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)     

Assessment of mycobacterial,propionibacterial, and human herpesvirus 8 DNA in tissues of greek patients with sarcoidosis

The causes of sarcoidosis are unknown. In this study, we report the presence of Mycobacterium tuberculosis complex and Propionibacterium granulosum DNA in a significant proportion of Greek patients with sarcoidosis. Human herpesvirus 8 DNA was not detected in sarcoid tissues from Greek patients. Our findings are discussed.     

Versagung einer Apothekenbetriebserlaubnis wegen Vereinbarung einer Umsatzmiete für ein Medizinisches Versorgungszentrum

Abstrakt 1. Die Vereinbarung einer am Umsatz oder Gewinn einer Apotheke ausgerichteten Miete ist nach § 8 S. 2 ApoG unzul?ssig. Das Verbot der Umsatzmiete gilt insbesondere für die Anmietung von Apothekenbetriebsr?umen. 2. Aus dem Gesamtgefüge der Vereinbarungen kann sich ergeben, dass die Vertragsparteien die Miete am Umsatz oder Gewinn ausgerichtet haben und der Vermieter dadurch an den Ertr?gnissen der Apotheke teilhat. 3. Ein immens hoher Mietzins engt die wirtschaftliche Bewegungsfreiheit des Apothekers erheblich ein und macht ihn zumindest indirekt vom Vermieter abh?ngig. 4. Der Umstand, dass die Apothekenansiedlung im Kontext eines Medizinischen Versorgungszentrums geplant ist, ?ndert nichts an der uneingeschr?nkten Geltung des § 8 S. 2 ApoG. (Leits?tze des Bearbeiters)     

Association of allelic imbalance at locus D13S171 (BRCA2) and p53 alterations with tumor kinetics and chromosomal instability (aneuploidy) in nonsmall cell lung carcinoma

BACKGROUND: BRCA2 gene, located at chromosome 13q12.3, frequently is altered in familial types of cancer in which a "double-hit" inactivation model seems to occur. In contrast, in sporadic forms of cancer there is frequent absence of a second event (point mutations) suggesting that allelic imbalance at the BRCA2 locus may be associated with a "gene dosage effect" of BRCA2 function. Little is known about BRCA2 allelic alterations in nonsmall cell lung carcinomas (NSCLCs). Furthermore, recent studies suggest that BRCA2 and p53 participate in a common pathway involved in DNA damage repair. In view of this putative link, the authors investigated in a series of 63 NSCLCs: 1) the allelic imbalance (AIm) at the D13S171 (BRCA2) locus, 2) the possible relation with tumor kinetics (proliferation [PI] and apoptotic indices [AI]) and chromosomal instability (aneuploidy) of the carcinomas, and 3) the mutual impact of D13S171 AIm and p53 altered status on the above-mentioned parameters. METHODS: Allelic status of the BRCA2 region was examined in a series of 63 NSCLCs, by using the polymorphic marker D13S171, which is located in the center of it. Most information regarding the status of p53 at the immunohistochemical and genetic levels was obtained from a previous analysis. Tumor kinetic parameters (proliferation and apoptotic indices) were determined using Ki-67 immunohistochemical analysis and Tdt-mediated dUTP nick end labeling assay, respectively. Chromosomal instability (aneuploidy) was assessed by measuring nuclear DNA ploidy with an image analysis system. RESULTS: Allelic imbalance at D13S171(BRCA2) was observed in 70% of the informative cases (H: heterozygous) with a rather high frequency of occurrence (50%) in Stage I disease, suggesting a possible early involvement in the development of NSCLCs. Although no association was found among loss of heterozygosity (LOH) at D13S171, kinetic parameters and ploidy status of the tumors and concurrent alterations in BRCA2 and p53 (BRCA2[LOH]/p53[P]), which was the most frequent profile (37.2%), had the highest growth index (PI/AI mean value ratio) that differed significantly only from the BRCA2(LOH)/p53(N) pattern (P = 0.027). This difference was attributed to the high AI of the BRCA2(LOH)/p53(N) pattern (P < 0.001), whereas PI was similar among all BRCA2/p53 profiles. Also the "full abnormal pattern" was associated with aneuploidy, whereas the BRCA2(LOH)/p53(N) profile was mainly diploid. When these indicators and conventional prognostic ones were examined for effect on patient survival, only stage and lymph node status showed a significant correlation, whereas LOH at D13S171 (BRCA2), p53 abnormalities, proliferative and apoptotic indices, ploidy status, smoking history, and histology and combinations of LOH and p53 abnormalities failed to show significant correlation with survival. CONCLUSIONS: These findings suggest that in BRCA2(LOH) NSCLCs the status of p53 (wild type or mutant) represents a decisive determinant of tumor growth and chromosomal instability. Nevertheless, a possible synergistic effect from loss of D13S171 region with p53 abnormalities cannot be excluded because the BRCA2(LOH)/p53(P) profile compared with the BRCA2(H)/p53(P) one had a higher PI/AI mean value ratio (31.05 vs. 22.97), although it was not statistically significant. However, we cannot exclude the possibility that LOH at D13S171 reflects deletion of other putative tumor suppressor gene(s) in the proximity of BRCA2. In this respect, more studies are needed to understand the involvement of BRCA2 region alterations in nonsmall cell lung carcinogenesis. (c) 2000 American Cancer Society.     

Expression of p16(INK4A) and alterations of the 9p21-23 chromosome region in non-small-cell lung carcinomas: relationship with tumor growth parameters and ploidy status

The 9p21-23 chromosome region harbors a number of known and putative tumor-suppressor genes (TSGs). The best characterized gene in this area is p16(INK4A) (CDKN2A). Alterations of its product have been observed in various malignancies, including non-small-cell lung carcinomas (NSCLCs). We earlier investigated the mechanisms underlying p16(INK4A) inactivation. In the present study, we examined, in a series of 87 NSCLCs, its relationship with the kinetic parameters [proliferation index (PI) and apoptotic index (Al)] and the ploidy status of the tumors. In addition, we extended our previous LOH analysis of the 9p21-23 region by examining flanking areas of p16(INK4A). Aberrant p16 expression was observed in 41.4% of the carcinomas. A significant association was found with increased PI (p = 0.037), but not with apoptosis. Aneuploid tumors were more frequently correlated with abnormal p16 staining (p = 0. 05). A high frequency of allelic imbalance (Alm) was noticed at the D9S161 (51.3%) and D9S157 (64.5%) loci, which lie approximately 4cM centromeric and 7cM telomeric, respectively, to CDKN2A. Abnormal p16(INK4A) expression was strongly correlated with Alm at D9S161 (p = 0.004). Allelic losses at D9S157 occurred more frequently in early stages (p = 0.018) and were significantly associated with deletions at D9S161 (p = 0.035). We conclude that, in a sub-set of NSCLCs, (i) abnormal p16 expression contributes to tumor growth mainly by increasing the proliferative activity in the initial stages of carcinogenesis; (ii) the association with aneuploidy merely reflects the impact of aberrant p16 on proliferative activity; and (iii) other putative TSGs possibly reside within the 9p21-23 region that possibly co-operate in certain cases with CDKN2A in the development of NSCLCs.