Berechnung des Pflichtbeitrags eines niedergelassenen Arztes zum ?rztlichen Versorgungswerk bei Insolvenz

1. Wird dem Insolvenzsschuldner von den Gl?ubigern die Fortführung seiner Arztpraxis gestattet (sog. Betriebsfortführung), stellen die Pflichtbeitr?ge zur Altersversorgung sonstige Massenverbindlichkeiten dar, die gem. § 53 InsO vorweg durch den Insolvenzverwalter zu berichtigen sind. 2. Der Umstand, dass die Gl?ubigerversammlung im Rahmen der Betriebsfortführung für den fortführenden Arzt einen bestimmten monatlichen Unterhalt festgesetzt hat, bedingt keine Umqualifizierung der T?tigkeit als niedergelassener Arzt in eine Angestelltent?tigkeit. Die Pflichtbeitr?ge zur Altersversorgung sind daher nach den für Niedergelassene geltenden Satzungsbestimmungen zu berechnen, so dass nach wie vor allein der in der Praxis erzielte Gesamtumsatz und nicht der dem Arzt gew?hrte Unterhaltsbetrag als Berechnungsgrundlage für den Beitragssatz heranzuziehen ist.     

Vorrang des EU-Rechts im Approbationsrecht

1. Nach § 2 Abs. 1 S. 7 ZHG wird die Approbation nicht erteilt, wenn die naturwissenschaftliche Vorprüfung, die zahn?rztliche Vorprüfung oder die zahn?rztliche Prüfung nach der ZAppO endgültig nicht bestanden wurde. 2. Diese Regelung ist in Hinblick auf Art. 12 GG nicht zu beanstanden; allerdings bestehen gegen die Gültigkeit des § 2 Abs. 1 S. 7 ZHG verfassungsrechtliche Bedenken in Hinblick auf eine fehlende übergangs- bzw. Vertrauensschutzregelung.     

Keine Rundfunkgebühr für den Praxisweg

Abstrakt Fahrten eines Selbst?ndigen von seiner Wohnung zur Arbeitsstelle und zurück stellen eine „private“ Nutzung des Kraftfahrzeuges dar. In diesem Fahrzeug befindliche Zweitger?te unterfallen deshalb nicht gesondert der Rundfunkgebührenpflicht. (Leitsatz der Bearbeiterin)     

Effect of adriamycin on expression and content of myocardial structural and regulatory proteins

The biochemical and morphological study of the cytoskeleton and extracellular matrix of rat heart was carried out after single injection of adriamycin (2.2 or 0.44 mg/kg). Hearts were taken for the study after 2 hours and 3 weeks after injection. The light and electronic microscopy, immunohistochemical determination of type I, III and IV collagens and fibronectin using specific antibodies were implied for morphological study; electrophoresis and immunoblotting were implied for the determination of the content of some proteins of cardiomyocytes (KRP or telokin, desmin, tubulin and vinculin), and extracellular matrix (fibronectin) and vascular smooth muscle cells (MLCK, myosin light chain kinase). Adriamycin injection in the dose 2.2 mg/kg which is close to therapeutic and known to alter intracellular membranes approximately in the half of cardiomyocytes, did not influence the relative volume and structure of collagen network but distinctly reduced the density of fibronectin-distribution. The content of tubulin, fibronectin, MLCK and KRP was significantly decreased by 18-24%, while contents of desmin and vinculin were changed insignificantly. After 3 weeks, an increased density and extension of collagen network indicating the development of diffuse fibrosis were observed. Contents of tubulin and KRP were increased above control level by 50 and 20%, respectively. Similar hyperrestitution of tubulin, fibronectin and KRP content by 15-25% was determined after smaller dose of adriamycin (0.44 mg/kg). Only content of MLCK out of proteins studied remained at lower level in both groups by 25-34%. Isolated chick embryo cardiomyocytes subjected to adriamycin responded by increased level of KRP expression by 20% in 4 days while the level of tubulin expression remained unchanged. Results showed that damage of cardiomyocytes and extracellular matrix after single injection of adriamycin in the dose close to therapeutic was followed by increased expression of some proteins of cytoskeleton and extracellular matrix. KRP seems to play active role in this reparative response while the steadily reduced level of MLCK expression may disturb the control of coronary vessels.     

Isoproterenol induced changes of protein expression and myocardial ultrastructure

AIM: To elucidate alterations in myocardial ultrastructure and protein expression caused by isoproterenol. METHODS: Biochemical, immunohistochemical and electron microscopic studies of rat myocardium were carried out 2 hours and 3 weeks after single injections of isoproterenol (50 and 10 mg/kg). Relative content of myospecific proteins (KRP - kinase-related protein, desmin), cytoskeletal proteins (tubulin, vinculin, and myosin light chain kinase - MLCK) and extracellular matrix protein, fibronectin, was determined by immunoblotting. RESULTS: In 2 hours after injection of 50 mg/kg of isoproterenol destruction of some cardiomyocytes, contracture of myofibrils, and mild edema of intercellular space occurred; the content of KRP decreased by l6%, and that of tubulin, vinculin and fibronectin - by 27-29%. Reduced level of these proteins and also of MLCK persisted until 3 weeks after injection and was associated with altered cardiomyocyte ultrastructure. Glycogen granules were sparse, mitochondria contained arrow-like inclusions characteristic for calcium overload, huge mitochondria connected by specialized intermitochondrial contacts were present. Enlarged intercellular space contained areas of fibrosis with increased amount of type I and II collagens and fibronectin. Lower dose of isoproterenol (10 mg/kg) did not cause noticeable damaging action in the acute period, but in 3 weeks thickening of extracellular matrix occurred accompanied by increases of KRP and tubulin contents (by 26-32% compared with control level). Similar rise in expression of these proteins, and also of MLCK was observed after addition of isoproterenol to culture of chicken cardiomyocytes. CONCLUSION: These results indicate that even single injection of isoproterenol causes long lasting structural alterations in cardiac muscle accompanied by increased expression of extracellular matrix proteins as well as sarcoplasmic proteins apparently involved in the hypertrophic response of the cardiomyocytes.