![Dipak Ramji BSc, PhD, FLSW, FISCB](https://profiles-cardiff.imgix.net/attachments/1182?w=200&h=200&auto=format&crop=faces&fit=crop&q=90")
Yr Athro Dipak Ramji
(e/fe)
BSc, PhD, FLSW, FISCB
- Ar gael fel goruchwyliwr ôl-raddedig
Timau a rolau for Dipak Ramji
Dirprwy Bennaeth yr Ysgol
Ysgol y Biowyddorau
Trosolwyg
Bywgraffiad
Mae Dipak Ramji yn Athro Gwyddor Cardiofasgwlaidd ac yn Ddirprwy Bennaeth Ysgol y Biowyddorau ym Mhrifysgol Caerdydd. Mae hefyd yn Gymrawd Cymdeithas Ddysgedig Cymru. Derbyniodd ei radd BSc (Anrh) (Biocemeg) a'i PhD (Bioleg Moleciwlaidd) o Brifysgol Leeds. Dilynwyd hyn gan ymchwil ôl-ddoethurol yn EMBL (Heidelberg) ac IRBM (Rhufain) gyda chymrodoriaethau gan y Gymdeithas Frenhinol a'r UE. Mae ei ymchwil gyfredol yn canolbwyntio ar glefyd cardiofasgwlaidd atherosglerotig ac anhwylderau llidiol eraill (gweler isod am fwy o fanylion). Mae wedi cyhoeddi dros 150 o erthyglau ymchwil gyda >10,000 o ddyfyniadau, gan gynnwys llyfr 880 tudalen yn 2022 ar Methods in Atherosclerosis. Mae'n aelod o Fwrdd Golygyddol nifer o gyfnodolion rhyngwladol, yn aelod o Bwyllgor Grantiau Prosiect Sefydliad Prydain y Galon, yn arholwr allanol rhaglenni a addysgir mewn tair prifysgol ac mae wedi goruchwylio 30 o fyfyrwyr PhD i'w cwblhau fel prif oruchwylydd.
llid, atherosglerosis, clefyd cardiofasgwlaidd a rheoleiddio mynegiant genynnau
Ffocws cyffredinol ymchwil yn fy labordy yw deall y mecanweithiau moleciwlaidd sy'n sail i'r newidiadau mewn prosesau cellog allweddol yn ystod anhwylderau llidiol fel atherosglerosis a chlefyd cardiofasgwlaidd gyda'r nod o nodi targedau / llwybrau therapiwtig/ataliol newydd.
Mae fy ymchwil yn defnyddio cyfuniad o systemau model diwylliant celloedd a llygoden ynghyd â dulliau moleciwlaidd, biocemegol, imiwnolegol a ffarmacolegol.
Mae ffocws penodol ar ddeall sut mae llid trwy cytocinau yn rheoleiddio prosesau allweddol sy'n gysylltiedig â datblygiad atherosglerosis ynghyd â'r mecanweithiau moleciwlaidd sy'n sail i weithredoedd cynhyrchion naturiol (nutraceuticals) wrth atal a thrin y clefyd hwn.
Mae Nutraceuticals a ymchwiliwyd yn cynnwys asidau brasterog amlannirlawn, polyphenols a bacteria probiotig.
Mae ymchwil flaenorol a chyfredol wedi'i ariannu gan grantiau gan Sefydliad Prydeinig y Galon, Ymddiriedolaeth Wellcome, BBSRC, MRC, YR UE, Llywodraethau Rhyngwladol a Diwydiant.
Rolau
- Dirprwy Bennaeth Ysgol y Biowyddorau Caerdydd
- Cymrawd Cymdeithas Ddysgedig Cymru
- Cymrawd Cymdeithas Cemegwyr a Biolegwyr India
- Aelod o Bwyllgor Grantiau Prosiect Sefydliad Prydain y Galon o fis Mai 2024
- Aelod o Bwyllgor y Grŵp Lipidau yng Nghymdeithas y Diwydiant Cemegol -SCI
- Cadeirydd Cronfa Cardiofasgwlaidd Sefydliad Ymchwil y Galon Cymru (WHRI)
- Aelod o Bwyllgor Craffu STEMM2 (Bioleg: Gwyddorau Moleciwlaidd i Ecosystemau) Cymdeithas Ddysgedig Cymru
- Aelod o Grŵp Modelu Llwyth Gwaith ym Mhrifysgol Caerdydd
- Aelod o'r Pwyllgor Safonau Biolegol ym Mhrifysgol Caerdydd
- Aelod o grŵp EDI Coleg y Gwyddorau Biofeddygol a Bywyd
- Aelod o Weithgor Arolwg Staff y Brifysgol 2023
- Arholwr Allanol ar gyfer Rhaglen Biocemeg BSc/MSci ym Mhrifysgol Keele
- Arholwr Allanol ar gyfer MSc mewn Meddygaeth Moleciwlaidd yng Ngholeg Imperial Llundain
- Arholwr Allanol ar gyfer MSc mewn Gwyddor Cardiofasgwlaidd yng Ngholeg Prifysgol Llundain
Oes gennych chi ddiddordeb mewn ymuno â'm labordy fel myfyriwr ôl-raddedig hunan-ariannu neu ôl-ddoethurwriaeth/cymrawd? Cysylltwch â mi drwy e-bost.
