Triceps motor branch transfer for isolated axillary nerve injury: Outcomes in 9 patients.

INTRODUCTION: Triceps motor branch transfer has been used for more than ten years to restore deltoid function after axillary nerve injury. However, there have been few reports of the outcome of this procedure in isolated axillary nerve injury. HYPOTHESIS: Triceps motor branch transfer could be an effective method to restore deltoid function for patients with isolated axillary nerve injury. MATERIALS AND METHODS: Nine patients who underwent triceps motor branch transfer for treatment of isolated axillary nerve injury were followed up for at least 22 months. Shoulder abduction was assessed for all patients. The DASH outcome questionnaire was completed by every patient. Electrophysiological study was performed on 7 patients. RESULTS: All patients regained≥90° (mean, 137°) shoulder abduction. Mean DASH score decreased from 35.2 before surgery to 13.1 at the last follow-up. There was no noticeable weakness of elbow extension in any patient. DISCUSSION: Triceps motor branch transfer provided good results and may be a feasible alternative to nerve grafting for the treatment of complete isolated axillary nerve injury. TYPE OF STUDY: IV, retrospective cohort study.

Targeting Bax interaction sites reveals that only homo-oligomerization sites are essential for its activation.

Bax is a proapoptotic Bcl-2 family member that has a central role in the initiation of mitochondria-dependent apoptosis. However, the mechanism of Bax activation during apoptosis remains unsettled. It is believed that the activation of Bax is mediated by either dissociation from prosurvival Bcl-2 family members, or direct association with BH3-only members. Several interaction sites on Bax that mediate its interactions with other Bcl-2 family members, as well as its proapoptotic activity, have been identified in previous studies by other groups. To rigorously investigate the functional role of these interaction sites, we knocked in their respective mutants using HCT116 colon cancer cells, in which apoptosis induced by several stimuli is strictly Bax-dependent. Bax-mediated apoptosis was intact upon knock-in (KI) of K21E and D33A, which were shown to block the interaction of Bax with BH3-only activators. Apoptosis was partially reduced by KI of D68R, which impairs the interaction of Bax with prosurvival members, and S184V, a constitutively mitochondria-targeting mutant. In contrast, apoptosis was largely suppressed by KI of L70A/D71A, which blocks homo-oligomerization of Bax and its binding to prosurvival Bcl-2 family proteins. Collectively, our results suggest that the activation of endogenous Bax in HCT116 cells is dependent on its homo-oligomerization sites, but not those previously shown to interact with BH3-only activators or prosurvival proteins only. We therefore postulate that critical interaction sites yet to be identified, or mechanisms other than protein-protein interactions, need to be pursued to delineate the mechanism of Bax activation during apoptosis.

Platelet cyclic GMP responses to nitroglycerin.

The present study further investigates the use of platelet cyclic guanosine monophosphate (GMP) as a biochemical measure of tolerance. Platelet cyclic GMP has been reported as a marker of the biochemical effects of nitroglycerin (GTN) and as an indicator of the development of tolerance. Platelet cyclic GMP levels and systolic blood pressure (SBP) were measured repeatedly in nine subjects who received continuous transdermal GTN therapy (0.6 mg/hour), and in nine control subjects who did not. These measurements were also made before and after sublingual GTN (0.6 mg) in both groups. Whole blood from five subjects was incubated with normal saline (as a control), with 22 nM GTN (representing a therapeutic GTN concentration), and with 100 microM GTN. Although the acute administration of transdermal GTN caused a significant decrease in SBP (112 +/- 3 to 96 +/- 3 mmHg, p = 0.003), SBP returned to baseline following 1 week of continuous therapy. Platelet cyclic GMP levels did not change in response to transdermal GTN, either acutely or following sustained therapy. Similarly, sublingual GTN caused no change in platelet cyclic GMP in either group. There was no change in platelet cyclic GMP concentration following incubation with 22 nM GTN. Platelet cyclic GMP did increase following incubation with 100 microM GTN (0.883 +/- 0.043 pmol/10(9) platelets, p < 0.001). These results demonstrate that platelet cyclic GMP levels do not change in response to clinically relevant doses of GTN. Literature supporting the use of platelet cyclic GMP levels as an index of GTN effects and/or tolerance should be interpreted with caution.

Reversible effect of testosterone undecanoate injection on spermatogenesis in rats.

AIM: To study the effect of testosterone undecanoate (TU) injection on spermatogenesis in rats. METHODS: Twenty adult SD rats received vehicle or TU (8 mg/kg, 19 mg/kg or 625 mg/kg) injection, im, every 15 days for 60 days, and another 38 animals received similar treatments for 130 days with half of them undergoing a recovery phase of 120 days (5 rats for each treatment). At the end of the treatment, testes were removed and the diameter of the seminiferous tubules and the number of late elongated spermatids (steps 15-19) per testis were estimated with stereological methods as a measure of the spermatogenic efficiency. RESULTS: Low dose (8 mg/kg) TU treatment virtually had no effect on spermatogenesis. A dose of 19 mg/kg slightly suppressed spermatogenesis 60 days after treatment, and severe suppression occurred after another 70 days of dosing. Spermatogenesis was completely recovered at the end of the recovery phase. Large dose (625 mg/kg) TU treatment did not significantly affect spermatogenesis and was well tolerated by animals. CONCLUSION: TU injection reversibly suppresses spermatogenesis in rats.