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In order to gain an understanding of the role of the sulfenyl group of nitrile hydratase (NHase), a new Co(III) complex with a sulfenyl-type ligand (LC=O:N2(SO)2), Na[CoIII(LC=O:N2(SO)2)(tBuNC)2] (2), was synthesized. The compound includes two amide groups, two sulfenate sulfurs in the equatorial plane, and two tBuNC molecules in the axial positions. Characterization of the compound was performed by UV-vis spectroscopic, IR spectral, thermogravimetric (TG), and X-ray structure analytical methods. The results are discussed in the context of Co(III) complexes containing the corresponding sulfur-type (LC=O:N2S2) (1) and sulfinyl-type ligands (LC=O:N2(SO2)2) (3). Complex 2 crystallized with the formula Na[CoIII(LC=O:N2(SO)2)(tBuNC)2].urea.2H2O.0.5EtOH. The X-ray structure revealed that the Co(III) complex has an octahedral geometry with Co-S=av. 2.221 A, Co-N=av. 1.998 A, and Co-C=av. 1.87 A. The sulfenyl oxygen and amidate carbonyl oxygen are linked to urea, water, EtOH, and Na+ and participate in a hydrogen-bond and an electrostatic interaction. IR and TG measurements demonstrated that the coordination strength of tBuNC to the Co atom increases as follows: 1<2<3. Complex 2 has almost the same stability as 3 in all solutions tested, although 1 exhibits a release of axial ligands in nonaqueous solutions. DFT calculations for 1, 2, and 3 demonstrated that Milliken atomic charges of the Co(III) centers are +1.466, +1.536, and +1.542, respectively, indicating that the extent of oxidation of the sulfur atoms increases the Lewis acidity of the Co(III) centers. Interestingly, the solution-state IR spectrum of 2 exhibits a solvent-dependent S-O stretching frequency. The frequency decreases with an increase in the electrophilicity (acceptor number) of the solvent. This solvent dependence was not observed for 3, which has a sulfinate (SO2) group, suggesting that the sulfenyl oxygen atom has nucleophilic character and promotes strong binding of the tBuNC molecule to lower the reaction barrier. These findings may suggest that the sulfenate oxygen in native NHase acts as a base (proton acceptor) and contributes to the activation of a water molecule and/or nitrile molecule.

Basketball is a major sport worldwide among different age groups that leads to a high frequency of injuries at multiple body sites. Upper and lower extremities and lower back are common pain sites in basketball players; however, there is little information about the relationship between upper or lower extremity pain and lower back pain. This study elucidated the associations between upper extremity (shoulder and elbow) pain and lower back pain (LBP) among young basketball players. We conducted a cross-sectional study using self-reported questionnaires mailed to 25,669 young athletes; the final study population comprised 590 basketball players, and their median age was 13 years (range: 6-15 years). The point prevalence rates of lower back, shoulder, elbow, and upper extremity pain among young basketball players were 12.9% (76/590), 4.6% (27/590), 2.7% (16/590), and 7.1% (42/590), respectively. Multivariate logistic regression analyses revealed that upper extremity pain was significantly associated with LBP (adjusted odds ratio [OR]: 7.86; 95% confidential interval [CI], 3.93-15.72). Shoulder pain was significantly associated with training per week (> 4 days) (adjusted OR: 4.15; 95% CI: 1.29-13.40) and LBP (adjusted OR: 13.77; 95% CI: 5.70-33.24). This study indicates that upper extremity and shoulder pain is associated with LBP among young basketball players. Assessing for lower back pain, as well as elbow and/or shoulder pain, may help prevent severe injuries in young basketball players. In conclusion, parents and coaches should be properly re-educated to help improve lower back, upper extremity, and shoulder pain among young basketball players.

Muscle pain is a common condition that relates to various pathologies. Muscle overuse induces muscle pain, and neutrophils are key players in pain production. Neutrophils also play a central role in chronic pain by secreting interleukin (IL)-18. The aim of this study was to investigate the involvement of neutrophils and IL-18 in a mouse model of muscle pain. The right hind leg muscles of BALB/c mice were stimulated electrically to induce excessive muscle contraction. The left hind leg muscles were not stimulated. The pressure pain threshold, number of neutrophils, and IL-18 levels were investigated. Furthermore, the effects of the IL-18-binding protein and Brilliant Blue G on pain were investigated. In stimulated muscles, pressure pain thresholds decreased, and neutrophil and IL-18 levels increased compared with that in non-stimulated muscles. The administration of IL-18-binding protein and Brilliant Blue G attenuated hyperalgesia caused by excessive muscle contraction. These results suggest that increased IL-18 secretion from larger numbers of neutrophils elicits mechanical hyperalgesia.

