. The technologies have been successfully commercialised as environmental and food safety consultancy service in Hong Kong (Vitargent (International) Biotechnology Ltd).
Ecotoxicology Molecular toxicology Obesogen screening Embryotoxicity assays Development of bioassays for EDC screening and detection
BIOL1003 Professional Skills for Biological Sciences, ENVS2004 Ecology, ENVS3004 Ecotoxicology, SCIT2500 Project and Advanced Studies, SCIT3500 Project and Advanced Studies II
BSc Merit Pathway Convenor
For years, I have been working in close collaboration with Prof Rudolf Wu (University of Hong Kong), Dr Richard Kong (City University of Hong Kong) and Prof John Giesy (University of Saskatchewan) on hypoxia and EDC research. Recent collaborative projects (funded) include: (1) National Natural Science Foundation of China – 2015 (Project no. 21577114), Investigators: A/P Richard Kong and Dr Richard Yu, Project title: Identification and molecular studies of environmental obesogens that cause overeating, Funding: $US 106,320. (2) CityU Strategic Research Grant, City University of Hong Kong – 2013 (Project no. 7003027), Investigators: A/P Richard Kong and Dr Richard Yu, Project Title: Pilot study to identify environmental obesogens (chemicals that cause overeating) using BRET (Bioluminescence Resonance Energy Transfer) and cell-based assays, Funding: $US 12,821. (3) SKLMP Seed Collaborative Research Fund, State Key Laboratory in Marine Pollution, China – 2012 (Project no. 9369101), Investigators: A/P Richard Kong, Prof Rudolf Wu and Dr Richard Yu, Project Title: Interactive effects of climate change and hypoxia on fish sex determination: estrogen synthesis and masculinisation, Funding: $US 115,384. (4) General Research Fund, Hong Kong Research Grants Council – 2011 (Project no. 160411), Investigators: A/P Richard Kong, Prof John Giesy and Dr Richard Yu, Project Title: Uncovering the molecular links between hypoxia and endocrine disruption: A functional study of zebrafish leptin, Funding: $US 108,974.
- PhD, City University of Hong Kong - China
- Bachelor of Science (Applied Biology)(Honours), City University of Hong Kong - China
- Endocrine disrupting chemicals
- Environmental estrogens
- Molecular Toxicology
- Sydney rock oyster
Fields of Research
|050199||Ecological Applications not elsewhere classified||20|
|060199||Biochemistry and Cell Biology not elsewhere classified||40|
|111599||Pharmacology and Pharmaceutical Sciences not elsewhere classified||40|
|Title||Organisation / Department|
|Lecturer||University of Newcastle
School of Environmental and Life Sciences
|Dates||Title||Organisation / Department|
|20/04/2016 - 20/04/2019||Editorial Board Member||Heliyon (Elsevier)
|Year||Title / Rationale|
Science Week Conference
Endocrine disrupting chemicals (EDCs) in the aquatic environment: Their mechanisms of action and detection strategies
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (31 outputs)
Tran TKA, MacFarlane GR, Kong RYC, O'Connor WA, Yu RMK, 'Mechanistic insights into induction of vitellogenin gene expression by estrogens in Sydney rock oysters, Saccostrea glomerata', Aquatic Toxicology, 174 146-158 (2016)
Â© 2016 Elsevier B.V.Marine molluscs, such as oysters, respond to estrogenic compounds with the induction of the egg yolk protein precursor, vitellogenin (Vtg), availing a biomark... [more]
Â© 2016 Elsevier B.V.Marine molluscs, such as oysters, respond to estrogenic compounds with the induction of the egg yolk protein precursor, vitellogenin (Vtg), availing a biomarker for estrogenic pollution. Despite this application, the precise molecular mechanism through which estrogens exert their action to induce molluscan vitellogenesis is unknown. As a first step to address this question, we cloned a gene encoding Vtg from the Sydney rock oyster Saccostrea glomerata (sgVtg). Using primers designed from a partial sgVtg cDNA sequence available in Genbank, a full-length sgVtg cDNA of 8498 bp was obtained by 5'- and 3'-RACE. The open reading frame (ORF) of sgVtg was determined to be 7980 bp, which is substantially longer than the orthologs of other oyster species. Its deduced protein sequence shares the highest homology at the N- and C-terminal regions with other molluscan Vtgs. The full-length genomic DNA sequence of sgVtg was obtained by genomic PCR and genome walking targeting the gene body and flanking regions, respectively. The genomic sequence spans 20 kb and consists of 30 exons and 29 introns. Computer analysis identified three closely spaced half-estrogen responsive elements (EREs) in the promoter region and a 210-bp CpG island 62 bp downstream of the transcription start site. Upregulation of sgVtg mRNA expression was observed in the ovaries following in vitro (explants) and in vivo (tank) exposure to 17Ã-estradiol (E2). Notably, treatment with an estrogen receptor (ER) antagonist in vitro abolished the upregulation, suggesting a requirement for an estrogen-dependent receptor for transcriptional activation. DNA methylation of the 5' CpG island was analysed using bisulfite genomic sequencing of the in vivo exposed ovaries. The CpG island was found to be hypomethylated (with 0-3% methylcytosines) in both control and E2-exposed oysters. However, no significant differential methylation or any correlation between methylation and sgVtg expression levels was observed. Overall, the results support the possible involvement of an ERE-containing promoter and an estrogen-activated receptor in estrogen signalling in marine molluscs.
