Tranexamic acid reduces postoperative blood loss of degenerative lumbar instability with stenosis in posterior approach lumbar surgery: a randomized controlled trial.

Study Design: This study is randomized controlled trial.

Purpose: To evaluate the effect of tranexamic acid (TXA) on reducing postoperative blood loss in posterior approach lumbar surgery for degenerative lumbar instability with stenosis.

Methods: Sixty patients with degenerative lumbar instability with stenosis were randomized into TXA and control groups, receiving 15 mg/kg body weight of TXA or placebo (0.

GIT1Y321 phosphorylation is required for ERK1/2- and PDGF-dependent VEGF secretion from osteoblasts to promote angiogenesis and bone healing.

Bone healing depends on vascular endothelial growth factor (VEGF) secretion from osteoblasts to promote angiogenesis. We examined the influence of the tyrosine 321 site of G protein-coupled receptor kinase interacting protein 1 (GIT1) on platelet-derived growth factor (PDGF)-induced VEGF synthesis in vitro and on bone healing in vivo. Cultured osteoblasts were prepared from calvaria of 1-2-day-old rats.

Phosphorylation of GIT1 tyrosine 321 is required for association with FAK at focal adhesions and for PDGF-activated migration of osteoblasts.

Osteoblast migration and proliferation are fundamental processes in bone healing. We demonstrated that the G-protein-coupled receptor kinase interacting protein 1(GIT1) is a key regulator of bone mass and osteoblast cell migration, but little is known about GIT1 regulation by upstream signaling systems or the impact of GIT1 on downstream effectors. We found that platelet-derived growth factor (PDGF) stimulated the GIT1 tyrosine phosphorylation in osteoblast cells and increased the association of GIT1 with focal adhesion kinase (FAK) at osteoblast focal adhesions.

A model of ischemia and reperfusion increases JNK activity, inhibits the association of BAD and 14-3-3, and induces apoptosis of rabbit spinal neurocytes.

It is now well established that the protein BAD (a pro-apoptotic Bcl-2 family protein) plays a pivotal role in determining cell death and survival. The c-Jun N-terminal kinase (JNK) pathway has been hypothesized to be involved in regulation of BAD. To clarify the role of BAD within the JNK pathway, a randomized, controlled study was designed using a rabbit model of ischemic spinal cord injury [5,8].