Clinical application of axonal repair technique for treatment of peripheral nerve injury

Objective: To evaluate the efficacy of axonal repair technique for treatment of peripheral nerve injury clinically. Methods: In 1998, the authors applied axonal repair technique to treat peripheral nerve injuries in 12 patients with 13 nerves. It consists of four steps, ie, stumps of the nerve being soaked in a modified Collins fluid, freezed, trimmed, and coapted with glue, making the injured nerve repaired at the axonal level. Results: The patients were followed up for an average of 13 months. Results showed that in 4 cases of first-stage contralateral C7 transfer, regenerating axons reached to the sternoclavicular joint or axilla at 4 to 7 months, offering the timing for performing the second-stage contralateral C7 transfer. In 5 cases of accessory nerve transferred to the suprascapular nerve, the abduction of the shoulder was 40° on average. In the other 3 patients with four different nerves repaired, results were also satisfactory. Conclusions: This technique is promising in the treatment of peripheral nerve injury.

Mechanism of macrophage injury following traumatic hemorrhagic shock: through PTX-sensitive G-protein-mediated signal transduction pathway

Objective: To study the mechanism of macrophage injury after trauma-hemorrhagic shock. Methods: Wistar male rats underwent trauma (closed bone fracture) and hemorrhage (mean arterial blood pressure of 35 mm Hg±5 mm Hg for 60 minutes, following fluid resuscitation). Rats without trauma, hemorrhage or fluid resuscitation served as controls. Peritoneal macrophages were harvested at 6 hours and 1, 2, 3, 7 days after traumatic hemorrhagic shock to determine the effects of pertussis toxin (PTX, as a specific inhibitor to Giα) and cholera toxin (CTX, as a stimulant to Gsα) on macrophage-Ia expression and TNF-α production and levels of Giα and Gsα. Results: The macrophages from the injured rats revealed a significant decrease of Ia positive number and TNF-α release in response to LPS. With pretreatment with PTX 10-100 ng/ml Ia positive cells and LPS-induced TNFα production in both control and impaired macrophages populations were dose-dependently increased. Both macrophages populations were not responding to CTX treatment (10-100 ng/ml). Western blot analyses showed that the levels of Giα protein expression increased as much as 116.5%- 148.8% of the control level from 6 hours through 7 days after traumatic hemorrhage. The levels of Gsα protein expression were reduced at 6 hours and decreased to the lowest degree; 36% of the control at day 1, began to return at day 2 and returned to the normal level at day 7, following traumatic hemorrhagic shock.Conclusions: PTX-sensitive G-protein may participate in the modulation of macrophage-Ia expression and TNF-α release following traumatic hemorrhagic shock. Analyses of the alteration of Giα and Gsα protein expressions further supports the concept that G-protein is involved in trauma-induced macrophage signal transduction pathways.

Ultrastructural changes of TMJ articular cartilage and synovial membrane following occlusal trauma in rabbit

Objective: To study the effects of occlusal trauma on the ultra structure of synovial membrane and articular cartilage in rabbits temporomandibular joints (TMJ). Methods: TMJs from six rabbits with occlusal trauma and three control rabbits were studied by transmission electron microscopy. Results: Degenerative changes in synovial membrane and articular cartilage of TMJ were induced following occlusal trauma. The structure of the articular surface was damaged, and chondrocytes in cartilage showed signs of degeneration. The synovial lining cells contained dense accumulations of vimentin intermediate filaments (IFs), which were especially prevalent in the cellular processes as well as paranuclearly. Microvilli on the synovial cell membrane were commonly seen. The “vermiform bodies” in the deeper interstitium of the synovial tissue were also found. Our findings of the punctate adherens between synovial lining cells were described in detail. Conclusions: The occlusal trauma is really a factor inducing degenerative changes of the TMJ.