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Hepatocellular carcinoma (HCC) is among the most malignant tumors with high recurrence and low 5-year survival rate. Lipid metabolism is essential in tumor metastasis, although how altered lipid metabolism promotes HCC progression has not been well elucidated. Fat Storage Inducing Transmembrane Protein 2 (FITM2) is a gene involved in lipid homeostasis and cytoskeletal organization; however, its role in regulating tumor biological behavior has not been evaluated.In this study, immunohistochemistry was performed to evaluate the expression of FITM2 in HCC. Univariate and multivariate analysis was performed to identify the prognostic factors. RNA interference wound healing and transwell experiments were performed to analyze the biological role of FITM2. Western blot analysis was performed to investigate the potential downstream signaling.The results revealed that FITM2 was highly expressed in the intratumoral tissues of HCC. Expression of intratumoral FITM2 was associated with microvascular invasion. FITM2 is an independent risk factor of HCC disease-free survival and overall survival. In vitro studies revealed that knockdown of FITM2 significantly inhibited the migration ability of HCC cells. FITM2 promotes HCC cell migration by regulating the expression of caveolin-1 and promoting the formation of caveolae. These results indicate that high intratumoral expression of FITM2 is associated with poor HCC prognosis, which may be applied to develop a new adjuvant therapy.

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

Objective: To investigate the effects of hemoperfusion combined with hemodialysis on target organ damage in patients with acute paraquat poisoning. Methods: A total of 42 patients with acute paraquat poisoning who were admitted and treated in our hospital between December 2013 and October 2017 were selected as the research subjects, and their therapies were reviewed and used to divide them into the control group (n=20) who received hemoperfusion alone and the combined treatment group (n=22) who received hemoperfusion combined with hemodialysis. The differences in the levels of liver and kidney function indexes in peripheral blood as well as lung function indexes in arterial blood were compared between the two groups of patients immediately after admission, after 1 d of treatment and after 3 d of treatment. Results: Immediately after admission, the differences in the levels of liver and kidney function indexes in peripheral blood as well as lung function indexes in arterial blood were not statistically significant between the two groups. After 1d of treatment and after 3 d of treatment, kidney function indexes Scr, BUN and β2-MG levels in peripheral blood of combined treatment group were lower than those of control group at corresponding time points respectively; liver function indexes ALT, AST, TB and ALP levels in peripheral blood were lower than those of control group at corresponding time points respectively; lung function indexes PaO2, BE and PCO3- levels in arterial blood were higher than those of control group at corresponding time points respectively whereas PaCO2 levels were lower than those of control group at corresponding time points respectively. Conclusion: Compared with hemoperfusion alone, hemoperfusion combined with hemodialysis is more advantageous in protecting the functions of liver, kidney, lungs and other target organs of patients with acute paraquat poisoning.

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.

// 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

MicroRNAs (miRNAs) are reported as vital participators in the pathophysiological course of neuropathic pain. However, the underlying mechanisms of the functional roles of miRNAs in neuropathic pain are largely unknown. This study was designed to explore the potential role of miR-150 in regulating the process of neuropathic pain in a rat model established by chronic sciatic nerve injury (CCI). Overexpression of miR-150 greatly alleviated neuropathic pain development and reduced inflammatory cytokine expression, including COX-2, interleukin IL-6, and tumor necrosis factor (TNF)-α in CCI rats. By bioinformatic analysis, 3'-untranslated region (UTR) of Toll-like receptor (TLR5) was predicted to be a target of miR-150. TLR5 commonly serves as an important regulator of inflammation. Overexpression of miR-150 significantly suppressed the expression of TLR5 in vitro and in vivo. Furthermore, upregulation of TLR5 decreased the miR-150 expression and downregulation of TLR5 increased miR-150, respectively. Overexpression of TLR5 significantly reversed the miR-150-induced suppressive effects on neuropathic pain. In conclusion, our current study indicates that miR-150 may inhibit neuropathic pain development of CCI rats through inhibiting TLR5-mediated neuroinflammation. Our findings suggest that miR-150 may provide a novel therapeutic target for neuropathic pain treatment.

