Contribution of rFVIIa to plasma thrombin generation assessed by the calibrated automated thrombogram and triggered with 0.25 (squares) or 4 (circles) pM tissue factor (TF) and 4 μM phospholipids.

<p>Left panel: Maximum thrombin generation presented as the peak height (A). Right panel: endogenous thrombin potential (ETP; B).</p

Thromboelastometry (TEM) analysis by means of ExTem (A, B and C) and plasma thrombin generation analysis (D, E, F; triggered by 0.25 pM TF) at baseline (Bl), after haemodilution (HD) and 10, 60 and 120 minutes after trauma.

<p>For TEM, the parameters clotting time (CT: A), clot formation time (CFT: B) and maximum clot firmness (MCF: C) are given, whereas for thrombin generation the lag time (D), endogenous thrombin potential (ETP; E) and peak height (F) are given. Data are presented as the median with inter-quartile ranges (IQR) for controls (solid black line, n = 7) and animals treated with 90 μg/kg rFVIIa (dotted black line, n = 7). For comparison, data from animals treated with either 180 or 360 μg/kg rFVIIa are presented as grey dotted lines. *<i>P</i><0.05 control versus rFVIIa; #<i>P</i><0.05 over time between baseline and haemodilution.</p

Prothrombin time (PT; A) and activated partial thromboplastin time (aPTT; B) at baseline (Bl), after haemodilution (HD) and at 10, 60 and 120 minutes after trauma.

<p>Data are presented as the median with inter-quartile ranges (IQR) for controls (solid black line, n = 7) and animals treated with 90 μg/kg rFVIIa (dotted black line, n = 7). For comparison, data from animals treated with either 180 or 360 μg/kg rFVIIa are presented as grey dotted lines. *<i>P</i><0.05 control versus rFVIIa; #<i>P</i><0.05 over time between baseline and haemodilution.</p

Total blood loss at the end of the observation period for animals not treated (control, black circles) or treated with 90 μg/kg (black squares), 180 μg/kg or 360 μg/kg rFVIIa.

<p>*<i>P</i><0.05 rFVIIa versus control.</p

Haemoglobin (A), platelet count (B), fibrinogen (C) and thrombin-antithrombin (TAT; D) levels at baseline (Bl), after haemodilution (HD) and 10, 60 and 120 minutes after trauma.

<p>Data are presented as the median with inter-quartile ranges (IQR) for controls (solid black line, n = 7) and animals treated with 90 μg/kg rFVIIa (dotted black line, n = 7). For comparison, data from animals treated with either 180 or 360 μg/kg rFVIIa are presented as grey dotted lines. *<i>P</i><0.05 control versus rFVIIa; #<i>P</i><0.05 over time between baseline and haemodilution.</p

Reduced astrocyte density underlying brain volume reduction in activity-based anorexia rats

<p><b>Objectives:</b> Severe grey and white matter volume reductions were found in patients with anorexia nervosa (AN) that were linked to neuropsychological deficits while their underlying pathophysiology remains unclear. For the first time, we analysed the cellular basis of brain volume changes in an animal model (activity-based anorexia, ABA).</p> <p><b>Methods:</b> Female rats had 24 h/day running wheel access and received reduced food intake until a 25% weight reduction was reached and maintained for 2 weeks.</p> <p><b>Results:</b> In ABA rats, the volumes of the cerebral cortex and corpus callosum were significantly reduced compared to controls by 6% and 9%, respectively. The number of GFAP-positive astrocytes in these regions decreased by 39% and 23%, total astrocyte-covered area by 83% and 63%. In neurons no changes were observed. The findings were complemented by a 60% and 49% reduction in astrocyte (GFAP) mRNA expression.</p> <p><b>Conclusions:</b> Volumetric brain changes in ABA animals mirror those in human AN patients. These alterations are associated with a reduction of GFAP-positive astrocytes as well as GFAP expression. Reduced astrocyte functioning could help explain neuronal dysfunctions leading to symptoms of rigidity and impaired learning. Astrocyte loss could constitute a new research target for understanding and treating semi-starvation and AN.</p