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<P>The use of radioisotopes has a long history in biomedical science, and the technique of accelerator mass spectrometry (AMS), an extremely sensitive nuclear physics technique for detection of very low-abundant, stable and long-lived isotopes, has now revolutionized high-sensitivity isotope detection in biomedical research, because it allows the direct determination of the amount of isotope in a sample rather than measuring its decay, and thus the quantitative analysis of the fate of the radiolabeled probes under the given conditions. Since AMS was first used in the early 90's for the analysis of biological samples containing enriched <SUP>14</SUP>C for toxicology and cancer research, the biomedical applications of AMS to date range from <I>in vitro </I>to <I>in vivo </I>studies, including the studies of 1) toxicant and drug metabolism, 2) neuroscience, 3) pharmacokinetics, and 4) nutrition and metabolism of endogenous molecules such as vitamins. In addition, a new drug development concept that relies on the ultrasensitivity of AMS, known as human microdosing, is being used to obtain early human metabolism information of candidate drugs. These various aspects of AMS are reviewed and a perspective on future applications of AMS to biomedical research is provided.</P>
<P><B>Background</B></P><P>Finding biomedical named entities is one of the most essential tasks in biomedical text mining. Recently, deep learning-based approaches have been applied to biomedical named entity recognition (BioNER) and showed promising results. However, as deep learning approaches need an abundant amount of training data, a lack of data can hinder performance. BioNER datasets are scarce resources and each dataset covers only a small subset of entity types. Furthermore, many bio entities are polysemous, which is one of the major obstacles in named entity recognition.</P><P><B>Results</B></P><P>To address the lack of data and the entity type misclassification problem, we propose CollaboNet which utilizes a combination of multiple NER models. In CollaboNet, models trained on a different dataset are connected to each other so that a target model obtains information from other collaborator models to reduce false positives. Every model is an expert on their target entity type and takes turns serving as a target and a collaborator model during training time. The experimental results show that CollaboNet can be used to greatly reduce the number of false positives and misclassified entities including polysemous words. CollaboNet achieved state-of-the-art performance in terms of precision, recall and F1 score.</P><P><B>Conclusions</B></P><P>We demonstrated the benefits of combining multiple models for BioNER. Our model has successfully reduced the number of misclassified entities and improved the performance by leveraging multiple datasets annotated for different entity types. Given the state-of-the-art performance of our model, we believe that CollaboNet can improve the accuracy of downstream biomedical text mining applications such as bio-entity relation extraction.</P>
<P><B>Background</B></P><P>Due to the advent of deep learning, the increasing number of studies in the biomedical domain has attracted much interest in feature extraction and classification tasks. In this research, we seek the best combination of feature set and hyperparameter setting of deep learning algorithms for relation classification. To this end, we incorporate an entity and relation extraction tool, PKDE4J to extract biomedical features (i.e., biomedical entities, relations) for the relation classification. We compared the chosen Convolutional Neural Networks (CNN) based classification model with the most widely used learning algorithms.</P><P><B>Results</B></P><P>Our CNN based classification model outperforms the most widely used supervised algorithms. We achieved a significant performance on binary classification with a weighted macro-average F1-score: 94.79% using pre-extracted relevant feature combinations. For multi-class classification, the weighted macro-average F1-score is estimated around 86.95%.</P><P><B>Conclusions</B></P><P>Our results suggest that our proposed CNN based model using the not only single feature as the raw text of the sentences of biomedical literature, but also coupling with multiple and highlighted features extracted from the biomedical sentences could improve the classification performance significantly. We offer hyperparameter tuning and optimization approaches for our proposed model to obtain optimal hyperparameters of the models with the best performance.</P>
