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Herpes zoster (HZ) is a localized, painful cutaneous eruption that occurs upon reactivation of the herpes virus. Postherpetic neuralgia (PHN) is the most common chronic complication of HZ. In this study, we examined the metabolomic and proteomic signatures of disease progression in patients with HZ and PHN. We identified differentially expressed metabolites (DEMs), differentially expressed proteins (DEPs), and key signaling pathways that transition from healthy volunteers to the acute or/and chronic phases of herpetic neuralgia. Moreover, some specific metabolites correlated with pain scores, disease duration, age, and pain in sex dimorphism. In addition, we developed and validated three optimal predictive models (AUC > 0.9) for classifying HZ and PHN from healthy individuals based on metabolic patterns and machine learning. These findings may reveal the overall metabolomics and proteomics landscapes and proposed the optimal machine learning predictive models, which provide insights into the mechanisms of HZ and PHN.

Background: Previous observational studies have suggested the involvement of 25-hydroxyvitamin D [25(OH)D] in chronic pain. However, whether the 25(OH)D is a novel target for management, the causality remains unclear.Methods: A two-sample Mendelian randomization (MR) study was conducted to identify the causal association between 25(OH)D and low back pain (LBP). The primary analysis was revealing causality from serum 25(OH)D level (n = 417,580) on LBP (21,140 cases and 227,388 controls). The replicated analysis was performing MR estimates from circulating 25(OH)D concentration (n = 79,366) on LBP experienced last month (118,471 cases and 343,386 controls). Inverse variance weighted (IVW) was used as the main analysis. In addition, we used weighted median and MR-Egger to enhance the robustness. Sensitivity analysis was conducted to evaluate the robustness of MR results.Results: IVW estimation indicated strong evidence that higher serum 25(OH)D levels exerted a protective effect on LBP (OR = 0.89, 95% CI = 0.83–0.96, p = 0.002). Similar trends were also found in replicate analysis (OR = 0.98, 95% CI = 0.96–1.00, p = 0.07). After meta-analysis combining primary and replicated analysis, the causal effect is significant (p = 0.03). Sensitivity analysis supported that the MR estimates were robust.Conclusion: In our MR study, genetically increased serum 25(OH)D levels were associated with a reduced risk of LBP in the European population. This might have an implication for clinicians that vitamin D supplements might be effective for patients with LBP in clinical practice.

Chronic pain remains to be a clinical challenge and is recognized as a major health problem with varying impacts on quality of life. Currently, the first-line therapy for chronic pain is opioids, which are often accompanied by unwanted psychoactive side effects. Thus, new and effective treatments for chronic pain are urgently needed and eagerly pursued. Inflammatory cytokines, especially interleukin-17 (IL-17), are reportedly potential therapeutic targets owing to their pivotal role in chronic pain from the neuroinflammation perspective. Recently, substantial evidence confirmed that IL-17 and IL-17 receptors (IL-17Rs) were increased in neuropathic, inflammatory, and cancer pain models. Notably, IL-17/IL-17R antibodies also reportedly relieve or cure inflammatory- and pain-related diseases. However, existing studies have reported controversial results regarding IL-17/IL-17Rs as potential therapeutic targets in diverse animal models of chronic pain. In this review, we present a summary of published studies and discuss the evidence, from basic to clinical to research, regarding the role and mechanism of action between IL-17 and diverse kinds of chronic pain in animal models and clinical patients. Furthermore, we evaluated IL-17-based therapy as a potential therapeutic strategy for inflammatory- and pain-related disease. Importantly, we also discussed clinical trials of IL-17/IL-17R targeting monoclonal antibodies. Overall, we found that IL-17 is a potential therapeutic target for chronic pain from the perspective of neuroinflammation.

