A Doctor Facing Turbulent Times: Antoni Tomasz Jurasz, Citizen of the World

The eponymous of the Jurasz procedure is Antoni Tomasz Jurasz (1882–1961). The procedure is a standard approach to treating mature pancreatic pseudocysts that are in contact with the stomach, although recent advances in instrumentation have empowered surgeons to perform pseudocystogastrostomy laparoscopically for this problem. Dr. Jurasz was born in Germany but felt himself as Polish as his ancestors. He graduated from Heidelberg with a degree in medicine. Over the following years, he developed a German surgery school, especially helping with the achievements of Erich Lexer and Erwin Payr. During the period between World Wars I and II, Jurasz chaired and led the Surgery Clinic of Poznan University in Poland; and he gave lectures and performed public operations abroad. These activities, together with articles published in German-, French-, and English-language medical journals, made him a world-renowned figure in the field of abdominal and thyroid surgery. During World War II, he revealed exceptional traits, taking part in the September Campaign in Poland as a surgeon. He then organized the Polish School of Medicine and the Paderewski Hospital in Edinburgh. Despite his outstanding mind, generosity, and merits, A. T. Jurasz became persona non grata in Communist Poland, which ultimately persuaded him to emigrate to the United States

Insights into Mechanisms of Blood-Brain Barrier Permeability – Roles of Free Radicals, Matrix Metalloproteinsases, and Caveolin-1

Free radicals, including reactive oxygen species (ROS) and reactive nitrogen species (RNS), are important mediators in cerebral ischemia-reperfusion injury and other neurological diseases. Accumulation of toxic free radicals not only increase the susceptibility of brain tissue to ischemic damage but also trigger numerous molecular cascades, leading to increased blood-brain barrier (BBB) permeability, brain edema, hemorrhage and inflammation, and brain death. Matrix metalloproteinases (MMPs) are one of the major targets in BBB breakdown. MMPs are proteolytic zinc-containing enzymes responsible for degradation of the extracellular matrix around cerebral blood vessels and neurons. Free radicals can activate MMPs and induce the degradations of tight junctions (TJs), leading to BBB breakdown. Recent studies indicate that caveolin-1, a 22 kDa membrane integral protein located at caveolae, can inhibit RNS production and MMPs activity, protect TJ proteins from degradation, and reduce the BBB permeability in cerebral ischemia-reperfusion injury. The interaction of RNS, caveolin-1, and MMPs forms a positive feedback loop which provides amplified impacts on BBB dysfunction during cerebral ischemia-reperfusion injury. Herein, we review the recent progress in the interaction of RNS, caveolin-1, and MMPs and the impact of the interaction on BBB permeability. For drug discovery, we summarize current evidence about antioxidant therapy in regulations of MMPs and caveolin-1 and anticipate the potential of developing antioxidants for the treatment of stroke and other neurological diseases. In conclusion, the interaction of RNS, caveolin-1, and MMPs could be a critical signal pathway in BBB disruption and infarction enlargement during cerebral ischemia-reperfusion injury and other neurological diseases