Cyhoeddiad
2026
- Alalawi, S. et al., 2026. Anti-atherogenic actions of pomegranate polyphenol punicalagin and its metabolites: In vitro effects on vascular cells and in vivo atheroprotection by urolithin A via anti-inflammatory and plaque-stabilising mechanisms. Antioxidants 15 (4) 507. (10.3390/antiox15040507)
- Alahmadi, A. et al. 2026. Resveratrol mediates anti-atherogenic actions in vitro and in LDL receptor-deficient mice fed a high fat diet via antioxidant, anti-inflammatory and plaque stabilising activities. Antioxidants 15 (1) 76. (10.3390/antiox15010076)
2023
- Mazzarino, M. et al. 2023. Therapeutic targeting of chronic kidney disease-associated DAMPs differentially contributing to vascular pathology. Frontiers in Immunology 14 1240679. (10.3389/fimmu.2023.1240679)
- Chan, Y. et al. 2023. (+)-catechin attenuates multiple atherosclerosis-associated processes in vitro, modulates disease-associated risk factors in C57BL/6J mice and reduces atherogenesis in LDL receptor deficient mice by inhibiting inflammation and increasing markers of plaque stability. Molecular Nutrition & Food Research 67 (14) 2200716. (10.1002/mnfr.202200716)
- Alalawi, S. , Albalawi, F. and Ramji, D. P. 2023. The role of punicalagin and its metabolites in atherosclerosis and risk factors associated with the disease. International Journal of Molecular Sciences 24 (10) 8476. (10.3390/ijms24108476)
- O'Morain, V. L. et al. 2023. Anti-Atherogenic actions of the Lab4b consortium of probiotics in vitro. International Journal of Molecular Sciences 24 (4) 3639. (10.3390/ijms24043639)
- Takala, R. , Ramji, D. P. and Choy, E. 2023. The beneficial effects of pine nuts and its major fatty acid, pinolenic acid, on inflammation and metabolic perturbations in inflammatory disorders. International Journal of Molecular Sciences 24 (2) 1171. (10.3390/ijms24021171)
2022
- Zabetakis, I. et al., 2022. Functional foods and their implications for health promotion. Elsevier. (10.1016/C2020-0-00556-6)
- Takala, R. et al. 2022. Pinolenic acid exhibits Anti-inflammatory and Anti-atherogenic effects in Peripheral blood- derived Monocytes from patients with Rheumatoid Arthritis. Scientific Reports 12 8807. (10.1038/s41598-022-12763-8)
- Takala, R. et al. 2022. Anti-inflammatory and immunoregulatory effects of pinolenic acid in rheumatoid arthritis. Rheumatology 61 (3), pp.992-1004. (10.1093/rheumatology/keab467)
- Ramji, D. P. ed. 2022. Atherosclerosis: Methods and protocols. Methods in Molecular Biology New York: Humana Press. (10.1007/978-1-0716-1924-7)
- Alahmadi, A. and Ramji, D. P. 2022. Monitoring modified lipoprotein uptake and macropinocytosis associated with macrophage foam cell formation. In: Ramji, D. ed. Atherosclerosis: Methods and Protocols. Vol. 2419, Methods in Molecular Biology Vol. 1064-3.New York, NY: Springer. , pp.247-255. (10.1007/978-1-0716-1924-7_14)
- Chan, Y. et al. 2022. Evaluation of plaque burden and in atherosclerotic plaques. In: Ramji, D. ed. Atherosclerosis: Methods and Protocols. Vol. 2419, Methods in Molecular Biology Springer. , pp.481-496. (10.1007/978-1-0716-1924-7_29)
- Chan, Y. et al. 2022. Monitoring cellularity and expression of key in atherosclerotic plaques. In: Ramji, D. ed. Atherosclerosis: Methods and Protocols. Vol. 2419, Methods in Molecular Biology Springer. , pp.497-506. (10.1007/978-1-0716-1924-7_30)
- Chan, Y. and Ramji, D. P. 2022. Atherosclerosis: pathogenesis and key cellular processes, current and emerging therapies, key challenges, and future research directions. In: Ramji, D. ed. Atherosclerosis: Methods and Protocols. Vol. 2419, Methods in Molecular Biology Vol. 1064-3.New York, NY: Springer. , pp.3-19. (10.1007/978-1-0716-1924-7_1)
- Chan, Y. and Ramji, D. P. 2022. Investigation of mitochondrial bioenergetic profile and dysfunction in atherosclerosis. In: Ramji, D. ed. Atherosclerosis: Methods and Protocols. Vol. 2419, Methods in Molecular Biology Vol. 1064-3.New York, NY: Springer(10.1007/978-1-0716-1924-7_19)
- Chan, Y. and Ramji, D. P. 2022. Key roles of inflammation in atherosclerosis: mediators involved in orchestrating the inflammatory response and its resolution in the disease along with therapeutic avenues targeting inflammation. In: Ramji, D. ed. Atherosclerosis: Methods and Protocols. Vol. 2419, Methods in Molecular Biology Vol. 1064-3.New York, NY: Springer. , pp.21-37. (10.1007/978-1-0716-1924-7_2)
- Chan, Y. and Ramji, D. P. 2022. Probing inflammasome activation in atherosclerosis. In: Ramji, D. ed. Atherosclerosis: Methods and Protocols. Vol. 2419, Methods in Molecular Biology Vol. 1064-3.New York, NY: Springer. , pp.313-331. (10.1007/978-1-0716-1924-7_20)
- Ramji, D. P. et al. 2022. Survey of approaches for investigation of atherosclerosis in vivo. In: Ramji, D. ed. Atherosclerosis: Methods and Protocols. Vol. 2419, Methods in Molecular Biology Vol. 1064-3.New York, NY: Springer. , pp.57-72. (10.1007/978-1-0716-1924-7_4)
- Ramji, D. P. et al. 2022. Survey of in vitro model systems for Investigation of key cellular processes associated with atherosclerosis. In: Ramji, D. P. ed. Atherosclerosis: Methods and Protocols. Vol. 2419, Vol. 1064-3.New York, NY: Springer. , pp.39-56. (10.1007/978-1-0716-1924-7_3)
2021
- Al-Ahmadi, W. et al., 2021. Pro-atherogenic actions of signal transducer and activator of transcription 1 serine 727 phosphorylation in LDL receptor deficient mice via modulation of plaque inflammation. FASEB Journal 35 (10) e21892. (10.1096/fj.202100571RR)
- O'Morain, V. L. et al. 2021. The Lab4P consortium of probiotics attenuates atherosclerosis in LDL receptor deficient mice fed a high fat diet and causes plaque stabilization by inhibiting inflammation and several pro-atherogenic processes. Molecular Nutrition & Food Research 65 (17) 2100214. (10.1002/mnfr.202100214)
- Moss, J. W. E. et al. 2021. Protective effects of a unique combination of nutritionally active ingredients on risk factors and gene expression associated with atherosclerosis in C57BL/6J mice fed a high fat diet. Food and Function 12 (8), pp.3657-3671. (10.1039/D0FO02867C)
2020
- Chan, Y. and Ramji, D. 2020. A perspective on targeting inflammation and cytokine actions in atherosclerosis. Future Medicinal Chemistry 12 (7), pp.613-626. (10.4155/fmc-2019-0301)
- O'Morain, V. and Ramji, D. P. 2020. The potential of probiotics in the prevention and treatment of atherosclerosis. Molecular Nutrition and Food Research 64 (4) 1900797. (10.1002/mnfr.201900797)
2019
- Gallagher, H. et al. 2019. Dihimo-γ-linolenic acid inhibits several key cellular processes associated with atherosclerosis. BBA - Molecular Basis of Disease 1865 (9), pp.2538-2550. (10.1016/j.bbadis.2019.06.011)
- Buckley, M. L. et al. 2019. The interleukin-33-mediated inhibition of expression of two key genes implicated in atherosclerosis in human macrophages requires MAP kinase, phosphoinositide 3-kinase and nuclear factor-κB signaling pathways. Scientific Reports 9 11317. (10.1038/s41598-019-47620-8)
- Ramji, D. P. 2019. Polyunsaturated fatty acids and atherosclerosis: insights from pre-clinical studies. European Journal of Lipid Science and Technology 121 (1) 1800029. (10.1002/ejlt.201800029)
2018
- Moss, J. , Williams, J. and Ramji, D. 2018. Nutraceuticals as therapeutic agents for atherosclerosis. Biochimica et Biophysica Acta - Molecular Basis of Disease 1864 (5. A.), pp.1562-1572. (10.1016/j.bbadis.2018.02.006)
2017
- Moss, J. and Ramji, D. 2017. Cytokines in Atherosclerosis. In: Foti, M. and Locati, M. eds. Cytokine Effector Functions in Tissues. Academic Press. , pp.109-118.
