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To reduce the bleeding time and to shorten the surgery time are vital to patients' prog-nosis, therefore, in this study, high moisture absorption nonwoven composites are proposed to attain hemostasis in time. Polyacrylate fiber and Tencel® fibers at different blending ratios (10:90, 20:80, 30:70, 40:60, and 50:50) are used to form PT composite nonwoven. Next, composed of a 50:50 ratio, PT composite nonwoven exhibits the maximal vertical wicking height of 4.4 cm along the cross direction. Additionally, the UV-Vis absorption spectra analysis shows that at absorption waves of 413-415 nm, the occurring of distinct peaks suggests the presence of nanoparticles. The XRD patterns indicate the presence of silver nanoparticles with corresponding crystal planes of characteristic peaks at (111), (200), and (220). Polyacrylate/Tencel® nonwoven composites exhibit comparable adsorption capacity of blood and water molecules. In particular, 30PT composite nonwoven outperforms the control group, exhibiting 3.8 times and 4.7 times greater the water absorption and blood absorption, respectively. Moreover, a great number of red blood cells with a size of 4-6 μm agglomerate among fibers as observed in SEM images, while 6hr-PT composite dressing demonstrates the optimal antibacterial efficacy against Escherichia coli and Staphylococcus aureus, proven by the zone of inhibition being 1.9 mm and 0.8 mm separately. When in contact with plasma, hemostasis composites have plasma hemostasis prothrombin time of 97.9%, and activated partial thromboplastin time of 96.7%. As for animal hemostasis model, the arteria over the rats' thigh bones is cut open perpendicularly, generating mass arteria hemorrhage. To attain hemostasis, it takes 46.5% shorter time when using composite dressings (experimental group) than the control group.
The cross-talk between the inflammatory complement system and hemostasis is becoming increasingly recognized. The interaction between complement C1q, initiation molecule of the classical pathway, and von Willebrand factor (vWF), initiator molecule of primary hemostasis, has been shown to induce platelet rolling and adhesion in vitro. As vWF disorders result in prolonged bleeding, a lack of C1q as binding partner for vWF might also lead to an impaired hemostasis. Therefore, this study aimed to investigate the in vivo relevance of C1q-dependent binding of vWF in hemostasis. For this purpose, we analyzed parameters of primary and secondary hemostasis and performed bleeding experiments in wild type (WT) and C1q-deficient (C1qa-/-) mice, with reconstitution experiments of C1q in the latter. Bleeding tendency was examined by quantification of bleeding time and blood loss. First, we found that complete blood counts and plasma vWF levels do not differ between C1qa-/- mice and WT mice. Moreover, platelet aggregation tests indicated that the platelets of both strains of mice are functional. Second, while the prothrombin time was comparable between both groups, the activated partial thromboplastin time was shorter in C1qa-/- mice. In contrast, tail bleeding times of C1qa-/- mice were prolonged accompanied by an increased blood loss. Upon reconstitution of C1qa-/- mice with C1q, parameters of increased bleeding could be reversed. In conclusion, our data indicate that C1q, a molecule of the first-line of immune defense, actively participates in primary hemostasis by promoting arrest of bleeding. This observation might be of relevance for the understanding of thromboembolic complications in inflammatory disorders, where excess of C1q deposition is observed.
Patients with severe hemophilia A and inhibitors are at risk of bleeding during invasive procedures. The standard of care for preventing perioperative bleeding has been replacement therapy with FVIII concentrates or for patients with high-titer inhibitors, bypassing agents. However, there is no consensus on the appropriate management of surgery in patients receiving the novel agent emicizumab. The aim of this study was to demonstrate a case of a patient on emicizumab undergoing major surgery with bypassing agents with preoperative use of the thrombin generation assay (TGA) and thromboelastography (TEG).
Adaptive immunity in jawless fishes is performed by a unique set of proteins termed variable lymphocyte receptors (VLRs). Here we compare the crystallographic structures of VLRs and the human primary hemostasis receptor, glycoprotein (GP) Ib. It has been estimated jawless fish vertebrates diverged from jawed vertebrates 500 million years ago. Identifying structural similarities provides insights into the origins of primary hemostasis and the unique adaptive immunity of jawless fishes.
