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Die fast vollständig zerlegbaren Gruppen bilden eine Teilklasse der Butlergruppen. Das Konzept des Regulators, d.h. der Durchschnitt aller regulierenden Untergruppen, ist unverzichtbar für fast vollständig zerlegbare Gruppen. Dieses Konzept lässt sich in natürlicher Weise auf die ganze Klasse der Butlergruppen fortsetzen. Allerdings lässt sich die Regulatorbildung im allgemeineren Fall der Butlergruppen a priori iterieren. Damit stellt sich erst einmal die Frage, ob es überhaupt Butlergruppen gibt mit Regulatorketten, der Länge größer als 1. Ein erstes Beispiel der Länge 2 wurde 1997 von Lehrmann und Mutzbauer konstruiert. In dieser Dissertation wurden mit konzeptionell neuen Techniken Butlergruppen mit beliebiger vorgegebener endlicher Kettenlänge angegeben. Grundsätzliche Schwierigkeiten bei diesem Unterfangen resultieren aus dem Fehlen, bzw. der Unmöglichkeit, einer kanonischen Darstellung von Butlergruppen. Man verwendet die allseits gebrauchte Summendarstellung für Butlergruppen. Genau an dieser Stelle bedarf es völlig neuer Methoden, verglichen mit den fast vollständig zerlegbaren Gruppen mit ihrer kanonischen Regulatordarstellung. Alle Teilaufgaben bei der anstehenden Konstruktion von Butlergruppen, die für fast vollständig zerlegbare Gruppen Standard sind, werden hierbei problematisch, u.a. die Bildung reiner Hüllen, die Bestimmung regulierender Untergruppen und die Regulatorbildung.
There is a debate on the optimal way of monitoring training loads in elite endurance athletes especially during altitude training camps. In this case report, including nine members of the German national middle distance running team, we describe a practical approach to monitor the psychobiological stress markers during 21 days of altitude training (~2100 m above sea‐level) to estimate the training load and to control muscle damage, fatigue, and/or chronic overreaching. Daily examination included: oxygen saturation of hemoglobin, resting heart rate, body mass, body and sleep perception, capillary blood concentration of creatine kinase. Every other day, venous serum concentration of blood urea nitrogen, venous blood concentration of hemoglobin, hematocrit, red and white blood cell were measured. If two or more of the above‐mentioned stress markers were beyond or beneath the athlete's normal individual range, the training load of the subsequent training session was reduced. Running speed at 3 mmol L\(^{−1}\) blood lactate (V\(_{3}\)) improved and no athlete showed any signs of underperformance, chronic muscle damage, decrease body and sleep perception as well as activated inflammatory process during the 21 days. The dense screening of biomarkers in the present case study may stimulate further research to identify candidate markers for load monitoring in elite middle‐ and long‐distance runners during a training camp at altitude.
Glycoprotein VI (GPVI) is a platelet-specific receptor for collagen and fibrin, regulating important platelet functions such as platelet adhesion and thrombus growth. Although the blockade of GPVI function is widely recognized as a potent anti-thrombotic approach, there are limited studies focused on site-specific targeting of GPVI. Using computational modeling and bioinformatics, we analyzed collagen- and CRP-binding surfaces of GPVI monomers and dimers, and compared the interacting surfaces with other mammalian GPVI isoforms. We could predict a minimal collagen-binding epitope of GPVI dimer and designed an EA-20 antibody that recognizes a linear epitope of this surface. Using platelets and whole blood samples donated from wild-type and humanized GPVI transgenic mice and also humans, our experimental results show that the EA-20 antibody inhibits platelet adhesion and aggregation in response to collagen and CRP, but not to fibrin. The EA-20 antibody also prevents thrombus formation in whole blood, on the collagen-coated surface, in arterial flow conditions. We also show that EA-20 does not influence GPVI clustering or receptor shedding. Therefore, we propose that blockade of this minimal collagen-binding epitope of GPVI with the EA-20 antibody could represent a new anti-thrombotic approach by inhibiting specific interactions between GPVI and the collagen matrix.