Die Schutzaufsicht im Jugendgerichtsgesetz und im Entwurf eines neuen deutschen Strafgesetzbuches

Ohne ZusammenfassungNach einem auf der XIV. Tagung der deutschen Gesellschaft für gerichtliche und soziale Medizin in Bonn, September 1925 gehaltenen Vortrage.     

Phosphoramidon abolishes the increases in endothelin-1 release induced by ischemia-hypoxia in isolated perfused guinea pig lungs.

Endothelin (ET)-1 is a potent vasoactive peptide elaborated by the vascular endothelial cells. In the present study we examined the effects of ischemia-hypoxia (I/H) on ET-1 release from isolated perfused guinea pig lungs and heart. Guinea pig lungs subjected to 15 min I/H followed by reperfusion and reventilation significantly (P less than .05) augmented ET-1 release from 14.1 +/- 2.7 to 30.4 +/- 5.6, 27.3 +/- 4.0 and 28.0 +/- 5.0 pg/g of dry weight of lung at 15, 30 and 45 min after I/H, respectively. Pretreatment of guinea pigs with phosphoramidon (10 mg/kg i.v.), an ET converting enzyme inhibitor, 10 min before the removal of lungs abrogated the I/H-induced increases in ET-1 release without affecting the base-line values of ET-1. Phosphoramidon also attenuated the elevations in pulmonary insufflation pressure (PIP) produced by I/H. Moreover, infusion of big ET-1 (BET-1; 30 micrograms/over 15 min) into isolated perfused guinea pig lungs enhanced PIP that was abolished by phosphoramidon. Isolated guinea pig hearts subjected to 15 or 30 min of global ischemia exhibited no disturbances in ET-1 release or mechanical activity. In addition, the increases in perfusion pressure elicited by BET-1 infusion (12 micrograms/over 30 min) into isolated guinea pig hearts was unaffected by phosphoramidon. In a separate study in anesthetized guinea pigs, phosphoramidon significantly attenuated the increases in blood pressure and PIP elicited by BET-1 (10 micrograms/kg i.v.); the pressor and PIP responses to ET-1 (4 micrograms/kg i.v.) were not affected.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical analysis of Fuchs' heterochromic cyclitis

Fuchs' heterochromic cyclitis (FHC) is an important diagnosis to make. Not only for the patient, because incorrect diagnosis may lead to unnecessary therapy and the failure to detect secondary glaucoma, but also for the comparison of studies on the etiology of FHC, which is still unknown. No clinical criteria for establishing the diagnosis of FHC have been internationally accepted yet. By means of clinical analyses of FHC patients in different parts of the world, predominant clinical features may be distinguished and combined to form (internationally accepted) diagnostic criteria. We report a clinical analysis of 51 FHC patients in the Netherlands. Acute symptoms (severe redness, pain or photophobia) were never (100%) encountered. Characteristic keratic precipitates (88%) and/or minimal aqueous cells and flare (60%) and/or vitreous opacities (84%) were major signs, indicating a chronic inflammatory activity, in which no synechiae (100%) were present. Heterochromia (82%) was not a constant sign, but iris stromal atrophy, which causes the heterochromia, was always present (100%). Cataract was present in 82% as a result of the chronic iridocyclitis. Secondary glaucoma was present in 22%. Based on the predominant clinical findings obtained from this analysis of FHC patients, and on data in the literature, we propose clinical diagnostic criteria for FHC. Future studies, also including other uveitis groups, are necessary to confirm these diagnostic criteria.Abbreviations FHC Fuchs' heterochromic cyclitis