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Urolithiasis is a common urological disease, and treatment strategy options vary between different stone types. However, accurate detection of stone composition can only be performed in vitro. The management of infection stones is particularly challenging with yet no effective approach to pre-operatively identify infection stones from non-infection stones. Therefore, we aimed to develop a radiomic model for preoperatively identifying infection stones with multicenter validation. In total, 1198 eligible patients with urolithiasis from three centers were divided into a training set, an internal validation set, and two external validation sets. Stone composition was determined by Fourier transform infrared spectroscopy. A total of 1316 radiomic features were extracted from the pre-treatment Computer Tomography images of each patient. Using the least absolute shrinkage and selection operator algorithm, we identified a radiomic signature that achieved favorable discrimination in the training set, which was confirmed in the validation sets. Moreover, we then developed a radiomic model incorporating the radiomic signature, urease-producing bacteria in urine, and urine pH based on multivariate logistic regression analysis. The nomogram showed favorable calibration and discrimination in the training and three validation sets (area under the curve [95% confidence interval], 0.898 [0.840-0.956], 0.832 [0.742-0.923], 0.825 [0.783-0.866], and 0.812 [0.710-0.914], respectively). Decision curve analysis demonstrated the clinical utility of the radiomic model. Thus, our proposed radiomic model can serve as a non-invasive tool to identify urinary infection stones in vivo, which may optimize disease management in urolithiasis and improve patient prognosis.

Background The incidence of breast cancer ranks the first among female malignant tumors. Although the effect of breast cancer treatment strategies has been very ideal and the mortality rate of breast cancer has decreased, some patients are still not sensitive to these, which eventually leads to rapid recurrence, metastasis and poor prognosis. Ferroptosis is a kind of Regulated cell death, which induced by accumulation of lipid peroxidation products and Reactive Oxygen Species (ROS). It is quite different from apoptosis and autophagy in cell morphological characteristics and biochemical indicators. According to the latest studies, ferroptosis can reduce the activity of GPX4 (Gutathione Peroxidase 4) in cells and accumulate ROS and lipid Peroxidase products through iron metabolism, ROS metabolism, amino acid metabolism and lipid metabolism, etc., thus causing ferroptosis. Ferroptosis is a hotspot in the study of drug resistance and metastasis of breast cancer. Simvastatin is a kind of commonly used oral cholesterol-lowering drugs, belongs to the HMG CoA reductase inhibitors. Some clinical studies have shown that statins can reduce the risk of a variety of cancers, including breast cancer, and the risk of recurrence. Other basic experiment show lipophilic statins have anti-cancer effect. Simvastatin is the most lipophilic of all statins in use. Recent studies have found that simvastatin can be used in combination with docetaxel to enhance the effect of chemotherapy in prostate cancer, but has not been reported in breast cancer. In this study, we investigated whether simvastatin could induce ferroptosis in breast cancer by inhibiting GPX4 and play the role of chemotherapy sensitization in combination with docetaxel. Methods (1) CCK8 assay was used for cell proliferation in vitro by simvastatin and docetaxel in breast cancer cells MDA-MB-231 and MCF-7. (2) The anti-cancer effect of simvastatin in vivo was verified by xenograft experiments in nude mice. (3) GPX4 mRNA and protein levels were detected by qPCR and Western blot. (4) GPXs activity test, ROS level test and MDA level test were used for ferroptosis detection.(5) the expression of ferroptosis-related genes ACSL4, PTGS2 and NOX1 was detected by qPCR.(6) anti-tumor effect of simvastatin combined with docetaxel in breast cancer cells mda-mb-231 and McF-7 was detected in vitro by CCK8 method.(7) By MDA-MB-231 tumor xenograft models surveyed anti-tumor activity of simvastatin and docetaxel. Results CCK8 results showed that simvastatin significantly inhibited cell proliferation in breast cancer cells MDA-MB-231 and MCF-7 (P Citation Format: Sihong Lu, Nan Shao, Jong Bi, Ying Lin. Simvastatin induces ferroptosis in breast cancer cells by inhibiting GPX4 and sensitizes chemotherapy [abstract]. In: Proceedings of the 2020 San Antonio Breast Cancer Virtual Symposium; 2020 Dec 8-11; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2021;81(4 Suppl):Abstract nr PS18-44.

