Heinrich Brinkmeier, Ph.D., is currently Prof. of Pathophysiology and Molecular Medicine at the University of Greifswald, Germany. He is also Director of the Institute of Pathophysiology since May 2002. Heinrich studied biology with a focus on developmental biology and cell differentiation. He obtained his Ph.D. from the University of Bielefeld, Germany, in 1989. In his thesis he discovered the underlying defect of mouse myotonia showing that lack of chloride channels in muscle fibers is the basic problem. He showed that reduced muscular chloride conductance can cause overexcitability of fibers and muscle stiffness in a mouse mutant abbreviated as ADR. After his Ph.D. he moved to the University of Ulm, south Germany and spent about twelve years investigating voltage-gated ion channels in nerve and muscle fibers, including pharmacology of ion channels and channelopathies. During the years in Ulm he became interested in intracellular Ca2+-regulation of muscle fibers and the pathomechanism of Duchenne muscular dystrophy. At Greifswald University his group is studying the role of transient receptor potential (TRP) channels in muscle under normal and pathophysiological conditions. Applied techniques are, besides electrophysiology, muscle force measurements, histology, analyses of gene expression, proteomics and pharmacology. Heinrich Brinkmeier organized meanwhile six international meetings and workshops, is reviewer for numerous scientific journals and obtained four scientific awards.

Pathomechanism and therapy of Duchenne muscular dystrophy; the role TRP channels, gene expression and fibrosis in normal and dystrophic muscle; muscle structure and function in aged animals