个人简介
2017 – present
Lecturer at School of Pharmacy and Pharmaceutical Sciences, Cardiff University
2012 – 2016
Career Development Research Fellow (NISCHR, National Institute of Social Care and Health Research, now Health and Care Research Wales) Institute of Infection & Immunity, School of Medicine, Cardiff University.
“Cross-interaction of the innate immune response (complement system) with coagulation proteins in blood disorders”.
2013 – 2014
Lecturer (fixed-term), Cardiff University Independent Researcher Secondment Scheme, School of Medicine, Cardiff University.
2011 – 2012
Post-Doctoral Research Associate, Institute of Psychological Medicine & Clinical Neurosciences and Institute of Infection & Immunity, School of Medicine, Cardiff University. “The role of complement regulators in Alzheimer’s disease”.
2008 – 2011
Post-Doctoral Research Associate, Department of Infection, Immunity & Biochemistry, School of Medicine, Cardiff University. “The role and diagnosis of complement dysregulation in disease” & “The Complotype: dictating risk for inflammation and infection”.
2004 – 2008
PhD in Applied Biochemistry, Cranfield Biotechnology Centre, Cranfield University. “Development of a screen-printed voltametric electrochemical sensor for the immunosuppressant mycotoxin ochratoxin A”.
研究领域
My past research has largely focussed on the characterisation of structure-function mechanisms leading to dysregulation of the complement system, part of the innate immune defence. This is relevant in renal disorders such as aHUS; atypical hemolytic uremic syndrome or DDD; dense deposit disease and a result of disease-associated polymorphisms or mutations.
Recent research focussed on the molecular characterisation of cross-talk between the two innate defence systems against pathogen invasion and bleeding, complement and coagulation. Both complement and coagulation systems are structurally and organisationally similar protein cascades that are activated by defined triggers, often in parallel. Dysregulation of these systems have been associated with many diseases.
We are currently studying complement and coagulation cross-talk on the protein and cellular level in vitro and investigating in vivo mechanisms. With clinical colleagues at the UHW Cardiff, a clinical biomarker study in a severe sepsis patient cohort is identifying key cross-talking complement and coagulation protein biomarkers as tools to predict disease severity.
近期论文
查看导师新发文章
(温馨提示:请注意重名现象,建议点开原文通过作者单位确认)
Heurich-Sevcenco, M.et al. 2016. Thrombomodulin enhances complement regulation through strong affinity interactions with factor H and C3b-Factor H complex. Thrombosis Research 145, pp. 84-92. (10.1016/j.thromres.2016.07.017) pdf
Szakmany, T. and Heurich-Sevcenco, M. 2015. Immunomodulation in sepsis - why blunting the response doesn't work?. Journal of Infection 71(2), pp. 147-149. (10.1016/j.jinf.2015.04.019) pdf
Martínez-Barricarte, R.et al. 2015. The molecular and structural bases for the association of complement C3 mutations with atypical hemolytic uremic syndrome. Molecular Immunology 66(2), pp. 263-273. (10.1016/j.molimm.2015.03.248) pdf
Ruseva, M. and Heurich-Sevcenco, M. 2014. Purification and characterization of human and mouse complement C3. Methods in Molecular Biology -Clifton then Totowa- 1100, pp. 75-91.
Harris, C.et al. 2012. The complotype: dictating risk for inflammation and infection. Trends in Immunology 33(10), pp. 513-521. (10.1016/j.it.2012.06.001)
Heurich, M.et al. 2011. Common polymorphisms in C3, factor B, and factor H collaborate to determine systemic complement activity and disease risk. Proceedings of the National Academy of Sciences of the United States of America 108(21), pp. 8761-8766. (10.1073/pnas.1019338108)
Martínez-Barricarte, R.et al. 2010. Human C3 mutation reveals a mechanism of dense deposit disease pathogenesis and provides insights into complement activation and regulation. Journal of Clinical Investigation 120(10), pp. 3702-3712. (10.1172/JCI43343) pdf