Patients with severe fever with thrombocytopenia syndrome (SFTS) commonly show liver function impairment. This study aimed to characterize the liver function indices in SFTS patients and investigate their association with mortality.Clinical information and laboratory results of 459 laboratory-confirmed SFTS patients, including 78 deceased and 381 surviving patients, were retrospectively analyzed. To explore the infectivity of SFTS caused by novel Bunyavirus (SFTSV) in hepatocytes, Huh7 human hepatoma cells were infected with various concentrations of SFTSVThe proportion of SFTS patients developing liver injury during hospitalization was 73.2% (336/459); the hepatocellular injury was the predominant type. The median time to occurrence of liver injury from disease onset was 8 d. Liver injury in the deceased group occurred earlier than that in the surviving group. Alanine aminotransferase (ALT) level between 2-5 times upper limit of normal (ULN) at 4-6 d and between 5-15 ULN at 7-12 d of disease course were independent predictors of mortality. Alkaline phosphatase (ALP)2 ULN at 7-9 d and elevated ALP at 10-12 days after disease onset were risk factors for death. ALT and aspartate transaminase (AST) levels were correlated with lymphocyte count and platelet-to-lymphocyte ratio (PLR). Total bilirubin (TB), ALT, AST levels showed positive correlation with viral load. In theLiver injury is common in SFTS patients. ALT and ALP were independent predictors of SFTS-related mortality. Frequent monitoring and evaluation of liver function indices are needed for SFTS patients.

Breast cancer (BC) is one of the most common female cancers, and its incidence has been increasing in recent years. Although treatments are continuously improving, the prognosis of patients in the advanced stage is still unsatisfactory. Thus, an in-depth understanding of its molecular mechanisms is necessary for curing breast cancer. KIF15 is a tetrameric spindle motor which can regulate mitosis in cellular process and exert the crucial functions in several cancers. The purpose of our research was to investigate the functions of KIF15 in breast cancer. We tested the expression of KIF15 in breast cancer tissues and the survival rate of breast cancer patients with high or low level of KIF15 through TCGA data. What's more, western blot and immunohistochemistry assay were utilized to evaluate the protein level and mRNA level of KIF15 in breast cancer tissues. Then CCK-8, wound healing, transwell and flow cytometry experiments were adopted separately to test cell viability, migration, invasion and cell cycle distribution. We discovered that KIF15 was highly expressed in breast cancer tissues and high level KIF15 was associated with a low survival rate of breast cancer patients. Moreover, silence of KIF15 suppressed cell viability, migration, invasion and cell cycle distribution. Following, we discovered that ZNF367 was the upstream transcription factor of KIF15. In addition, silenced ZNF367 could also repress the growth of breast cancer cells. And rescue experiments indicated that overexpressed KIF15 could counteract the inhibition effect of silencing ZNF367 on the progression of breast cancer. Importantly, we discovered that KIF15 and ZNF367 were associated with the regulation of cell cycle. In short, ZNF367-activated KIF15 accelerated the progression of breast cancer by regulating cell cycle progress.

Approximately half of the SARS-CoV-2 infections occur without apparent symptoms, raising questions regarding long-term humoral immunity in asymptomatic individuals. Plasma levels of immunoglobulin G (IgG) and M (IgM) against the viral spike or nucleoprotein were determined for 25,091 individuals enrolled in a surveillance program in Wuhan, China. We compared 405 asymptomatic individuals with 459 symptomatic COVID-19 patients. The well-defined duration of the SARS-CoV-2 endemic in Wuhan allowed a side-by-side comparison of antibody responses following symptomatic and asymptomatic infections without subsequent antigen re-exposure. IgM responses rapidly declined in both groups. However, both the prevalence and durability of IgG responses and neutralizing capacities correlated positively with symptoms. Regardless of sex, age, and body weight, asymptomatic individuals lost their SARS-CoV-2-specific IgG antibodies more often and rapidly than symptomatic patients. These findings have important implications for immunity and favour immunization programs including individuals after asymptomatic infections.One-Sentence SummaryPrevalence and durability of SARS-CoV-2-specific IgG responses and neutralizing capacities correlate with COVID-19 symptoms.

