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Li-Hui Li,1,2 Qiang-Min Huang,1 Marco Barbero,2 Lin Liu,3 Thi-Tham Nguyen,4 Matteo Beretta-Piccoli,2 An-Le Xu,1 Li-Juan Ji1 1Department of Sport Medicine and Rehabilitation Center, Shanghai University of Sport, Shanghai, China; 2Rehabilitation Research Laboratory 2rLab, Department of Business Economics Health and Social Care, University of Applied Sciences and Arts of Southern Switzerland, Manno, Switzerland; 3Nanjing Sport Institute, Sport and Health Science Department, Nanjing, China; 4Faculty of Sport Science, Ton Duc Thang University, Ho Chi Minh City, Vietnam Background: Proteomics analysis may provide important information regarding the pathogenesis of chronic myofascial pain and the mechanisms underlying the treatment effects of dry needling. Materials and methods: This study used a rat model of myofascial trigger points (MTrPs) to perform a proteomics analysis. Three biological replicate experiments were used to compare the proteomes of healthy control rats, a rat model of MTrP, MTrP model rats following dry needling of MTrPs, and MTrP model rats following dry needling of non-MTrPs. Tandem mass tag (TMT) labeling technology based on nanoscale liquid chromatography-tandem mass spectrometry was used. Hierarchical clustering, gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and protein–protein interaction network analysis were performed to characterize the proteins. To validate the TMT results, three candidate biomarker proteins were verified using parallel reaction monitoring and Western blot analysis. Results: A total of 2,635 proteins were identified. GO and KEGG enrichment analyses showed that the glycolysis/gluconeogenesis pathways played dominant roles in the pathogenesis of chronic myofascial pain. The three candidate biomarker proteins were the pyruvate kinase muscle isozyme (encoded by the PKM gene), the muscle isoform of glycogen phosphorylase (encoded by the PYGM gene), and myozenin 2 (encoded by the MYOZ2 gene). The validation results were consistent with the TMT results.Conclusion: This is the first proteomics study that has investigated the pathogenesis of chronic myofascial pain and the mechanisms underlying the treatment effects of dry needling in an in vivo rat model of MTrPs, which might promote our understanding of the molecular mechanisms underlying chronic myofascial pain. Keywords: musculoskeletal pain, acupuncture, bioinformatics, mass spectrometry, tandem mass tag, parallel reaction monitoring

Neuropathic pain (NP) is a substantial clinical problem causing great injury to people word-widely. Although gene expression analyses had been performed previously, the mechanisms underlying the etiology and development of NP are still poorly understood. To understand the function genes involved in the etiology and development of NP, we built the co-expression modules and performed function enrichment analysis for neuropathic pain. In the present study, from a public microarray data set (GSE69901) from NCBI, gene co-expression modules were contributed with the help of WGCNA for 12 neuropathic pain samples and 13 control samples, respectively. And functional enrichment analyses were followed by DAVID database. Firstly, we established 21 co-expression modules and 19 co-expression modules out of 5,000 high-express genes in NP and control samples, respectively. Then, it showed great difference in interaction relationships of total genes and hub-genes between pairwise modules, which indicated the high confidence of gene co-expression modules. Finally, functional enrichment analysis of the top five co-expression modules in NP exhibited great differences and significant enrichment in transcription regulation of RNA polymerase II promoter and ubiquitin mediated proteolysis pathway. RNA polymerase II promoter and ubiquitin-mediated proteolysis pathway played important role in etiology and development of NP. Anyhow, our findings provided the framework of gene co-expression modules of NP and furthered the understanding of these modules from functional aspect. J. Cell. Biochem. 118: 4436-4443, 2017. © 2017 Wiley Periodicals, Inc.