BRAF inhibitors (BRAFi) that target BRAF V600E kinase, a driver mutation found in 50% of melanomas, show a significant antitumor response, but the common emergence of acquired resistance remains a challenge. Abnormal expression of RAF isoforms CRAF and ARAF reactivates pERK1/2, which plays crucial roles in the acquisition of resistance of melanoma cells. However, the mechanisms of dysregulation of RAF isoforms in resistant melanoma cells remain unknown. Here, we identified NONO interacted with and stabilized both CRAF and ARAF in melanoma cells, and that NONO was acetylated at 198K by p300 acetyltransferase, which stabilized NONO via antagonizing its ubiquitination/degradation mediated by RNF8. The upregulation of both p300 and NONO promoted the rebound of pERK1/2 and the subsequent resistance of melanoma cells to BRAFi, and the activation of ERK1/2 in turn induced p300 to form a positive feedback loop in resistant melanoma cells. There was a positive correlation between p300 and NONO in resistant melanoma cells and clinical samples, and p300 inhibitor C646 overcame the resistance of resistant melanoma cells to BRAF inhibitors in vitro and in vivo. Our findings reveal that targeting the positive feedback loop of p300-NONO-CRAF/ARAF-pERK1/2 may be excellent strategies to overcome the resistance of BRAF inhibitors for melanoma patients.

IntroductionA patient record review study conducted in 2006 in a random sample of 21 Dutch hospitals found that 51%–77% of adverse events are related to perioperative care, while Centers for Disease Control and Prevention data in USA in 2013 estimated that the medical error is the third-leading cause of mortality. To capitalise on the potential of apps to enhance perioperative medical quality, there is a need for interventions developed in consultation with real-world users designed to support integrated management for perioperative adverse events (PAEs). This study aims: (1) to access the knowledge, attitude and practices for PAEs among physicians, nurses and administrators, and to identify the needs of healthcare providers for a mobile-based PAEs tool; (2) to develop a data-driven app for integrated PAE management that meets those needs and (3) to test the usability, clinical efficacy and cost-effectiveness of the developed app.Methods and analysisWe will adopt an embedded mixed-methods research technique; qualitative data will be used to assess user needs and app adoption, while quantitative data will provide crucial insights to establish the demand for the app, and measure the app effects. Phase 1 will enrol surgery-related healthcare providers from the West China Hospital and identify their latent demand for mobile-based PAEs management using a self-designed questionnaire underpinned by the knowledge, attitude and practice model, as well as expert interviews. In phase 2, we will develop the app for integrated PAE management and test its effectiveness and sustainability. In phase 3, the effects on the total number and severity of reported PAEs will be evaluated using Poisson regression with interrupted time-series analysis over a 2-year period, while users’ engagement, adherence, process evaluation and cost-effectiveness will be evaluated using quarterly surveys and interviews.Ethics and disseminationThe West China Hospital of Sichuan University’s Institutional Review Board authorised this study after approving the study protocol, permission forms and questionnaires (number: 2022-1364). Participants will be provided with study information, and informed written consent will be obtained. Study findings will be disseminated through peer-reviewed publications and conference presentations.

Chemotherapy-induced peripheral neuropathy (CIPN) is among the most disabling and frustrating problems for cancer survivors. The neurotoxicity caused by cisplatin varies greatly among patients, and few predictors of appearance, duration of symptoms, susceptibility, or severity are available. A deeper understanding of the mechanisms underlying individual differences in status, severity, or sensitivity in response to cisplatin treatment is therefore required. By analyzing the GSE64174 gene expression profile and constructing a weighted gene co-expression network analysis (WGCNA) network, we screened gene modules and hub genes related to CIPN status, severity and sensitivity. We first identified the transcriptome profile of mouse dorsal root ganglion (DRG) samples and transformed their genes to human DRG counterparts. We then constructed WGCNA gene modules via optimal soft-threshold power-identification and module-preservation analysis. Comprehensive analysis and identification of module hub genes were performed via functional-enrichment analysis and significant common hub genes were identified, including "Cytoscape_cytoHubba," "Cytoscape_MCODE," and "Metascape_MCODE." Brown, green, and blue modules were selected to represent CIPN sensitivity, status, and severity, respectively, via trait-module correlational analysis. Additionally, functional enrichment analysis results indicated that these three modules were associated with some crucial biological functions, such as neutrophil migration, chemokine-mediated signaling pathway, and PI3K-Akt signaling pathway. We then identified seven common hub genes via three methods, including CXCL10, CCL21, CCR2, CXCR4, TLR4, NPY1R, and GALR2, related to CIPN status, severity and sensitivity. Our results provide possible targets and mechanism insights into the development and progress of CIPN, which can guide further transformation and pre-clinical research.

