Elgaardbarefoot6977

Heparins represent one of the most frequently used pharmacotherapeutics. Discovered around 1926, routine clinical anticoagulant use of heparin was initiated only after the publication of several seminal papers in the early 1970s by the group of Kakkar. It was shown that heparin prevents venous thromboembolism and mortality from pulmonary embolism in patients after surgery. With the subsequent development of low-molecular-weight heparins and synthetic heparin derivatives, a family of related drugs was created that continues to prove its clinical value in thromboprophylaxis and in prevention of clotting in extracorporeal devices. Fundamental and applied research has revealed a complex pharmacodynamic profile of heparins that goes beyond its anticoagulant use. Recognition of the complex multifaceted beneficial effects of heparin underscores its therapeutic potential in various clinical situations. In this review we focus on the anticoagulant and nonanticoagulant activities of heparin and, where possible, discuss the underlying molecular mechanisms that explain the diversity of heparin's biological actions.The venom of the Australian snake Pseudonaja textilis comprises powerful prothrombin activators consisting of factor X (v-ptFX)- and factor V-like proteins. While all vertebrate liver-expressed factor X (FX) homologs, including that of P. textilis, comprise an activation peptide of approximately 45 to 65 residues, the activation peptide of v-ptFX is significantly shortened to 27 residues. In this study, we demonstrate that exchanging the human FX activation peptide for the snake venom ortholog impedes proteolytic cleavage by the intrinsic factor VIIIa-factor IXa tenase complex. Troglitazone Furthermore, our findings indicate that the human FX activation peptide comprises an essential binding site for the intrinsic tenase complex. Conversely, incorporation of FX into the extrinsic tissue factor-factor VIIa tenase complex is completely dependent on exosite-mediated interactions. Remarkably, the shortened activation peptide allows for factor V-dependent prothrombin conversion while in the zymogen state. This indicates that the active site of FX molecules comprising the v-ptFX activation peptide partially matures upon assembly into a premature prothrombinase complex. Taken together, the shortened activation peptide is one of the remarkable characteristics of v-ptFX that has been modified from its original form, thereby transforming FX into a powerful procoagulant protein. Moreover, these results shed new light on the structural requirements for serine protease activation and indicate that catalytic activity can be obtained without formation of the characteristic Ile16-Asp194 salt bridge via modification of the activation peptide.

 Extensive osseous defects of the extremities following trauma and tumour resection represent a major challenge for plasticreconstructive surgical teams. Defect reconstruction by free microsurgical fibula transplantation has become a standard method but is associated with a considerable rate of complications. The aim of the present work is to provide an up-to-date overview of the various reconstruction methods and to report our personal experiences with free fibula transplantation in a case series.

 The literature search on the subject was performed on Pubmed and Web of Science, and a retrospective collection of data was conducted based on our own cases, including clinical and radiological data.

 From 2007 to 2018, free fibula transplantation was performed in 11 patients under the guidance of the senior author (MS). The defects were a result of pseudarthrosis in four cases, osteitis in three, and a tumour in two cases. Two patientssustained a primary defect due to a high-energy trauma. In nine cases the Close cooperation between the disciplines of plastic reconstructive surgery and trauma orthopaedics is indispensable.Hidradenitis suppurativa is a chronic inflammatory disease of apocrine gland-bearing skin, especially in the axilla. The coverage of large defects in the region of the axilla after radical resection poses a challenge to reconstructive surgery. The lateral chest offers, among others, two options for perforator flaps the thoracodorsal artery perforator flap and the lateral thoracic artery perforator flap. This article introduces the lateral thoracic artery flap as an additional option for defect restoration alongside the thoracodorsal artery perforator flap. A total of 13 flaps (10 lateral thoracic artery perforator flaps and 3 thoracodorsal artery perforator flaps) were used for defect reconstruction in 10 patients with axillary hidradenitis suppurativa stages II or III. All patients were assessed for surgical complications pursuant to the classification of Clavien-Dindo, subjective aesthetic results, recurrence rate, and maximum abduction angle evaluated by measuring the range of motion. All flaps healed without major or partial flap necrosis. In 12 out of 13 flaps, the aesthetic result was rated very good or good.Only one patient complained of a visible scar, but rated the overall result as satisfactory. The range of motion in the shoulder was unlimited in all cases with a maximum abduction angle of 178.8 ± 4.2°. Recurrence was not observed in any case during the postsurgical follow-up of 27.2 ± 14.4 months. The use of the two perforator-based fasciocutaneous flaps of the thoraco dorsal artery and the lateral thoracic artery offers a useful and reliable option for the reconstruction of large axillary defects while maintaining full shoulder movement and providing cosmetically satisfactory results.Bleeding and thrombosis are both common complications that patients with advanced liver disease experience. While hemostatic pathways remain largely intact with cirrhosis, this balance can quickly shift in the direction of bleeding or clotting in an unpredictable manner. A growing body of literature is attempting to shed light on difficult scenarios that clinicians often face, ranging from predicting and mitigating bleeding risk in those who need invasive procedures to determining the best strategies to manage both bleeding and thrombotic complications when they occur. Studies examining hemostasis in those with advanced liver disease, however, often include heterogeneous cohorts with varied methodology. While these studies often select a cohort of all types and degrees of cirrhosis, emerging evidence suggests significant differences in underlying systemic inflammation and hemostatic abnormalities among specific phenotypes of liver disease, ranging from compensated cirrhosis to decompensated cirrhosis and acute-on-chronic liver failure.