- Gallagher, H. et al. 2017. Nutraceuticals in the prevention and treatment of Atherosclerosis. Cardiology 137 (S1), pp.264. (10.1159/000477751)
- Michael, D. R. et al., 2017. The anti-cholesterolaemic effect of a consortium of probiotics: An acute study in C57BL/6J mice. Scientific Reports 7 2883. (10.1038/s41598-017-02889-5)
2016
- Salter, R. C. et al. 2016. The role of mitogen-activated protein kinases and sterol receptor coactivator-1 in TGF-β-regulated expression of genes implicated in macrophage cholesterol uptake. Scientific Reports 6 34368. (10.1038/srep34368)
- Moss, J. W. E. and Ramji, D. P. 2016. Nutraceutical therapies for atherosclerosis. Nature Reviews Cardiology 13 (9), pp.513-532. (10.1038/nrcardio.2016.103)
- Davies, T. et al., 2016. The action of Nutraceuticals on key macrophage processes associated with Atherosclerosis. Cardiology 134 (S1), pp.314-314. (10.1159/000447505)
- Moss, J. and Ramji, D. P. 2016. Cytokines: roles in atherosclerosis disease progression and potential therapeutic targets. Future Medicinal Chemistry 8 (11), pp.1317-1330. (10.4155/fmc-2016-0072)
- Ramji, D. et al. 2016. Cytkines in atherosclerosis: molecular mechanisms underlying their actions and promising therapeutic targets [Abstract]. Journal of Clinical and Experimental Cardiology 7 (6), pp.52-52.
- Ramji, D. et al. 2016. Nutraceuticals as preventative and therapeutic agents in atherosclerosis. Journal of Clinical and Experimental Cardiology 7 (6), pp.31-31. (10.4172/2155-9880.C1.029)
- Michael, D. R. et al., 2016. Lactobacillus plantarum CUL66 can impact cholesterol homeostasis in Caco-2 enterocytes. Beneficial Microbes 7 (3), pp.443-451. (10.3920/BM2015.0146)
- Moss, J. W. E. et al. 2016. A unique combination of nutritionally active ingredients can prevent several key processes associated with atherosclerosis in vitro. PLoS ONE 11 (3) e0151057. (10.1371/journal.pone.0151057)
2015
- Moss, J. and Ramji, D. P. 2015. Interferon-γ: Promising therapeutic target in atherosclerosis. World Journal of Experimental Medicine 5 (3), pp.154-159. (10.5493/wjem.v5.i3.154)
- Buckley, M. and Ramji, D. P. 2015. The influence of dysfunctional signaling and lipid homeostasis in mediating the inflammatory responses during atherosclerosis. Biochimica et Biophysica Acta - Molecular Basis of Disease 1852 (7), pp.1498-1510. (10.1016/j.bbadis.2015.04.011)
- Davies, T. S. et al., 2015. Interferon gamma signalling in atherosclerosis: pro-atherogenic actions and therapeutic approaches. Cardiology 131 , pp.292-292.
- Huwait, E. A. et al., 2015. Protein Kinase C is involved in the induction of ATP-Binding cassette transporter A1 expression by liver X receptor/retinoid X receptor agonist in human macrophages. Journal of Cellular Biochemistry 116 (9), pp.2032-2038. (10.1002/jcb.25157)
- Michael, D. R. et al. 2015. The phosphoinositide 3-kinase signaling pathway is involved in the control of modified low-density lipoprotein uptake by human macrophages. Lipids 50 (3), pp.253-260. (10.1007/s11745-015-3993-0)
- Ramji, D. P. and Davies, T. S. 2015. Cytokines in atherosclerosis: key players in all stages of disease and promising therapeutic targets. Cytokine & Growth Factor Reviews 26 (6), pp.673-685. (10.1016/j.cytogfr.2015.04.003)
2014
- Willis, G. R. et al. 2014. Young women with polycystic ovary syndrome have raised levels of circulating annexin V-positive platelet microparticles. Human Reproduction 29 (12), pp.2756-2763. (10.1093/humrep/deu281)
- Ashlin, T. G. et al. 2014. The anti-atherogenic cytokine interleukin-33 inhibits the expression of a disintegrin and metalloproteinase with thrombospondin motifs-1,-4 and-5 in human macrophages: Requirement of extracellular signal-regulated kinase, c-Jun N-terminal kinase and phosphoinositide 3-kinase signaling pathways. The International Journal of Biochemistry & Cell Biology 46 , pp.113-123. (10.1016/j.biocel.2013.11.008)
- Davies, T. S. et al., 2014. Pro- therogenic actions of interferon-gamma on macrophages in atherosclerosis. Cardiology 128 (S1), pp.278-278. (10.1159/000365062)
2013
- Ashlin, T. G. , Kwan, A. P. L. and Ramji, D. P. 2013. Regulation of ADAMTS-1, -4 and -5 expression in human macrophages: differential regulation by key cytokines implicated in atherosclerosis and novel synergism between TL1A and IL-17. Cytokine 64 (1), pp.234-242. (10.1016/j.cyto.2013.06.315)
- Michael, D. R. et al. 2013. Differential regulation of macropinocytosis in macrophages by cytokines: Implications for foam cell formation and atherosclerosis. Cytokine 64 (1), pp.357-361. (10.1016/j.cyto.2013.05.016)
2012
- Michael, D. R. et al. 2012. Liver X receptors, atherosclerosis and inflammation. Current Atherosclerosis Reports 14 (3), pp.284-293. (10.1007/s11883-012-0239-y)
- Michael, D. R. et al. 2012. Macrophages, lipid metabolism and gene expression in atherogenesis: a therapeutic target of the future?. Clinical Lipidology 7 (1), pp.37-48. (10.2217/clp.11.73)
