Suppression of lncRNA HOTAIR alleviates RCC angiogenesis through regulating miR-126/EGFL7 axis.

Renal cell carcinoma (RCC) has the highest mortality rate among urological cancers and tumor angiogenesis that plays a critical role in RCC progress. Epidermal growth factor-like domain multiple 7 (EGFL7) has been recently identified as a regulator in RCC tumor angiogenesis and progression. Long noncoding RNA (LncRNA) HOTAIR has been considered as a pro-oncogene in multiple cancers, but its precise mechanism of tumor angiogenesis has rarely been reported. MicroRNA-126 (miR-126) functions as a tumor suppressor in RCC. However, the underlying tumor angiogenesis mechanism of HOTAIR/miR-126 axis in RCC has not been studied. The proliferation, migration, angiogenesis, and expression of EGFL7 and related proteins in extracellular signal-regulated kinase (ERK)/activators of transcription 3 (STAT3) signal pathway were determined to examine the effect and mechanism of HOTAIR and miR-126 on RCC progress. The regulatory relationship of HOTAIR and miR-126, as well as miR-126 and EGFL7 were tested using dual-luciferase reporter assay. Aenograft RCC mice model was used to examine the effect of HOTAIR on RCC tumor growth and metastasis in vivo. HOTAIR knockdown and miR-126 overexpression suppressed the proliferation, migration, and angiogenesis of RCC cells. HOTAIR regulated EGFL7 expression by competitively binding to miR-126. Knockdown of HOTAIR significantly suppressed the RCC tumor progression and lung metastasis in vivo. These findings suggest that lncRNA HOTAIR regulate RCC angiogenesis through miR-126/EGFL7 axis and provide a new perspective on the molecular pathways of angiogenesis in RCC development, which might be potential therapeutic targets for RCC treatment.

Fabrication and characterization of SiC/Ge/graphene heterojunction with Ge micro-nano structures.

To widen the detection wavelength range and improve the detection sensitivity of SiC-based optoelectronic devices, the SiC/Ge/graphene heterojunction was fabricated by using wet transfer of the graphene following chemical vapor deposition. The Ge films on 4H-SiC(0001) have polycrystalline structure with nano-wire (NWs) and submicron spherical island (SIs) features. Due to the distinct light trapping effect of the Ge NWs, the SiC/GeNWs/graphene heterojunction has an absorbance of more than 90% in the 500-1600 nm range, which is higher than the SiC/GeSIs/graphene heterojunction. And the SiC/GeNWs/graphene heterojunction photodetector exhibits rectification ratio up to 25 at ±2 V and stable photoresponse to the NIR light at zero voltage bias.

Identification of potential crucial genes and key pathways in osteosarcoma.

BACKGROUND: The aim of this study is to identify the potential pathogenic and metastasis-related differentially expressed genes (DEGs) in osteosarcoma through bioinformatic analysis of Gene Expression Omnibus (GEO) database. RESULTS: Gene expression profiles of GSE14359, GSE16088, and GSE33383, in total 112 osteosarcoma tissue samples and 7 osteoblasts, were analyzed. Seventy-four normal-primary DEGs (NPDEGs) and 764 primary-metastatic DEGs (PMDEGs) were screened. VAMP8, A2M, HLA-DRA, SPARCL1, HLA-DQA1, APOC1 and AQP1 were identified continuously upregulating during the oncogenesis and metastasis of osteosarcoma. The enriched functions and pathways of NPDEGs include procession and presentation of antigens, activation of MHC class II receptors and phagocytosis. The enriched functions and pathways of PMDEGs include mitotic nuclear division, cell adhesion molecules (CAMs) and focal adhesion. With protein-protein interaction (PPI) network analyzed by Molecular Complex Detection (MCODE) plug-in of Cytoscape software, one hub NPDEG (HLA-DRA) and 7 hub PMDEGs (CDK1, CDK20, CCNB1, MTIF2, MRPS7, VEGFA and EGF) were eventually selected, and the most significant pathways in NPDEGs module and PMDEGs module were enriched in the procession and presentation of exogenous peptide antigen via MHC class II and the nuclear division, respectively. CONCLUSIONS: By integrated bioinformatic analysis, numerous DEGs related to osteosarcoma were screened, and the hub DEGs identified in this study are possibly part of the potential biomarkers for osteosarcoma. However, further experimental studies are still necessary to elucidate the biological function and mechanism of these genes.