Long-term antibody responses and neutralizing activities in response to SARS-CoV-2 infection are not yet clear. Here we quantify immunoglobulin M (IgM) and G (IgG) antibodies recognizing the SARS-CoV-2 receptor-binding domain (RBD) of the spike (S) or the nucleocapsid (N) protein, and neutralizing antibodies during a period of 6 months from COVID-19 disease onset in 349 symptomatic COVID-19 patients who were among the first be infected world-wide. The positivity rate and magnitude of IgM-S and IgG-N responses increase rapidly. High levels of IgM-S/N and IgG-S/N at 2-3 weeks after disease onset are associated with virus control and IgG-S titers correlate closely with the capacity to neutralize SARS-CoV-2. Although specific IgM-S/N become undetectable 12 weeks after disease onset in most patients, IgG-S/N titers have an intermediate contraction phase, but stabilize at relatively high levels over the 6 month observation period. At late time points, the positivity rates for binding and neutralizing SARS-CoV-2-specific antibodies are still >70%. These data indicate sustained humoral immunity in recovered patients who had symptomatic COVID-19, suggesting prolonged immunity., A better understanding of longitudinal changes in antibody responses in COVID-19 patients is needed. Here the authors analyze anti-spike and anti-nucleocapsid antibody responses to Sars-CoV-2 over a course of 6 months in a large cohort of patients with COVID-19, showing that IgM is mostly not detectable after 3 months, whereas IgG responses contract, yet remain at high levels at 6 months.

Objective To illustrate the effect of corticosteroids and heparin, respectively, on coronavirus disease 2019 (COVID-19) patients’ CD8+ T cells and D-dimer. Methods In this retrospective cohort study involving 866 participants diagnosed with COVID-19, patients were grouped by severity. Generalized additive models were established to explore the time-course association of representative parameters of coagulation, inflammation and immunity. Segmented regression was performed to examine the influence of corticosteroids and heparin upon CD8+ T cell and D-dimer, respectively. Results There were 541 moderate, 169 severe and 156 critically ill patients involved in the study. Synchronous changes of levels of NLR, D-dimer and CD8+ T cell in critically ill patients were observed. Administration of methylprednisolone before 14 DFS compared with those after 14 DFS (β = 0.154%, 95% CI=(0, 0.302), p=.048) or a dose lower than 40 mg per day compared with those equals to 40 mg per day (β = 0.163%, 95% CI=(0.027, 0.295), p=.020) significantly increased the rising rate of CD8+ T cell in 14–56 DFS. Conclusions The parameters of coagulation, inflammation and immunity were longitudinally correlated, and an early low-dose corticosteroid treatment accelerated the regaining of CD8+ T cell to help battle against SARS-Cov-2 in critical cases of COVID-19.

Additional file 1. Detailed materials and methods, and supplementary tables and figure.

Background Patients with severe Coronavirus Disease 2019 (COVID-19) will progress rapidly to acute respiratory failure or death. We aimed to develop a quantitative tool for early predicting mortality risk of patients with COVID-19. Methods 301 patients with confirmed COVID-19 admitted to Main District and Tumor Center of the Union Hospital of Huazhong University of Science and Technology (Wuhan, China) between January 1, 2020 to February 15, 2020 were enrolled in this retrospective two-centers study. Data on patient demographic characteristics, laboratory findings and clinical outcomes was analyzed. A nomogram was constructed to predict the death probability of COVID-19 patients. Results Age, neutrophil-to-lymphocyte ratio, d-dimer and C-reactive protein obtained on admission were identified as predictors of mortality for COVID-19 patients by LASSO. The nomogram demonstrated good calibration and discrimination with the area under the curve (AUC) of 0.921 and 0.975 for the derivation and validation cohort, respectively. An integrated score (named ANDC) with its corresponding death probability was derived. Using ANDC cut-off values of 59 and 101, COVID-19 patients were classified into three subgroups. The death probability of low risk group (ANDC 101) was more than 50%, respectively. Conclusion The prognostic nomogram exhibited good discrimination power in early identification of COVID-19 patients with high mortality risk, and ANDC score may help physicians to optimize patient stratification management.