- Michael, D. R. , Salter, R. C. and Ramji, D. P. 2012. TGF-β inhibits the uptake of modified low density lipoprotein by human macrophages through a Smad-dependent pathway: A dominant role for Smad-2. Biochimica et Biophysica Acta - Molecular Basis of Disease 1822 (10), pp.1608-1616. (10.1016/j.bbadis.2012.06.002)
2011
- Salter, R. et al., 2011. The expression of a disintegrin and metalloproteinase with thrombospondin motifs 4 in human macrophages is inhibited by the anti-atherogenic cytokine transforming growth factor-β and requires Smads, p38 mitogen-activated protein kinase and c-Jun. The International Journal of Biochemistry & Cell Biology 43 (5), pp.805-811. (10.1016/j.biocel.2011.02.005)
- Huwait, E. et al., 2011. A novel role for c-Jun N-terminal kinase and phosphoinositide 3-kinase in the liver X receptor-mediated induction of macrophage gene expression. Cellular Signalling 23 (3), pp.542-549. (10.1016/j.cellsig.2010.11.002)
- Li, N. , Salter, R. C. and Ramji, D. P. 2011. Molecular mechanisms underlying the inhibition of IFN-γ-induced, STAT1-mediated gene transcription in human macrophages by simvastatin and agonists of PPARs and LXRs. Journal of Cellular Biochemistry 112 (2), pp.675-683. (10.1002/jcb.22976)
- McLaren, J. E. et al. 2011. Cytokines, macrophage lipid metabolism and foam cells: implications for cardiovascular disease therapy. Progress in Lipid Research 50 (4), pp.331-347. (10.1016/j.plipres.2011.04.002)
- McLaren, J. E. et al. 2011. Eicosapentaenoic acid and docosahexaenoic acid regulate modified LDL uptake and macropinocytosis in human macrophages. Lipids 46 (11), pp.1053-1061.
2010
- McLaren, J. E. et al. 2010. IL-33 reduces macrophage foam cell formation. The Journal of Immunology 185 (2), pp.1222-1229. (10.4049/jimmunol.1000520)
- Salter, R. C. et al. 2010. ADAMTS proteases: key roles in atherosclerosis?. Journal of Molecular Medicine 88 (12), pp.1203-1211. (10.1007/s00109-010-0654-x)
- Ali, S. et al., 2010. Requirement for nuclear factor kappa B signalling in the interleukin-1-induced expression of the CCAAT/enhancer binding protein-delta gene in hepatocytes. International Journal of Biochemistry & Cell Biology 42 (1), pp.113-119. (10.1016/j.biocel.2009.09.018)
- Li, N. et al. 2010. ERK is integral to the IFN-γ-mediated activation of STAT1, the expression of key genes implicated in atherosclerosis, and the uptake of modified lipoproteins by human macrophages. The Journal of Immunology 185 (5), pp.3041-3048. (10.4049/jimmunol.1000993)
- McLaren, J. E. et al., 2010. In vitro promotion of macrophage foam cell formation by Death Receptor 3 and its ligand TL1A. Immunology 131 (1), pp.103-103.
- McLaren, J. E. et al. 2010. The TNF-like protein 1A-death receptor 3 pathway promotes macrophage foam cell formation in vitro. Journal of Immunology 184 (10), pp.5827-5834. (10.4049/jimmunol.0903782)
2009
- Foka, P. et al., 2009. The tumour necrosis factor-a-mediated suppression of the CCAAT/enhancer binding protein-a gene transcription in hepatocytes involves inhibition of autoregulation. International Journal of Biochemistry & Cell Biology 41 (5), pp.1189-1197. (10.1016/j.biocel.2008.10.024)
- McLaren, J. E. and Ramji, D. P. 2009. Interferon gamma: A master regulator of atherosclerosis. Cytokine & Growth Factor Reviews 20 (2), pp.125-135. (10.1016/j.cytogfr.2008.11.003)
- Ramji, D. P. 2009. Growth hormone-releasing peptides, CD36, and stimulation of cholesterol efflux: cyclooxygenase-2 is the link. Cardiovascular Research 83 (3), pp.419-420. (10.1093/cvr/cvp195)
2008
- Harris, S. M. et al., 2008. The interferon-γ-mediated inhibition of lipoprotein lipase gene transcription in macrophages involves casein kinase 2- and phosphoinositide-3-kinase-mediated regulation of transcription factors Sp1 and Sp3. Cellular Signalling 20 (12), pp.2296-2301. (10.1016/j.cellsig.2008.08.016)
- Ramji, D. P. et al. 2008. Cytokine signalling in macrophages and the expression of key genes implicated in atherosclerosis [Abstract]. Atherosclerosis Supplements 9 (1), pp.53. (10.1016/S1567-5688(08)70209-5)
- Singh, N. N. and Ramji, D. P. 2008. Protein kinase CK2, an important regulator of the inflammatory response?. Journal of Molecular Medicine 86 (8), pp.887-897. (10.1007/s00109-008-0352-0)
- Singh, N. N. , Salter, R. C. and Ramji, D. P. 2008. Molecular mechanisms underlying transforming growth factor-beta-induced expression of the apolipoprotein E gene [Abstract]. Atherosclerosis Supplements 9 (1), pp.21. (10.1016/S1567-5688(08)70078-3)
2007
- Harvey, E. J. , Li, N. and Ramji, D. P. 2007. Critical role for casein kinase 2 and phosphoinositide-3-kinase in the interferon- -induced expression of monocyte chemoattractant protein-1 and other key genes implicated in atherosclerosis. Arteriosclerosis Thrombosis and Vascular Biology 27 (4), pp.806-812. (10.1161/01.ATV.0000258867.79411.96)
- Singh, N. N. et al., 2007. Signaling pathways underlying cytokine regulated expression of key genes in macrophages implicated in atherosclerosis. Atherosclerosis Supplements 8 (1), pp.4-4.