Chemoradiation phase II trials: re-exploring a world of missed opportunities.

Background: Phase II trials are designed to assess the efficacy/toxicity ratio of experimental treatments and select those worth being tested in phase III trials. Although crucial limitations were identified when concurrent chemoradiation (cCRT) phase III trials characteristics were assessed, features of cCRT phase II trials have never been reported. The objective was to describe features of all cCRT phase II trials. Methods and material: Requests were performed in the Medline database (via PubMed). The latest update was performed in April 2016, using the following MESH terms: 'clinical trials: phase II as topic', 'chemoradiotherapy'. Results: Four hundred and fifty-eight cCRT phase II trials were identified. They were mainly multicenter (51.5%), single arm studies (77.7%) published after 2011 (55.0%). The median number of included patients was 52. Primary endpoints were mainly response rate (20.5%), pathological complete response (14.4%) and overall survival (12.6%). The primary endpoint was not defined in 22% of studies. Tumors were mostly lung (23.1%), head and neck (20.3%), colorectal (16.6%) and esophagogastric cancer (14.6%) treated at a locally advanced setting (81.7%). 55.2% of trials used 3D-conformal radiotherapy and 9.1% intensity-modulated radiotherapy, mainly with normo-fractionation (82.0% of the 573 arms with radiotherapy). Radiation technique was not reported in 19.9% of studies. Associated anticancer drugs (563 arms) were mainly conventional chemotherapies (559 arms): cisplatin (46.2%) and 5-fluorouracil (28.3%). Non cytotoxic agents (targeted therapies, immunotherapies) were tested in 97 arms (17%). With a median follow-up of 31 months, acute grades 3-5 were reported in 98.5% of studies and late toxicities in 44.5%. Follow-up was not reported in 17% of studies. Conclusions: cCRT phase II trials featured severe limitations, with outdated radiation techniques, insufficient reporting of crucial data and a small number of included patients. This certainly limited the impact of conclusions and hindered the development of successful phase III trials.

LINC00470 Coordinates the Epigenetic Regulation of ELFN2 to Distract GBM Cell Autophagy.

The epigenetics and genomics of glioblastoma (GBM) are complicated. Previous reports indicate that ELFN2 is widely distributed in the cerebral cortex neurons, striatum, and hippocampus cone and in granular cells. However, the function and mechanism of ELFN2, particularly in GBM, have rarely been explored. In this study, we identified ELFN2 as a new hypomethylation gene that acts as an oncogene in GBM. ELFN2 promoted cell autophagy by interacting with AurkA and eIF2α and inhibiting the activation of AurkA. We also demonstrated that aberrantly high ELFN2 expression is obtained due to hypomethylation of its promoter and abnormal miR-101 and LINC00470 expression in GBM. LINC00470 not only enhanced the expression of ELFN2 through adsorption of miR-101 but also affected the methylation level of ELFN2 by decreasing H3K27me3 occupancy. In addition, LINC00470 played a dominant role in the regulation of GBM cell autophagy, even though it upregulated ELFN2 expression. The results indicate that the combination of LINC00470 and ELFN2 has important significance for evaluating the prognosis of astrocytoma patients.

Liver X receptors agonists suppress NLRP3 inflammasome activation.