<P>Avian leukosis virus (ALV) is a retrovirus that causes tumors in avian species, and its vertical and horizontal transmission in poultry flocks results in enormous economic losses. Despite the discovery of specific host receptors, there have been few reports on the modulation of viral susceptibility via genetic modification. We therefore engineered acquired resistance to ALV subgroup B using CRISPR/Cas9-mediated genome editing technology in DF-1 chicken fibroblasts. Using this method, we efficiently modified the tumor virus locus B (<I>tvb</I>) gene, encoding the TVB receptor, which is essential for ALV subgroup B entry into host cells. By expanding individual DF-1 clones, we established that artificially generated premature stop codons in the cysteine-rich domain (CRD) of TVB receptor confer resistance to ALV subgroup B. Furthermore, we found that a cysteine residue (C80) of CRD2 plays a crucial role in ALV subgroup B entry. These results suggest that CRISPR/Cas9-mediated genome editing can be used to efficiently modify avian cells and establish novel chicken cell lines with resistance to viral infection.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1186/s13567-017-0454-1) contains supplementary material, which is available to authorized users.</P>
<P><B>Introduction</B></P><P>Liver X receptors are established sensors of lipid and cholesterol homeostasis. Recent studies have reported that these receptors are involved in the regulation of inflammation and immune responses. We attempted to identify single nucleotide polymorphisms (SNPs) of the <I>NR1H3</I> gene associated with the susceptibility to systemic lupus erythematosus (SLE).</P><P><B>Methods</B></P><P>SNPs were genotyped using SNaPSHOT assay in 300 Korean patients with SLE and 217 normal controls (NC), and in replication samples (160 SLE patients and 143 NC). Also, the functional effects of <I>NR1H3</I> gene promoter polymorphisms were analyzed using a luciferase assay, real-time polymerase chain reaction, B cell proliferation assay and an electrophoretic mobility shift assay.</P><P><B>Results</B></P><P>We identified five polymorphisms: -1851 T > C (rs3758673), -1830 T > C (rs3758674), -1003 G > A (new), -840 C > A (rs61896015) and -115 G > A (rs12221497). There was a significant and reproducible difference in the -1830 T > C, -1003 G > A and -115 G > A polymorphisms between the SLE and the NC. Luciferase activity of the structure containing -1830 C was less enhanced compared to the structure containing -1830 T in basal, GW3965 and T0901317 treated Hep3B cells (<I>P</I> = 0.009, <I>P</I> = 0.034 and <I>P</I> <0.001, respectively). Proliferation of the -1830 TC type was increased compared to the -1830 TT type in basal, GW3965 and T0901317 treated B cells from SLE patients (<I>P</I> = 0.011, <I>P</I> = 0.040 and <I>P</I> = 0.017, respectively). Transcription factor GATA-3 preferentially bound the -1830 T allele in the promoter.</P><P><B>Conclusions</B></P><P><I>NR1H3</I> genetic polymorphisms may be associated with disease susceptibility and clinical manifestations of SLE. Specifically, -1830 T > C polymorphism within <I>NR1H3</I> promoter region may be involved in regulation of <I>NR1H3</I> expression.</P>
<P><B>Background</B></P><P>The overexpression of histone deacetylase (HDAC) and a subsequent decrease in the acetylation levels of nuclear histones are frequently observed in cancer cells. Generally it was accepted that the deacetylation of histones suppressed expression of the attached genes. Therefore, it has been suggested that HDAC might contribute to the survival of cancer cells by altering the NKG2D ligands transcripts. By the way, the translational regulation of NKG2D ligands remaines unclear in cancer cells. It appears the modulation of this unclear mechanism could enhance NKG2D ligand expressions and the susceptibility of cancer cells to NK cells. Previously, it was reported that irradiation can increase the surface expressions of NKG2D ligands on several cancer cell types without increasing the levels of NKG2D ligand transcripts via ataxia telangiectasia mutated and ataxia telangiectasia and Rad3 related (ATM-ATR) pathway, and suggested that radiation therapy might be used to increase the translation of NKG2D ligands.