2006
- Monslow, J. et al., 2006. Sp1 and Sp3 mediate constitutive transcription of the human hyaluronan synthase 2 gene. The Journal of Biological Chemistry 281 (26), pp.18043-18050. (10.1074/jbc.M510467200)
- Foka, P. et al., 2006. Signalling pathways underlying transforming growth factor-beta regulated expression of key genes implicated in the control of foam cell formation. Atherosclerosis Supplements 7 (3), pp.237-237.
- Irvine, S. A. et al., 2006. Lipoprotein lipase is expressed by glomerular mesangial cells. The International Journal of Biochemistry & Cell Biology 38 (1), pp.12-16. (10.1016/j.biocel.2005.07.008)
- Kockar, F. , Yildirim, H. and Ramji, D. P. 2006. Molecular characterisation and comparative analysis of the human C/EBP delta promoter to mammalian homologues. FEBS Letters 273 , pp.334-334.
- Singh, N. N. et al., 2006. Transforming growth factor-b-regulated expression of genes in macrophages implicated in the control of cholesterol homoeostasis. Biochemical Society Transactions 34 (6), pp.1141-1141. (10.1042/BST0341141)
- Singh, N. N. and Ramji, D. P. 2006. The role of transforming growth factor-β in atherosclerosis. Cytokine & Growth Factor Reviews 17 (6), pp.487-499. (10.1016/j.cytogfr.2006.09.002)
- Singh, N. N. and Ramji, D. P. 2006. Transforming growth factor-β-induced expression of the apolipoprotein e gene requires c-Jun N-terminal kinase, p38 kinase, and casein kinase 2. Arteriosclerosis Thrombosis and Vascular Biology 26 (6), pp.1323-1329. (10.1161/01.ATV.0000220383.19192.55)
2005
- Irvine, S. A. et al., 2005. A critical role for the Sp1-binding sites in the transforming growth factor-β-mediated inhibition of lipoprotein lipase gene expression in macrophages. Nucleic Acids Research , pp.1423-1434. (10.1093/nar/gki280)
- Foka, P. et al., 2005. Molecular mechanisms involved in the cytokine-regulated expression of genes in macrophages implicated in foam cell formation and atherosclerosis. Arteriosclerosis Thrombosis and Vascular Biology 25 (5), pp.E71-E71.
- Greenow, K. , Pearce, N. J. and Ramji, D. P. 2005. The key role of apolipoprotein E in atherosclerosis. Journal of Molecular Medicine 83 (5), pp.329-342. (10.1007/s00109-004-0631-3)
- Harvey, E. J. and Ramji, D. P. 2005. Interferon-γ and atherosclerosis: pro- or anti-atherogenic?. Cardiovascular Research 67 (1), pp.11-20. (10.1016/j.cardiores.2005.04.019)
- Harvey, E. J. and Ramji, D. P. 2005. Up-regulation of monocyte chemoattractant protein-1 and the monocyte chemoattractant protein-1 receptor (CCR2) in macrophages by the pro-inflammatory cytokine interferon-gamma. Arteriosclerosis Thrombosis and Vascular Biology 25 (5), pp.E64-E64.
2004
- Foka, P. , Irvine, S. and Ramji, D. P. 2004. Regulation of CCAAT/enhancer binding protein-alpha gene transcription by interleukin-6. Atherosclerosis Supplements 5 (1), pp.31-31.
- Greenow, K. R. , Pearce, N. and Ramji, D. P. 2004. A critical role for the phosphoinositide-3-kinase signal transduction pathway in the activation of apolipoprotein E gene expression. Atherosclerosis Supplements 5 (1), pp.25-25. (10.1016/S1567-5688(04)90110-4)
- Irvine, S. A. , Foka, P. and Ramji, D. P. 2004. Transcriptional regulation of macrophage lipoprotein lipase gene expression by transforming growth factor-beta. Atherosclerosis Supplements 5 (1), pp.31-32. (10.1016/S1567-5688(04)90137-2)
- Ramji, D. P. et al. 2004. Signal transduction pathways and transcriptional control mechanisms involved in the cytokine-mediated, regulation of key genes in macrophages implicated in foam cell formation and atherosclerosis. Atherosclerosis Supplements 5 (1), pp.29-30.
2003
- Foka, P. et al. 2003. Interleukin-6 represses the transcription of the CCAAT/enhancer binding protein-α in hepatoma cells by inhibiting its ability to autoactivate the proximal promoter region. Nucleic Acids Research , pp.6722-6732. (10.1093/nar/gkg861)
- Mead, J. R. et al., 2003. Interferon-γ stimulates the expression of the inducible cAMP early repressor in macrophages through the activation of casein kinase 2: A Potentially novel pathway for interferon-γ-mediated inhibition of gene transcription. Journal of Biological Chemistry , pp.17741-17751. (10.1074/jbc.M301602200)
- Ramji, D. P. et al. 2003. Novel pathways for cytokine-mediated regulation of macrophage lipoprotein lipase gene expression. Atherosclerosis Supplements 4 (2), pp.62-62. (10.1016/S1567-5688(03)90263-7)
2002
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- Kockar, F. T. et al., 2001. Analysis of the Xenopus laevis CCAAT-enhancer binding protein α gene promoter demonstrates species-specific differences in the mechanisms for both auto-activation and regulation by Sp1. Nucleic Acids Research 29 (2), pp.362-372. (10.1093/nar/29.2.362)
- Foka, P. , Kousteni, S. and Ramji, D. P. 2001. Molecular characterization of the xenopus CCAAT-enhancer binding protein β gene promoter. Biochemical and Biophysical Research Communications 285 (2), pp.430-436. (10.1006/bbrc.2001.5203)
- Davies, G. E. et al., 2000. The ovine CCAAT-enhancer binding protein δ gene: cloning, characterization, and species-specific autoregulation. Biochemical and Biophysical Research Communications 271 (2), pp.346-352. (10.1006/bbrc.2000.2630)
- Granger, R. L. , Hughes, T. R. and Ramji, D. P. 2000. Gene, stimulus and cell-type specific regulation of activator protein-1 in mesangial cells by lipopolysaccharide and cytokines. Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 1492 (1), pp.100-107. (10.1016/S0167-4781(00)00089-0)