Inflammasomes are multiprotein complexes that control the production of IL-1ß and IL-18. NLRP3 inflammasome, the most characterized inflammasome, plays prominent roles in defense against infection, however aberrant activation is deleterious and leads to diseases. Therefore, its tight control offers therapeutic promise. Liver X receptors (LXRs) have significant anti-inflammatory properties. Whether LXRs regulate inflammasome remains unresolved. We thus tested the hypothesis that LXR's anti-inflammatory properties may result from its ability to suppress inflammasome activation. In this study, LXRs agonists inhibited the induction of IL-1ß production, caspase-1 cleavage and ASC oligomerization by NLRP3 inflammasome. The agonists also inhibited inflammasome-associated mtROS production. Importantly, the agonists inhibited the priming of inflammasome activation. In vivo data also showed that LXRs agonist prevented NLRP3-dependent peritonitis. In conclusion, LXRs agonists are identified to potently suppress NLRP3 inflammasome and the regulation of LXRs signaling is a potential therapeutic for inflammasome-driven diseases.

NGL-2 Is a New Partner of PAR Complex in Axon Differentiation.

Neuronal polarization is pivotal for neural network formation during brain development. Axon differentiation is a hallmark of initial neuronal polarization. Here, we report that the leucine-rich repeat-containing protein netrin-G ligand-2 (NGL-2) as a polarity regulator that localizes asymmetrically in rat hippocampal neurons and is required for differentiation of the future axon. NGL-2 was associated with PAR complex, and this interaction resulted in local stabilization of axonal microtubules. Further study showed that the C terminal of NGL-2 binds to the PDZ domain of PAR6, and NGL-2 interacts with PAR3 and atypical PKCζ (aPKCζ), with PAR6 acting as a bridge or modifier. Then, NGL-2 regulates the local stabilization of microtubules and promotes axon differentiation by the aPKCζ/microtubule affinity-regulating kinase 2 pathway. These findings reveal the critical role of NGL-2 in regulating axon differentiation in rat hippocampal neurons and reveal a novel partner of the PAR complex.

Chemokine CXCL16 expression suppresses migration and invasiveness and induces apoptosis in breast cancer cells.

BACKGROUND: Increasing evidence argues that soluble CXCL16 promotes proliferation, migration, and invasion of cancer cells in vitro. However, the role of transmembrane or cellular CXCL16 in cancer remains relatively unknown. In this study, we determine the function of cellular CXCL16 as tumor suppressor in breast cancer cells. METHODS: Expression of cellular CXCL16 in breast cancer cell lines was determined at both RNA and protein levels. In vitro and in vivo studies that overexpressed or downregulated CXCL16 were conducted in breast cancer cells. RESULTS: We report differential expression of cellular CXCL16 in breast cancer cell lines that was negatively correlated with cell invasiveness and migration. Overexpression of CXCL16 in MDA-MB-231 cells led to a decrease in cell invasion and migration and induced apoptosis of the cells; downregulation of CXCL16 in MCF-7 cells increased cell migration and invasiveness. Consistent with the in vitro data, CXCL16 overexpression inhibited tumorigenesis in vivo. CONCLUSIONS: Cellular CXCL16 suppresses invasion and metastasis of breast cancer cells in vitro and inhibits tumorigenesis in vivo. Targeting of cellular CXCL16 expression is a potential therapeutic strategy for breast cancer.

[Expression of non-secretory CXCL16 and its impact on biological characteristics in breast cancer cell lines].

OBJECTIVE: To detect the expression of non-secretory CXCL16 and its impact on malignant biological behaviors in breast cancer cell lines. METHODS: RT-PCR was carried out to examine the expression of CXCL16 mRNA in breast cancer cell lines with different aggressiveness SK-BR-3, MCF-7, MDA-MB-231, MDA-MB-435S and human mammary normal epithelial cell; MCF-10A. The eukaryotic expression plasmid of CXCL16 was transfected into MDA-MB-231 cells and overexpression of CXCL16 was confirmed by Real time PCR and Western blot. Boyden Chamber assay was used to determine cell migration and invasion, while MTT assay was performed to determine cell proliferation. RESULTS: Among four breast cancer cell lines, CXCL16 mRNA was highly expressed in MCF-7, lowly expressed in MDA-MB-231, while MCF-10A faintly expressed CXCL16. Overexpression of CXCL16 led to a decrease in cell migration, invasion but not proliferation in MDA-MB-231 cells. CONCLUSION: Expression of non-secretory CXCL16 is associated with aggressiveness of breast cancer cell lines, and CXCL16 expression inhibits cell migration and invasion in vitro.