Introduction Breast cancer metastasis suppressor 1 like (BRMS1-like)was first reported to be a component of the Sin3-HDAC complex, but the role in the progression of cancers was largely unknown. Our previous study reported that BRMS1L promoted the metastasis of breast cancer through facilitating the recruitment of HDAC complex to the promoter FZD10, and hence suppressing the transcription of FZD10. Methods In this study, we detected the expression level of BRMS1L in esophageal squamous cell carcinoma (ESCC). The effect of BRMS1L in TE-1D (knockdown) and ECA-109 (overexpression) cell lines was explored by transwell assays, wound healing assays, and cell adhesion assays. Quantitative real‑time PCR, Western blot analysis, and luciferase assays were used to detect the interaction of the CBP/P300-BRMS1L-ITGA7 axis. Results In the present study, we found that knockdown of BRMS1L promoted the migration, invasion, and epithelial-mesenchymal transition (EMT). Conversely, overexpression of BRMS1L inhibited the migration and invasion of ESCC. Mechanistically, BRMS1L exerted their metastasis-suppressing role via transcriptionally repress ITGA7 expression. Moreover, we revealed that CBP/p 300 regulated the expression of BRMS1L and might be responsible for the down-regulation of BRMS1L in ESCC. Conclusion Collectively, we identified the role of CBP/p300-BRMS1L-ITGA7 axis in the metastasis of ESCC.

Background: WT161 is a recently discovered histone deacetylase 6 (HDAC6) inhibitor which shows anti-tumor effects on multiple myelomas and breast cancer. However, the role of WT161 in retinoblastoma remains unclear. The aim of this study is to explore the role of WT161 in retinoblastoma and its underlying mechanisms. Methods: The anti-proliferation of WT161 on retinoblastoma cells was examined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and soft agar colony formation assay. Cell apoptosis was analyzed using flow cytometer. WT161 and DDP synergistic effect was evaluated by isobologram analysis using CompuSyn software. Results: WT161 suppressed the cell growth and induced apoptosis of retinoblastoma cells in a dose- and time-dependent manner. Mechanistically, WT161 increases the transcription of Bad through activating Bad promoter. Chromatin immunoprecipitation (ChIP) assay showed WT161 treatment increased acetylated histone H3 (AcH3) and acetylated histone H4 (AcH4) on the Bad promoter in retinoblastoma cells. In addition, WT161 shows synergistically inhibitory effects on retinoblastoma cell combined with cisplatin. Conclusions: These results indicate that WT161, as a selective HDAC6 inhibitor, is a promising agent against retinoblastoma.

Retinoblastoma (RB) is the most common type of intraocular malignant tumor that occurs in childhood. AR-42, a member of a newly discovered class of phenylbutyrate-derived histone deacetylase inhibitors, exerts antitumor effects on many cancers. In the present study, we initially evaluated the effect of AR-42 towards RB cells and explored the underlying mechanism in this disease. Our results found that AR-42 showed powerful antitumor effects at low micromolar concentrations by inhibiting cell viability, blocking cell cycle, stimulating apoptosis in vitro, and suppressing RB growth in a mouse subcutaneous tumor xenograft model. Furthermore, the AKT/nuclear factor-kappa B signaling pathway was disrupted in Y79 cells treated with AR-42. In conclusion, we propose that AR-42 might be a promising drug treatment for RB.

A giant retrosternal goiter can lead to compression of vital organs in the mediastinum with high risk of acute cardiorespiratory decompensation. Additionally, patients with acromegaly are prone to developing severe airway obstruction and ventilation difficulties during anesthetic induction, leading to hypoxia and an increased partial pressure of carbon dioxide. Therefore, more comprehensive airway management strategies are needed. We herein describe a 57-year-old man with acromegaly and severe tracheal obstruction caused by a giant retrosternal goiter. He presented with a 1-week history of progressive dyspnea and was scheduled to undergo right lobe thyroidectomy and retrosternal goiter thyroidectomy. We created a comprehensive emergency plan for a difficult airway, including regional and topical anesthesia for awake endotracheal intubation, sevoflurane inhalation, small doses of midazolam and sufentanil to increase tolerance, self-made extended-length tracheostomy, video laryngoscope-assisted fiber-optic bronchoscopy, extracorporeal membrane oxygenation, and surgical tracheostomy. Importantly, tetracaine was inhaled through an atomizer, and a laryngotracheal topical anesthesia applicator was used to spray the larynx with 1% tetracaine to reduce stimulation during intubation. The giant goiter was successfully removed through the cervical approach. A carefully designed airway management strategy and close communication among a multidisciplinary operation team are the basis of perioperative anesthetic management for these patients.

