Understanding aliasing effects and their removal in SPEN MRI: A k-space perspective.

PURPOSE: To characterize the mechanism of formation and the removal of aliasing artifacts and edge ghosts in spatiotemporally encoded (SPEN) MRI within a k-space theoretical framework. METHODS: SPEN's quadratic phase modulation can be described in k-space by a convolution matrix whose coefficients derive from Fourier relations. This k-space model allows us to pose SPEN's reconstruction as a deconvolution process from which aliasing and edge ghost artifacts can be quantified by estimating the difference between a full sampling and reconstructions resulting from undersampled SPEN data. RESULTS: Aliasing artifacts in SPEN MRI reconstructions can be traced to image contributions corresponding to high-frequency k-space signals. The k-space picture provides the spatial displacements, phase offsets, and linear amplitude modulations associated to these artifacts, as well as routes to removing these from the reconstruction results. These new ways to estimate the artifact priors were applied to reduce SPEN reconstruction artifacts on simulated, phantom, and human brain MRI data. CONCLUSION: A k-space description of SPEN's reconstruction helps to better understand the signal characteristics of this MRI technique, and to improve the quality of its resulting images.

Superparamagnetic iron oxide (SPIO) nanoparticles labeled endothelial progenitor cells (EPCs) administration inhibited heterotopic ossification in rats.

Heterotopic ossification (HO) is a painful disease characterized by unwanted bone ectopic formation outside of the skeleton after injury. SPIO nanoparticles therapy has been widely used in diverse orthopedic diseases. However, the effect of SPIO nanoparticles on heterotopic ossification remains unknown. Here, we prepared the SPIO nanoparticles carrying mothers against decapentaplegic homolog 7 (SMAD7) and evaluated their mechanism function to HO in a rat model. The results revealed that SPIO nanoparticles containing SMAD7 treatment lead to a decrease in epithelial-mesenchymal transition (EMT) relevant protein expression in vitro. Moreover, SPIO nanoparticles labeled EPCs transplantation effectively prevented heterotopic ossification and inhibited endothelial-mesenchymal transition (EndMT) in HO rats. In addition, SPIO nanoparticles labeled EPCs transplantation suppressed osteogenic and adipogenic differentiation of embryonic fibroblasts (EFs) in HO rats. Our results demonstrated that administration of SPIO nanoparticles labeled EPCs could inhibit heterotopic ossification in rats, which might be a potential therapy method for a medical intervention to treat HO in clinic.

Retraction Note: Long noncoding RNA ANRIL is activated by hypoxia-inducible factor-1α and promotes osteosarcoma cell invasion and suppresses cell apoptosis upon hypoxia.

[This retracts the article DOI: 10.1186/s12935-016-0349-7.].

Long noncoding RNA ANRIL is activated by hypoxia-inducible factor-1α and promotes osteosarcoma cell invasion and suppresses cell apoptosis upon hypoxia.

BACKGROUND: Osteosarcoma is the most common malignancy of bone. Intratumoral hypoxia occurs in many solid tumors, where it is associated with the development of aggressive phenotype. ANRIL has been shown to be a long noncoding RNA that facilitates the progression of a number of malignancies. Yet, few studies have explored the expression pattern of ANRIL in osteosarcoma and the effect of hypoxia on ANRIL. METHODS: We evaluated the expression levels of ANRIL in osteosarcoma tissues, adjacent normal tissues and cells with quantitative real-time polymerase chain reaction. Multiple approaches including luciferase reporter assay with nucleotide substitutions, chromatin immunoprecipitation assay and electrophoretic mobility shift assay were used to confirm the direct binding of HIF-1α to the ANRIL promoter region. SiRNA-based knockdown and other molecular biology techniques were employed to measure the effect of HIF-1α on the expression of ANRIL. RESULTS: We found that the expression of ANRIL was upregulated in 15 pairs of osteosarcoma compared with adjacent normal tissues. We found that hypoxia is sufficient to upregulate ANRIL expression in osteosarcoma cells (MNNG and U2OS). HIF-1α directly binds to the putative hypoxia response element in the upstream region of ANRIL. What's more, siRNA and small molecular inhibitors-mediated HIF-1α suppression attenuated ANRIL upregulation under hypoxic conditions. Upon hypoxia, ANRIL promoted cancer cell invasion and suppressed cell apoptosis. CONCLUSION: Taken together, these data suggest that HIF-1α may contribute to the upregulation of ANRIL in osteosarcoma under hypoxic conditions. ANRIL is involved in hypoxia-induced aggressive phenotype in osteosarcoma.