Quantitative CT Metrics for the Prediction of Therapeutic Effect in Asthma.

Background: Few studies have explored the correlation between asthma medication and features on HRCT images. We aim to analyse the differences and temporal changes of lung function and airway resistance in asthma with diverse HRCT phenotypes in a short period after inhalation of budesonide/formoterol. Method: This observational study recruited 55 adult patients with varying severities of asthma. We performed detailed airway metrics measurements of chest CT scans, such as airway wall thickness (WT), wall area percentage (WA%), wall thickness percentage (T/OR), and airways with an inner perimeter of 10 mm (Pi10). The effect of lung structural features on asthma medication response was explored according to the WA% and T/OR twelve hours post-drug administration. Using multivariable regression models, we then assessed the influence of WA% on lung function. Results: WA% (p < 0.001) and T/OR (p < 0.001) significantly increased in asthma than in healthy control subjects. Compared to mild asthma, airway walls were further thickened (WA%, p = 0.023; T/OR: p = 0.029) and associated with lumen narrowing (Pi10, p = 0.055) in moderate to severe asthma. WA% and T/OR correlated well with lung function (FEV1, FVC, MMEF, and PEF) and airway resistance (R5, R20, Rp, and Fres). Regression analysis showed that MEF25 decreased with increasing age and WA% (R2 = 0.58, p < 0.001). Patients with thickened airway walls experienced a maximal increase in FVC, FEV1, and PEF at 2 h (p < 0.001) and a maximal decrease of R5, Z5, and Rp at 2 h (p < 0.001) in those with a thickened airway pattern. Conclusions: Asthma patients with different bronchial wall thicknesses exhibited variable lung function changes. Specifically, patients with thick airway wall patterns were more sensitive to inhaled budesonide in the short term.

Gross Tumor Volume Segmentation for Stage III NSCLC Radiotherapy Using 3D ResSE-Unet.

INTRODUCTION: Radiotherapy is one of the most effective ways to treat lung cancer. Accurately delineating the gross target volume is a key step in the radiotherapy process. In current clinical practice, the target area is still delineated manually by radiologists, which is time-consuming and laborious. However, these problems can be better solved by deep learning-assisted automatic segmentation methods. METHODS: In this paper, a 3D CNN model named 3D ResSE-Unet is proposed for gross tumor volume segmentation for stage III NSCLC radiotherapy. This model is based on 3D Unet and combines residual connection and channel attention mechanisms. Three-dimensional convolution operation and encoding-decoding structure are used to mine three-dimensional spatial information of tumors from computed tomography data. Inspired by ResNet and SE-Net, residual connection and channel attention mechanisms are used to improve segmentation performance. A total of 214 patients with stage III NSCLC were collected selectively and 148 cases were randomly selected as the training set, 30 cases as the validation set, and 36 cases as the testing set. The segmentation performance of models was evaluated by the testing set. In addition, the segmentation results of different depths of 3D Unet were analyzed. And the performance of 3D ResSE-Unet was compared with 3D Unet, 3D Res-Unet, and 3D SE-Unet. RESULTS: Compared with other depths, 3D Unet with four downsampling depths is more suitable for our work. Compared with 3D Unet, 3D Res-Unet, and 3D SE-Unet, 3D ResSE-Unet can obtain superior results. Its dice similarity coefficient, 95th-percentile of Hausdorff distance, and average surface distance can reach 0.7367, 21.39mm, 4.962mm, respectively. And the average time cost of 3D ResSE-Unet to segment a patient is only about 10s. CONCLUSION: The method proposed in this study provides a new tool for GTV auto-segmentation and may be useful for lung cancer radiotherapy.

Radiation-induced eosinophil increase ratio predicts patient outcomes in non-small celllung cancer.