Tran TKA, MacFarlane GR, Kong RYC, O'Connor WA, Yu RMK, 'Potential mechanisms underlying estrogen-induced expression of the molluscan estrogen receptor (ER) gene', Aquatic Toxicology, 179 82-94 (2016)
Â© 2016 Elsevier B.V.In vertebrates, estrogens and estrogen mimicking chemicals modulate gene expression mainly through a genomic pathway mediated by the estrogen receptors (ERs).... [more]
Â© 2016 Elsevier B.V.In vertebrates, estrogens and estrogen mimicking chemicals modulate gene expression mainly through a genomic pathway mediated by the estrogen receptors (ERs). Although the existence of an ER orthologue in the mollusc genome has been known for some time, its role in estrogen signalling has yet to be deciphered. This is largely due to its constitutive (ligand-independent) activation and a limited mechanistic understanding of its regulation. To fill this knowledge gap, we cloned and characterised an ER cDNA (sgER) and the 5'-flanking region of the gene from the Sydney rock oyster Saccostrea glomerata. The sgER cDNA is predicted to encode a 477-amino acid protein that contains a DNA-binding domain (DBD) and a ligand-binding domain (LBD) typically conserved among both vertebrate and invertebrate ERs. A comparison of the sgER LBD sequence with those of other ligand-dependent ERs revealed that the sgER LBD is variable at several conserved residues known to be critical for ligand binding and receptor activation. Ligand binding assays using fluorescent-labelled E2 and purified sgER protein confirmed that sgER is devoid of estrogen binding. In silico analysis of the sgER 5'-flanking sequence indicated the presence of three putative estrogen responsive element (ERE) half-sites and several putative sites for ER-interacting transcription factors, suggesting that the sgER promoter may be autoregulated by its own gene product. sgER mRNA is ubiquitously expressed in adult oyster tissues, with the highest expression found in the ovary. Ovarian expression of sgER mRNA was significantly upregulated following in vitro and in vivo exposure to 17Ã-estradiol (E2). Notably, the activation of sgER expression by E2 in vitro was abolished by the specific ER antagonist ICI 182, 780. To determine whether sgER expression is epigenetically regulated, the in vivo DNA methylation status of the putative proximal promoter in ovarian tissues was assessed using bisulfite genomic sequencing. The results showed that the promoter is predominantly hypomethylated (with 0Â¿3.3% methylcytosines) regardless of sgER mRNA levels. Overall, our investigations suggest that the estrogen responsiveness of sgER is regulated by a novel ligand-dependent receptor, presumably via a non-genomic pathway(s) of estrogen signalling.