BackgroundKinesin superfamily (KIFs) has a long-reported significant influence on the initiation, development, and progress of breast cancer. However, the prognostic value of whole family members was poorly done. Our study intends to demonstrate the value of kinesin superfamily members as prognostic biomarkers as well as a therapeutic target of breast cancer.MethodsComprehensive bioinformatics analyses were done using data from TCGA, GEO, METABRIC, and GTEx. LASSO regression was done to select tumor-related members. Nomogram was constructed to predict the overall survival (OS) of breast cancer patients. Expression profiles were testified by quantitative RT-PCR and immunohistochemistry. Transcription factor, GO and KEGG enrichments were done to explore regulatory mechanism and functions.ResultsA total of 20 differentially expressed KIFs were identified between breast cancer and normal tissue with 4 (KIF17, KIF26A, KIF7, KIFC3) downregulated and 16 (KIF10, KIF11, KIF14, KIF15, KIF18A, KIF18B, KIF20A, KIF20B, KIF22, KIF23, KIF24, KIF26B, KIF2C, KIF3B, KIF4A, KIFC1) overexpressed. Among which, 11 overexpressed KIFs (KIF10, KIF11, KIF14, KIF15, KIF18A, KIF18B, KIF20A, KIF23, KIF2C, KIF4A, KIFC1) significantly correlated with worse OS, relapse-free survival (RFS) and distant metastasis-free survival (DMFS) of breast cancer. A 6-KIFs-based risk score (KIF10, KIF15, KIF18A, KIF18B, KIF20A, KIF4A) was generated by LASSO regression with a nomogram validated an accurate predictive efficacy. Both mRNA and protein expression of KIFs are experimentally demonstrated upregulated in breast cancer patients. Msh Homeobox 1 (MSX1) was identified as transcription factors of KIFs in breast cancer. GO and KEGG enrichments revealed functions and pathways affected in breast cancer.ConclusionOverexpression of tumor-related KIFs correlate with worse outcomes of breast cancer patients and can work as potential prognostic biomarkers.

Additional file 2: Table S2. The association between different risk groups and actual outcome in the derivation cohort.

Additional file 3: Table S3. The association between different risk groups and actual outcome in the validation cohort.

Additional file 5: Figure S2. LASSO coefficient profiles of the 24 candidate predictors.

Additional file 4: Figure S1. Five-fold cross-validation to select the Lambda.1SE for LASSO based on binominal deviance.

Background: The dynamic changes of lymphocyte subsets and cytokines profiles of patients with novel coronavirus disease (COVID-19) and their correlation with the disease severity remain unclear. Method: Peripheral blood samples were longitudinally collected from 40 confirmed COVID-19 patients and examined for lymphocyte subsets by flow cytometry and cytokine profiles by specific immunoassays. Findings: Of the 40 COVID-19 patients enrolled, 13 severe cases showed significant and sustained decreases in lymphocyte counts but increases in neutrophil counts than 27 mild cases. Further analysis demonstrated significant decreases in the counts of T cells, especially CD8 + T cells, as well as increases in IL-6, IL-10, IL-2 and IFN-γ levels in the peripheral blood in the severe cases compared to those in the mild cases. T cell counts and cytokine levels in severe COVID-19 patients who survived the disease gradually recovered at later time points to levels that were comparable to those of the mild cases. Moreover, the neutrophil-to-CD8+ T cell ratio (N8R) were identified as the most powerful prognostic factor affecting the prognosis for severe COVID-19. Interpretation: The degree of lymphopenia and a proinflammatory cytokine storm is higher in severe COVID-19 patients than in mild cases, and is associated with the disease severity. N8R may serve as a useful prognostic factor for early identification of severe COVID-19 cases. Funding Statement: This work is supported by the National Natural Science Foundation of China (81861138044, 91742114 and 91642118), the National Science and Technology Major Project (2018ZX10723203, 2018ZX10302206, 2017ZX10202201, 2017ZX10202202 and 2017ZX10202203), the Innovation Team Project of Health Commission of Hubei Province (WJ2019C003), the Integrated Innovative Team for Major Human Diseases Program of Tongji Medical College and the “Double-First Class” Project for the International Cooperation Center on Infection and Immunity, HUST, and a special joint project of University Hospital Essen, University of Duisburg-Essen. Declaration of Interests: The authors disclose no conflicts of interest. Ethics Approval Statement: A written informed consent was regularly obtained from all patients upon admission into Wuhan Union Hospital, China. The study was approved by the Ethics Committee of Tongji Medical College of Huazhong University of Science and Technology.

Additional file 1: Table S1. Total points in nomogram and corresponding death probability of patients with COVID-19.

Background: Chest CT image guided handling of pneumonia patients with negative RT-PCR detection of SARS-CoV-2 in high endemic areas is still controversial b