BRAF inhibitors (BRAFi) that target BRAF V600E kinase, a driver mutation found in 50% of melanomas, show a significant antitumor response, but the common emergence of acquired resistance remains a challenge. Abnormal expression of RAF isoforms CRAF and ARAF reactivates pERK1/2, which plays crucial roles in the acquisition of resistance of melanoma cells. However, the mechanisms of dysregulation of RAF isoforms in resistant melanoma cells remain unknown. Here, we identified NONO interacted with and stabilized both CRAF and ARAF in melanoma cells, and that NONO was acetylated at 198K by p300 acetyltransferase, which stabilized NONO via antagonizing its ubiquitination/degradation mediated by RNF8. The upregulation of both p300 and NONO promoted the rebound of pERK1/2 and the subsequent resistance of melanoma cells to BRAFi, and the activation of ERK1/2 in turn induced p300 to form a positive feedback loop in resistant melanoma cells. There was a positive correlation between p300 and NONO in resistant melanoma cells and clinical samples, and p300 inhibitor C646 overcame the resistance of resistant melanoma cells to BRAF inhibitors in vitro and in vivo. Our findings reveal that targeting the positive feedback loop of p300-NONO-CRAF/ARAF-pERK1/2 may be excellent strategies to overcome the resistance of BRAF inhibitors for melanoma patients.

Aim: To develop an oxidative phosphorylation (OXPHOS)-related gene signature of lung adenocarcinoma (LUAD). Materials & methods: We split The Cancer Genome Atlas LUAD cohort into a training set and a test set; we used the least absolute shrinkage and selection operator Cox method to structure the OXPHOS-related prognostic signature in the training set and verified in the test set and GSE30219 dataset. Meanwhile, the diagnostic model was constructed using the logistic Cox method. Results: The signature consisted of seven genes ( LDHA, CFTR, HSPD1, SNHG3, MAP1LC3C, COX6B2, and TWIST1). LUAD patients were divided into high- and low-risk groups, demonstrating good diagnostic and prognostic capabilities. Conclusion: We developed the first-ever OXPHOS-related signature with both prognostic predictive power and diagnostic efficacy.

During the COVID-19 pandemic, ensuring the gradual recovery of anesthesia nursing unit and avoiding cross-infection between surgical patients and staff are difficult problems for hospital managers. We outlined the emergency response measures and the transition to normal operation of the anesthesia nursing unit in West China Hospital, which is a large teaching hospital. This mainly included hospital and operating room channel management, three-level screening management of patients and medical staff, classification management of patients undergoing anesthesia and recovery, training management of medical personnel, strict environmental management, and online teaching management.

Aim: This study aimed to explore the genetic and epigenetic similarities between chronic obstructive pulmonary disease (COPD) and lung adenocarcinoma (LUAD). Materials & methods: We mainly used Weighted correlation network analysis, protein–protein interaction network and pivot analysis to identify hub modules, bridge regulators, bridge genes and hub-driving genes in both diseases and carried out verifying using external datasets. Results: We identified eight bridge regulators, 19 key molecules in the COPD model and ten key molecules in the LUAD model. Moreover, we validated that CDC5L could be a reliable biomarker in COPD and may regulate cell proliferation and metastasis in LUAD via promoter methylation. Conclusion: Our results might form a theoretical foundation for future study at an epigenetic level.