Li VWT, Tsui MPM, Chen X, Hui MNY, Jin L, Lam RHW, et al., 'Effects of 4-methylbenzylidene camphor (4-MBC) on neuronal and muscular development in zebrafish (Danio rerio) embryos', Environmental Science and Pollution Research, 23 8275-8285 (2016) [C1]
Â© 2016, Springer-Verlag Berlin Heidelberg.The negative effects of overexposure to ultraviolet (UV) radiation in humans, including sunburn and light-induced cellular injury, are o... [more]
Â© 2016, Springer-Verlag Berlin Heidelberg.The negative effects of overexposure to ultraviolet (UV) radiation in humans, including sunburn and light-induced cellular injury, are of increasing public concern. 4-Methylbenzylidene camphor (4-MBC), an organic chemical UV filter, is an active ingredient in sunscreen products. To date, little information is available about its neurotoxicity during early vertebrate development. Zebrafish embryos were exposed to various concentrations of 4-MBC in embryo medium for 3Â¿days. In this study, a high concentration of 4-MBC, which is not being expected at the current environmental concentrations in the environment, was used for the purpose of phenotypic screening. Embryos exposed to 15Â¿ÂµM of 4-MBC displayed abnormal axial curvature and exhibited impaired motility. Exposure effects were found to be greatest during the segmentation period, when somite formation and innervation occur. Immunostaining of the muscle and axon markers F59, znp1, and zn5 revealed that 4-MBC exposure leads to a disorganized pattern of slow muscle fibers and axon pathfinding errors during the innervation of both primary and secondary motor neurons. Our results also showed reduction in AChE activity upon 4-MBC exposure both in vivo in the embryos (15Â¿ÂµM) and in vitro in mammalian Neuro-2A cells (0.1Â¿ÂµM), providing a possible mechanism for 4-MBC-induced muscular and neuronal defects. Taken together, our results have shown that 4-MBC is a teratogen and influences muscular and neuronal development, which may result in developmental defects.
Yu RMK, Chaturvedi G, Tong SKH, Nusrin S, Giesy JP, Wu RSS, Kong RYC, 'Evidence for microRNA-mediated regulation of steroidogenesis by hypoxia', Environmental Science and Technology, 49 1138-1147 (2015) [C1]
Â© 2014 American Chemical Society.Environmental hypoxia can occur in both natural and occupational environments. Over the recent years, the ability of hypoxia to cause endocrine d... [more]
Â© 2014 American Chemical Society.Environmental hypoxia can occur in both natural and occupational environments. Over the recent years, the ability of hypoxia to cause endocrine disruption via perturbations in steroid synthesis (steroidogenesis) has become increasingly clear. To further understand the molecular mechanism underlying hypoxia-induced endocrine disruption, the steroidproducing human cell line H295R was used to identify microRNAs (miRNAs) affecting steroidogenic gene expression under hypoxia. Hypoxic treatment of H295R cells resulted in the downregulation of seven steroidogenic genes and one of these, CYP19A1 (aromatase), was shown to be regulated by the transcription factor hypoxia-inducible factor-1 (HIF-1). Using bioinformatic and luciferase reporter analyses, miR-98 was identified to be a CYP19A1- targeting miRNA from a subset of HIF-1-inducible miRNAs. Gain- and loss-of-function analysis suggested that under hypoxia, the increased expression of miR-98 led to the downregulation of CYP19A1 mRNA and protein expression and that it may have contributed to a reduction in estradiol (E2) production. Intriguingly, luciferase reporter assays using deletion constructs of a proximal 5'-flanking region of miR-98 did not reveal a hypoxia-responsive element (HRE)-containing promoter. Overall, this study provided evidence for the role of miRNAs in regulating steroidogenesis and novel insights into the molecular mechanisms of hypoxia-induced endocrine disruption. (Figure Presented).
Lu X, Yu RMK, Murphy MB, Lau K, Wu RSS, 'Hypoxia disrupts gene modulation along the brain-pituitary-gonad (BPG)-liver axis', Ecotoxicology and Environmental Safety, 102 70-78 (2014) [C1]
Hypoxia alters sex hormone concentrations leading to reproductive impairment in fish; however the mechanisms underlying these effects remain largely unknown. Using zebrafish (Dani... [more]
Hypoxia alters sex hormone concentrations leading to reproductive impairment in fish; however the mechanisms underlying these effects remain largely unknown. Using zebrafish (Danio rerio), this study is the first to demonstrate that hypoxia causes endocrine disruption by simultaneously acting on multiple targets along the brain-pituitary-gonadal (BPG)-liver axis in fish. Alterations in the expression of key genes associated with reproductive endocrine pathways in the brain (sGnRH), pituitary (FSHÃ and LHÃ), gonads (FSH-R, LH-R, HMGR, StAR, CYP19A, CYP11A, CYP11Ã and 20Ã-HSD), and liver were correlated with significant reductions of estradiol in females and testosterone in males. Hypoxia also induced sex-specific and tissue-specific changes in the expression of estrogen, androgen, and membrane progestin receptors along the BPG axis, suggesting disruption of the feedback and synchronization of hormone signals. Furthermore, the hypoxia-induced upregulation of hepatic sex hormone-binding globulin suggests an increase in hormone transport and reduced bioavailability in blood, while upregulation of hepatic CYP3A65 and CYP1A in females suggests an increase in estrogen biotransformation and clearance. Given that the regulation of reproductive hormones and the BPG-liver axis are highly conserved, this study provides new insights into the hypoxia-induced endocrine disrupting mechanisms and reproductive impairment in other vertebrates. Â© 2014 Elsevier Inc.