Background and purpose: Radiotherapy (RT) is a double-edged sword in regulating immune responses. This study aimed to investigate the impact of thoracic RT on circulating eosinophils and its association with patient outcomes in non-small cell lung cancer (NSCLC). Materials and methods: This retrospective study included 240 patients with advanced NSCLC treated with definitive thoracic RT from January 2012 to January 2020. Statistics included Kaplan-Meier analysis of overall survival (OS) and progression-free survival (PFS), multivariate Cox analyses to identify significant variables, and Spearman's correlation to qualify the relationship between dose-volume histogram (DVH) parameters and EIR. Results: Absolute eosinophil counts (AECs) showed an increasing trend during RT and an obvious peak in the 1st month after RT. Thresholds of eosinophil increase ratio (EIR) at the 1st month after RT for both OS and PFS were 1.43. Patients with high EIR above 1.43 experienced particularly favorable clinical outcomes (five-year OS: 21% versus 10%, P<0.0001; five-year PFS: 10% versus 8%, P=0.014), but may not derive PFS benefit from the addition of chemotherapy to RT. The higher a patient's EIR, the larger the potential benefit in the absence of chemotherapy. DVH parameters including heart mean dose and heart V10 were negatively associated with EIR. None of these DVH parameters was correlated with the clinical outcomes. Conclusion: EIR may serve as a potential biomarker to predict OS and PFS in NSCLC patients treated with RT. These findings require prospective studies to evaluate the role of such prognostic marker to identify patients at risk to tailor interventions.

CXCR6/CXCL16 functions as a regulator in metastasis and progression of cancer.

Metastasis is considered the obvious mark for most aggressive cancers. However, little is known about the molecular mechanism of the regulation of cancer metastasis. Recent evidence increasingly suggests that the interaction between chemokines and chemokine receptors is pivotal in the process of metastasis. The chemokine receptor CXCR4 and its ligand CXCL12, for example, have been reported to play a vital role in cancer metastasis. Another chemokine and chemokine receptor pair, the CXCL16/CXCR6 axis, has been studied by several independent research groups. Here, we summarize recent advances in our knowledge of the function of CXC chemokine receptor CXCR6 and its ligand CXCL16 in regulating metastasis and invasion of cancer. CXCR6 and CXCL16 are up-regulated in multiple cancer tissue types and cancer cell lines relative to normal tissues and cell lines. In addition, both CXCR6 and CXCL16 levels increase as tumor malignancy increases. Trans-membranous CXCL16 chemokine reduces proliferation while soluble CXCL16 chemokine enhances proliferation and migration. TM-CXCL16 functions as an inducer for lymphocyte build-up around tumor sites. High trans-membranous CXCL16 expression correlates with a good prognosis. Moreover, the Akt/mTOR signal pathway is involved in activating the CXCR6/CXCL16 axis. These findings suggest multiple opportunities for blocking the CXCR6/CXCL16 axis and the Akt/mTOR signal pathway in novel cancer therapies.

The role of significantly deregulated MicroRNAs in osteosarcoma based on bioinformatic analysis.

OBJECTIVE: This study aimed to identify potential key microRNAs (miRNAs) in osteosarcoma and construct miRNA-mRNA negative regulatory networks through analysis of the Gene Expression Omnibus (GEO) database. METHODS: The differentially expressed miRNAs (DE-miRNAs) in GSE28423 were screened, and their prognostic value was assessed with the prognostic data of GSE39058. The target genes of prognostic DE-miRNAs were predicted and underwent Gene Ontology (GO) classification and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. In addition, the expression of all predicted target genes were assessed using the mRNA array data of GSE28424. Finally, the gene-drug interaction network was constructed. RESULTS: We identified 205 DE-miRNAs between osteosarcoma cells and normal bone. Among them, high expression of miR-411-3p and miR-487b-5p were correlated with prolonged survival. Furthermore, 2659 genes predicted as targets of miR-411-3p or miR-487b-5p were clustered in 42 significant GO categories, including "regulation of neurotransmitter secretion" and "phosphoprotein binding", as well as 23 significant KEGG pathways, such as "MAPK signaling pathway" and "Ras signaling pathway". Five of the 75 overlapping target genes of miR-411-3p and miR-487b-5p were downregulated in osteosarcoma, including ZBTB20, ADAMTS4, GLIPR2, CLIC5 and CBX7. CONCLUSIONS: Our findings might help clarify molecular mechanisms underlying the oncogenesis and development, and offer potential targets for osteosarcoma.