</P><P><B>Methods</B></P><P>Two NSCLC cell lines, that is, A549 and NCI-H23 cells, were used to investigate the combined effects of ionizing radiation and HDAC inhibitors on the expressions of five NKG2D ligands. The mRNA expressions of the NKG2D ligands were quantitated by multiplex reverse transcription-PCR. Surface protein expressions were measured by flow cytometry, and the susceptibilities of cancer cells to NK cells were assayed by time-resolved fluorometry using the DELFIA® EuTDA cytotoxicity kit and by flow cytometry.</P><P><B>Results</B></P><P>The expressions of NKG2D ligands were found to be regulated at the transcription and translation levels. Ionizing radiation and HDAC inhibitors in combination synergistically increased the expressions of NKG2D ligands. Furthermore, treatment with ATM-ATR inhibitors efficiently blocked the increased translations of NKG2D ligands induced by ionizing radiation but did not block the increased ligand translations induced by HDAC inhibitors. The study confirms that increased NKG2D ligand levels by ionizing radiation and HDAC inhibitors could synergistically enhance the susceptibilities of cancer cells to NK-92 cells.</P><P><B>Conclusions</B></P><P>This study suggests that the expressions of NKG2D ligands are regulated in a complex manner at the multilevel of gene expression, and that their expressions can be induced by combinatorial treatments in lung cancer cells.</P>
<P><B>Introduction</B></P><P>Wnt ligands bind to low-density lipoprotein receptor–related protein (LRP) 5 or 6, triggering a cascade of downstream events that include β-catenin signaling. Here we explored the roles of LRP5 in interleukin 1β (IL-1β)- or Wnt-mediated osteoarthritic (OA) cartilage destruction in mice.</P><P><B>Methods</B></P><P>The expression levels of LRP5, type II collagen, and catabolic factors were determined in mouse articular chondrocytes, human OA cartilage, and mouse experimental OA cartilage. Experimental OA in wild-type, <I>Lrp5</I> total knockout (<I>Lrp5</I><SUP>-/-</SUP>) and chondrocyte-specific knockout (<I>Lrp5</I><SUP><I>fl/fl</I></SUP>;<I>Col2a1-cre</I>) mice was caused by aging, destabilization of the medial meniscus (DMM), or intra-articular injection of collagenase. The role of LRP5 was confirmed <I>in vitro</I> by small interfering RNA–mediated knockdown of <I>Lrp5</I> or in <I>Lrp5</I><SUP>-/-</SUP> cells treated with IL-1β or Wnt proteins.</P><P><B>Results</B></P><P>IL-1β treatment increased the expression of LRP5 (but not LRP6) via JNK and NF-κB signaling. LRP5 was upregulated in human and mouse OA cartilage, and <I>Lrp5</I> deficiency in mice inhibited cartilage destruction. Treatment with IL-1β or Wnt decreased the level of <I>Col2a1</I> and increased those of <I>Mmp3</I> or <I>Mmp13</I>, whereas <I>Lrp5</I> knockdown ameliorated these effects. In addition, we found that the functions of LRP5 in arthritic cartilage were subject to transcriptional activation by β-catenin. Moreover, <I>Lrp5</I><SUP>-/-</SUP> and <I>Lrp5</I><SUP><I>fl/fl</I></SUP>;<I>Col2a1-cre</I> mice exhibited decreased cartilage destruction (and related changes in gene expression) in response to experimental OA.</P><P><B>Conclusions</B></P><P>Our findings indicate that LRP5 (but not LRP6) plays an essential role in Wnt/β-catenin-signaling-mediated OA cartilage destruction in part by regulating the expression levels of type II collagen, MMP3, and MMP13.</P>
Kim, Dong Wook,Chung, Kwangzoo,Chung, Weon Kuu,Bae, Sun Hyun,Shin, Dong Oh,Hong, Seongeon,Park, Sung Ho,Park, Sung-Yong,Hong, Chae-Seon,Lim, Young Kyung,Shin, Dongho,Lee, Se Byeong,Lee, Hyun-ho,Sung, BioMed Central 2014 Radiation oncology Vol.9 No.-
