Transcriptional activation of CBFβ by CDK11p110 is necessary to promote osteosarcoma cell proliferation.

BACKGROUND:Aberrant expression of cyclin-dependent protein kinases (CDK) is a hallmark of cancer. CDK11 plays a crucial role in cancer cell growth and proliferation. However, the molecular mechanisms of CDK11 and CDK11 transcriptionally regulated genes are largely unknown. METHODS:In this study, we performed a global transcriptional analysis using gene array technology to investigate the transcriptional role of CDK11 in osteosarcoma. The promoter luciferase assay, chromatin immunoprecipitation assay, and Gel Shift assay were used to identify direct transcriptional targets of CDK11. Clinical relevance and function of core-binding factor subunit beta (CBFβ) were further accessed in osteosarcoma. RESULTS:We identified a transcriptional role of protein-DNA interaction for CDK11p110, but not CDK11p58, in the regulation of CBFβ expression in osteosarcoma cells. The CBFβ promoter luciferase assay, chromatin immunoprecipitation assay, and Gel Shift assay confirmed that CBFβ is a direct transcriptional target of CDK11. High expression of CBFβ is associated with poor outcome in osteosarcoma patients. Expression of CBFβ contributes to the proliferation and metastatic behavior of osteosarcoma cells. CONCLUSIONS:These data establish CBFβ as a mediator of CDK11p110 dependent oncogenesis and suggest that targeting the CDK11- CBFβ pathway may be a promising therapeutic strategy for osteosarcoma treatment

High Resolution Technology in Digital Imaging and its Remote Sensing Applications

Remote Sensing is a markable achievement in- last century. High resolution is a vital technol- ogy to digital image characteristics. Especially, in recent 20 years, digital technology promotes the development of spatial information field. As the increasing requirement of people, achieving high resolution images is urgent. For this target, we work from four parts: spatial resolution, ra- diant resolution, spectral resolution, temporal resolution and proposed schemes for each of them with different imaging manners, designed several prototype systems and carried out many experiments to verify their feasibilities

Correction to: Transcriptional activation of CBFβ by CDK11p110 is necessary to promote osteosarcoma cell proliferation.

Following publication of the original article [1], it was reported that Figs. 4 and 5 were not updated during the production process

Development，Reliability and Validity of the Chinese Version of the Return-to-Work Self-Efficacy Questionnaire among Young and Middle-aged Stroke Patients

BackgroundThe prevalence of varying degrees of post-stroke dysfunctions commonly found in an increasing number of young and middle-aged stroke patients, has hindered them from returning to work quickly, and caused serious socioeconomic burdens. Return-to-work self-efficacy is an important predictor of returning to work, and the assessment of which may provide guidance for promoting patients to return to work. However, there is no scale measuring the return-to-work self-efficacy of Chinese stroke patients.ObjectiveTo develop a Chinese version of the Return-to-work Self-efficacy Questionnaire (RTW-SE) by translating the English version of the RTW-SE, then assess its reliability and validity in young and middle-aged Chinese stroke patients.MethodsBy use of forward and backward translation of the English version of the RTW-SE, the Chinese version of the scale was developed. Then the scale was tested in a sample of 130 cases, and was analyzed for item analysis and exploratory factor analysis. Then, the scale was retested in another sample (n=255) from November 2020 to April 2021 for confirmatory factor analysis. The Pearson correlation and critical ratio were used as parameters for item analysis, and the Cronbach's α and split-half reliability were used as parameters of the reliability of the scale. Content validity and structural validity were adopted as parameters of the scale validity. Content validity was expressed by scale- and item-level content validity indices. Structural validity was evaluated by factor analysis, including exploratory factor analysis and confirmatory factor analysis.ResultsThe response rates of the test, and retest for the scale were 93.1% (121/130) , and 96.1% (245/255) , respectively. The results of item analysis showed that item-total correlation coefficients ranged from 0.636 to 0.897, with critical ratios greater than 3 for all items (P<0.001) . Reliability analysis showed that the Cronbach's α and split-half reliability of the scale were 0.942, and 0.940, respectively. The scale- and item-level content validity indices were 0.95 and 0.80~1.00, respectively. By exploratory factor analysis, one common factor was extracted, and the factor loadings of items ranged from 0.628 to 0.901, with 63.919% as the percentage of explained total variance. The confirmatory factor analysis showed that the model fit was good.ConclusionThe Chinese version of RTW-SE may be a reliable and valid tool for measuring return-to-work self-efficacy in young and middle-aged Chinese patients with stroke

Enhancement in Interfacial Adhesion of Ti/Polyetheretherketone by Electrophoretic Deposition of Graphene Oxide