Background The dynamic changes of lymphocyte subsets and cytokines profiles of patients with novel coronavirus disease (COVID-19) and their correlation with the disease severity remain unclear. Methods Peripheral blood samples were longitudinally collected from 40 confirmed COVID-19 patients and examined for lymphocyte subsets by flow cytometry and cytokine profiles by specific immunoassays. Findings Of the 40 COVID-19 patients enrolled, 13 severe cases showed significant and sustained decreases in lymphocyte counts [0·6 (0·6-0·8)] but increases in neutrophil counts [4·7 (3·6-5·8)] than 27 mild cases [1.1 (0·8-1·4); 2·0 (1·5-2·9)]. Further analysis demonstrated significant decreases in the counts of T cells, especially CD8+ T cells, as well as increases in IL-6, IL-10, IL-2 and IFN-γ levels in the peripheral blood in the severe cases compared to those in the mild cases. T cell counts and cytokine levels in severe COVID-19 patients who survived the disease gradually recovered at later time points to levels that were comparable to those of the mild cases. Moreover, the neutrophil-to-lymphocyte ratio (NLR) (AUC=0·93) and neutrophil-to-CD8+ T cell ratio (N8R) (AUC =0·94) were identified as powerful prognostic factors affecting the prognosis for severe COVID-19. Interpretation The degree of lymphopenia and a proinflammatory cytokine storm is higher in severe COVID-19 patients than in mild cases, and is associated with the disease severity. N8R and NLR may serve as a useful prognostic factor for early identification of severe COVID-19 cases. Funding The National Natural Science Foundation of China, the National Science and Technology Major Project, the Health Commission of Hubei Province, Huazhong University of Science and Technology, and the Medical Faculty of the University of Duisburg-Essen and Stiftung Universitaetsmedizin, Hospital Essen, Germany.

Background Breast cancer angiogenesis is key for metastasis and predicts a poor prognosis. Angiotensin-converting enzyme 2 (ACE2), as a member of the renin-angiotensin system (RAS), was reported to restrain the progression of hepatocellular carcinoma (HCC) and non-small cell lung cancer (NSCLC) through inhibiting angiogenesis. However, the relationship between ACE2 and breast cancer angiogenesis remains unclear. Methods The prognosis and relative gene selection were analysed using the GEPIA, GEO, TCGA and STRING databases. ACE2 expression in breast cancer tissue was estimated by reverse transcription-quantitative polymerase chain reaction (qPCR). Breast cancer cell migration, proliferation and angiogenesis were assessed by Transwell migration, proliferation, tube formation, and wound healing assays. The expression of vascular endothelial growth factor A (VEGFa) was detected by qPCR and Western blotting. The phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2), mitogen-activated protein kinase 1/2 (MEK1/2), and extracellular signal-regulated protein kinase 1/2 (ERK1/2) was examined by Western blotting. Breast cancer metastasis and angiogenesis in vivo were measured using a zebrafish model. Results ACE2 was downregulated in breast cancer patients. Patients with higher ACE2 expression had longer relapse-free survival (RFS). In vitro, ACE2 inhibited breast cancer migration. Meanwhile, ACE2 in breast cancer cells inhibited human umbilical vascular endothelial cell (HUVEC) proliferation, tube formation and migration. In the zebrafish model, ACE2 inhibited breast cancer cell metastasis, as demonstrated by analyses of the number of disseminated foci and the metastatic distance. Neo-angiogenesis was also decreased by ACE2. ACE2 downregulated the expression of VEGFa in breast cancer cells. Furthermore, ACE2 in breast cancer cells inactivated the phosphorylation of VEGFR2, MEK1/2, and ERK1/2 in HUVECs. Conclusions Our findings suggest that ACE2, as a potential resister to breast cancer, might inhibit breast cancer angiogenesis through the VEGFa/VEGFR2/ERK pathway. Trial registration Retrospectively registered. Electronic supplementary material The online version of this article (10.1186/s13046-019-1156-5) contains supplementary material, which is available to authorized users.

Table S3. Hub gene selection. (DOCX 19 kb)

Table S2. TCGA breast cancer clinical data stratified by the ACE2 expression level. (DOCX 20 kb)

Table S1. Clinical and pathological characteristics of breast cancer patients. (DOCX 17 kb)

Table S4. KEGG pathways between ACE2 and VEGFa. (DOCX 32 kb)