Recent mounting studies showed that neuroinflammation caused by surgery or anesthesia is closely related to postoperative cognitive dysfunction (POCD). This study investigated the effect of mineralocorticoid receptor (MR) on neuroinflammation and POCD. To detect the MR effect in an animal model, we randomly divided rats into control, anesthesia, and surgery groups. To determine whether the MR-specific blocker eplerenone (EPL) could improve cognitive dysfunction, we assigned other animals into the control, surgery and EPL treatment, and surgery groups. Cognitive function was detected using the Morris water maze. Serum cytokine levels were measured by ELISA, and the histopathological changes of hippocampal neurons were identified by hematoxylin/eosin and Nissl staining. Our research confirmed that anesthesia and surgical stimulation could lead to IL-1β, IL-6, and TNF-α activation and hippocampal neuronal degeneration and pathological damage. MR was upregulated in the hippocampus under cognitive impairment condition. Additionally, EPL could alleviate inflammatory activation and neuronal damage by exerting neuroprotective effects. The preclinical model of sevoflurane anesthesia/splenectomy implied that MR expression is upregulated by regulating the neuroinflammation in the brain under POCD condition. Manipulating the MR expression by EPL could improve the inflammation activation and neuronal damage.

Background: Postherpetic neuralgia (PHN) is one of the most common types of chronic neuropathic pain, which seriously affects quality of the life because of pain severity and poor response to the currently available treatments. The main strategies for PHN management are medication and invasive interventional therapies; however, these approaches have many adverse effects, so it is important to find another effective and safe treatment for PHN. Methods: A single-center, single-blind randomized clinical trial will evaluate 98 study participants randomized in a 1:1 ratio into control and experimental groups. The control group will receive conventional treatment including medication therapy and invasive interventional therapy. The experimental group will be receive extracorporeal shockwave therapy (ESWT) in addition to conventional therapy. The primary outcome is pain intensity assessed on a visual analogue scale (VAS); the secondary outcomes are the following: quality of life assessed by the 36-Item Short-Form Health Survey (SF-36); psychological state for anxiety and depression measured by the Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS); and sleep quality measured by the Pittsburgh Sleep Quality Index (PSQI). Assessors blinded to the randomization will collect data during the intervention period at baseline and weeks 1, 4, and 12. The plasma levels of tumor necrosis factor-α and interleukin 6 will be assessed before and after ESWT to explore the biochemical mechanisms of ESWT in the treatment of PHN. Discussion: This randomized controlled trial will evaluate the effectiveness and safety of ESWT in patients with PHN, and thus will provide clinical evidence for its use in the management of PHN and explore the potential biochemical mechanisms of this treatment. Trial registration: www.ChiCTR.org.cn, identifier: ChiCTR1900025828. Registered on 10th September 2019

Background Postherpetic neuralgia (PHN) is one of the most common types of chronic neuropathic pain, which seriously affects quality of the life because of pain severity and poor response to the currently available treatments. The main strategies for PHN management are medication and invasive interventional therapies; however, these approaches have many adverse effects, so it is important to find another effective and safe treatment for PHN. Methods A single-center, single-blind randomized clinical trial will evaluate 98 study participants randomized in a 1:1 ratio into control and experimental groups. The control group will receive conventional treatment including medication therapy and invasive interventional therapy. The experimental group will receive extracorporeal shockwave therapy (ESWT) in addition to conventional therapy. The primary outcome is pain intensity assessed on a visual analogue scale (VAS); the secondary outcomes are the following: quality of life assessed by the 36-Item Short-Form Health Survey (SF-36), psychological state for anxiety and depression measured by the Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS), and sleep quality measured by the Pittsburgh Sleep Quality Index (PSQI). Assessors blinded to the randomization will collect data during the intervention period at baseline and weeks 1, 4, and 12. The plasma levels of tumor necrosis factor-α and interleukin-6 will be assessed before and after ESWT to explore the biochemical mechanisms of ESWT in the treatment of PHN. Discussion This randomized controlled trial will evaluate the effectiveness and safety of ESWT in patients with PHN and thus will provide clinical evidence for its use in the management of PHN and explore the potential biochemical mechanisms of this treatment. Trial registration www.ChiCTR.org.cn, identifier: ChiCTR1900025828. Registered on 10 September 2019

Additional file 1 Standard Protocol Items: Recommendations for Interventional Trials (SPIRIT) Checklist for the protocol of a clinical trial.