<P><B>Purpose</B></P><P>To evaluate and compare the risks of secondary cancers from therapeutic doses received by patients with hepatocellular carcinoma (HCC) during intensity-modulated radiotherapy (IMRT), volumetric arc therapy (VMAT), and tomotherapy (TOMO).</P><P><B>Methods</B></P><P>Treatments for five patients with hepatocellular carcinoma (HCC) were planned using IMRT, VMAT, and TOMO. Based on the Biological Effects of Ionizing Radiation VII method, the excess relative risk (ERR), excess absolute risk (EAR), and lifetime attributable risk (LAR) were evaluated from therapeutic doses, which were measured using radiophotoluminescence glass dosimeters (RPLGDs) for each organ inside a humanoid phantom.</P><P><B>Results</B></P><P>The average organ equivalent doses (OEDs) of 5 patients were measured as 0.23, 1.18, 0.91, 0.95, 0.97, 0.24, and 0.20 Gy for the thyroid, lung, stomach, liver, small intestine, prostate (or ovary), and rectum, respectively. From the OED measurements, LAR incidence were calculated as 83, 46, 22, 30, 2 and 6 per 10<SUP>4</SUP> person for the lung, stomach, normal liver, small intestine, prostate (or ovary), and rectum.</P><P><B>Conclusions</B></P><P>We estimated the secondary cancer risks at various organs for patients with HCC who received different treatment modalities. We found that HCC treatment is associated with a high secondary cancer risk in the lung and stomach.</P>
Jin, Hye Mi,Kim, Tae-Jong,Choi, Jung-Ho,Kim, Moon-Ju,Cho, Young-Nan,Nam, Kwang-Il,Kee, Seung-Jung,Moon, Jang Bae,Choi, Seok-Yong,Park, Dong-Jin,Lee, Shin-Seok,Park, Yong-Wook BioMed Central 2014 ARTHRITIS RESEARCH AND THERAPY Vol.16 No.2
<P><B>Introduction</B></P><P>Gout is characterized by episodes of intense joint inflammation in response to intra-articular monosodium urate monohydrate (MSU) crystals. miR-155 is crucial for the proinflammatory activation of human myeloid cells and antigen-driven inflammatory arthritis. The functional role of miR-155 in acute gouty arthritis has not been defined. Therefore, the aim of this study was to examine the role of miR-155 in pathogenesis of acute gouty arthritis.</P><P><B>Methods</B></P><P>Samples from 14 patients with acute gouty arthritis and 10 healthy controls (HCs) were obtained. Peripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) were cultured <I>in vitro</I> with MSU crystals, and gene expression (human miR-155 and SHIP-1) were assessed by real-time PCR. THP-1 cells were stimulated by MSU crystals and/or miR-155 transfection and then subjected to Western blot analysis. Levels of human tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-1β in cell culture supernatants were measured by Luminex. Immunohistochemistry was performed on formalin-fixed gout tissues with anti–SHIP-1 antibody. A C57BL/6 J male mouse model of gout was used to analyze the expressions of miR-155, SHIP-1, and inflammatory cytokines.</P><P><B>Results</B></P><P>The samples from gouty arthritis were highly enriched in miR-155, with levels of expression being higher than those found in PBMC from HC. Treatment of the cells with MSU crystals strongly induced miR-155. In addition, overexpression of miR-155 in the cells decreased levels of SHIP-1 and promoted production of MSU-induced proinflammatory cytokines, such as TNF-α and IL-1β. Consistent with <I>in vitro</I> observations, miR-155 expression was elevated in the mouse model of gout. The production of inflammatory cytokines was markedly increased in MSU crystal induced peritonitis mice.</P><P><B>Conclusions</B></P><P>Overexpression of miR-155 in the gouty SFMC leads to suppress SHIP-1 levels and enhance proinflammatory cytokines.</P>
<P><I>Cordyceps</I> belongs to a genus of acormycete fungi and is known to exhibit various pharmacological effects. The aim of this study was to investigate the effect of <I>Cordyceps</I> species on the proliferation of vascular smooth muscle cells (VSMC) and their underlying molecular mechanism. A cell proliferation assay showed that <I>Cordyceps bassiana</I> ethanol extract (CBEE) significantly inhibited VSMC proliferation. In addition, neointimal formation was significantly reduced by treatment with CBEE in the carotid artery of balloon-injured rats. We also investigated the effects of CBEE on the extracellular signal-regulated kinase (ERK) signal pathway. Western blot analysis revealed increased ERK 1/2 phosphorylation in VSMCs treated with CBEE. Pretreatment with U0126 completely abrogated CBEE-induced ERK 1/2 phosphorylation. In conclusion, CBEE exhibited anti-proliferative properties that affected VSMCs through the ERK1/2 MAPK signaling pathway. Our data may elucidate the inhibitory mechanism of this natural product<I>.</I></P>