Background/Aims: Hypoxia has recently been proposed as one of the most important factors in progressive renal injury. Hypoxia-induced vascular endothelial growth factor (VEGF) expression may play a critical role in maintaining peritubular capillary endothelium in renal disease. This study was designed to investigate the effect and underlying mechanism of all-trans retinoic acid (ATRA) on hypoxia-induced injury in NRK52E cells. Methods: For mimicking hypoxia, cells were treated with 100 µM of cobalt chloride (CoCl2). The cell viability, expression of VEGF, p65, transforming growth factor-β2 (TGF-β2) and serine carboxypeptidase 1 (Scpep1), and nuclear factor of kappaB (NF-κB) activities after ATRA treatment were determined by MTT, western blot and electrophoretic mobility shift assay. Co-immunoprecipitation analysis was performed to demonstrate whether Scpep1 interacted with TGF-β2. Results: It was found that CoCl2 triggered hypoxia injury and significantly reduced cell viability. ATRA pretreatment increased the cell survival rate. Under hypoxic conditions, the expression of VEGF, p65 and TGF-β2 increased. Addition of ATRA significantly attenuated the expression of VEGF, p65 and TGF-β2. There was a corresponding variation of NF-κB/DNA binding activities. In addition, ATRA stimulated Scpep1 expression under normoxic and hypoxia condition. Furthermore, TGF-β2 interacted with Scpep1. Conclusions: This study indicated that ATRA may attenuate hypoxia-induced injury in NRK52E cells via inhibiting NF-κB/VEGF and TGF-β2/VEGF pathway.

// Xiao-Jie Lu 1,* , Jing Dong 2,* , Li-Juan Ji 3,* , Li-Xin Xiao 4 , Chang-Quan Ling 5 and Jun Zhou 6 1 Department of Gastroenterology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China 2 Outpatient Department, Zhejiang Provincial People’s Hospital, Hangzhou, Zhejiang Province, China 3 Department of Rehabilitation, The Affiliated Huai’an Hospital of Xuzhou Medical College and The Second People’s Hospital of Huai’an, Huai’an, China 4 Department of Gamma Knife, The 411st Hospital of Chinese People’s Liberation Army, Shanghai, China 5 Changhai Hospital of Traditional Chinese Medicine, Second Military Medical University, Shanghai, China 6 Department of Oncology and Hematology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China * Co-first authors Correspondence to: Jun Zhou, email: // Keywords : hepatocellular carcinoma; portal vein tumor thrombosis; gamma knife; adverse events; overall survival Received : August 14, 2015 Accepted : September 24, 2015 Published : October 14, 2015 Abstract This is a retrospective study on the safety and efficacy of gamma knife radiosurgery (GKR) in treating hepatocellular carcinoma (HCC) with portal vein tumor thrombosis (PVTT). Patients with confirmed HCC and PVTT were allocated into two groups based on the treatments they received (palliative or GKR). A total of 138 patients were included (74 in the palliative group, 64 in GKR group). No significant differences in baseline characteristics existed between the two groups. Treatment-related adverse events (AEs) were recorded and compared between groups. The majority of AEs were mild to moderate and subsided naturally or after medication. There was no AE-induced death. The influences of baseline characteristics and treatment options on patients’ OS were analyzed. The median OS of patients in the palliative and GKR group were 3.0 months (95% CI: 2.719-3.281) and 6.1 months (95% CI: 4.706-7.494) respectively ( p = 0.003). Multivariate analysis revealed that GKR treatment, performance status 0-1, Child A, smaller tumor diameter and monolobar distribution were significant favorable prognosticators. Subgroup analyses showed OS benefit of GKR regardless of PVTT location (main or branch of PVTT). In conclusion, GKR is well tolerated in selected HCC-PVTT patients and can confer OS benefit, which needs validation in future prospective studies.