Impact of high-dose rate radiotherapy on B and natural killer (NK) cell polarization in peripheral blood mononuclear cells (PBMCs) via inducing non-small cell lung cancer (NSCLC)-derived exosomes.

BACKGROUND: Non-small cell lung cancer (NSCLC) is the most commonly diagnosed solid tumor. While it has been established that stereotactic body radiotherapy for NSCLC plays an important role in antitumor immune response, the possible effects of the dose rate on this response has not been fully clarified. METHODS: In vitro, A549 cells were irradiated on a Varian TrueBeam® Linear Accelerator with dose and dose rate escalation using the flattening filter-free (FFF) technique, which was followed by coculturing with peripheral blood mononuclear cells (PBMCs). The exosomes from irradiated A549 cells were isolated and then cocultured with PBMCs. Flow cytometry was performed to analyze the proportion of lymph cell clusters in PBMCs. RESULTS: The proportion of CD3- immune cell clusters in PBMCs was significantly higher in the 10 Gy treatment group than in the nonirradiated group and other lower-dose (2, 6 Gy) treatment groups at the dose rate of 1,000 MU/min. However, no influence was observed on the proportion of CD3+ T cell subsets. Further results showed that both natural killer (NK) and B cell proportions reached peaks in the 14 Gy treatment group when a dose rate of 1,200 MU/min was used. Notably, the peak values of these two cell proportions were reached at a lower radiation dose of 10 Gy when a greater dose rate, ranging from 1,600 to 2,400 MU/min, was used. We further found that a single, high dose of irradiation (10 Gy), as compared with a single, low dose of irradiation (2 Gy), could markedly stimulate the A549-related exosome secretion in a radiation dose rate-dependent manner. The ultrahigh dose rate radiation-derived exosomes contributed to the polarization of B and NK cell subsets in PBMCs. CONCLUSIONS: The optimized radiation regime, which depends on the appropriate radiation dose and dose rate, results in the production of exosomes derived from NSCLC cells and eventually the redistribution of immune cells in PBMCs.

Higher mortality in lung cancer patients with COVID-19? A systematic review and meta-analysis.

OBJECTIVE: Given that the coronavirus disease 2019 (COVID-19) mainly spreads through the respiratory system and is associated with severe pulmonary complications, lung cancer patients may have worse outcomes than those with other tumors. There is no confirmed evidence about the mortality comparison between COVID-19 patients with lung cancer and other tumors. We performed a systematic review and pooled analysis to provide precise estimates of the mortality rate of COVID-19 patients with lung cancer and other tumors. MATERIALS AND METHODS: Our study systemically included and reviewed 13 studies on the characteristics of COVID-19 patients with lung cancer published up to November 1, 2020. The primary endpoint was all-cause mortality. We also compared the all-cause mortality rates in China and other regions as a secondary endpoint. The mortality rate was assessed with a fixed-effects model, which was used to derive the pooled mortality and 95 % confidence interval (CI). RESULTS: Thirteen studies from different countries, involving 1,229 patients with both COVID-19 and cancer, were selected for the pooled analysis. A total of 343 deaths were recorded in this population: 86 for lung cancers and 257 for other tumors. The mortality rate varies from 18 % to 60 % for patients with lung cancer and COVID-19 and 10%-41% for other tumor patients with COVID-19. The overall meta-analysis did not show a significant mortality difference for the lung cancer and other tumor subgroups (OR = 1.47, 95 %CI = 0.98-2.20, p = 0.06, I2 = 23 %). Nevertheless, in regions other than China, the pooled mortality of lung cancer patients with COVID-19 was 42 %, which was significantly higher than that of other tumors (24 %) (OR = 2.73, 95 % CI = 1.54-4.86, p = 0.0006, I2 = 16 %). CONCLUSION: Appropriate and aggressive preventive measures should be implemented to reduce the risk of COVID-19 in patients with cancer and optimally manage those who contract the infection.

