Despite the discovery and application of many parenteral (unfractionated and low-molecular-weight heparins) and oral anticoagulant vitamin K antagonist (VKA) drugs, the prevention and treatment of venous and arterial thrombotic phenomena remain major medical challenges. Furthermore, VKAs are the only oral anticoagulants used during the past 60 years. The main objective of this study is to present recent data on non-vitamin K antagonist oral anticoagulants (NOACs) and to analyze their advantages and disadvantages compared with those of VKAs based on a large number of recent studies. NOACs are novel direct-acting medications that are selective for one specific coagulation factor, either thrombin (IIa) or activated factor X (Xa). Several NOACs, such as dabigatran (a direct inhibitor of FIIa) and rivaroxaban, apixaban and edoxaban (direct inhibitors of factor Xa), have been used for at least 5 years but possibly 10 years. Unlike traditional VKAs, which prevent the coagulation process by suppressing the synthesis of vitamin K-dependent factors, NOACs directly inhibit key proteases (factors IIa and Xa). The important indications of these drugs are the prevention and treatment of deep vein thrombosis and pulmonary embolisms, and the prevention of atherothrombotic events in the heart and brain of patients with acute coronary syndrome and atrial fibrillation. They are not fixed, and dose-various strengths are available. Most studies have reported that more advantages than disadvantages for NOACs when compared with VKAs, with the most important advantages of NOACs including safety issues (ie, a lower incidence of major bleeding), convenience of use, minor drug and food interactions, a wide therapeutic window, and no need for laboratory monitoring. Nonetheless, there are some conditions for which VKAs remain the drug of choice. Based on the available data, we can conclude that NOACs have greater advantages and fewer disadvantages compared with VKAs. New studies are required to further assess the efficacy of NOACs.

The antithrombotic action of aspirin has long been recognized. Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity. Until recently, aspirin has been mainly used for primary and secondary prevention of arterial antithrombotic events. The aim of this study was to review the literature with regard to the various mechanisms of the newly discovered effects of aspirin in the prevention of the initiation and development of venous thrombosis. For this purpose, we used relevant data from the latest numerous scientific studies, including review articles, original research articles, double-blinded randomized controlled trials, a prospective combined analysis, a meta-analysis of randomized trials, evidence-based clinical practice guidelines, and multicenter studies. Aspirin is used in the prevention of venous thromboembolism (VTE), especially the prevention of recurrent VTE in patients with unprovoked VTE who were treated with vitamin K antagonists (VKAs) or with non-vitamin K antagonist oral anticoagulants (NOACs). Numerous studies have shown that aspirin reduces the rate of recurrent VTE in patients, following cessation of VKAs or NOACs. Furthermore, low doses of aspirin are suitable for long-term therapy in patients recovering from orthopedic or other surgeries. Aspirin is indicated for the primary and secondary prevention as well as the treatment of cardiovascular diseases, including acute coronary syndrome, myocardial infarction, peripheral artery disease, acute ischemic stroke, and transient ischemic attack (especially in atrial fibrillation or mechanical heart valves). Aspirin can prevent or treat recurrent unprovoked VTEs as well as VTEs occurring after various surgeries or in patients with malignant disease. Recent trials have suggested that the long-term use of low-dose aspirin is effective not only in the prevention and treatment of arterial thrombosis but also in the prevention and treatment of VTE. Compared with VKAs and NOACs, aspirin has a reduced risk of bleeding.

Traumatic injuries of the peripheral nerves are very common. Surgical repair of the damaged nerve is often complicated by scar tissue formation around the damaged nerve itself. The main objective of this study is to present the recent data from animal experimental studies where pharmacological topical agents are used at the site of peripheral nerve repair. Some of the most commonly topical agents used are tacrolimus (FK506), hyaluronic acid and its derivatives, and melatonin, whereas methylprednisolone and vitamin B12 have been used less. These studies have shown that the abovementioned substances have neuroprotective and neuroregenerative properties though different mechanisms. The successes of the regenerative process of the nerve repair in experimental research, using topical agents, can be evaluated using variety of methods such as morphological, electrophysiologic, and functional evaluation. However, most authors agree that despite good microsurgical repair and topical application of these substances, full regeneration and functional recovery of the nerve injured are almost never achieved.

Based on our findings, topical application of HA and FK506 exhibits equally positive effects, preventing perineural scar formation and enhancing nerve regeneration after peripheral nerve repair.

Introduction Traumatic brain injuries (TBIs) are very common in paediatric populations, in which they are also a leading cause of death. Computed tomography (CT) overuse in these populations results in ionization radiation exposure, which can lead to lethal malignancies. The aims of this study were to investigate the accuracy of serum S100B levels with respect to the detection of cranial injury in children with mild TBI and to determine whether decisions regarding the performance of CT can be made based on biomarker levels alone. Materials and Methods This was a single-center prospective cohort study that was carried out from December 2016 to December 2017. A total of 80 children with mild TBI who met the inclusion criteria were included in the study. The patients were between 2 and 16 years of age. We determined S100B protein levels and performed head CTs in all the patients. Results Patients with cranial injury, as detected by CT, had higher S100B protein levels than those without cranial injury (p < 0.0001). We found that patients with cranial injury (head CT+) had higher mean S100B protein levels (0.527 μg L−1, 95% confidence interval (CI) 0.447–0.607 μg L−1) than did patients without cranial injury (head CT−) (0.145 μg L−1, 95% CI 0.138–0.152 μg L−1). Receiver operating characteristic (ROC) curve analysis clearly showed that S100B protein levels differed between patients with and without cranial injury at 3 hours after TBI (AUC = 0.893, 95% CI 0.786–0.987, p = 0.0001). Conclusion Serum S100B levels cannot replace clinical examinations or CT as tools for identifying paediatric patients with mild head injury; however, serum S100B levels can be used to identify low-risk patients to prevent such patients from being exposed to radiation unnecessarily.