Supporting methods. (DOCX 19 kb)

e12040 Background: Chemotherapy followed by endocrine therapy is the standard adjuvant treatment strategy for estrogen receptor-positive breast cancer patients. However, no direct evidence so far demonstrated better efficacy of sequential use of chemotherapy and endocrine therapy over concurrent. Objective: To evaluate the efficacy between sequential and concurrent use of chemotherapy and endocrine therapy in the adjuvant treatment of ER positive breast cancer. Methods: Randomized clinical trials comparing chemotherapy and/or endocrine therapy in the adjuvant treatment of ER positive breast cancer were included. Hazard ratios (HRs) of disease-free survival (DFS) and overall survival (OS) were extracted and analyzed in Bayesian analysis. Patients were stratified by menopause status for subgroup analysis. Results: 37 trials were identified with 37225 patients enrolled in total, 37 trials with DFS results and 24 with OS. 3 comparisons were done between sequential and concurrent arms. In DFS analysis, no statistical significance was found in all 3 comparisons [CHE seq/con TAM (HR 1.01, 95%CI 0.8497 - 1.199); CHE seq/con OFS+TAM (HR 0.9119, 95%CI 0.5666 - 1.49); CHE seq/con OFS+AI (HR 1.032, 95%CI 0.6291 - 1.776)]. The same were seen in OS analysis [CHE seq/con TAM (HR 0.9512, 95%CI 0.8053 - 1.125); CHE seq/con OFS+TAM (HR 1.065, 95%CI 0.6344 - 1.789); CHE seq/con OFS+AI (HR 1.069, 95%CI 0.665 - 1.717)]. Rankings were done for preferable treatment recommendations. In DFS analyses, sequential arms ranked higher than concurrent arms [CHE seq/con OFS+AI (1 vs. 3); CHE seq/con OFS+TAM (6 vs. 7); CHE seq/con TAM (8 vs. 8)]. The same tendency was seen in OS analyses [CHE seq/con OFS+AI (1 vs. 2); CHE seq/con TAM (4 vs. 5)] except for CHE seq/con OFS+TAM (11 vs. 6-9). In subgroup ranking results, CHE seq/con OFS+AI and CHE seq/con OFS+TAM showed consistency among comparisons with concurrent arms ranked higher than sequential arms. However, CHE seq TAM ranked higher than CHE con TAM in all comparisons. Conclusions: The combination of chemotherapy and endocrine therapy in the adjuvant treatment of ER positive breast cancer demonstrated equal efficacy either used sequentially or concurrently. However, concurrent arms were recommended over sequential arms in premenopausal patients for better DFS and OS, except for the combination of chemotherapy and tamoxifen which was recommended to be used sequentially. Others: This study has been registered in PROSPERO (CRD42018104889).

e12573 Background: Angiogenesis is key for metastasis and predicts a poor prognosis in breast cancer. Among the pro-angiogenic factors, interleukin-8 (IL-8) could be secreted by tumor cells mediated by microRNA-200 family (miR-200s). Long non-coding RNA (LncRNA), was reported to absorb microRNA to play multiple roles in various diseases including breast cancer. Our preliminary results recognized lncRNA NR2F1 through Agilent Human LncRNA array from breast cancer cells overexpressing IL-8. However, the relationship between LncRNA NR2F1 and breast cancer angiogenesis remains unknown. Methods: Breast cancer cell migration, invasion, proliferation and angiogenesis were assessed by Transwell, CCK8, tube formation, and wound healing assays. The expression of LncRNA NR2F1, miR-200s and IL-8 were detected by qPCR, Western blotting and ELISA. Breast cancer metastasis and angiogenesis in vivo were measured in a zebrafish model. Results: We found that the basal expression of lncRNA NR2F1 is higher in breast cancer cell lines than it in normal cells. In vitro, lncRNA NR2F1 induced breast cancer migration, invasion, and proliferation. Meanwhile, lncRNA NR2F1 promoted human umbilical vascular endothelial cell (HUVEC) proliferation, tube formation, and migration both via breast cancer conditioned medium and via direct HUVEC transfection. In the zebrafish model, lncRNA NR2F1 promoted breast cancer cell metastasis and neo-angiogenesis. Further study disclosed that lncRNA NR2F1 downregulated the expression of miR-200s, which in turn upregulated the expression of IL-8 in breast cancer cells. Conclusions: Our findings suggest that LncRNA NR2F1, as a potential promoter of breast cancer, may induce breast cancer angiogenesis through IL-8/lncRNA NR2F1/miR-200s/IL-8 loop.

Ordered mesoporous carbon/carbon aerogel (OMC/CA) composites have been obtained by a simple ultrasonic mixing technique. It is found that there exists a synergistic effect between OMC’s channel-like mesopores and CA’s network-like mesopores during electrochemical charge–discharge process; and the maximum synergistic coefficient arrives at 0.37 when CA content is 30 wt.%. As a result, the as-prepared OMC/CA composites can make full use of the two-dimensional order of mesoporous structure of OMC and the three-dimensional connectivity of mesoporous structure of CA, and thus, exhibit much better electrochemical properties as compared to OMC and CA alone.