Background Low back pain (LBP) is a common problem among young basketball players in addition to lower extremity injuries. However, studies that focus on LBP with lower extremity pain are limited. From the perspective of the kinematic chain, disrupted lower extremity function can lead to LBP. The association between these two symptoms in basketball players, however, has not been reported. Therefore, this study aimed to clarify the association between lower extremity pain and LBP among young basketball players. Methods This cross-sectional study was conducted on school-aged basketball players (n = 592). Information regarding their sporting activities was collected using a self-reported questionnaire. Musculoskeletal pain such as low back, knee, and ankle pain was assessed. The sports players with knee and/or ankle pain were defined as having lower extremity pain. Multivariate logistic regression analysis was used to assess the association between lower extremity pain and LBP. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated. The associations of knee or ankle pain with LBP were similarly assessed. Results School-aged basketball players had a point prevalence of 12.8% for LBP. Compared with the players without lower extremity pain, the players with lower extremity pain had higher rates of LBP, with an adjusted OR (95% CI) of 6.21 (3.57–10.80). There was also a significant association of knee and ankle pain with LBP. Compared with the players without knee or ankle pain, the adjusted ORs (95% CI) for LBP were 4.25 (2.55–7.07) in the players with knee pain and 3.79 (2.26–6.36) in the players with ankle pain. Conclusions Lower extremity pain was associated with LBP among school-aged basketball players. Further research is needed to clarify the mechanism of this association, which will provide useful information for prevention and treatment of LBP among young basketball players.

}(tBuNC) 2 ] (3) were synthesized and characterized on the basis of electronic absorption spectroscopy, IR spectroscopy, cyclic voltammetry, and X-ray structural analysis. Both of the crystal structures of complexes 1-Na and 1-PPh 4 revealed a square planar structure with N 2 S 2 donating atoms, and 2 exhibited an octahedral structure coordinated with two tert-butylisocyanide (tBuNC) molecules at the axial sites of complex 1-PPh 4 . Complex 3, which showed an octahedral structure with sulfinate sulfur atoms equatorially coordinated to the center, was synthesized by the treatment of 2 with a suitable oxidant. The reduction potential values from Co III to Co II for complex 3 in solution demonstrated a larger positive shift when compared with those of complexes 1-PPh 4 and 2, which indicates that the oxygenation of the sulfur atoms increased the Lewis acidity of the Co III center. Interestingly, the coordination equilib-

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Muscle pain is a common condition in many diseases and is induced by muscle overuse. Muscle overuse induces an increase in uric acid, which stimulates the nucleotide-binding oligomerization domain-like receptor (NLR). This receptor contains the pyrin domain NLRP-3 inflammasome which when activated, results in the secretion of potent pro-inflammatory cytokines such as interleukin-1β (IL-1β). The aim of this study was to investigate the involvement of inflammasome activation via the elevation of uric acid level in nociception in a mouse model of muscle pain. The right hind leg muscles of BALB/c mice were stimulated electrically to induce excessive muscle contraction. The left hind leg muscles were not stimulated as a control. Mechanical withdrawal thresholds, levels of uric acid, IL-1β, and NLRP3, caspase-1 activity, and the number of macrophages were investigated. Furthermore, the effects of xanthine oxidase inhibitors, such as Brilliant Blue G, caspase-1 inhibitor, and clodronate liposome, on pain were investigated. In the stimulated muscles, mechanical withdrawal thresholds decreased, and the levels of uric acid, NLRP3, and IL-1β, caspase-1 activity, and the number of macrophages increased compared to that in the non-stimulated muscles. Administration of the inhibitors attenuated hyperalgesia caused by excessive muscle contraction. These results suggested that IL-1β secretion and NLRP3 inflammasome activation in macrophages produced mechanical hyperalgesia by elevating uric acid level, and xanthine oxidase inhibitors may potentially reduce over-exercised muscle pain.