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This contribution argues that the European crisis in general and Brexit in particular, can be seen to reflect the partial loss of the ethos of a principle that has been at the heart of the EU, namely mutual recognition. While familiar to legal scholars as a norm governing the integration of markets and the management of conflicts of law, the essay seeks to show how this principle bears on our current European predicament as a philosophical concept and a form of governance between states before dwelling on the intricacies of mutual recognition in the EU single market. Because recognition is sought, obtained or denied in all social spheres, every discipline has its own complex variation on this simple theme requiring to connect legal theory with anthropology, philosophy, history, sociology and international relations. The essay spans all these fields through eight takes (mutual Recognition shunned, invented, enshrined, constitutionalised, managed, 'on trial', lost, and for grabs) which can also be interpreted as different time horizons (from Sapiens to Brexit through Westphalia). Each take provides a variation on what is referred to as "mutual recognition paradox", eg how to increase mutual engagement and mutual deference at the very same time. [ABSTRACT FROM AUTHOR]

The pharmacokinetics of ceftazidime were studied in 12 patients during peritoneal dialysis. In five patients given 1 g iv the mean serum levels (mg/l) at 0.25, 2 and 12 h after starting peritoneal dialysis were 50.6±11.2, 35.6±3.7 and 22.7±7.9, respectively. The mean ceftazidime peak level was 13.2±5.5 mg/l in peritoneal effluent, approximately 3 h after start of dialysis. The peritoneal clearance was 9 ml/min and the mean half-life during and after peritoneal dialysis was 8.7±3.1 h and 26.9±11 h, respectively.In four patients, 1 g ceftazidime was given via an intraperitoneal catheter. The mean serum levels (mg/l) at 0.25, 2 and 8 h were 14.2±3.1, 40.0±13.0 and 32.5±6.4 respectively.In three patients given ceftazidime 200 mg, in 21 dialysate treatments each with 12 cycles, mean serum levels increased from 1.3±1.5 mg/l at 1 h to 25.3±3.1 mg/l at 12 h. Mean levels in the dialysis effluent were 47.2±14.3 mg/l and the mean percentage of the dose recovered in the effluent was 47.1%.We concluded that (1) 1 g ceftazidime as an iv bolus maintained serum and peritoneal effluent levels adequate to treat patients; (2) its peritoneal absorption produced high ceftazidime levels in serum; (3) in infected patients undergoing peritoneal dialysis ceftazidime may be given either by the intravenous or intraperitoneal route. [ABSTRACT FROM PUBLISHER]

Chromosomal aneuploidy is one of the major causes of pregnancy wastage. In this review we summarize the knowledge about the origin and mechanisms of non-disjunction in human autosomal trisomies 8, 13, 15, 16, 18, and 21, accumulated during the last decade by using DNA polymorphism analysis. Maternal meiosis I non-disjunction is the most important single class, but chromosome-specific patterns exist. For the acrocentric chromosomes 15 and 21, meiosis I errors predominate among the maternal errors, in contrast to trisomy 18 where meiosis II errors predominate. For trisomy 16, virtually all cases are due to maternal meiosis I non-disjunction. Postzygotic (mitotic) non-disjunction constitutes 5-15% of cases of trisomies 15, 18, and 21, whereas for trisomy 8 and trisomy 8 mosaicism the majority of cases are due to mitotic non-disjunction. For paternal non-disjunction of chromosomes 18 and 21, meiosis II or mitotic errors predominate. There is aberrant meiotic recombination associated with maternal meiotic non-disjunction in all trisomies studied in detail so far. Advanced maternal age remains the only well documented risk factor for maternal meiotic non-disjunction, but there is, however, still a surprising lack of understanding of the basic mechanism(s) behind the maternal age effect. [ABSTRACT FROM AUTHOR]

Chromosomal aneuploidy is one of the major causes of pregnancy wastage. In this review we summarize the knowledge about the origin and mechanisms of non-disjunction in human autosomal trisomies 8, 13, 15, 16, 18, and 21, accumulated during the last decade by using DNA polymorphism analysis. Maternal meiosis I non-disjunction is the most important single class, but chromosome-specific patterns exist. For the acrocentric chromosomes 15 and 21, meiosis I errors predominate among the maternal errors, in contrast to trisomy 18 where meiosis II errors predominate. For trisomy 16, virtually all cases are due to maternal meiosis I non-disjunction. Postzygotic (mitotic) non-disjunction constitutes 5-15% of cases of trisomies 15, 18, and 21, whereas for trisomy 8 and trisomy 8 mosaicism the majority of cases are due to mitotic non-disjunction. For paternal non-disjunction of chromosomes 18 and 21, meiosis II or mitotic errors predominate. There is aberrant meiotic recombination associated with maternal meiotic non-disjunction in all trisomies studied in detail so far. Advanced maternal age remains the only well documented risk factor for maternal meiotic non-disjunction, but there is, however, still a surprising lack of understanding of the basic mechanism(s) behind the maternal age effect. [ABSTRACT FROM PUBLISHER]