Kaplan Meier survival plot for the three models of noncompressible hemorrhage.

<p>Time zero = moment of injury; CLI = central liver injury (N = 6); PVR = portal vein resection (N = 6); LLLH = hepatic left lower lobe hemitransection (N = 10).</p

Select endpoints (at time of death or 1 hr post-injury) for the three injury mechanisms of noncompressible hemorrhage.

<p>CLI = central liver injury; PVR = portal vein resection; LLLH = hepatic left lateral lobe hemitransection; MAP = mean arterial pressure. Continuous data expressed as mean ± standard deviation.</p><p>*Categorical data compared with the Fisher Exact Test;</p>†<p>continuous data compared with the Kruskal-Wallis nonparametric analysis of variance.</p><p>Select endpoints (at time of death or 1 hr post-injury) for the three injury mechanisms of noncompressible hemorrhage.</p

Vital sign data for three porcine models of noncompressible truncal hemorrhage.

<p>(A) Temperature. (B) Heart rate. (C) Mean arterial pressure (MAP). Time zero = moment of injury; CLI = central liver injury (N = 6); PVR = portal vein resection (N = 6); LLLH = hepatic left lower lobe hemitransection (N = 10). Values shown are mean ± sd; *p<0.05, Kruskal–Wallis one-way analysis of variance on all three time points for a given injury; **p<0.05, Kruskal–Wallis one-way analysis of variance on all three injuries at the indicated time point. Also refer to Table S2 in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0108293#pone.0108293.s002" target="_blank">file S2</a>.</p

Dissection demonstrating the anatomy of the porcine intrahepatic portal venous system.

<p><i>Ex vivo</i> porcine liver, inferior aspect (scale in cm). The soft tissues overlying the portal venous system have been dissected and retracted with silk stay sutures. RL = right lateral lobe; RM = right medial lobe; LM = left medial lobe; LL = left lateral lobe; Q = quadrate lobe; Gb = gallbladder; 1 = cut orifice of main portal vein; 2 = intrahepatic portal vein; 3 = RM lobe portal vein branch; 4 = 1^st LL lobe portal vein branch; 5 = cut orifice of 2^nd LL lobe portal vein branch (proximal end); 6 = distal end of structure 5; 7 = pedicle containing the common bile duct and hepatic artery (reflected laterally by stitch). In this dissection the 2^nd LL lobe portal vein branch was transected (the two ends are labeled as 5 and 6). The hepatic veins were not exposed in this dissection. The dashed blue polygon indicates the portion of the portal vein that was resected for the PVR injury mechanism. The dashed yellow line indicates where the cut was made across base of LL lobe for the LLLH injury mechanism. Scale = cm. [201 words].</p

Hematologic testing for three porcine models of noncompressible truncal hemorrhage.

<p>(A) Serum hemoglobin. (B) Protime. (C) Serum fibrinogen. Time zero = moment of injury; CLI = central liver injury (N = 6); PVR = portal vein resection (N = 6); LLLH = hepatic left lower lobe hemitransection (N = 10). Values shown are mean ± sd; *p<0.05, Kruskal–Wallis one-way analysis of variance on all three time points for a given injury; **p<0.05, Kruskal–Wallis one-way analysis of variance on all three injuries at the indicated time point. Also refer to Table S2 in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0108293#pone.0108293.s002" target="_blank">file S2</a>.</p

Postmortem liver ex vivo, demonstrating the standard injury.

<p>(A) Inferior aspect; anterior toward top of image. (B) Left inferior oblique aspect; anterior toward right of image. Scale in cm. RL = right lateral lobe; RM = right medial lobe; LM = left medial lobe; LL = left lateral lobe; Q = quadrate lobe; C = caudate lobe (black arrow indicates location of infrahepatic IVC); Gb = gallbladder. The scissors in panel A has been inserted through the cut orifice of the main portal vein, and the scissors tip are emerging through the transected 2^nd portal vein branch to the LL lobe (1); the distal end of this portal vein branch also is indicated (2). The gap in the liver parenchyma created by the injury is indicated with a dashed yellow line. The 1^st portal vein branch to the LL lobe (3), visible at the bottom of the wound, was not injured in this subject. The soft tissues (including the common bile duct and hepatic artery) overlying the portal venous system have been dissected and flipped anteriorly (4). White arrow indicates orifice of transected hepatic vein to the LL lobe; the latter has a dusky appearance relative to the other lobes.</p

Recombinant Human Fibrinogen That Produces Thick Fibrin Fibers with Increased Wound Adhesion and Clot Density

Human fibrinogen is a biomaterial used in surgical tissue sealants, scaffolding for tissue engineering, and wound healing. Here we report on the post-translational structure and functionality of recombinant human FI (rFI) made at commodity levels in the milk of transgenic dairy cows. Relative to plasma-derived fibrinogen (pdFI), rFI predominately contained a simplified, neutral carbohydrate structure and >4-fold higher levels of the γ′-chain transcriptional variant that has been reported to bind thrombin and Factor XIII. In spite of these differences, rFI and pdFI were kinetically similar with respect to the thrombin-catalyzed formation of protofibrils and Factor XIIIa-mediated formation of cross-linked fibrin polymer. However, electron microscopy showed rFI produced fibrin with much thicker fibers with less branching than pdFI. In vivo studies in a swine liver transection model showed that, relative to pdFI, rFI made a denser, more strongly wound-adherent fibrin clot that more rapidly established hemostasis