Zu-yun Liu,1,* Yan-yu Shen,2,* Li-juan Ji,3 Xiao-yan Jiang,4 Xiao-feng Wang,5 Yan Shi6 1Department of Internal Medicine, Yale School of Medicine, New Haven, CT, USA; 2Department of Nephrology, People’s Hospital of Xuyi, Xuyi, Jiangsu, China; 3Department of Sport Medicine and Pain Clinic, Center of Sports Rehabilitation, School of Sport Science, Shanghai University of Sport, 4Key Laboratory of Arrhythmias of the Ministry of Education of China, Tongji University School of Medicine, 5Unit of Epidemiology, Ministry of Education Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Shanghai, China, 6Department of Emergency, Huai’an Second People’s Hospital, The Affiliated Huai’an Hospital of Xuzhou Medical University, Huai’an, China *These authors contributed equally to this work Objective: To examine the association between serum β2-microglobulin (B2M) levels and frailty in an elderly Chinese population.Design: A population-based cohort study.Setting and participants: We used data on 1,663 elderly participants (aged 70–84 years) from the aging arm of the Rugao Longevity and Ageing study, a population-based observational two-arm cohort study conducted in Rugao, China.Measurements: The serum B2M was measured with chemiluminescence immunoassay by a technician in the biochemistry laboratory of the Rugao People’s Hospital. Information on the frailty index and phenotype was collected.Results: The mean B2M levels and frailty index were 1.8 mg/L and 0.16, respectively; 188 (11.3%) participants were classified as frail (frailty phenotype). For a standard deviation increase in B2M, the adjusted odds ratio for frailty phenotype was 1.20 (95% CI: 1.05, 1.39; P=0.009) and the standardized coefficient for frailty index was 0.07 (95% CI: 0.02, 0.11; P=0.004). Relative to the lowest quartile, the highest B2M quartile had a greater risk of prevalent frailty with adjusted odds ratios of 1.68 (95% CI: 1.04, 2.71; P=0.034) for frailty phenotype and 1.51 (95% CI: 1.01, 2.27; P=0.044) for frailty index (≥0.25). In addition, estimated glomerular filtration rate (based on B2M) or chronic kidney disease (estimated glomerular filtration rate

Emerging evidence suggests that microRNAs (miRNAs) play a critical role in the pathogenesis of neuropathic pain. However, the exact role of miRNAs in regulating neuropathic pain remains largely unknown. In this study, we aimed to investigate the potential role of miR-93 in a rat model of neuropathic pain induced by chronic constriction sciatic nerve injury (CCI). We found a significant decrease of miR-93 in the spinal cord of CCI rats compared with sham rats. Overexpression of miR-93 significantly alleviated neuropathic pain development and reduced inflammatory cytokine expression, including interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and IL-6 in CCI rats. By bioinformatic analysis and dual-luciferase reporter assay, we found that miR-93 directly targeted the 3'-untranslated region (UTR) of signal transducer and activator of transcription 3 (STAT3), an important regulator of inflammation. Overexpression of miR-93 markedly suppressed the expression of STAT3 in vitro and in vivo. Furthermore, overexpression of STAT3 significantly reversed the miR-93 overexpression-induced suppressive effects on neuropathic pain development and neuroinflammation. Taken together, our study suggests that miR-93 inhibits neuropathic pain development of CCI rats possibly through inhibiting STAT3-mediated neuroinflammation. Our findings indicate that miR-93 may serve as a novel therapeutic target for neuropathic pain intervention.

We read with interest the comment letter by *** et, al. regarding our article “Identification of Key Gene Modules of Neuropathic Pain by Co-expression Analysis” [1] and we are grateful for their interest in our study. The authors pointed out that our bioinformatics methods are inappropriate and provided their methods of improvement. We read with interest their suggestions and reevaluated our bioinformatics methods as well as their suggestions. However, we do not agree with their claims after careful assessment.This article is protected by copyright. All rights reserved

We read with interest the article by Bruix et al 1 in which Sorafenib was regarded as the standard treatment for hepatocellular carcinoma (HCC) patients with portal vein tumour thrombosis (PVTT). However, Sorafenib can only confer 2–3 months of overall survival (OS) benefit2 ,3 and is inapplicable to many patients due to extensive side effects and high price. Zhong et al 4 proposed that liver resection might provide survival benefit to patients with HCC-PVTT with adequate liver function. However, this proposal was based on literature survey, lacked definite patient inclusion criteria and failed to provide information on patients’ baseline characteristics. Therefore, explorations of alternative therapeutics for patients with HCC-PVTT are still needed. Although not recommended by mainstream guidelines5 ,6 for patients with HCC-PVTT, transarterial chemoembolisation (TACE) has long been practiced in the clinic in selected patients with HCC-PVTT.7 ,8 Gamma knife surgery (GKS) has shown favourable effects in treating brain …