[Myxovirus resistance protein A (MxA) induces the expression of interferon-stimulated genes in HepG2 cells by enhancing the activity of the interferon-stimulated response element (ISRE)].

Objective To explore the effects of Myxovirus resistance protein A (MxA) on the Janus kinase/Signal transducer and activator of transcription (JAK/STAT) pathway in HepG2 cells. Methods HepG2 cells were transfected with the pcDNA3.1-Flag-MxA construct, and subsequent localization and expression of the MxA protein were detected through immunofluorescence cytochemistry. The presence of MxA protein was further confirmed by using Western blot analysis. Following transfection with MxA small interfering RNA (si-MxA) and subsequent treatment with alpha interferon (IFN-α), real-time fluorescent quantitative PCR was employed to measure the mRNA levels of myxovirus resistance protein A (MxA), protein kinase R (PKR), and oligoadenylate synthase (OAS). Western blot analysis was used to detect the protein expression of MxA, PKR, OAS, signal transducer and activator of transcription 1 (STAT1), phosphorylated STAT1 (pSTAT1), STAT2, phosphorylated STAT2 (p-STAT2) and interferon regulatory factor 9 (IRF9). Additionally, pcDNA3.1-Flag-MxA and pISRE-TA-luc were co-transfected into HepG2 and HepG2.2.15 cells, respectively, to assess the activity of the interferon-stimulated response element (ISRE) by using a luciferase activity assay. Results MxA protein was expressed in both the cytoplasm and nucleus of HepG2 cells, with higher expression levels in the cytoplasm than in the nucleus. Knocking down MxA expression in HepG2 cells did not affect the expression of STAT1, p-STAT1, STAT2, p-STAT2, and IRF9 proteins induced by IFN-α, but significantly reduced the expression of antiviral proteins PKR and OAS. Overexpression of MxA in HepG2 cells enhanced ISRE activity and increased the expression of PKR and OAS proteins, but this effect was inhibited in HepG2.2.15 cells. Conclusion MxA induces the expression of antiviral proteins by enhancing the activity of the JAK/STAT signaling pathway ISRE.

Identification of pivotal genes and pathways for spinal cord injury via bioinformatics analysis.

The present study aimed to identify key genes and pathways associated with spinal cord injury (SCI) and subsequently investigate possible therapeutic targets for the condition. The array data of GSE20907 was downloaded from the Gene Expression Omnibus database and 24 gene chips, including 3­day, 4­day, 1­week, 2­week and 1­month post­SCI together with control propriospinal neurons, were used for the analysis. The raw data was normalized and then the differentially expressed genes (DEGs) in the (A) 2­week post­SCI group vs. control group, (B) 1­month post­SCI group vs. control group, (C) 1­month and 2­week post­SCI group vs. control group, and (D) all post­SCI groups vs. all control groups, were analyzed with a limma package. Gene Ontology annotation and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses for DEGs were performed. Cluster analysis was performed using ClusterOne plugins. All the DEGs identified were associated with immune and inflammatory responses. Signal transducer and activator of transcription 3 (STAT3), erb­B2 receptor tyrosine kinase 4 (ERBB4) and cytochrome B­245, α polypeptide (CYBA) were in the network diagrams of (A), (C) and (D), respectively. The enrichment analysis of DEGs identified in all samples demonstrated that the DEGs were also enriched in the chemokine signaling pathway (enriched in STAT3) and the high­affinity immunoglobulin E receptor (FcεRI) signaling pathway [enriched in proto­oncogene, src family tyrosine kinase (LYN)]. Immune and inflammatory responses serve significant roles in SCI. STAT3, ERBB4 and CYBA may be key genes associated with SCI at certain stages. Furthermore, STAT3 and LYN may be involved in the development of SCI via the chemokine and FcεRI signaling pathways, respectively.