This study shows that oxygen equilibration relevant for clinical interpretation requires only 10 minutes following an increase and 16 minutes following a decrease in FIO2. over the range studied.

PNMT (phenylethanolamine-N-methyl-transferase) is the enzyme that catalyzes the formation of epinephrine from norepinephrine. In transgenic mice over-expressing PNMT, observations revealed a very high level of aggression compared to their background strain, C57BL/6J. To evaluate the influence of PNMT on aggression and emotionality in this transgenic line, single-sex male and female groups were independently established that consisted of either four wild-type mice or four transgenic mice overexpressing PNMT. The members of each group were littermates. Mixed single-sex groups consisting of two transgenic mice and two wild-type mice were also established. Almost no fights were observed within the female groups. In males, the transgenic line showed a significantly higher level of fighting than controls (p=0.007) and mixed male groups (p=0.02). Housing mice from the transgenic line in mixed groups with wild-type mice seems to decrease the level of aggression in the transgenic line. In conclusion, this is the first study to demonstrate a clear, significant increase in aggression arising from PNMT overexpression. This suggests an important role for central epinephrine levels in aggressive behavior.

Muscle function tests of the triceps brachii muscle were performed before operation and on the third postoperative day in ten patients undergoing elective cholecystectomy. Electromyograms (EMGs) were recorded by surface electrodes during sustained isotonic and isometric muscle contraction with a constant force of 20 per cent of the preoperative maximal voluntary contraction. Root-mean-square of the EMG was calculated together with the neuromuscular efficiency and measures of the fatiguability. These parameters were compared with changes in the simultaneously measured serum phosphate concentrations. Mean (s.e.m.) neuromuscular efficiency measured after 32-40 s of muscle contraction decreased 14(5) per cent after operation (P less than 0.01), whereas the mean fatiguability of the muscle was unchanged. Mean serum phosphate concentration was 0.87(0.06) mmol/l before operation and 0.79(0.06) mmol/l 3 days after the operation (P greater than 0.05). Two patients developed severe postoperative hypophosphataemia (serum phosphate concentration less than 0.50 mmol/l). Postoperative muscle function deterioration was not associated with changes in the serum phosphate level (P greater than 0.10; r = 0.03). We conclude that patients undergoing cholecystectomy develop postoperative deterioration in skeletal muscle function, which is not associated with serum phosphate concentration.

Tibial hypo-/aplasia with preaxial syn- and polydactyly is a rare autosomal dominant condition. Fewer than 20 cases have so far been described. One is presented here.

GLP‐1 is a gut hormone and has been in focus for its role in response to food intake. An analogue of GLP‐1 has been constructed by adding a palmitoyl chain to the GLP‐1 peptide making it adhere to albumin. Here we have explored the potential roles of GLP‐1 and Liraglutide in vascular function by studying signaling in human dermal endothelial cells (HDMEC), human umbilical vein endothelial cells (HUVEC) and rat mesenteric resistance arteries. We found that HDMEC expresses the GLP‐1R by use of RT‐PCR. By use of Ca2+ imaging we found that preincubation with GLP‐1 (500 nM) caused a reduction in VEGF‐A (25 ng/ml) induced Ca2+ signaling due to a reduction in phosphorylation of PLCγ and that GLP‐1 causes phosphorylation of Src, Akt, ERK 1/2 and p38. In HUVEC, VEGF‐A (3 h, 20 ng/ml) causes a 2 times upregulation of mRNA for I‐CAM which is attenuated by 20% in the presence of Liraglutide (100 nM) and a 5 times upregulation of mRNA for V‐CAM which is attenuated 25% by Liraglutid. Liraglutide, but not GLP‐1, caused a small transient increase in [Ca2+]i. Our data are consistent with the GLP‐1 signaling being evoked through an enhanced Gs/βγ signaling since Gi inhibition with pertussis toxin elicits a similar response by favoring the Gs/βγ signaling pathway. The attenuating responses on VEGF‐induced Ca2+ transients and VEGF‐induced mRNA expression for surface proteins implicate that GLP‐1 signaling could affect endothelial cell function in relation to inflammatory processes.