bluuebunny/crossref_metadata_2025_split huggingface dataset:
HANDBOOK OF ATTACHMENT, THIRD EDITION: THEORY, RESEARCH, AND CLINICAL APPLICATIONSJudeCassidy and Phillip R.Shaver (Eds.), New York: Guilford Press, 2016, 1,068 pp., ISBN 978‐1‐4625‐2529‐4
Authors: Negrini Lisa S. 
Published: August 2018

ABSTRACTJude Cassidy and Phillip R. Shaver's third edition of the Handbook of Attachment has emerged and set a new bar for formative texts on pivotal issues related to the field of attachment. This state‐of‐the‐science reference on attachment eloquently intertwines attachment theory, research, and clinical applications, giving us innovative conceptualizations and perspectives on both implications for clinical advancement and directions for future research. This handbook moves basic research findings quickly into the realm of clinical and community applications, providing the field with new information about intervention procedures and outcomes while setting the stage for theoretical advancement. New chapters reflect the way we think about the interweaving of attachment, development, and infant mental health research and application. From the authors’ opening “Overview of Attachment” to the summary overview and evaluation of the field, “The Place of Attachment in Development” by attachment‐research pioneer L. Alan Sroufe, this third edition broadly delivers the most significant and important information that the field has on attachment. Researchers, clinicians, and professionals will benefit from this handbook as it presents with the most up‐to‐date, innovative, and thorough presentation of attachment theory.
Biomineralization improves mechanical and osteogenic properties of multilayer‐modified PLGA porous scaffolds
Authors: Kong Junchao , Wei Bo , Groth Thomas , Chen Zhuming , Li Lihua , He Dongning , Huang Rui , Chu Jiaqi , Zhao Mingyan 
Published: August 2018

AbstractPoly‐(lactide‐co‐glycolide acid) (PLGA) has been widely investigated as scaffold material for bone tissue engineering owing to its biosafety, biodegradability, and biocompatibility. However, the bioinert surface of PLGA may fail in regulating cellular behavior and directing osteointegration between the scaffold and the host tissue. In this article, oxidized chondroitin sulfate (oCS) and type I collagen (Col I) were assembled onto PLGA surface via layer by layer technique (LbL) as an adhesive coating for the attachment of inorganic minerals. The multilayer‐modified PLGA scaffold was mineralized in vitro to ensure the deposition of nanohydroxyapatite (nHAP). It was found that nHAP crystals were more uniformly and firmly attached on the multilayer‐modified PLGA as compared with the pure PLGA scaffold, which remarkably improved PLGA surface and mechanical properties. Additionally, in vitro biocompatibility of PLGA scaffold, in terms of bone mesenchymal stem cells (BMSCs) attachment, spreading and proliferation was greatly enhanced by nHAP coating and multilayer deposition. Furthermore, the fabricated composite scaffold also shows the ability to promote the osteogenic differentiation of BMSCs through the up‐regulation of osteogenic marker genes. Thus, this novel biomimetic composite scaffold might achieve a desirable therapeutic result for bone tissue regeneration. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 2714–2725, 2018.
The efficacy of curcuminoids in improvement of ulcerative colitis symptoms and patients’ self‐reported well‐being: A randomized double‐blind controlled trial
Authors: Masoodi Mohsen , Mahdiabadi Mohammad Ali , Mokhtare Marjan , Agah Sharam , Kashani Amir Hossein Faghihi , Rezadoost Amir Mansoor , Sabzikarian Mohammad , Talebi Atefeh , Sahebkar Amirhossein 
Published: August 2018