- Granger, R. L. , Hughes, T. R. and Ramji, D. P. 2000. Stimulus- and cell-type-specific regulation of CCAAT-enhancer binding protein isoforms in glomerular mesangial cells by lipopolysaccharide and cytokines. Biochimica et Biophysica Acta - Molecular Basis of Disease 1501 (2-3), pp.171-179. (10.1016/S0925-4439(00)00016-8)
- Tengku-Muhammad, T. S. et al., 2000. Cytokine-mediated differential regulation of macrophage activator protein-1 genes. Cytokine 12 (6), pp.720-726. (10.1006/cyto.1999.0620)
- Tengku-Muhammad, T. S. et al., 2000. Differential regulation of macrophage ccaat- enhancer binding protein isoforms by lipopolysaccharide and cytokines. Cytokine 12 (9), pp.1430-1436. (10.1006/cyto.2000.0711)
- Kousteni, S. , Tura-Kockar, F. and Ramji, D. P. 1999. Sequence and expression analysis of a novel Xenopus laevis cDNA that encodes a protein similar to bacterial and chloroplast ribosomal protein L24. Gene 235 (1-2), pp.13-18. (10.1016/S0378-1119(99)00221-8)
- Mead, J. R. , Cryer, A. and Ramji, D. P. 1999. Lipoprotein lipase, a key role in atherosclerosis?. FEBS Letters 462 (1-2), pp.1-6. (10.1016/S0014-5793(99)01495-7)
- Tengku-Muhammad, T. S. et al., 1999. Involvement of both the tyrosine kinase and the phosphatidylinositol-3 ' kinase signal transduction pathways in the regulation of lipoprotein lipase expression in J774.2 macrophages by cytokines and lipopolysaccharide. Cytokine 11 (7), pp.463-468. (10.1006/cyto.1998.0460)
- Tengku-Muhammad, T. S. et al., 1999. Synergism between lipopolysaccharide and interferon gamma in the regulation of lipoprotein lipase in macrophages. Cytokine 11 (6), pp.408-415. (10.1006/cyto.1998.0447)
- Kousteni, S. et al., 1998. Characterisation and developmental regulation of the Xenopus laevis CCAAT-enhancer binding protein β gene. Mechanisms of Development 77 (2), pp.143-148. (10.1016/S0925-4773(98)00128-2)
- Sabatakos, G. et al., 1998. Rapid communication: Nucleotide sequence of ovine C/EBP epsilon gene. Journal of Animal Science 76 (11), pp.2953-2954.
- Kousteni, S. et al., 1997. Sequence and expression analysis of a Xenopus laevis cDNA which encodes a homologue of mammalian 14-3-3 zeta protein. Gene 190 (2), pp.279-285. (10.1016/S0378-1119(97)00013-9)
Llyfrau
- Zabetakis, I. et al., 2022. Functional foods and their implications for health promotion. Elsevier. (10.1016/C2020-0-00556-6)
- Ramji, D. P. ed. 2022. Atherosclerosis: Methods and protocols. Methods in Molecular Biology New York: Humana Press. (10.1007/978-1-0716-1924-7)
Ymchwil
llid, atherosglerosis, clefyd cardiofasgwlaidd a rheoleiddio mynegiant genynnau
Nod cyffredinol ymchwil yn fy labordy yw deall sut mae cytocinau a ffactorau eraill sy'n gysylltiedig â chlefydau yn rheoleiddio prosesau cellog allweddol yn ystod anhwylderau llidiol gyda'r nod o nodi targedau / llwybrau therapiwtig/ataliol newydd. Yn benodol, rydym yn egluro'r llwybrau sy'n arwain o ryngweithio ffactorau o'r fath â'u derbynyddion, trwy'r rhaeadrau signalau mewngellog, i reoli mynegiant genynnau yn y niwclews a rheoleiddio prosesau cellog dillynol. Mae ymchwil yn defnyddio cyfuniad o systemau model diwylliant celloedd a llygoden ynghyd â dulliau moleciwlaidd, biocemegol, imiwnolegol a ffarmacolegol. Mae ymchwil flaenorol a chyfredol wedi'i ariannu gan grantiau gan Sefydliad Prydeinig y Galon, Ymddiriedolaeth Wellcome, BBSRC, MRC, YR UE, Llywodraethau Rhyngwladol a Diwydiant. Mae ein hymchwil yn canolbwyntio ar ddau brif faes:
Rheoleiddio prosesau macroffag yn ystod atherosglerosis gyda ffocws ar weithredoedd cytocinau
Mae atherosglerosis a'i gymhlethdodau, fel cnawd myocardaidd a damwain cerebrofasgwlaidd, yn gyfrifol am fwy o farwolaethau ledled y byd nag unrhyw glefyd arall. Mae atherosglerosis yn anhwylder llidiol rhydwelïau canolig a mawr wedi'i drefnu gan cytocinau. Mae macroffagau yn chwarae rhan amlwg yn pathogenesis y clefyd hwn gyda'u defnydd heb ei reoli o lipoproteinau atherogenig a'u trawsnewid dilynol yn gelloedd ewyn, sy'n cynrychioli cam cynnar hanfodol mewn atherogenesis. Mae prif ffocws ymchwil yn fy labordy yn neilltuo i ddeall y mecanweithiau moleciwlaidd y mae cytocinau yn rheoleiddio prosesau macroffag allweddol yn ystod atherosglerosis. Mae ffocws penodol ar weithredoedd interferon-gamma, gan drawsnewid ffactor twf-beta ac interleukin-33.
Nutraceuticals wrth atal a thrin atherosglerosis
Mae therapïau fferyllol cyfredol yn erbyn atherosglerosis yn gysylltiedig â risg weddilliol sylweddol ar gyfer clefyd cardiofasgwlaidd ynghyd â materion eraill fel sgîl-effeithiau ac effeithiolrwydd sy'n ddibynnol ar gleifion. Yn ogystal, mae llawer o raglenni darganfod cyffuriau wedi methu â dod o hyd i ddewisiadau amgen. Mae Nutraceuticals yn cynrychioli asiantau addawol naill ai ar gyfer atal atherosglerosis neu drin y clefyd ar y cyd ag asiantau fferyllol. Fodd bynnag, mae hyn yn gofyn am ddealltwriaeth fanwl o'u mecanweithiau gweithredu ac yn y pen draw treialon clinigol mawr i brofi eu heffeithiolrwydd. Rydym yn ymchwilio i weithredoedd gwrth-atherogenig sawl nutraceuticals, gan gynnwys asid dihomo-gamma-linolenig, asid gamma-linolenig, asid pinolenig, asidau brasterog omega-3, hydroxytyrosol, catechin, resveratrol, punicalagin, ffytosterolau a probiotegau.