Objectives- The prediction of patients at risk for poor clinical outcome after acute ischemic stroke remains challenging. An imbalance of coagulation factors may play an important role in progression and prognosis of these patients. In this systematic review, we assessed the current literature on hemostasis biomarkers and the association with poor clinical outcome in acute ischemic stroke. Approach and Results- A systematic search of Embase, Medline, Cochrane Library, Web of Science, and Google Scholar was performed on studies reporting on hemostasis biomarkers and clinical outcome after acute ischemic stroke. Studies were considered eligible if blood samples were collected within 72 hours after symptom onset. Additionally, clinical outcome should be assessed using a disability score (Barthel Index or modified Rankin scale). Methodological quality of included studies was assessed with an adapted version of the Quality Assessment of Diagnostic Accuracy Studies questionnaire. A total of 80 articles were read full text, and 41 studies were considered eligible for inclusion, reporting on 37 different hemostasis biomarkers. No single biomarker appeared to be effective in predicting poor clinical outcome in acute ischemic stroke patients. Conclusions- Based on current literature, no clear recommendations can be provided on which hemostasis biomarkers are a predictor of clinical outcome after acute ischemic stroke. However, some biomarkers show promising results and need to be further investigated and validated in large populations with clear defined study designs.
There is no established hemostasis method or protocol for the transdistal radial approach. Therefore, this study aimed to determine whether "the PreludeSYNC DISTAL" radial compression device (PSD; Merit Medical Systems, Inc., South Jordan, UT) can effectively prevent distal radial artery (dRA) occlusion following catheterization procedures. This retrospective study analyzed patients who underwent hemostasis using the PSD from January 1, 2019, to March 31, 2019. The primary endpoint was occlusion or excessive stenosis of the radial artery (RA) 1 month after catheterization. Pulsatile blood flow and vessel diameters of the dRA and forearm RA (fRA) were measured using vascular ultrasound before and 1 month after catheterization to determine arterial damage. Secondary endpoints were achievement of hemostasis, bleeding, hematoma, aneurysm, neurological abnormality, and functional disturbance of the fingers or hand. Fifty patients (mean age, 70.9 ± 10.7 years; male, 72.0%) were enrolled in this study. Complete hemostasis was achieved in all cases. Total hemostasis time was 161 ± 45 min. No procedure-associated complications were noted. Pulsations of the dRA and fRA were maintained at 1 month. No functional disturbance or neurological abnormality was observed. Vessel diameters of the dRA and fRA were not significantly different before and 1 month after catheterization. No dissection, pseudoaneurysm, or occlusion/stenosis was observed on ultrasound. Distal radial access with a unique device and protocol effectively achieved hemostasis and prevented injury and occlusion of the dRA and fRA.
Management of bleeding is critical for improving patient outcomes. While various hemostatic products are used in daily practice, technical improvement is still needed. To addresses this problem, we newly developed a microneedle hemostatic sheet based on microneedle technology. We demonstrated the unique features of this microneedle hemostatic sheet, including reduced hemostatic time, biodegradable polymer composition that allows intracorporeal use without increasing infectious risk incorporation of microneedles to fix the sheet to the wound even on the left ventricular wall of a swine while beating, and a mesh structure with flexibility comparable to that of bonding surgical tape and sufficient rigidity to penetrate human aorta tissue and swine left ventricular wall. One potential application of the microneedle hemostatic sheet is intracorporeal topical hemostasis for parenchymatous organs, large vessels, and heart wall during trauma or surgery, in addition to new, widespread applications.