Yu MKR, Chu DLH, Tan T-F, Li VWT, Chan AKY, Giesy JP, et al., 'Leptin-mediated modulation of steroidogenic gene expression in hypoxic zebrafish embryos: Implications for the disruption of sex steroids', Environmental Science & Technology, 46 9112-9119 (2012) [C1]
Lo KH, Hui MNYH, Yu MKR, Wu RSS, Cheng SH, 'Hypoxia impairs primordial germ cell migration in zebrafish (danio rerio) embryos', PLoS ONE, 6 e24540 (2011) [C1]
Ng PKS, Yu MKR, Kwong TFN, Wong MML, Kong RYC, 'Transcriptional regulation and functional implication of the grass carp CITED1 (gcCITED1) in the negative regulation of HIF-1', International Journal of Biochemistry and Cell Biology, 42 1544-1552 (2010) [C1]
Chu DLH, Li VWT, Yu MKR, 'Leptin: Clue to poor appetite in oxygen-starved fish', Molecular and Cellular Endocrinology, 319 143-146 (2010) [C1]
Ng PKS, Chiu S-K, Kwong TFN, Yu MKR, Wong MML, Kong RYC, 'Functional characterization of two CITED3 homologs (gcCITED3a and gcCITED3b) in the hypoxia-tolerant grass carp, Ctenopharyngodon idellus', BMC Molecular Biology, 10 1-14 (2009) [C1]
Kong RYC, Law SHL, Chu JKY, Ng PKD, Yu RMK, Wu RSS, 'Functional and molecular plasticity of the HIF transcription factors', COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR & INTEGRATIVE PHYSIOLOGY, 148 S7-S7 (2007)
Shang EHH, Yu RMK, Wu RSS, 'Hypoxia alters sex hormones, sex ratio and favors a male-dominated population in fish', COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR & INTEGRATIVE PHYSIOLOGY, 148 S118-S118 (2007)
Chen X, Kinoshita M, Hirata T, Yu RMK, Cheng SH, 'Transgenic marine medaka (Oryzias melastigma): a sensitive sentinel for estrogenic pollutants', MOLECULAR & CELLULAR TOXICOLOGY, 3 34-34 (2007)
Wong MML, Yu RMK, Ng PKS, Law SHW, Tsang AKC, Kong RYC, 'Characterization of a hypoxia-responsive leptin receptor (omLepR(L)) cDNA from the marine medaka (Oryzias melastigma)', MARINE POLLUTION BULLETIN, 54 797-803 (2007) [C1]
Gracia T, Hilscherova K, Jones PD, Newsted JL, Higley EB, Zhang X, et al., 'Modulation of steroidogenic gene expression and hormone production of H295R cells by pharmaceuticals and other environmentally active compounds', TOXICOLOGY AND APPLIED PHARMACOLOGY, 225 142-153 (2007) [C1]
Xu Y, Yu RMK, Zhang XW, Murphy MB, Giesy JP, Lam MHW, et al., 'Effects of PCBs and MeSO2-PCBs on adrenocortical steroidogenesis in H295R human adrenocortical carcinoma cells', CHEMOSPHERE, 63 772-784 (2006) [C1]
Yu RMK, Lin CC, Chan PK, Chow ESH, Murphy MB, Chan BP, et al., 'Four-dimensional imaging and quantification of gene expression in early developing zebrafish (Danio rerio) embryos', TOXICOLOGICAL SCIENCES, 90 529-538 (2006) [C1]
Gracia T, Hilscherova K, Jones PD, Newsted JL, Zhang X, Hecker M, et al., 'The H295R system for evaluation of endocrine-disrupting effects', ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY, 65 293-305 (2006) [C1]
Yu RMK, Wong MML, Kong RYC, Wu RSS, Cheng SH, 'Induction of hepatic choriogenin mRNA expression in male marine medaka: A highly sensitive biomarker for environmental estrogens', AQUATIC TOXICOLOGY, 77 348-358 (2006) [C1]
Law SHW, Wu RSS, Ng PKS, Yu RMK, Kong RYC, 'Cloning and expression analysis of two distinct HIF-alpha isoforms - gcHIF-1alpha and gcHIF-4alpha - from the hypoxia-tolerant grass carp, Ctenopharyngodon idellus', BMC MOLECULAR BIOLOGY, 7 (2006) [C1]