Cydweithrediadau
- Yr Athro Foo Liew (FRS), Prifysgol Glasgow
- Yr Athro Thomas Decker, Labordai Max F. Perutz, Fienna
- Yr Athro Shinji Takai, Ysgol Feddygol Osaka
- Prof. Sammy Boussiba ac Inna Khozin-Goldberg, Prifysgol Ben-Gurion
- Drs. Frank Flider a Riccardo LoCascio, Arcadia Biosciences
- Drs. Daryn Michael, Tom Davies a Sue Plummer, Cultech Ltd
- Dr. Rob Winwood, DSM Nutraceuticals
- Dr Jason Johnson, Sefydliad y Galon Bryste
- Yr Athro Jonathan Napier a Dr. Olga Sayanova, Rothamsted Research
- Dr. Nigel Pearce, GlaxoSmithKline
- Dr. Ahmed Ali, International Gums & Oils Limited
- Yr Athro Gavin Wilkinson, a Dr Timothy Hughes, John Martin, Tim Bowen, Eddie Wang, Ian Humphreys ac Anne-Catherine Raby, Ysgol Feddygaeth, Caerdydd
- Dr Xiaoqing Wei, Ysgol Deintyddiaeth, Caerdydd
- Yr Athro John Harwood a'r Dr Alvin Kwan a Neil Rodrigueac Irina Guschina
Aelodau'r grŵp
- Dr. Jessica Williams
- Miss Hayley Gallagher
- Mr Joe Moss
- Miss Wajdan Al-Ahmadi
- Mrs Faizah Binti Jaafar
- Mr Alex Joseph
- Mrs Victoria O'Morain
- Mrs Alaa Ismail
- Mrs Rabaa Takala
- Miss Yee-Hung Chan
- Miss Alaa Alahmadi
- Mrs Reem Alotibi
- Miss Jing Chen
- Mr Sulaiman Al Alawi
- Mr Fahad Alradi
- Mrs Nouf Alshehri
- Mrs Faizah Albalawi
- Mrs Daniah Rifqi
- Mr Abdulaziz Almalki
- Mrs Hanaa Surrati
- Mrs Alanood Alenezi
- Mr Alexander Bera
Addysgu
Darlithoedd ar Lid ac Atherosglerosis i fyfyrwyr Blwyddyn 2 yn y modiwl Cysyniadau o Glefyd (BI2332).
Bywgraffiad
Ionawr 2025-presennol: Cymrawd Cymdeithas Cemegwyr a Biolegwyr India
Ebrill 2022-presennol: Cymrawd Cymdeithas Ddysgedig Cymru
Hydref 2021-presennol: Dirprwy Bennaeth, Ysgol y Biowyddorau, Prifysgol Caerdydd
Hydref 2020-Medi 2021: Dirprwy Bennaeth Is-adran Biofeddygaeth, Ysgol y Biowyddorau Caerdydd, Prifysgol Caerdydd
Hydref 2019-Medi 2020: Pennaeth Dros Dro Is-adran Biofeddygaeth, Ysgol y Biowyddorau Caerdydd , Prifysgol Caerdydd
Awst 2017-presennol: Athro Gwyddor Gardiofasgwlaidd, Ysgol y Biowyddorau, Prifysgol Caerdydd
Hydref 2009-Medi 2021: Tiwtor Ôl-raddedig ar gyfer Is-adran Biofeddygaeth, Ysgol y Biowyddorau Caerdydd , Prifysgol Caerdydd
Awst 2006-Gorffennaf 2017: Darllenydd, Ysgol y Biowyddorau Caerdydd , Prifysgol Caerdydd
Awst 2003-Gorffennaf 2006: Uwch Ddarlithydd, Ysgol y Biowyddorau Caerdydd , Prifysgol Caerdydd
Awst 1992-Gorffennaf 2003: Darlithydd, Ysgol Biowyddorau Moleciwlaidd a Meddygol, Prifysgol Caerdydd
Ionawr 1991-Mehefin 1992: Cymrawd Ymchwil Ôl-ddoethurol, Istituto di Ricerche di Biologia Molecolare P. Angeletti (IRBM), Rhufain. Cymrodoriaeth o'r UE
Hydref 1988-Rhagfyr 1990: Cymrawd Ymchwil Ôl-ddoethurol, Labordy Bioleg Moleciwlaidd Ewropeaidd (EMBL), Heidelberg. Cymrodoriaeth gan y Gymdeithas Frenhinol
1988: PhD (Bioleg Moleciwlaidd), Adran Biocemeg, Prifysgol Leeds
1984: BSc (Anrh) Biocemeg, Dosbarth 2(1), Adran Biocemeg, Prifysgol Leeds
Anrhydeddau a dyfarniadau
- Cymrawd Cymdeithas Ddysgedig Cymru
- Cymrawd Cymdeithas Cemegwyr a Biolegwyr India
- Cymrodoriaethau Ôl-ddoethurol gan y Gymdeithas Frenhinol a'r UE
Aelodaethau proffesiynol
- Cymrawd Cymdeithas Ddysgedig Cymru
- Academi Ryngwladol Cardioleg
- Cymdeithas Atherosclerosis Prydain
- International Chemical Biology Society
Pwyllgorau ac adolygu
- Aelod o Bwyllgor Grantiau Prosiect Sefydliad Prydain y Galon o fis Mai 2024
- Gwerthuswr Arbenigol ar gyfer yr alwad 'Rhwydweithiau Doethurol Marie Skłodowska-Curie yn 2022-2026
- Adolygydd Grant Rhaglen MRC a Grant Prosiect MRC
- Adolygydd ar gyfer Cymrodoriaeth Ymchwil Gwyddoniaeth Sylfaenol Canolradd BHF a Grant Prosiect BHF
- Adolygydd ar gyfer Heart Research UK
- Arholwr Allanol ar gyfer MSc mewn Meddygaeth Gardiofasgwlaidd Drosiadol ym Mhrifysgol Bryste (2021-2025)
- Arholwr Allanol ar gyfer rhaglenni MBiol/BSc Gwyddorau Biolegol a MBiol/BSc Gwyddorau Biolegol (Biotechnoleg gyda Menter) ym Mhrifysgol Leeds (2021-2025)
- Arholwr Allanol ar gyfer BSc mewn Biowyddoniaeth ym Mhrifysgol Limerick (2020-2024)
- Gwerthuswr arbenigol ac aelod o'r panel ar gyfer Horizon 2020 (2015)
- Arholwr Allanol ar gyfer BSc mewn Biocemeg yng Ngholeg y Brenin Llundain (2016-2020)
- Arholwr Allanol ar gyfer BSc mewn Gwyddorau Biolegol ym Mhrifysgol Reading (2015-2019)
- BSc mewn Gwyddorau Biolegol ym Mhrifysgol Huddersfield (2013-2017)
- Cronfa Arbenigwyr BBSRC (2009-2010)
- Aelod o'r Panel a Chadeirydd y Pwyllgor Asesu ar gyfer Cynllun Cymrodoriaeth Ôl-ddoethurol IRCSET, Iwerddon (2008-2009)
- Arholwr Allanol ar gyfer rhaglenni MSc a addysgir ym Mhrifysgol Sheffield Hallam (2006-2011)
- Aelod o Fwrdd Cynghori MRC (2004-2005)
- Aelod o Bwyllgor Gwaith Gwyddonol yr Academi Ryngwladol Cardioleg.