BACKGROUND The long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) is expressed in solid malignant tumors. The aim of this systematic review and meta-analysis was to determine whether expression of the lncRNA SNHG1 was associated with prognosis in patients with malignancy. MATERIAL AND METHODS A literature review from Jan 1970 to July 2018 identified publications in the English language. Databases searched included: PubMed, OVID, Web of Science, the Cochrane Database, Embase, EBSCO, Google Scholar. Systematic review and meta-analysis were performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The Newcastle-Ottawa Scale (NOS) assessment tool for risk of bias was used. RESULTS Eight publications (570 patients) and eight solid tumors were identified, including osteosarcoma, colorectal cancer, hepatocellular carcinoma, non-small cell lung cancer, esophageal cancer, ovarian cancer, glioma, and gastric cancer. Meta-analysis showed that expression of the lncRNA SNHG1 was significantly correlated with reduced overall survival (OS) (HR=1.917; 95% CI, 1.58-2.31) (P

Introduction Breast cancer metastasis suppressor 1 like (BRMS1-like)was first reported to be a component of the Sin3-HDAC complex, but the role in the progression of cancers was largely unknown. Our previous study reported that BRMS1L promoted the metastasis of breast cancer through facilitating the recruitment of HDAC complex to the promoter FZD10, and hence suppressing the transcription of FZD10. Methods In this study, we detected the expression level of BRMS1L in esophageal squamous cell carcinoma (ESCC). The effect of BRMS1L in TE-1D (knockdown) and ECA-109 (overexpression) cell lines was explored by transwell assays, wound healing assays, and cell adhesion assays. Quantitative real‑time PCR, Western blot analysis, and luciferase assays were used to detect the interaction of the CBP/P300-BRMS1L-ITGA7 axis. Results In the present study, we found that knockdown of BRMS1L promoted the migration, invasion, and epithelial–mesenchymal transition (EMT). Conversely, overexpression of BRMS1L inhibited the migration and invasion of ESCC. Mechanistically, BRMS1L exerted their metastasis-suppressing role via transcriptionally repress ITGA7 expression. Moreover, we revealed that CBP/p 300 regulated the expression of BRMS1L and might be responsible for the down-regulation of BRMS1L in ESCC. Conclusion Collectively, we identified the role of CBP/p300-BRMS1L-ITGA7 axis in the metastasis of ESCC.

Mesenchymal stem cells (MSCs) have the ability to differentiate into multiple cell types, including osteogenic, chondrogenic and adipogenic lineages. Osteogenic differentiation of MSCs plays a critical role in bone tissue engineering. Inducing MSC osteogenesis represents a potential treatment that promotes bone formation and bone regeneration. Recently, long non-coding RNA (lncRNA) was shown to participate in the occurrence and development of various diseases. Different lncRNA expression patterns can regulate the cell cycle, proliferation, metastasis, immunobiology and differentiation. With the recent extensive study of lncRNAs, an increasing number of lncRNAs are being studied in the MSC field. Furthermore, some lncRNAs have been confirmed to regulate MSC osteogenesis. Therefore, here, we review research concerning lncRNA in osteogenic differentiation of MSCs and highlight the importance of lncRNA in bone formation and bone regeneration.

AR-42 is a member of a novelly discovered class of phenylbutyrate-derived histone deacetylase inhibitors, and has a number of antitumor effects in a variety of tumor types; however, the role of AR-42 and its possible mechanisms have not been reported in the treatment of breast cancer. The aim of the present study was to investigate the antitumor effects of AR-42 and its associated mechanisms in breast cancer. MTT assays and colony formation assays were conducted to measure the proliferation of MCF-7 cells, and flow cytometry was used to analyze cell apoptosis. The results revealed that AR-42 induced cell apoptosis and suppressed cell growth in a dose- and time-dependent manner. Mechanistically, AR-42 treatment increased the acetylation of the p53 protein and prolonged the half-life of the p53 protein; furthermore, AR-42 treatment upregulated p21 and PUMA expression. Notably, AR-42 had a synergistic effect on MCF-7 cells in combination with fluorouracil, which is one of the most commonly used chemotherapeutic agents. In conclusion, the results indicated that AR-42 inhibits breast cancer cell proliferation and induces apoptosis, indicating that AR-42 is a potential therapeutic agent.

Timeline. A timeline of the important discoveries in exosome research, focusing on the breakthroughs in exosomal RNA research. (PPTX 90 kb)

Exosomal RNA articles published per year. Graph showing the number of articles published relating to exosome-derived RNA per year since 2007. (DOCX 58 kb)