The efficacy of combined vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR) inhibition in patients with advanced non-small-cell lung cancer (NSCLC) was well studied. However, few studies focused on the risk and adverse events (AEs) of combined targeted therapy. The aim of this meta-analysis was to evaluate the safety profile of combined targeted therapy against EFGR and VEGF in patients with advanced NSCLC. A comprehensive literature search in MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL), ASCO Abstracts and ESMO Abstracts was conducted. Eligible studies were randomized clinical trials (RCTs) that compared safety profile of combined therapy inhibiting EFGR and VEGF pathways with control groups (placebo, single EGFR or VEGF inhibition therapy, chemotherapy or a combination of them) in patients with advanced NSCLC. The endpoints included treatment discontinuation, treatment-related deaths and AEs. The search identified 15 RCTs involving 6,919 patients. The outcomes showed that three of four pairwise comparisons detected more discontinuation due to AEs in combined targeted therapy, with odds ratio (OR) compared with the control groups ranged from 1.97 to 2.29. Treatment with combined inhibition therapy was associated with several all-grade and grade 3 or 4 AEs (e.g. rash, diarrhea and hypertension). Also, there was a significantly higher incidence of treatment-related deaths in combined inhibition using vandetanib versus single EGFR inhibition therapy (OR = 1.97, 95% CI 1.19-3.28). In conclusion, combined inhibition therapy against EGFR and VEGF in patients with advanced NSCLC was associated with increased toxicity. Increased AEs hinder patient compliance and reduce their quality of life, leading to dose reduction or discontinuation.

CRISPR-Cas9 is an RNA-guided site-specific DNA editing tool which, together with its reprogrammed versions such as nickase Cas9 and dead Cas9, enables quick modeling of desired combinations of cancer-associated genomic and/or epigenetic aberrations simultaneously or sequentially, thus facilitating massive functional interrogations and therapy testing.

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.

A quantitative proteomic analysis of the response to dry needling combined with static stretching treatment was performed in a rat model of active myofascial trigger points (MTrPs). 36 rats were divided into a model group (MG), a stretching group (SG) and a dry needling combined with stretching group (SDG). We performed three biological replicates to compare large-scale differential protein expression between groups by tandem mass tag (TMT) labeling technology based on nanoscale liquid chromatography mass spectrometry analysis (LC&ndash, MS/MS). Hierarchical clustering, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment and protein-protein interaction network analyses were performed for the general characterization of overall enriched proteins. For validation of the results of TMT, the candidate proteins were verified by parallel reaction monitoring (PRM) analysis. 285 differentially expressed proteins between groups were identified and quantified. Tight junction pathway played a dominant role in dry needling combined with static stretching treatment for the rat model of active MTrPs. Three candidate proteins, namely actinin alpha 3, calsequestrin-1 and parvalbumin alpha, were further validated, consistent with the results of LC&ndash, MS/MS. This is the first proteomics-based study to report the therapeutic mechanism underlying dry needling and static stretching treatment for MTrPs. Further functional verification of the potential signaling pathways and the enriched proteins is warranted.

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.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-x03BA;B) 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.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-x03BA;B/DNA binding activities. In addition, ATRA stimulated Scpep1 expression under normoxic and hypoxia condition. Furthermore, TGF-β2 interacted with Scpep1.This study indicated that ATRA may attenuate hypoxia-induced injury in NRK52E cells via inhibiting NF-x03BA;B/VEGF and TGF-β2/VEGF pathway.

