Published by Elsevier B.V.”
“Objectives: To investigate the impact of hypovolaemic shock on the aortic diameter in a porcine model, and to determine the implications

for the endovascular management of hypovolaemic patients with traumatic thoracic aortic injury (TTAI).

Materials and methods: The circulating blood volume of seven Yorkshire pigs was gradually lowered in 10% increments. At 40% volume loss, an endograft was deployed in the descending thoracic aorta, followed by gradual fluid resuscitation. Potential changes in aortic diameter during the experiment were recorded using intravascular ultrasound (IVUS).

Results: The aortic diameter decreased significantly at all evaluated levels during blood loss. Selleckchem Proteasome inhibitor The ascending aortic diameter decreased on average with 38% after 40% blood loss (range 24 -62%, p = 0.018), the descending thoracic aorta with 32% (range 18-52%, p = 0.018) and the abdominal aorta with 28% (range 15-39%, p = 0.018). The aortic diameters regained their initial size during fluid resuscitation.

Conclusion: The aortic diameter significantly decreases during blood loss in this porcine model. If these changes take place in hypovolaemic TTAI patients as well, it may have implications for thoracic endovascular aortic repair

(TEVAR). Increased oversizing of the endograft, or additional computed tomography (CT) or IVUS imaging after fluid resuscitation for more adequate aortic measurements, may be needed in TTAI patients with considerable blood JPH203 in vivo loss. (C) 2010 European Society for

Vascular Surgery. Published by Elsevier Ltd. All rights reserved.”
“The cellular prion protein (PrPc) undergoes alpha-secretase-derived processing by disintegrins. This cleavage occurs within the 106-126 putative toxic domain of PrPc, yielding two complementary N- and C-terminal fragments referred to as N1 Selleck INCB018424 and C1, respectively. Here we review our recent data showing that these two PrPc-derived products harbor distinct p53-dependent functions. Thus, C1 potentiates staurosporine (STS)-induced caspase-3 activation by upregulating p53 transcription, mRNA levels and activity. Conversely, N1 is protective both in vitro and in vivo. Thus, N1 inhibits STS-induced caspase-3 activation by downregulating p53 in various cell systems and protects rat retinal ganglion cells from hypoxia-induced apoptosis. Furthermore, N1 protects cells against C1-induced toxicity. Therefore, our data show that disintegrin-associated processing of PrPc gives rise to two fragments that display opposite effects on p53-dependent cell death and that can functionally interact. Copyright (C) 2012 S. Karger AG, Basel”
“Background: The early resuscitation occurs in the emergency department (ED) where intensive care unit protocols do not always extend and monitoring capabilities vary.