AbstractBackgroundCurcuminoids are polyphenols with documented anti‐inflammatory activity and has been shown to improve the symptoms of several inflammatory diseases. We aimed to evaluate the effectiveness of a nanoformulation of curcuminoids in the treatment of ulcerative colitis.MethodsThis randomized double‐blinded controlled trial was conducted on 56 patients aged 18 years or older with the final diagnosis of mild to moderate ulcerative colitis according to the Simple Clinical Colitis Activity Index (SCCAI). The patients were randomly assigned (using a computerized random sampling table) to receive curcuminoids nanomicelles (80 mg, three times daily, orally) plus mesalamine (3 g/24 hours, orally) as the treatment group and placebo plus mesalamine (3 g/24 hours, orally) as the control group for a period of four weeks. The severity of disease was assessed at baseline and at the end of the second and fourth weeks of the treatment according to the SCCAI.ResultsThe score for urgency of defecation reduced significantly more in case group as compared with control group at four weeks after beginning the treatment. The patients in case group experienced better general condition than the control ones after 4 weeks of treatment. Overall, the mean SCCAI score was significantly lower in the patients received curcuminoids nanomicelles plus mesalamine as compared with the group received placebo plus mesalamine at fourth week after the treatment (1.71 ± 1.84 vs 2.68 ± 2.09, p = 0.050).ConclusionAdding curcuminoids nanomicelles to routine treatment of patients with ulcerative colitis is associated with a significant improvement of symptoms, including reduced frequency of urgent defecation, improved patients’ self‐reported well‐being and reduced clinical activity of ulcerative colitis. ClinicalTrials. “IRCT2017052634142N1”.
The dietary flavone luteolin epigenetically activates the Nrf2 pathway and blocks cell transformation in human colorectal cancer HCT116 cells
Authors: Zuo Qian , Wu Renyi , Xiao Xi , Yang Caizhi , Yang Yuqing , Wang Chao , Lin Lizhu , Kong Ah‐Ng 
Published: August 2018

AbstractColorectal cancer remains a leading malignancy in humans. The importance of epigenetic modification in the development of this disease is now being recognized. The reversible and dynamic nature of epigenetic modifications provides a promising strategy in colorectal cancer chemoprevention and treatment. Luteolin (LUT), a flavone dietary phytochemical, can modulate various signaling pathways involved in carcinogenesis. Many studies have demonstrated that LUT inhibits colorectal carcinogenesis by activating the Nuclear factor erythroid 2‐related factor 2 (Nrf2)/antioxidant‐responsive element (ARE) pathway. However, the potential epigenetic mechanism underlying Nrf2/ARE pathway activation remains unclear. In this study, we aimed to explore the anticancer potential of LUT in human colon cancer cells and the epigenetic regulation of the Nrf2/ARE pathway. Specifically, our data showed that LUT suppressed cell proliferation and cellular transformation of HCT116 and HT29 cells in a dose‐dependent manner. Additionally, quantitative real‐time polymerase chain reaction and Western blot analysis were performed to determine the mRNA and protein expression of Nrf2 and its downstream genes after LUT treatment. Bisulfite genomic sequencing revealed that methylation of the Nrf2 promoter region was decreased by LUT, corresponding with the increased mRNA expression of Nrf2. Decreased protein levels and enzyme activities of epigenetic modifying enzymes, such as DNA methyltransferases (DNMTs) and histone deacetylases (HDACs), were also observed in LUT‐treated HCT116 cells. In summary, our findings suggest that LUT may exert its antitumor activity in part via epigenetic modifications of the Nrf2 gene with subsequent induction of its downstream antioxidative stress pathway.
The prognostic value of long noncoding RNA MEG3 expression in the survival of patients with cancer: A meta‐analysis
Authors: Binabaj Maryam Moradi , Bahrami Afsane , Bahreyni Amirhossein , Shafiee Mojtaba , Rahmani Farzad , Khazaei Majid , Soleimanpour Saman , Ghorbani Elnaz , Fiuji Hamid , Ferns Gordon A. , Ryzhikov Mikhail , Avan Amir , Hassanian Seyed Mahdi 
Published: August 2018