CRISPR-Cas9 (clustered regularly interspaced short palindromic repeats-CRISPR associated nuclease 9) systems have emerged as versatile and convenient (epi)genome editing tools and have become an important player in medical genetic research. CRISPR-Cas9 and its variants such as catalytically inactivated Cas9 (dead Cas9, dCas9) and scaffold-incorporating single guide sgRNA (scRNA) have been applied in various genomic screen studies. CRISPR screens enable high-throughput interrogation of gene functions in health and diseases. Compared with conventional RNAi screens, CRISPR screens incur less off-target effects and are more versatile in that they can be used in multiple formats such as knockout, knockdown and activation screens, and can target coding and non-coding regions throughout the genome. This powerful screen platform holds the potential of revolutionising functional genomic studies in the near future. Herein, we introduce the mechanisms of (epi)genome editing mediated by CRISPR-Cas9 and its variants, introduce the procedures and applications of CRISPR screen in functional genomics, compare it with conventional screen tools and at last discuss current challenges and opportunities and propose future directions.

Leukemia cells can acquire a multidrug resistant (MDR) phenotype in response to a wide variety of chemotherapeutic agents including doxorubicin (Dox). In addition to the constitutive expression in the leukemia prior to chemotherapy, a complex phenotype of pleiotropic resistance is presented in the residual or recurrent leukemia. Recent studies showed Dox-induced coexpression of COX2 and MDR1 genes in human leukaemia cells, and whether Dox-induced MDR1 up-regulation in acute leukaemia cells is dependent on COX2-transcriptional activity and thus might be overcome or prevented with COX2-promotor inhibitor quercetin interfering with COX2 expression and activity. This study was purposed to investigate the impacts of quercetin on Dox-induced mRNA expression of MDR1 and COX2 genes in HL-60 leukemia cells.The MDR1 and COX2 mRNA expression in HL-60 cells was detected by RT-PCR; the prostaglandin E2 (PGE2) release was measured by ELISA; the cytotoxicity of Dox was determined by MTT test.The incubation of HL-60 cells with Dox not only up-regulated MDR1 mRNA, but also COX2 mRNA expression, and after co-incubation with quercetin or celecoxib, Dox-induced overexpression of MDR1 and COX2 mRNA were reduced by quercetin, not by celecoxib, whereas PGE2 release was significantly decreased with subsequent enhancement of Dox cytotoxic efficacy by both of them.Dox-induced MDR1 up-regulation may be dependent on COX2-transcriptional activity, not PGE2, suggesting that the existence of causal link between COX2 and MDR1 expression induced by Dox, and modulation of COX2 transcriptional expression by quercetin would not only sensitize leukemia cells to Dox, but also prevent the acquisition of MDR during chemotherapy.

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

The efficacy of combined vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR) inhibition in patients with advanced non-small-cell lung cancer (NSCLC) was well studied. However, few studies focused on the risk and adverse events (AEs) of combined targeted therapy. The aim of this meta-analysis was to evaluate the safety profile of combined targeted therapy against EFGR and VEGF in patients with advanced NSCLC. A comprehensive literature search in MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL), ASCO Abstracts and ESMO Abstracts was conducted. Eligible studies were randomized clinical trials (RCTs) that compared safety profile of combined therapy inhibiting EFGR and VEGF pathways with control groups (placebo, single EGFR or VEGF inhibition therapy, chemotherapy or a combination of them) in patients with advanced NSCLC. The endpoints included treatment discontinuation, treatment-related deaths and AEs. The search identified 15 RCTs involving 6,919 patients. The outcomes showed that three of four pairwise comparisons detected more discontinuation due to AEs in combined targeted therapy, with odds ratio (OR) compared with the control groups ranged from 1.97 to 2.29. Treatment with combined inhibition therapy was associated with several all-grade and grade 3 or 4 AEs (e.g. rash, diarrhea and hypertension). Also, there was a significantly higher incidence of treatment-related deaths in combined inhibition using vandetanib versus single EGFR inhibition therapy (OR = 1.97, 95% CI 1.19-3.28). In conclusion, combined inhibition therapy against EGFR and VEGF in patients with advanced NSCLC was associated with increased toxicity. Increased AEs hinder patient compliance and reduce their quality of life, leading to dose reduction or discontinuation.

