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The lack of standardization made it difficult to compare x-ray treatments from one centre to another, let alone within the same centre. A 1937 paper entitled "Effect of Roentgenotherapy on Gliomas" reflected this with a disclaimer that irradiation techniques had varied considerably, even though they were all treated at the same location. This was due in part to differences in dosage unit measurements, differences in filters used, and in part to early voltage limitations of equipment which was later upgraded 12 ; . One of the earliest improvements in radiotherapy was the discovery of fractionation. With fractionation, radiotherapy is administered in a series of fractions of the total dose, usually once a day for several weeks, in order to minimize damage to normal tissue. This important discovery remains the basis for most radiotherapy treatments given to this day. Using normal tissue with a high mitotic index as a model for cancer, Regaud and Ferroux performed experiments in Paris, France in the 1920s and 1930s in an attempt to deliver radiation to a target while minimizing damage to normal tissue. In these experiments, the testes of rams were irradiated with x-rays. It was known that if attempts were made to sterilize the animals in a single dose, a severe reaction to the skin of the scrotum would develop. However, Regaud and Ferroux discovered that if the dose was fractionated over a period of time, sterilization could be achieved with little apparent skin damage 6 ; . With this evidence, fractionation was introduced into clinical practise for all cancer treatments, including brain tumors. However, much higher energy radiation was needed to effectively penetrate the skull than the 200 kV roentgen rays that were available during those years. Much of the radiation acted on the surface. Skin damage was thus still the limiting factor in the irradiation of brain tumors. Tarlov defined the "threshold skin dose" in the treatment of gliomas in 1937 as the quantity of radiation that produced a visible skin pigmentation in 80 percent of patients within one month 12 ; . It wasn't until the late 1930s when the effect of radiotherapy on gliomas, the most common lethal form of primary brain cancer, was described 13 ; . With standards not yet established, variation between prescribed dosages were huge. For example, initial doses ranged from 1600 rads radiation absorbed dose a measurement of energy absorbed per unit mass ; up to 9500 rads. To put this in perspective, the total dose to gliomas now is usually between 5000 and 6000 rads, and a routine chest x-ray delivers approximately 0.015 rads 15 millirads ; to the chest. Some patients were re-irradiated upon recurrence, which is no longer done today due to late toxic effects. Some patients did poorly, and length of survival was not related to dosage. As well, survival was not influenced by the temporal sequence of irradiation. For example, a single series of radiotherapy versus three smaller series spread out over three months was compared - in either case, the mean survival was 11 months 12, 13 ; . Sachs concluded in his 1936 paper that larger doses of roentgen radiation should be used, and proposed various ways to try to accomplish this 14. T. Kottmann 1 , M. Farr 1 , M. Wiemer 1 , M. Steinberg 1 , M. Schmidt 1 , K. Kleesiek 2 , D. Horstkotte 1 , C. Piper 1 . 1 Heart Center NRW, Ruhr Univ Bochum, Department of Cardiology, Bad Oeynhausen, Germany; 2 Heart Center NRW, Ruhr Univ Bochum, Dept Laboratory Transfusion Medicine, Bad Oeynhausen, Germany Background: Enhanced fibrinolytic activity is a risk factor for coronary artery disease but there is less data about its influence on restenosis after coronary stent implantation ST ; . The fibrinogen polymorphisms may affect fibrinolytic processes and influence coronary in-stent restenosis. Methods: 120 patients 88% men, mean age: 649 years ; were enrolled prior to ST. Genotypes of fibrinogen -455G A, -854G A, and HaeIII ; were analyzed and levels of D-dimers, fibrinogen, F1 + 2 and CRP were determined before ST, as well as 3h, 6h, 12h, and 7 days thereafter. After 6 months, all patients underwent control coronary angiography to quantify restenosis. Results: The genotypes of the various fibrinogen polymorphisms presented as: 455G A: 62% GG, 34% GA and 4% AA. 854G A: 85% GG, 14%GA and 1% AA. HaeIII: 58% H1H1, 37% H1H2 and 5% H2H2 Table 1 ; . Independent of the genotypes, most fibrinolytic and inflammatory markers increased after ST and reached their maximum after 48h fibrinogen: p 0.001; CRP: p 0.001 ; and 7days Ddimers: p 0.01 ; , but no enhancement of F1 + was observed. In an univariate analysis, fibrinogen and CRP levels were not influenced by any fibrinogen polymorphisms, wereas levels of D-dimers were higher in patients with GA or AA genotype of 854G A and H1H2 or H2H2 genotype of HaeIII p 0.05 ; . F1 + was slightly influenced by HaeIII and 854G A genotypes p: n.s. ; . Coronary in-stent restenosis 50% ; was angiographically documented in 32% of all patients. In an univariate analysis, restenosis was not correlated with any of the determined fibrinogen polymorphisms or with one of the fibrinolytic markers and vicoprofen.

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