Shang EHH, Yu RMK, Wu RSS, 'Hypoxia affects sex differentiation and development, leading to a male-dominated population in zebrafish (Danio rerio)', ENVIRONMENTAL SCIENCE & TECHNOLOGY, 40 3118-3122 (2006) [C1]
Zhang XW, Yu RMK, Jones PD, Lam GKW, Newsted JL, Gracia T, et al., 'Quantitative RT-PCR methods for evaluating toxicant-induced effects on steroidogenesis using the H295R cell line', ENVIRONMENTAL SCIENCE & TECHNOLOGY, 39 2777-2785 (2005) [C1]
Yu RMK, Wong MML, Jack RW, Kong RYC, 'Structure, evolution and expression of a second subfamily of protein phosphatase 2A catalytic subunit genes in the rice plant (Oryza sativa L.)', PLANTA, 222 757-768 (2005) [C1]
Hilscherova K, Jones PD, Gracia T, Newsted JL, Zhang XW, Sanderson JT, et al., 'Assessment of the effects of chemicals on the expression of ten steroidogenic genes in the H295R cell line using real-time PCR', TOXICOLOGICAL SCIENCES, 81 78-89 (2004) [C1]
Yu RMK, Zhou Y, Xu ZF, Chye ML, Kong RYC, 'Two genes encoding protein phosphatase 2A catalytic subunits are differentially expressed in rice', PLANT MOLECULAR BIOLOGY, 51 295-311 (2003) [C1]
|Show 28 more journal articles|
Conference (3 outputs)
Priestley MN, Dunstan RH, O'Connor W, Van Zweiten R, Yu MKR, Macfarlane GR, 'Molluscan bio-monitor for quantification and impcat assessment of estrogenically active compounds in Australian marine ecosystems', 20th SETAC Europe Annual Meeting, Seville, Spain: Science and Technology Environmental Protection: Programme Book (2010) [E3]
|2010||Yu MKR, Chu DLH, Li VWT, 'Leptin: A molecular link between hypoxia and endocrine disruption in fish?', 6th International Conference on Marine Pollution and Ecotoxicology. Programme & Abstracts (2010) [E3]|
|2009||Yu MKR, 'Leptin: A molecular link between hypoxia and endocrine disruption in fish?', 13th Australasian Society for Ecotoxicology Conference: Posters (2009) [E3]|
Number of supervisions
Total current UON EFTSL
|Commenced||Level of Study||Research Title / Program / Supervisor Type|
Assessing of Potential Estrogenic Effects on Freshwater Mussel (Hyridelladepressa) in New South Wales, Australia
PhD (Environmental Sc), Faculty of Science, The University of Newcastle
Molecular cloning and characterisation of insulin-like growth factor binding protein (IGFBP) genes in the Sydney rock oyster
PhD (Environmental Sc), Faculty of Science, The University of Newcastle
Investigation of the Molecular Mechanisms Underlying Chemical-induced Endocrine Disruption in Sydney Rock Oysters (Saccostrea glomerata)
PhD (Environmental Sc), Faculty of Science, The University of Newcastle
|Year||Level of Study||Research Title / Program / Supervisor Type|
Influence of Metal Exposure History on Metal Tolerance in the Sydney Rock Oyster (Saccostrea Glomerata)
PhD (Biological Sciences), Faculty of Science, The University of Newcastle
The map is a representation of a researchers co-authorship with collaborators across the globe. The map displays the number of publications against a country, where there is at least one co-author based in that country. Data is sourced from the University of Newcastle research publication management system (NURO) and may not fully represent the authors complete body of work.
|Country||Count of Publications|
Dr Richard Yu
Environmental Water Science Group
School of Environmental and Life Sciences
Faculty of Science
Environmental Science and Management
|Phone||(02) 4921 6990|
|Fax||(02) 4921 8977|
Callaghan, NSW 2308