Axons in the adult mammalian central nervous system (CNS) exhibit little regeneration after injury. It has been suggested that several axonal growth inhibitors prevent CNS axonal regeneration. Recent research has demonstrated that semaphorin3A (Sema3A) is one of the major inhibitors of axonal regeneration. We identified a strong and selective inhibitor of Sema3A, SM-216289, from the fermentation broth of a fungal strain. To examine the effect of SM-216289 in vivo, we transected the spinal cord of adult rats and administered SM-216289 into the lesion site for 4 weeks. Rats treated with SM-216289 showed substantially enhanced regeneration and/or preservation of injured axons, robust Schwann cell-mediated myelination and axonal regeneration in the lesion site, appreciable decreases in apoptotic cell number and marked enhancement of angiogenesis, resulting in considerably better functional recovery. Thus, Sema3A is essential for the inhibition of axonal regeneration and other regenerative responses after spinal cord injury (SCI). These results support the possibility of using Sema3A inhibitors in the treatment of human SCI.

Adipocyte differentiation requires a well‐defined programme of gene expression in which the transcription factor C/EBPα (CCAAT/enhancer‐binding protein) has a central function. Here, we show that Hzf (haematopoietic zinc‐finger), a previously identified p53 transcriptional target, regulates C/EBPα expression. Hzf is induced during differentiation of preadipocyte cell lines, and its suppression by short hairpin RNA disrupts adipogenesis. In Hzf's absence, expression of C/EBPα is severely impaired because of reduced translation of its mRNA. Hzf physically interacts with the 3′ untranslated region of C/EBPα mRNA to enhance its translation. Taken together, these findings underscore a critical role of Hzf in the adipogenesis regulatory cascade.

This model will be useful for investigating the ability of rhythmic muscular electrical stimulation therapy to promote motor recovery, in addition to the efficacy of combining treatments with spinal cord regeneration therapy after spinal cord injuries.

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BackgroundRehabilitation facilitates the reorganization of residual/regenerated neural pathways and is key in improving motor function following spinal cord injury. Neuromuscular electrical stimulation (NMES) has been reported as being clinically effective. Although it can be used after the acute phase post-injury, the optimal stimulation conditions to improve motor function remain unclear. In this paper, we examined the effectiveness of NMES with alternating currents in the kilohertz (kHz) frequency in gait rhythm stimulation therapy.MethodsTests were performed using 20 mature female Fischer rats. Incomplete spinal cord injuries (T9 level) were made with an IH impactor using a force of 150 kdyn, and NMES was administered for 3 days from the 7th day post-injury. The needle electrodes were inserted percutaneously near the motor point of each muscle in conscious rats, and each muscle on the left and right leg was stimulated for 15 min at two frequencies, 75 Hz and 8 kHz, to induce a gait rhythm. Motor function was evaluated using Basso, Beattie, Bresnahan (BBB) scores and three-dimensional (3D) gait analysis. Rats were divided into four groups (5 rats/group), including the NMES treatment 75-Hz group (iSCI-NMES 75 Hz), 8-kHz group (iSCI-NMES 8 kHz), injury control group (iSCI-NT), and normal group (Normal-CT), and were compared.ResultsThere was no significant difference in BBB scores among the three groups. In 3D gait analysis, compared with the injury control group, the 8-kHz group showed a significant improvement in synergistic movement of both hindlimbs.ConclusionWe suggest that kHz stimulation is effective in gait rhythm stimulation using NMES.

Aims/Introduction An increased risk of diabetes mellitus has been reported in primary aldosteronism, but the pathogenesis of glucose intolerance between the primary aldosteronism subtypes remains unclear. This study aimed to evaluate glucose metabolism in oral glucose tolerance test between aldosterone‐producing adenoma and idiopathic hyperaldosteronism, and characterize patients with improved glucose intolerance after primary aldosteronism treatment. Materials and Methods Oral glucose tolerance test was carried out in 116 patients who were diagnosed with primary aldosteronism and received adrenal venous sampling for subtyping. Oral glucose tolerance test was re‐evaluated after starting the treatment of primary aldosteronism for those who had glucose intolerance before the treatment. Results A total of 46.4% and 52.3% of patients with aldosterone‐producing adenoma and idiopathic hyperaldosteronism, respectively, were diagnosed with impaired glucose tolerance or diabetes. The insulinogenic index was significantly lower in aldosterone‐producing adenoma than in idiopathic hyperaldosteronism ( P = 0.045), whereas the Matsuda insulin sensitivity index was significantly higher in aldosterone‐producing adenoma than in idiopathic hyperaldosteronism ( P = 0.022). After the treatment of primary aldosteronism, glucose intolerance was improved in 66.6% and 45.8% of aldosterone‐producing adenoma and idiopathic hyperaldosteronism, respectively. The presence of obesity and central obesity were significantly lower in patients who improved glucose intolerance after the treatment of primary aldosteronism as compared with those not improved ( P = 0.013 and P = 0.033, respectively). Conclusions Insulin secretion impairment and insulin resistance play pathogenic roles for glucose intolerance in aldosterone‐producing adenoma and idiopathic hyperaldosteronism, respectively. In addition, primary aldosteronism treatments can ameliorate glucose intolerance more effectively in patients without obesity and/or central obesity.

For tumors that are located beside the main peripheral nerve, combined wide resection of both the tumor and peripheral nerve is mandatory. We here present an interesting case with synovial sarcoma of the wrist. An 8 cm of ulnar nerve defect was reconstructed by vascularized, folded sural nerve graft with the peroneal flap, whereas an 8 cm of distal ulna was reconstructed using extracorporeally irradiated osteochondral autograft. Our case showed excellent nerve regeneration. Extracorporeal irradiated osteochondral graft was a good option for reconstruction of the distal ulna. This procedure should be indicated for the reconstruction of non-weight-bearing joints. These kinds of reconstruction have been addressed in only a few cases of oncological reconstruction.