AbstractLong noncoding RNAs (lncRNAs) play an important role in carcinogenesis and cancer progression. lncRNA maternally expressed gene 3 (MEG3) is a tumor suppressor that is downregulated in several cancers. However, its prognostic value in human malignancies remains controversial. We have therefore undertaken a meta‐analysis to explore the relationship between cancer survival and the expression of lncRNA MEG3. A systematic literature search identified 13 potentially eligible investigations comprising 1733 patients in nine different cancer types. In the pooled analysis, a low expression of MEG3 was associated with low overall survival (OS) in patients with cancer having a combined hazard ratio (HR) of 0.830 (HR = 0.83; 95% CI: 0.70‐0.98; p = 0.03; random effect model). However, subgroup analysis according to cancer type revealed that MEG3 expression was not associated with better OS in gastrointestinal cancer (HR = 0.58, 95% CI = 0.33‐1.03; p = 0.06), and patients with breast cancer (HR = 0.85, 95% CI: 0.12‐5.88; p = 0.87). In conclusion, our results demonstrate that only in the pooled analysis, there was a significant relationship between MEG3 expression and cancer survival. Further investigation of other molecular biomarkers involved in tumorigenesis‐related pathways is necessary.
Transcriptome analysis reveals an altered expression profile of zinc transporters in colorectal cancer
Authors: Barresi Vincenza , Valenti Giovanna , Spampinato Giorgia , Musso Nicolò , Castorina Sergio , Rizzarelli Enrico , Condorelli Daniele Filippo 
Published: August 2018

AbstractZinc is a transition metal and catalytic cofactor involved in many biological processes including proliferation, development, differentiation, and metabolism. Zinc transporters (ZnTs) play a fundamental role in cellular zinc homeostasis. ZnTs are responsible of zinc efflux and are encoded by 10 genes belonging to solute carrier family 30A (SLC30A1‐10), while zinc‐regulated transporter (ZRT)/iron‐regulated transporter (IRT)‐like protein (ZIP) transporters are responsible for the influx of zinc into the cytoplasm and are encoded by 14 genes belonging to solute carrier family 39A (SLC39A1‐14). In this study, we analyzed, by transcriptome analysis, the microRNA levels of ZnT‐encoding and ZIP‐encoding genes in colorectal cancer (CRC) samples matched to normal colon tissues and in CRC cell lines. Results revealed an upregulation of specific ZnT and ZIP transcripts in CRC. Upregulation of SLC30A5, SLC30A6, SLC30A7 transcripts, encoding zinc efflux transporters ZnT5, ZnT6, ZnT7, localized on endoplasmic reticulum membranes, might be part of a coordinated transcriptional program associated to the increased activity of the early secretory pathway, while transcriptional upregulation of several specific ZIP transporters (SLC39A6, SLC39A7, SLC39A9, SLC39A10, and SLC39A11) could contribute in meeting the increased demand of zinc in cancer cells. Moreover, exon‐level analysis of SLC30A9, a nuclear receptor coactivator involved in the transcriptional regulation of Wnt‐responsive genes, revealed the differential expression of alternative transcripts in CRC and normal colonic mucosa.
Integrative analysis of significant RNA‐binding proteins in colorectal cancer metastasis
Authors: Zhou Bin , Guo Rui 
Published: August 2018

AbstractThe aberrant expression of RNA‐binding proteins (RBPs) plays a crucial role in the occurrence and progression of human cancer. However, the key functions of RBPs in the metastasis of colorectal cancer have not yet been fully elucidated. Here, we integrated multi‐omics data and identified four differentially expressed RBPs (APOBEC3G, EEF1A2, EIF5AL1 and CELF3) in patients with colorectal cancer metastasis. To clarify the underlying molecular mechanisms, we systematically analyzed the genomic features and downstream regulatory relationships of the four RBPs. In a genomic level, the copy number variations of APOBEC3G, EEF1A2, and CELF3 demonstrated significantly differential distributions between metastatic and nonmetastatic patients. Besides that, combining sequence and expression information, we identified 436 putative RNA targets regulated by the four RBPs through strict multistep bioinformatics screening. For the downstream analysis, the evidence from functional enrichment analysis and public literature indicated the roles of these target genes in the carcinogenesis and progression of colorectal cancer. Furthermore, through the machine learning algorithm and statistical analysis, we obtained two gene candidates that had obvious effects on the metastasis and overall survival status of patients with colorectal cancer. In summary, our study comprehensively explored the influence of APOBEC3G, EEF1A2, EIF5AL1, and CELF3 in colorectal cancer metastasis, which may offer favorable perspectives for clinical diagnosis and therapy.
The oncoprotein Myc controls the phosphorylation of S6 kinase and AKT through protein phosphatase 2A
Authors: Chellini Lidia , Monteleone Valentina , Lombari Malinska , Caldarola Sara , Loreni Fabrizio 
Published: August 2018