Improvement of Flavonoids in Lemon Seeds on Oxidative Damage of Human Embryonic Kidney 293T Cells Induced by H2O2.

In this study, flavonoids in lemon seeds (FLS) were used to assess its improvement on the oxidative damage of human embryonic kidney 293T cells (HEK 293T cells) induced by H2O2. In vitro experiments showed that the survival rates of HEK 293T cells treated with different flavonoid concentrations (50 µg/mL, 100 µg/mL, and 150 µg/mL) exceeded 95%, indicating no significant toxic effect. Compared with the normal group, H2O2 (0.3 mmol/L) resulted significantly in oxidative stress injury of HEK 293T cells. The survival rate of the damaged cells increased after treatment with flavonoids, and the survival rate of cells treated with a high concentration (150 µg/mL) of flavonoids was 76.2%. Flavonoids also effectively inhibited H2O2-induced apoptosis. At the same time, flavonoid treatment significantly reduced the malondialdehyde content in cells and increased the levels of catalase (CAT), superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-Px). Quantitative polymerase chain reaction (qPCR) and Western blot analysis also suggested that FLS upregulated mRNA and protein expressions of CAT, SOD (SOD1, SOD2), GSH (GSH1), and GSH-Px in H2O2-induced oxidative damage of HEK 293T cells. The high-performance liquid chromatography analysis demonstrated that FLS contained six compounds, including gallocatechin, caffeic acid, epicatechin, vitexin, quercetin, and hesperidin. FLS were proven to have a good antioxidant capacity in vitro and improve significantly the oxidative damage of HEK 293T cells induced by H2O2. The biological activity value warrants investigation in additional studies.

Correction: MiR-101 reverses the hypomethylation of the LMO3 promoter in glioma cells.

[This corrects the article DOI: 10.18632/oncotarget.3181.].

Stuck-moving needle acupuncture myofascial trigger point to treat idiopathic frozen shoulder: study protocol for a randomized controlled trial.

BACKGROUND: There are evidence for the efficacy of acupuncture treatment for chronic shoulder pain, however, it remains unclear the best acupuncture modes for effective treatment. We compared the effect of the myofascial trigger point (MTrp) stuck-moving needle acupuncture with that of common acupuncture treatments. Further, we evaluated the efficacy and safety of stuck-moving needle acupuncture for the MTrp in improving pain and range of motions in patients with idiopathic frozen shoulder. The aim of present study is to select an effective therapy for patients with idiopathic frozen shoulder. METHODS: Randomized controlled trial will be conducted in the three clinical centers of Qingyang Traditional Chinese Medicine Hospital, Qingyang Xifeng district People's Hospital, and Qingyang Second People's Hospital in China from February 2020 to January 2021. One hundred and eight frozen shoulder patients will be recruited and randomized into one of three groups in a 1:1:1 ratio of the stuck-moving needle acupuncture group, common acupuncture control group, and physical exercise control group. This trial will include a 1-week baseline period, a 3-week treatment period, and a 12-week follow-up period. During the 3 weeks of the treatment period, patients will receive nine sessions of acupuncture. The primary outcome will be related to change in the Visual Analogue Scale (VAS) and measurement of range of joint motion (ROM) from the baseline period to the 12-week follow-up period. Secondary outcome measures will include measurement of pressure pain threshold (PPT), pressure pain tolerance (PTT), Oxford Shoulder Score (OSS), 36-item short form survey, and patient satisfaction evaluation. Adverse events also will be recorded for safety assessment. DISCUSSION: The results of this trial will allow us to compare the difference in efficacy between stuck-moving needle acupuncture MTrP with that of common acupuncture treatments. The findings from this trial will be published in the peer-reviewed journals. TRIAL REGISTRATION: Acupuncture-Moxibustion Clinical Trial Registry (ChiMCTR1900002862) and Chinese Clinical Trial Registry (ChiCTR1900028452). Registered on 22 December 2019. http://www.chictr.org.cn/showproj.aspx?proj=47354.