Evaluating soreness symptoms of fibromyalgia: Establishment and validation of the Revised Fibromyalgia Impact Questionnaire with Integration of Soreness Assessment.

BACKGROUND: Fibromyalgia is a chronic disorder characterized by widespread musculoskeletal pain. A common complaint is soreness. However, until now, no assessment tool is available to address soreness and evaluate its impact on disease severity. We aimed to establish a questionnaire for soreness assessment and to evaluate its validity in fibromyalgia patients. METHODS: Patients diagnosed with fibromyalgia per the American College of Rheumatology criteria (2011) were recruited. The Revised Fibromyalgia Impact Questionnaire with an integration of Soreness Assessment (FIQRS) was established by adding five items pertinent to soreness sensation to the existing FIQR. The participants were asked to evaluate their soreness symptoms by filling out the FIQRS twice. The test-retest reliability and internal consistency were assessed. Construct validity was evaluated by correlations with the FIQR and fibromyalgia symptom severity (SS) score. RESULTS: Sixty-two patients with fibromyalgia were recruited, including 57 females (91.9%; mean age: 51.4 years). The intraclass correlation coefficient (ICC) of test-retest reliability was 0.92 for the FIQRS overall score. The Cronbach's α of all the items in the FIQRS was 0.93. The correlation coefficient of the FIQRS total score with the FIQR was 0.97 (p < 0.0001) and that with the fibromyalgia SS scale was 0.52 (p < 0.0001). CONCLUSION: The FIQRS has good reliability and internal consistency for the assessment of disease impact on fibromyalgia patients, thus providing a reliable tool for soreness evaluation. Future studies are warranted for further validation regarding its correlation with other psychometric properties and life quality measurements.

Glucose Transporter Type 4 Redistribution on the Membrane Induced by Insulin through Akt in Hydrocortisone Treatment in Rat Skeletal Muscles.

Hydrocortisone is a growth hormone frequently used in the treatment of low back pain. Hydrocortisone treatment has an anti-inflammation effect, which also inactivates glucose transporter type 4 (GLUT4) by p38 mitogen-activated protein kinase (MAPK) inhibition. Translocation of GLUT4 regulates body glucose homeostasis and muscle repair and is induced by insulin. In this study, 56 SD rats were divided into seven groups, and were treated with insulin or hydrocortisone in sedentary or exercise training groups. The muscle proteins and biochemical blood parameters were analyzed after 7 days of treatments. The results showed that the serum glucose increased in hydrocortisone treatment accompanied by GLUT4 inactivation in both the sedentary and exercise training rats. In the exercise training groups, GLUT4 was redistributed on the plasma membrane on co-treatment with insulin and hydrocortisone through Akt phosphorylation. Insulin treatment exerted a compensatory feedback effect on the GLUT4 translocation on hydrocortisone co-treatment, which was the cause of GLUT4 inactivation.

The potential roles of EZH2 in regenerative medicine.

Enhancer of zeste homolog 2 (EZH2), a catalytic component of polycomb repressive complex 2, serves as a histone methyltransferase toward histone H3K27 trimethylation and also recruits DNA methyltransferases to regulate gene expression and chromatin structure. Accumulating evidence indicates the critical roles of EZH2 in stem cell maintenance and cell fate decision in differentiation into specific cell lineages. In this article, we review the updated progress in the field and the potential application of EZH2 in regenerative medicine including nervous system, muscle, pancreas, and dental pulp regeneration.

PACAP38/PAC1 signaling induces bone marrow-derived cells homing to ischemic brain.

Understanding stem cell homing, which is governed by environmental signals from the surrounding niche, is important for developing effective stem cell-based repair strategies. The molecular mechanism by which the brain under ischemic stress recruits bone marrow-derived cells (BMDCs) to the vascular niche remains poorly characterized. Here we report that hypoxia-inducible factor-1α (HIF-1α) activation upregulates pituitary adenylate cyclase-activating peptide 38 (PACAP38), which in turn activates PACAP type 1 receptor (PAC1) under hypoxia in vitro and cerebral ischemia in vivo. BMDCs homing to endothelial cells in the ischemic brain are mediated by HIF-1α activation of the PACAP38-PAC1 signaling cascade followed by upregulation of cellular prion protein and α6-integrin to enhance the ability of BMDCs to bind laminin in the vascular niche. Exogenous PACAP38 confers a similar effect in facilitating BMDCs homing into the ischemic brain, resulting in reduction of ischemic brain injury. These findings suggest a novel HIF-1α-activated PACAP38-PAC1 signaling process in initiating BMDCs homing into the ischemic brain for reducing brain injury and enhancing functional recovery after ischemic stroke.