AbstractThis study focuses on the effects of Myc oncoprotein on the translational apparatus of the cell. Translation is an energy consuming process that involves a large number of accessory factors. The production of components of the protein synthesis machinery can be regulated at the transcriptional level by specific factors. It has been shown that the product of the oncogene Myc, a transcription factor frequently activated in cancer, can control translational activity through an increase in the transcription of the eIF4F complex components (eIF4E, eIF4AI, and eIF4GI). However, additional effects at the posttranslational level have also been described. For instance, it has been shown that Myc upregulation can induce mammalian target of rapamycin (mTOR)–dependent 4E‐binding protein 1 (4E‐BP1) hyperphosphorylation. We induced overexpression or inhibition of Myc through transfection of complementary DNA constructs or specific small interfering RNA in PC3 (prostate carcinoma) and HeLa (cervical carcinoma) cells. We have observed that overexpression of Myc causes an increase in 4E‐BP1 phosphorylation and activation of protein synthesis. Unexpectedly, we detected a parallel decrease in the phosphorylation level of S6 kinase (in PC3 and HeLa) and AKT (in HeLa). We report evidence that these changes are mediated by an increase in protein phosphatase 2A activity.
Exploring the effect of E76K mutation on SHP2 cause gain‐of‐function activity by a molecular dynamics study
Authors: Li Wei‐Ya , Wei Hui‐Yu , Sun Ying‐Zhan , Zhou Hui , Ma Ying , Wang Run‐Ling 
Published: August 2018

AbstractJuvenile myelomonocytic leukemia (JMML), an invasive myeloproliferative neoplasm, is a childhood disease with very high clinical lethality. Somatic mutation E76K in SHP2 is the most commonly identified mutation found in up to 35% of patients with JMML. To investigate the effect of gain‐of‐function mutation‐E76K on SHP2 activity, molecular dynamic simulations on the wild‐type SHP2 (SHP2‐WT) system and the mutated E76K (SHP2‐E76K) system were performed. The evaluation of stability of these two systems indicated that the simulated trajectories were stable after simulation for 3 nanoseconds. The root mean square fluctuation and the per‐residue root mean square deviation illustrated that there were two regions (residues Tyr 81‐Glu 83 and Glu 258‐Leu 261) in the wild‐type system and the mutated system, which had large differences. The principal component analysis, dynamic cross correlation maps analysis, as well as secondary structure analysis suggested that the mutated E76K impacted the movement of these two regions in SHP2 protein. Furthermore, residue interaction network analysis, hydrogen bond occupancy, and binding free energies analysis were used to explain how the two regions were specifically affected by the mutant. The results indicated that the primary variances between SHP2‐WT and SHP2‐E76K were the different interactions between Glu/Lys 76 and Arg 265, Tyr 80 and Leu 77, Leu 77 and Tyr 81, Thr 73 and Glu 258, Ala 75 and Cys 259, Phe 71 and Tyr 81, Ala 75 and Glu 258, and Tyr 73 and Glu/Lys 76. Consequently, these findings here might provide insights into the increased activity in SHP2‐E76K.
Oxidative damage in glutaric aciduria type I patients and the protective effects of l‐carnitine treatment
Authors: Guerreiro Gilian , Faverzani Jéssica , Jacques Carlos Eduardo Diaz , Marchetti Desirèe P. , Sitta Angela , de Moura Coelho Daniella , Kayser Aline , Kok Fernando , Athayde Larissa , Manfredini Vanusa , Wajner Moacir , Vargas Carmen Regla 
Published: August 2018