- Gwerthuswr arbenigol o gyflwyniadau poster / llafar mewn dros 11 o gynadleddau rhyngwladol, gan gynnwys 16eg Cyngres ac Expo Lipid Euro Fed a Chynhadledd Ryngwladol ar Ddatblygiadau mewn Gwyddor Fferyllol ac Iechyd.
- Aelod o Fwrdd Golygyddol 10 cyfnodolyn rhyngwladol, gan gynnwys Frontiers in Clinical Diabetes and Healthcare, American Journal of Clinical and Experimental Immunology and Immunometabolism.
- Adolygydd ad hoc ar gyfer dros 20 o sefydliadau ariannu, gan gynnwys 14 y tu allan i'r DU.
- Adolygydd ad hoc o dros 36 o gyfnodolion rhyngwladol.
- Arholwr allanol ar gyfer dros 25 o fyfyrwyr PhD/MSc, gan gynnwys rhyngwladol (Iwerddon, India, a Malaysia).
Meysydd goruchwyliaeth
Goruchwyliodd 30 o fyfyrwyr PhD i'w gwblhau fel prif oruchwylydd.
Ar gael i oruchwylio myfyrwyr PhD hunan-ariannu neu a ariennir ar gyfer y prosiect canlynol.
Mecanweithiau moleciwlaidd sy'n sail i weithredoedd gwrth-atherogenig cynhyrchion naturiol
Mae atherosglerosis, achos sylfaenol cnawd myocardaidd, strôc a chlefyd fasgwlaidd ymylol, yn gyfrifol am y rhan fwyaf o farwolaethau yn y byd gorllewinol gyda marwolaethau yn cynyddu ar gyfradd sylweddol mewn gwledydd sy'n datblygu. Disgwylir i'r baich economaidd o atherosglerosis a'i gymhlethdodau waethygu oherwydd cynnydd byd-eang mewn ffactorau risg fel diabetes a gordewdra. Mae atherosglerosis yn anhwylder llidiol rhydwelïau mawr a chanolig sy'n cael ei reoleiddio gan cytocinau allweddol. Mae trin ymateb llidiol o'r fath yn ffordd addawol ar gyfer atal a thrin y clefyd hwn. Mae gan lawer o gynhyrchion naturiol a'u metabolitau briodweddau gwrth-atherogenig er bod y mecanweithiau moleciwlaidd sylfaenol yn parhau i gael eu deall yn wael. Felly, rydym yn ymchwilio i'r agwedd hon gan ddefnyddio cyfuniad o ddulliau in vitro ac in vivo .
Bydd y prosiect hwn yn canolbwyntio ar ymchwilio i weithredoedd amddiffynnol cynnyrch naturiol a ddewiswyd neu ei fetabolion ar brosesau mawr sy'n gysylltiedig ag atherosglerosis in vitro yn y tri math o gelloedd allweddol sy'n gysylltiedig â'r clefyd hwn (h.y. macroffagau, celloedd endothelaidd a chelloedd cyhyrau llyfn fasgwlaidd) ac in vivo gan ddefnyddio'r system model llygoden diffygiol derbynnydd lipoprotein dwysedd isel (mewn cydweithrediad â Dr. Timothy Hughes, Ysgol Feddygaeth, Prifysgol Caerdydd). Bydd y llygod hyn yn cael eu bwydo â diet atherogenig o fath gorllewinol am 12 wythnos a 24 wythnos wedi'i ategu â cherbyd neu metabolitau. Bydd paramedrau a fydd yn cael eu dadansoddi yn cynnwys: pwysau'r corff a phwysau organau; Proffil lipid plasma; morffometreg plac, dyddodiad colagen, a chronni macroffagau, celloedd cyhyrau llyfn a T-lymffocytau (imiwnohistocemeg). Yn ogystal, defnyddir RNA-Dilyniannu i bennu newidiadau byd-eang mewn mynegiant genynnau. Bydd yr effeithiau ar lwybrau signalau allweddol (e.e. kinasau MAP) hefyd yn cael eu dadansoddi. Bydd yr astudiaethau yn darparu dealltwriaeth fanwl o weithredoedd gwrth-atherogenig yr asiant in vitro ac in vivo.
Goruchwyliaeth gyfredol
Jing Chen
Sulaiman Amur Said Alalawi Al Alawi
Fahad Mohammed Alradi Alradi
Nouf Alshehri
Faizah Albalawi
Abdulaziz Almalki
Hanaa Surrati
Alanood Basher S Alenezi Alenezi
Alex Bera
Daniah Rifqi
Ymgysylltu
ArrayContact Details
[email protected]
+44 29208 76753
Adeilad Syr Martin Evans, Ystafell C/4.17, Rhodfa'r Amgueddfa, Caerdydd, CF10 3AX
+44 29208 76753
Adeilad Syr Martin Evans, Ystafell C/4.17, Rhodfa'r Amgueddfa, Caerdydd, CF10 3AX
Themâu ymchwil
Arbenigeddau
- Clefydau cardiofasgwlaidd
- Biocemeg a bioleg celloedd
- Bioleg foleciwlaidd
- Imiwnoleg
- Ffarmacoleg glinigol a therapiwteg