Hemostasis is a defense mechanism which protects the organism in the event of injury to stop bleeding. Recently, we established that all the known major mammalian hemostatic factors are conserved in early vertebrates. However, since their highly vascularized gills experience high blood pressure and are exposed to the environment, even very small injuries could be fatal to fish. Since trypsins are forerunners for coagulation proteases and are expressed by many extrapancreatic cells such as endothelial cells and epithelial cells, we hypothesized that trypsin or trypsin-like proteases from gill epithelial cells may protect these animals from gill bleeding following injuries. In this paper we identified the release of three different trypsins from fish gills into water under stress or injury, which have tenfold greater serine protease activity compared to bovine trypsin. We found that these trypsins activate the thrombocytes and protect the fish from gill bleeding. We found 27 protease-activated receptors (PARs) by analyzing zebrafish genome and classified them into five groups, based on tethering peptides, and two families, PAR1 and PAR2, based on homologies. We also found a canonical member of PAR2 family, PAR2-21A which is activated more readily by trypsin, and PAR2-21A tethering peptide stops gill bleeding just as trypsin. This finding provides evidence that trypsin cleaves a PAR2 member on thrombocyte surface. In conclusion, we believe that the gills are evolutionarily selected to produce trypsin to activate PAR2 on thrombocyte surface and protect the gills from bleeding. We also speculate that trypsin may also protect the fish from bleeding from other body injuries due to quick contact with the thrombocytes. Thus, this finding provides evidence for the role of trypsins in primary hemostasis in early vertebrates.
Collagen is a major component of the extracellular matrix and plays a wide variety of important roles in blood clotting, healing, and tissue remodeling. Natural, animal derived, collagen is used in many clinical applications but concerns exist with respect to its role in inflammation, batch-to-batch variability, and possible disease transfection. Therefore, development of synthetic nanomaterials that can mimic the nanostructure and properties of natural collagen has been a heavily pursued goal in biomaterials. Previously, we reported on the design and multihierarchial self-assembly of a 36 amino acid collagen mimetic peptide (KOD) that forms nanofibrous triple helices that entangle to form a hydrogel. In this report, we utilize this nanofiber forming collagen mimetic peptide as a synthetic biomimetic matrix useful in thrombosis. We demonstrate that nanofibrous KOD synthetic collagen matrices adhere platelets, activate them (indicated by soluble P-selectin secretion), and clot plasma and blood similar to animal derived collagen and control surfaces. In addition to the thrombotic potential, THP-1 monocytes incubated with our KOD collagen mimetic showed minimal proinflammatory cytokine (TNF-α or IL-1β) production. Together, the data presented demonstrates the potential of a novel synthetic collagen mimetic as a hemostat.
There have been numerous recent advances in wound care management. Nevertheless, the assessment of hemostatic dressing is essential to enable surgeons and other physicians and healthcare professionals to make the correct decisions regarding the disposition of severe hemorrhage. Here, we investigated the relative efficacies of chitosan-based and conventional gauze dressings in a rat model of femoral artery hemorrhage and in patients with surgical wounds. Dressing effectiveness was evaluated based on hemostatic profiles, biocompatibility, antimicrobial activity, and blood factor responses in coagulation. Relative to standard gauze dressing, the chitosan fiber (CF) dressing treatment significantly shortened the time to hemostasis in injured rats. Moreover, the CF dressing significantly prolonged partial thromboplastin time, enhanced blood absorption, and reduced antithrombin production without altering the prothrombin ratio. Unlike regular gauze bandages, the CF dressing demonstrated remarkable antibacterial activity. The results of this study indicate the effectiveness of chitosan as a hemostatic dressing and elucidate its underlying mechanism. It is possible that chitosan surgical dressings could serve as first-line intervention in hospital emergency care for uncontrolled hemorrhage.
Blood flow is a major regulator of hemostasis and arterial thrombosis. The current view is that low and intermediate flows occur in intact healthy vessels, whereas high shear levels (>2000 s-1) are reached in stenosed arteries, notably during thrombosis. To date, the shear rates occurring at the edge of a lesion in an otherwise healthy vessel are nevertheless unknown. The aim of this work was to measure the shear rates prevailing in wounds in a context relevant to hemostasis. Three models of vessel puncture and transection were developed and characterized for a study that was implemented in mice and humans. Doppler probe measurements supplemented by a computational model revealed that shear rates at the edge of a wound reached high values, with medians of 22 000 s-1, 25 000 s-1, and 7000 s-1 after puncture of the murine carotid artery, aorta, or saphenous vein, respectively. Similar shear levels were observed after transection of the mouse spermatic artery. These results were confirmed in a human venous puncture model, where shear rates in a catheter implanted in the cubital vein reached 2000 to 27 000 s-1. In all models, the high shear conditions were accompanied by elevated levels of elongational flow exceeding 1000 s-1. In the puncture model, the shear rates decreased steeply with increasing injury size. This phenomenon could be explained by the low hydrodynamic resistance of the injuries as compared with that of the downstream vessel network. These findings show that high shear rates (>3000 s-1) are relevant to hemostasis and not exclusive to arterial thrombosis.