This is the peer reviewed version of the following article: Pan, L., Lv, Y., Nipon, R., Wang, Y., Duan, L., Hu, J., ... & Shi, Y. (2019). Enhancement in Interfacial Adhesion of Ti/Polyetheretherketone by Electrophoretic Deposition of Graphene Oxide. Polymer Composites, 40(S2), E1243-E1251, which has been published in final form at https://doi.org/10.1002/pc.24955. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.This article discusses about the significance of graphene oxide (GO) deposition on the surface of a titanium plate by electrophoretic deposition (EPD) method to improve the adhesive strength of Ti/polyetheretherketone (PEEK) interfacial adhesive. Firstly, the anodic EPD method was applied to a water dispersion solution of GO, and then the morphology and the properties of titanium plate surface were characterized by scanning electron microscopy and contact angle measurements before and after GO deposition. Furthermore, the changes in the properties of GO after heating at 390°C were characterized by Raman and Fourier transform infrared spectroscopies. According to the results of single lap tensile shear test, the adhesion strength of Ti/PEEK interface after the anodization and deposition of GO was 34.94 MPa, an increase of 29.2% compared with 27.04 MPa of sample with only anodization. Also, the adhesion strengths were 58.1 and 76.5% higher compared with the samples of only GO deposited (22.1 MPa) and pure titanium (19.8 MPa), respectively

Resident Immune Cells of the Liver in the Tumor Microenvironment

The liver is a central immunomodulator that ensures a homeostatic balance between protection and immunotolerance. A hallmark of hepatocellular carcinoma (HCC) is the deregulation of this tightly controlled immunological network. Immune response in the liver involves a complex interplay between resident innate, innate, and adaptive immune cells. The immune response in the liver is modulated by its continuous exposure to toxic molecules and microorganisms that requires a degree of immune tolerance to protect normal tissue from damage. In HCC pathogenesis, immune cells must balance a dual role that includes the elimination of malignant cells, as well as the repair of damaged liver tissue to maintain homeostasis. Immune response in the innate and adaptive immune systems extends to the cross-talk and interaction involving immune-regulating non-hematopoietic cells, myeloid immune cells, and lymphoid immune cells. In this review, we discuss the different immune responses of resident immune cells in the tumor microenvironment. Current FDA-approved targeted therapies, including immunotherapy options, have produced modest results to date for the treatment of advanced HCC. Although immunotherapy therapy to date has demonstrated its potential efficacy, immune cell pathways need to be better understood. In this review article, we summarize the roles of specific resident immune cell subsets and their cross-talk subversion in HCC pathogenesis, with a view to identifying potential new biomarkers and therapy options

Assessing the Cumulative Contribution of New and Established Common Genetic Risk Factors to Early-Onset Prostate Cancer

We assessed the evidence for association between 23 recently reported prostate cancer (PCa) variants and early-onset PCa and the aggregate value of 63 PCa variants for predicting early-onset disease using 931 unrelated men diagnosed with PCa prior to age 56 years and 1126 male controls

PERK-Mediated Cholesterol Excretion from IDH Mutant Glioma Determines Anti-Tumoral Polarization of Microglia

Isocitrate dehydrogenase (IDH) mutation, a known pathologic classifier, initiates metabolic reprogramming in glioma cells and has been linked to the reaction status of glioma-associated microglia/macrophages (GAMs). However, it remains unclear how IDH genotypes contribute to GAM phenotypes. Here, it is demonstrated that gliomas expressing mutant IDH determine M1-like polarization of GAMs, while archetypal IDH induces M2-like polarization. Intriguingly, IDH-mutant gliomas secrete excess cholesterol, resulting in cholesterol-rich, pro-inflammatory GAMs without altering their cholesterol biosynthesis, and simultaneously exhibiting low levels of tumoral cholesterol due to expression remodeling of cholesterol transport molecules, particularly upregulation of ABCA1 and downregulation of LDLR. Mechanistically, a miR-19a/LDLR axis-mediated novel post-transcriptional regulation of cholesterol uptake is identified, modulated by IDH mutation, and influencing tumor cell proliferation and invasion. IDH mutation-induced PERK activation enhances cholesterol export from glioma cells via the miR-19a/LDLR axis and ABCA1/APOE upregulation. Further, a synthetic PERK activator, CCT020312 is introduced, which markedly stimulates cholesterol efflux from IDH wild-type glioma cells, induces M1-like polarization of GAMs, and consequently suppresses glioma cell invasion. The findings reveal an essential role of the PERK/miR-19a/LDLR signaling pathway in orchestrating gliomal cholesterol transport and the subsequent phenotypes of GAMs, thereby highlighting a novel potential target pathway for glioma therapy