Zinc deficiency impairs axonal regeneration and functional recovery after spinal cord injury by modulating macrophage polarization via NF-κB pathway.

Background: Spinal cord injury (SCI) is a devastating disease that results in permanent paralysis. Currently, there is no effective treatment for SCI, and it is important to identify factors that can provide therapeutic intervention during the course of the disease. Zinc, an essential trace element, has attracted attention as a regulator of inflammatory responses. In this study, we investigated the effect of zinc status on the SCI pathology and whether or not zinc could be a potential therapeutic target. Methods: We created experimental mouse models with three different serum zinc concentration by changing the zinc content of the diet. After inducing contusion injury to the spinal cord of three mouse models, we assessed inflammation, apoptosis, demyelination, axonal regeneration, and the number of nuclear translocations of NF-κB in macrophages by using qPCR and immunostaining. In addition, macrophages in the injured spinal cord of these mouse models were isolated by flow cytometry, and their intracellular zinc concentration level and gene expression were examined. Functional recovery was assessed using the open field motor score, a foot print analysis, and a grid walk test. Statistical analysis was performed using Wilcoxon rank-sum test and ANOVA with the Tukey-Kramer test. Results: In macrophages after SCI, zinc deficiency promoted nuclear translocation of NF-κB, polarization to pro-inflammatory like phenotype and expression of pro-inflammatory cytokines. The inflammatory response exacerbated by zinc deficiency led to worsening motor function by inducing more apoptosis of oligodendrocytes and demyelination and inhibiting axonal regeneration in the lesion site compared to the normal zinc condition. Furthermore, zinc supplementation after SCI attenuated these zinc-deficiency-induced series of responses and improved motor function. Conclusion: We demonstrated that zinc affected axonal regeneration and motor functional recovery after SCI by negatively regulating NF-κB activity and the subsequent inflammatory response in macrophages. Our findings suggest that zinc supplementation after SCI may be a novel therapeutic strategy for SCI.

Effects of high-dose major components in oral disinfectants on the cell cycle and apoptosis in primary human gingival fibroblasts in vitro.

We evaluated the effects of high-dose major components in oral disinfectants on oral cells from the standpoints of the cell cycle and apoptosis. We examined the viability and cell cycle of human gingival fibroblasts (HGFs) treated with the components of dental disinfectants, benzethonium chloride (BEC), benzalkonium chloride (BAC), and povidone iodine (PVD-I) using a cell counting kit and flow cytometry. The IC(50) inhibitory concentration value in HGF cultures at 24 hours was 1.3x10(-2) mM BEC, 6.0x10(-3) mM BAC, and 2.6x10(-1) mM PVD-I. In the cell cycle analysis, propidium iodide-stained HGFs were arrested in G(0)/G(1) of the cell cycle by all three disinfectants, and in the apoptosis assay, annexin V-FITC/PI-stained HGFs that became apoptotic at 5.0x10(-2) and 1.0x10(-1) mM BEC and 5.0x10(-2) and 1.0x10(-1) mM BAC, but not in PVD-I at concentrations as high as 5.0x10(-1) mM. Our findings describe the effects of high-dose oral disinfectants, rather than clinical concentrations. Nevertheless, appreciating the effects of high-dose disinfectants absorbed into the human body is important, where they may accumulate in specific tissues and cells.

Monitoring masseter muscle evoked responses enables faster tracheal intubation.

PURPOSE: The aim of this study was to investigate whether monitoring neuromuscular block at the masseter muscle (MM) would allow faster tracheal intubation when compared with that at the adductor pollicis muscle (APM). METHODS: Twenty female patients undergoing gynecological surgery were enrolled into this study. Immediately after inducing anesthesia with fentanyl and propofol, both the left masseter and ulnar nerves were stimulated in a 2 Hz train-of-four (TOF) mode using peripheral nerve stimulators. Contractions of the MM were felt with the anesthesiologist's left hand lifting the patient's jaw and holding an anesthesia facemask, while those of the APM were visually observed. Immediately after the contracting responses of the muscles were confirmed, all of the patients received an iv bolus of vecuronium 0.1 mg kg(-1). Onset times after vecuronium were defined as the duration until the contractions became impalpable at the MM or invisible at the APM. When the contraction of the MM could no longer be felt, the conditions for laryngoscopy and tracheal intubation were assessed. RESULTS: Onset time evaluated tactually at the MM (mean +/- SD, 108.4 +/- 27.7 s) was significantly shorter than that evaluated visually at the APM (181.2 +/- 32.1 s, P < 0.0001). The intubating conditions for all patients were graded as either excellent or good. CONCLUSION: Tactual evaluation of muscle paralysis of the MM during induction of anesthesia is clinically useful since it leads to faster tracheal intubation.

Basidiomycosis: Schizophyllum commune osteomyelitis in a dog.

A six-year-old female Labrador retriever dog was suffering from osteomyelitis in her hindlimb. A puncture wound caused by a rotted bamboo stick was presumed as the source of infection. The dog suffered from pre-existing aortic stenosis, but otherwise exhibited no significant abnormality in her systemic conditions excluding claudication of the left hindlimb. The results of cytology and pathological examinations of biopsy samples revealed the diagnosis of mycotic osteomyelitis in this dog. Mycological and DNA tests showed the pathogen as the mushroom Schizophyllum commune. Antibiotic sensitivity testing also revealed susceptibility to itraconazole, which was used to successfully treat the dog. This is a rare case of canine basidiomycosis with S. commune as the etiologic agent.