The aim of this study was to investigate the features of overweight or obese individuals with a BMI >25 kg/m² who complained of low back pain, knee pain, and neck stiffness. The subjects comprised 88 overweight or obese individuals who were divided into a symptomatic group and an asymptomatic group prior to the weight–loss intervention in order to compare several parameters of each group. Symptomatic patients were divided into groups of subjects whose symptoms did or did not improve as a result of the 6–month weight–loss intervention. Changes in the test paramete­rs from before and after the intervention were compared between the two groups. The results revealed no differences in any parameters between the two groups (symptomatic and asymptomatic) at baseline in neck stiffness or low back pain. However, for knee pain, the maximal oxygen uptake (VO₂max) was significantly lower in the symptomatic group than in the asymptomatic group (p<0.01). Furthermore, the weight–loss intervention revealed a significant increase in VO₂max in the “improved” group compared to the “no change” group (p<0.05). The study results showed that both weight loss and the acquisition of aerobic capacity were important in relieving knee pain in overweight or obese individuals.

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   Recently, the involvement of inflammatory mediators such as chemokines in neuropathic pain has been focused. Among inflammatory cells recruited into the injured peripheral nerves, macrophages play key roles in chronic neuroinflammation through cytokine–chemokine network. As epigenetic histone modifications induce long–lasting expression of inflammatory mediators, we highlight the contribution of histone modifications in the injured peripheral nerves to neuropathic pain.
   After partial sciatic nerve ligation (PSL) in mice, F4⁄80⁺ macrophages were accumulated in the injured sciatic nerve (SCN). By microarray analysis, several inflammatory chemokine ligands and those receptors were upregulated in the injured SCN on day 7 after PSL. Indeed, the expression levels of CC–chemokine ligand (CCL) 3 and CCL8 showed the highest upregulation, and were confirmed by quantitative RT–PCR. Moreover, those receptors including CCR1, CCR2 and CCR5 were markedly upregulated after PSL. Chromatin precipitation assay revealed the acetylation in K9 residue (H3K9Ac) and trimethylation in K4 residue (H3K4me³) of histone H3, facilitating gene transcriptions associated with chromatin remodeling, on the promoter regions of CCLs in the injured SCN. By immunohistochemistry, upregulated CCL3 or CCL8 was located on the accumulated F4⁄80⁺ macrophages. Expressions of H3K9Ac and H3K4me³ were also increased in the injured SCN, and those were detected in the nuclei of macrophages expressing CCLs.
   These findings indicate that facilitation of chemokine signaling through histone H3 modifications in macrophages largely contributes to peripheral neuroinflammation leading to neuropathic pain. Further research considering the critical components of peripheral neuroinflammation exploit novel therapeutic strategy of neuropathic pain.

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   Although the application of aroma–oil compounds contained in plants such as lavender to the skin produces a local anesthetic effect, cellular mechanisms for this effect have not been fully examined yet. Since some of aroma oil–derived chemicals modulate transient receptor potential (TRP) channels expressed in primary–afferent neurons, this modulation may be involved in the local anesthetic effect. We have previously reported that plant–derived chemicals (capsaicin, menthol and allyl isothiocyanate, which activate TRPV1, TRPM8 and TRPA1 channels, respectively) at high concentrations inhibit fast–conducting and Na⁺–channel blocker tetrodotoxin–sensitive compound action potentials (CAPs) recorded from the frog sciatic nerve without TRP activation. The CAPs were also inhibited by opioids and adrenoceptor agonists without the activation of receptors for the agonists. The inhibitory actions were specific to their chemical structures. The present study examined how various aroma–oil compounds affect frog sciatic nerve CAPs by using the air–gap method. Lavender–oil compounds, linalyl acetate and linalool, reduced CAP peak amplitudes with the half–maximal inhibitory concentration (IC₅₀) values of 0.49 mM and 1.65 mM, respectively. When compared with local anesthetics’ actions reported previously in the frog sciatic nerve, the linalyl acetate activity was similar to those of lidocaine, ropivacaine and cocaine (0.74, 0.34 and 0.80 mM, respectively), while the linalool one was comparable to that (2.2 mM) of procaine. Citral, which activated TRPV1, TRPM8, TRPA1 and TRPV3 channels, attenuated CAP peak amplitudes with the IC₅₀ value of 0.48 mM; this action was resistant to a non–selective TRP antagonist ruthenium red (0.3 mM). Camphor, a TRPV1 and TRPV3 agonist, also reduced CAP peak amplitudes (by 30％ at 5 mM) in a manner insensitive to ruthenium red. With respect to other aroma–oil compounds, citronellal and rose oxide reduced CAP peak amplitudes with the IC50 values of 0.50 mM and 2.0 mM, respectively, while myrcene at a high concentration such as 5 mM hardly reduced CAP peak amplitudes. Taking into consideration previously–reported frog sciatic nerve data, an efficacy sequence of aroma–oil compounds for the CAP inhibi­tions was phenols (carbacrol: 0.35 mM; thymol: 0.42 mM; eugenol: 0.81 mM) ≧ aldehydes (citral and citronellal) ≧ esters (linaryl acetate) ＞ alcohols (linalool; menthol: 0.93 – 1.1 mM) ＞ ketones (pulegone: 1.4 mM; carbone: 1.4 – 1.6 mM; menthone: 1.5 – 2.3 mM) ＞ oxides (rose oxide; cineole: 6.6 – 7.5 mM) ≫ hydrocarbons (myrcene; limonene: 8％ inhibition at 10 mM), except for a ketone camphor that was less effective than oxides. It is suggested that aroma–oil compounds inhibit nerve conduction in a manner specific to their chemical structures; some of the compounds have efficacies comparable to those of local anesthetics. This result would serve to know aroma–oil compounds which may be useful as local anesthetics.

