Dr Guozheng Wang MBChB, MD, PhD.

Personal Statement

1978-1982 undergraduate study of medicine in the Medical School of Southeast University (originally Nanjing Railway Medical School). After 3 years of HO, SHO, I began my research work while I was doing my MD degree in China (1985-1988). In 1992, I have been awarded a scholarship and gained the opportunity to work in Cambridge University (Laboratory of Molecular Biology and Babraham Institute), where I received an excellent training in molecular biology, protein biochemistry and cell biology. From 1994-1997, I was supported by BBSRC to work on fission yeast and mouse genetic projects as an employee of Oxford University, where I knocked out yeast and mouse genes as well as their structure-function relationship. In 1997 with support from Wellcome Trust, I moved to the School of Biological Sciences, University of Liverpool, where I found that S100P is a metastasis-promoting gene and gained a leading position in the study of S100P by solving its crystal structure, metastasis-promoting property in animal model and its prognostic role in human breast cancer. Now the underlying molecular mechanism is still under investigation.

Since 2006, I have focused on critical illnesses, particularly on sepsis. At the beginning, I did some work on CRP-VLDL complexes in diagnosis and their effects on blood bacterial clearance. Since 2009, a new discovery that extracellular histones are toxic have attracted my attention and most of the group have been studying the roles of circulating histones in the pathophysiology of critical illnesses as well as their diagnostic and prognostic values in critical illnesses, such as in severe trauma, sepsis and pancreatitis. In this direction, we are very successful and productive. Through our work, we have first linked the circulating histone levels to disease severity, for example in severe trauma, and pancreatitis. We also first demonstrate that high levels of circulating histones are the major mediators of acute lung injury and cardiac complications in sepsis. On the other hand, we have also established a new concept that circulating histones are important regulators of innate immunity, including cytokine release, acute phase response, complement inhibition and neutrophil extracellular trap (NETs) formation. Recently, our works on histone-induced coagulation activation in critical ill patients have made a great progress. For example, histones directly enhancing thrombin activation, platelet drop and disseminate intravascular coagulation (DIC) have been completed and some has been published in high impact journal, JAMA. All those works have established our world leading position in this field.