Radial artery obstruction is the most common complication of coronary angiography performed via transradial access. Patent hemostasis can significantly reduce the risk of radial artery occlusion. Previous studies utilized sophisticated methods to evaluate radial artery patency. Simplified and easily applicable methods for successful patent hemostasis are currently lacking.
Thrombosis is the fatal and disabling consequence of cardiovascular diseases, the leading cause of mortality and morbidity in Western countries. Two inbred mouse strains, C57BL/6J and A/J, have marked differences in susceptibility to obesity, atherosclerosis, and vessel remodeling. However, it is unclear how these diverse genetic backgrounds influence pathways known to regulate thrombosis and hemostasis. The objective of this study was to evaluate thrombosis and hemostasis in these two inbred strains and determine the phenotypic response of A/J chromosomes in the C57BL/6J background.
Physical inactivity is considered a risk factor for cardiovascular disease and is strongly associated with changes in arterial structure. Regular physical activity and exercise contributes to the prevention of coronary artery disease. Therefore, cardiovascular and resistance training improve hemostatic parameters and promote a less thrombotic blood profile. This review highlights the studies, mechanisms, and outcomes relating to the effectiveness of resistance training on the process of hemostasis. The Pubmed, Scopus, Medline, Scielo, Lilacs, Ibecs, and Cochrane databases were used to locate the original articles. Seventeen studies were found during the research process. Of these, ten articles were excluded. Those protocols using a high volume of training for young adults showed a greater fibrinolytic response, and training protocols with intensities above 80% of 1 maximum repetition showed an increased platelet activity. In subjects with coronary artery disease, just one session of resistance training resulted in improvement in the fibrinolytic system (tissue plasminogen activator) without raising potential thrombotic markers.
Our recent studies suggest that sphingomyelin levels in the plasma membrane influence TF (tissue factor) procoagulant activity. The current study was performed to investigate how alterations to sphingomyelin metabolic pathway would affect TF procoagulant activity and thereby affect hemostatic and thrombotic processes.
The challenge for the treatment of severe traumas poses an urgent clinical need for the development of biomaterials to achieve rapid hemostasis and wound healing. In the past few decades, active inorganic components and their derived composites have become potential clinical products owing to their excellent performances in the process of hemorrhage control and tissue repair. In this review, we provide a current overview of the development of inorganic-based biomaterials used for hemostasis and wound healing. We highlight the methods and strategies for the design of inorganic-based biomaterials, including 3D printing, freeze-drying, electrospinning and vacuum filtration. Importantly, inorganic-based biomaterials for rapid hemostasis and wound healing are presented, and we divide them into several categories according to different chemistry and forms and further discuss their properties, therapeutic mechanisms and applications. Finally, the conclusions and future prospects are suggested for the development of novel inorganic-based biomaterials in the field of rapid hemostasis and wound healing.
Platelet degranulation is crucial for hemostasis and may participate in inflammation. Exocytosis in platelets is mediated by SNARE proteins and should be controlled by Munc13 proteins. We found that platelets express Munc13-2 and -4. We assessed platelet granule exocytosis in Munc13-2 and -4 global and conditional knockout (KO) mice, and observed that deletion of Munc13-4 ablates dense granule release and indirectly impairs alpha granule exocytosis. We found no exocytic role for Munc13-2 in platelets, not even in the absence of Munc13-4. In vitro, Munc13-4-deficient platelets exhibited defective aggregation at low doses of collagen. In a flow chamber assay, we observed that Munc13-4 acted as a rate-limiting factor in the formation of thrombi. In vivo, we observed a dose-dependency between Munc13-4 expression in platelets and both venous bleeding time and time to arterial thrombosis. Finally, in a model of allergic airway inflammation, we found that platelet-specific Munc13-4 KO mice had a reduction in airway hyper-responsiveness and eosinophilic inflammation. Taken together, our results indicate that Munc13-4-dependent platelet dense granule release plays essential roles in hemostasis, thrombosis and allergic inflammation.
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