Hypertension disorders (HD) and pre-eclampsia (PRE) are leading causes of maternal deaths worldwide. PRE is associated with vascular endothelial dysfunction and with deregulation of the fibrinolysis pathway genes. Fibrinolysis is the fibrin clot hydrolysis process catalyzed by plasmin, a proteolytic enzyme formed from plasminogen. Plasminogen is cleaved by tissue-type (tPA) and urokinase-type (uPA) activators and inhibited by the plasminogen activator inhibitors type-1 (PAI-1) and type-2 (PAI-2). The whole process maintains blood hemostasis. This study aims to assess PAI-1, PAI-2, tPA and uPA mRNA expression in primary cultured human umbilical vein endothelial cells (HUVEC) isolated and cultured from healthy, HD and PRE women. Results show that PAI-1 and PAI-2 mRNA decreased in HD-HUVEC, whereas PAI-1 and uPA decreased in PRE-HUVEC cultures compared to control ones. Notably, the expression ratio between pro- and anti-fibrinolytic actors remained unchanged among the studied groups. It seems that newborn's hemostasis is maintained balanced probably by a compensatory mechanism that involves changes in the fibrinolysis gene expression profile. The real impact of these changes in mRNA expression is unknown, however, it is suggested that these changes could be associated with an increased predisposition to vascular disease development in the progeny.

Renal vein thrombosis in a transplanted kidney is an uncommon but critical complication that can result in graft loss if management is delayed. A 31-year-old male with known atresia of the inferior vena cava who received a deceased donor renal transplant 7 years previously presented to hospital with severe graft site pain and a week of nausea, vomiting, and chills. Serum creatinine was markedly elevated from baseline. Sonographic examination revealed external iliac vein thrombosis with extension of the thrombus into the transplant renal vein. Urgent angiographic administration of tissue plasminogen activator and suction thrombectomy was performed, then followed by heparin and clopidogrel post procedure. Within 24 h, his serum creatinine improved, and within 2 weeks returned to his baseline. He was started on lifelong warfarin anti-coagulation to reduce the risk of rethrombosis secondary to his uncorrectable aberrant venous anatomy. Due to the turbulent and sometimes reversed flow in the major veins, lifelong anticoagulation should be strongly considered for such transplant patients with recipient aberrancy of the large veins.

Now well-established throughout Europe, mobile stroke unit (MSU) programs are in the early stages of development in the United States. The concept aims to improve outcomes by bringing diagnostic capabilities and clot-busting care to the patients experiencing stroke, thereby reducing the time to treatment. In October, New York Presbyterian/Weill Cornell Medical Center in New York became the first medical center on the East Coast to deploy an MSU, and in July, the University of Tennessee College of Medicine in Memphis deployed a first-of-its-kind MSU that is larger and more robust than other MSUs currently in use. In the first month of operation, the MSU in New York responded to 29 calls and brought 12 patients to the hospital with suspected strokes. Two of these patients received tissue plasminogen activator in the field and both made full recoveries by the next day. The MSU deployed in Memphis is larger and carries more sophisticated diagnostic equipment than other MSUs. The program also replies on doctorally prepared, vascular neurology fellowship-trained nurse practitioners, instead of relying on telemedicine connections to external experts. Now operating with the assistance of grant funding, leaders of both programs hope that strong outcomes will prove convincing to hospitals and prayers, although the U.S. healthcare model complicates the establishment of a reimbursement structure for MSUs.

The present study aimed to investigate the effect of the expression of interleukin (IL)‑18 and related markers on deep venous thrombosis (DVT) to examine their correlation. Sprague‑Dawley rats of different models were established and were randomly assigned into three groups. The expression of IL‑18, nuclear factor (NF)‑κB and von Willebrand factor (vWF) were detected in blood samples. The inferior vena cava (IVC) was ligated to establish the DVT model. Rat IL‑18 overexpression and inhibition vectors were constructed. The expression levels of IL‑18 and related markers in the venous wall were compared between the model group and the control group using reverse transcription‑quantitative polymerase chain reaction and western blot analyses. Following the culture of human umbilical vein endothelial cells (HUVECs), IL‑18 was added to the cells, following which the growth of the HUVECs, and changes in vWF and other endothelial functional markers were analyzed. The IVC model demonstrated complete thrombosis at 8 h and stable thrombosis at 24 h. At 24 h following model establishment, the expression levels of IL‑18, NF‑κB and vWF were high in the blood samples with the occurrence and development of thrombosis (P<0.05). The weight, length and weight/length ratio of thrombi in each model group showed significant differences from those in the control group (P<0.05) with the overexpression of IL‑18, and the expression levels of NF‑κB and vWF in venous tissues were altered with abnormal expression levels of IL‑18. IL‑18 damaged HUVECs and significantly increased viability in early‑stage apoptosis, promoted the upregulation of vWF and P‑selectin, and reduced tissue plasminogen activator. IL‑18 and the related markers were closely associated with the occurrence and development of DVT.