Competing endogenous RNAs (ceRNAs) refer to RNA transcripts, such as mRNAs, non-coding RNAs, pseudogene transcripts, and circular RNAs, that can regulate each other by competing for the same pool of miRNAs. ceRNAs involve in the pathogenesis of several common cancers such as prostate cancer, liver cancer, breast cancer, lung cancer, gastric cancer, endometrial cancer, and so on. ceRNA activity is determined by factors such as miRNA/ceRNA abundance, ceRNAs binding affinity to miRNAs, RNA editing, and RNA-binding proteins. The alteration of any of these factors may lead to ceRNA network imbalance and thus contribute to cancer initiation and progression. There are generally three steps in ceRNA research conductions: ceRNA prediction, ceRNA validation, and ceRNA functional investigation. Deciphering ceRNA interplay in cancer provides new insight into cancer pathogenesis and opportunities for therapy exploration. In this review, we try to give readers a concise and reliable illustration on the mechanism, functions, research approaches, and perspective of ceRNA in cancer.

Most cancers develop upon the accumulation of genetic alterations that provoke and sustain the transformed phenotype. Several metabolomic approaches now allow for the global assessment of intermediate metabolites, generating profound insights into the metabolic rewiring associated with malignant transformation. The metabolomic profiling of neoplastic lesions growing in mice, irrespective of their origin, can provide invaluable information on the mechanisms underlying oncogenesis, tumor progression, and response to therapy. Moreover, the metabolomic profiling of tumors growing in mice may result in the identification of novel diagnostic or prognostic biomarkers, which is of great clinical significance. Several methods can be applied to the metabolomic profiling of neoplastic lesions in mice, including mass spectrometry-based techniques (e.g., gas chromatography-, capillary electrophoresis-, or liquid chromatography-coupled mass spectrometry) as well as nuclear magnetic resonance. Here, we compare and discuss the advantages and disadvantages of all these techniques to provide a concise and reliable guide for readers interested in this active area of investigation.

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 …

Most cancers develop upon the accumulation of genetic alterations that provoke and sustain the transformed phenotype. Several metabolomic approaches now allow for the global assessment of intermediate metabolites, generating profound insights into the metabolic rewiring associated with malignant transformation. The metabolomic profiling of neoplastic lesions growing in mice, irrespective of their origin, can provide invaluable information on the mechanisms underlying oncogenesis, tumor progression, and response to therapy. Moreover, the metabolomic profiling of tumors growing in mice may result in the identification of novel diagnostic or prognostic biomarkers, which is of great clinical significance. Several methods can be applied to the metabolomic profiling of neoplastic lesions in mice, including mass spectrometry-based techniques (e.g., gas chromatography-, capillary electrophoresis-, or liquid chromatography-coupled mass spectrometry) as well as nuclear magnetic resonance. Here, we compare and discuss the advantages and disadvantages of all these techniques to provide a concise and reliable guide for readers interested in this active area of investigation.

Background: A prospective randomized controlled trial was designed to observe the effect of tramadol on T-lymphocyte subsets, activated T cell and natural killer (NK) cells of patients undergoing gastric cancer surgeries. Subjects and Methods: Thirty patients undergoing elective gastric cancer surgeries under general anesthesia were randomly divided into two groups. Before anesthesia induction, Group I did not receive any drugs and Group II received intramuscular tramadol 1 mg/kg. Peripheral venous blood samples were taken before anesthesia, 1 h after incision and postoperation. CD3+, CD3+ CD4+, CD3+ CD8+, CD3–CD16+ CD56+ (NK) cells and CD3+ human leukocyte antigen (HLA)-DR+ (activated T cell) were measured by flow cytometer. Results: One hour after incision, CD3+, CD3+ CD4+, CD3+ CD4+/CD3+ CD8+, CD3-CD16+ CD56+, and CD3+ HLA-DR+ cells in the experimental and control group were significantly decreased compared with their baselines (P < 0.05), while the values of Group I were lower than those of Group II (P < 0.05). After surgery, the values of Group I were lower than their baselines (P < 0.05). But the values of Group II had no significant difference compared with their baselines. Conclusion: Tramadol can reduce the decrease of T-lymphocytes subsets and NK cells, thus improve the cellular immune function in the perioperation of gastric cancer.