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   Musculoskeletal pain and other clinical complaints are known to increase with age, however its relationship to these symptoms remains unclear. In this study, we investigated the correlation between musculoskeletal pain and other clinical complaints. Questionnaires containing self–reported complaints collected from 3891 people over 30 years old were used for our study. Serf–reported complaints comprised of 33 items including three musculo­skeletal disorders (knee, low back, neck) and another thirty complaints. Firstly, we divided subjects into the following eight different categories by their musculoskeletal condition; a group without musculoskeletal disorder (Control), a group with knee pain alone, a group with low back pain alone, a group with neck stiffness alone, three groups which had overlapping pain in above two regions and a group with overlapping pain in all regions. Secondly, we investigated the epidemiological background and analyzed the number of other complaints in each group.
   In terms of epidemiological background, the ages in groups with any musculoskeletal disorders were significantly higher than those in control. Moreover, groups with musculoskeletal disorders except low back pain alone were significantly more prevalent in women. Groups with any musculo­skeletal disorders had significantly greater numbers of other complaints compared to control. Comparing the three groups with mono–regional pain, we discovered the number of other complaints was more significant in the group with neck stiffness than in the other two groups. The theoretical number of other complaints in a group with pain in all regions was significantly greater than the sum in each group with mono–regional pain.
   These findings suggest that musculoskeletal disorders are not only a regional problem but also affect other organs in the human body, followed by an increase of other unidentified complaints.

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   Background: Physical exercise may facilitate the improvement of pain–associated symptoms in patients with chronic pain. Moreover, motor cortex activation causes pain reduction via actions in pain–related central nervous system areas. Thus, physical exercise is believed to activate this pain control mechanism in the central nervous system. Cognitive tasks may also modulate pain, as these pain–related areas of the central nervous system play a vital role in cognitive functions. However, the mechanisms underlying pain reduction when performing cognitive tasks are unclear. Here, we aimed to investigate the effect of a cognitive–motor task on pain control.
   Methods: Thirty healthy subjects participated in this study. All participants performed 3 different tasks: a motor task involving the pressing of a button on a keyboard with the dominant hand (M task), a cognitive task involving thinking about the answers to the Stroop task (C task), and a cognitive–motor task involving the pressing of a button on a keyboard cor­responding to the answer to the Stroop task (CM task). Furthermore, the participants were classified according to the rate of correct answers given on the CM task (low rate, LS group; high rate, HS group). The pressure pain threshold (PPT) of the non–dominant forearm was estimated, and electro­encephalography (EEG) was performed over the frontal region to determine the attention and concentration given to each task. The EEG data were used to analyze the power of the theta, alpha, and beta frequency bands.
   Result: The PPT of the CM task significantly increased after the task period compared to that before the test, and was significantly higher compared to that of other tasks after the task period. Moreover, the power of the theta and alpha bands for the CM task significantly increased during the task period compared to that before the task, and was significantly higher compared to that of the other tasks during the task period. Moreover, the PPT of the HS group was significantly higher compared to the LS group after the task period, whereas the power of the theta and alpha bands significantly increased during the task period in the HS group.
   Conclusion: Compared to the motor or cognitive task alone, the CM task significantly reduced pain sensitivity. Moreover, a significant increase in the power of the theta and alpha bands was only noted in the CM task. Thus, the cognitive–motor task that required attention and concentration was effective in pain inhibition.

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   The purpose of this study was to establish an only–ankle–immobilization model. We divided 10 Wistar male rats into a control group (Cont, n=5) and immobilization group (IM, n=5). IM had their right ankle immobilized in planter flexion (PF) using external fixation for 4 weeks, while Cont were observed without immobilization for 4 weeks. All rats gained weight during the 4 weeks without significant differences between groups. Range of motion (ROM), pain threshold, and body weight were measured in all rats once a week for the 4 weeks. ROM of ankle dorsiflexion (DF) and PF, knee extension, and flexion were measured using X–ray fluoroscopy with a tension gauge, and pain thresholds were evaluated by behavioral response with the von Frey test and Hargreaves Assay using a plantar test. All data were shown as ％ of right limb ⁄ left limb. Ankle DF in IM was significantly limited 1 week after immobilization (83.7％ vs. Cont: 98％, p<0.05), and it continued decrease to 70.4％, 51.5％, and 61.9％ after 2, 3, and 4 weeks, respective­ly (vs. Cont: 99.4％, p<0.01). Ankle PF, knee extension, and flexion showed no significant difference between the groups. In the von Frey test, the mechanical hyperalgesia threshold in IM was significantly decreased to 45.8％ after 1 week compared to the Cont rats (90.4％, p<0.01), and then further to 21.4％, 17.7％, and 20％ after 2, 3, and 4 weeks, respectively (vs. Cont, p<0.01). In the plantar test, thermal nociceptive thresholds significantly decreased to 62.9％ after 1 week in IM (vs. Cont: 96.7％, p<0.01), and then further to 83.3％, 70.6％, and 76％ after 2, 3, and 4 weeks, respectively (vs. Cont, p<0.01). The model shown here will be useful for further studies to investigate the mechanisms and treatments of immobilization.

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