AbstractThe deficiency of the enzyme glutaryl‐CoA dehydrogenase, known as glutaric acidemia type I (GA‐I), leads to the accumulation of glutaric acid (GA) and glutarilcarnitine (C5DC) in the tissues and body fluids, unleashing important neurotoxic effects. l‐carnitine (l‐car) is recommended for the treatment of GA‐I, aiming to induce the excretion of toxic metabolites. l‐car has also demonstrated an important role as antioxidant and anti‐inflammatory in some neurometabolic diseases. This study evaluated GA‐I patients at diagnosis moment and treated the oxidative damage to lipids, proteins, and the inflammatory profile, as well as in vivo and in vitro DNA damage, reactive nitrogen species (RNS), and antioxidant capacity, verifying if the actual treatment with l‐car (100 mg kg−1 day−1) is able to protect the organism against these processes. Significant increases of GA and C5DC were observed in GA‐I patients. A deficiency of carnitine in patients before the supplementation was found. GA‐I patients presented significantly increased levels of isoprostanes, di‐tyrosine, urinary oxidized guanine species, and the RNS, as well as a reduced antioxidant capacity. The l‐car supplementation induced beneficial effects reducing these biomarkers levels and increasing the antioxidant capacity. GA, in three different concentrations, significantly induced DNA damage in vitro, and the l‐car was able to prevent this damage. Significant increases of pro‐inflammatory cytokines IL‐6, IL‐8, GM‐CSF, and TNF‐α were shown in patients. Thus, the beneficial effects of l‐car presented in the treatment of GA‐I are due not only by increasing the excretion of accumulated toxic metabolites, but also by preventing oxidative damage.
Licochalcone C induced apoptosis in human oral squamous cell carcinoma cells by regulation of the JAK2/STAT3 signaling pathway
Authors: Oh Ha‐Na , Seo Ji‐Hye , Lee Mee‐Hyun , Kim Cheolhee , Kim Eunae , Yoon Goo , Cho Seung‐Sik , Cho Young Sik , Choi Hyun Woo , Shim Jung‐Hyun , Chae Jung‐Il 
Published: August 2018

AbstractOral cancer is of an aggressive malignancy that arises on oral cavity and lip, 90% of cancers histologically originated in the squamous cells. Licochalcone (LC)C has been known as natural phenolic chalconoid substances, and its origin is the root of Glycyrrhiza glabra or Glycyrrhiza inflata. LCC inhibited oral squamous cell carcinoma (OSCC) cell viability, mitochondrial function, and anchorage‐independent growth in a dose‐dependent manner. To investigate the ability of LCC to target Janus kinase 2 (JAK2), we performed pull‐down binding assay, kinase assay, and docking simulation. The molecular docking studies were performed between JAK2 and the potent inhibitor LCC. It was shown that LCC tightly interacted with ATP‐binding site of JAK2. In addition, LCC inhibited the JAK2/signal transducer and activator of transcription 3 pathway, upregulated p21, and downregulated Bcl‐2, Mcl‐1, and Survivin, while it disrupted mitochondrial membrane potential and subsequently caused cytochrome c release with activation of multi‐caspase, eventually leading to apoptosis in HN22 and HSC4 cells. LCC elevated the protein levels of Bax, cleaved Bid and PARP, and increased Apaf‐1, and this effect was reversed by LCC treatment. Our results demonstrated that treatment of OSCC cells with LCC induced the death receptor (DR)4 and DR5 expression level with the generation of reactive oxygen species and the upregulation of CHOP protein expression. Taken together, these results could provide the basis for clinical application as a new therapeutic strategy in the treatment of oral cancer.
Isolation of AccGalectin1 from Apis cerana cerana and its functions in development and adverse stress response
Authors: Wang Lijun , Wang Chen , Li Han , Yang Xinxin , Wang Ying , Guo Xingqi , Xu Baohua 
Published: August 2018

AbstractThe galectins are a family of lectins that play important roles in development, immunity, and the regulation of cellular responses. Much research has focused on the functions of galectins in mammals, though less in insects. Here, we identified the AccGalectin1 gene in Apis cerana cerana for the first time and explored its functions. The open reading frame of AccGalectin1 is 1449 base pairs and encodes a 482‐amino‐acid protein. AccGalectin1 expression was high during the transition between developmental stages and was high in the head, thorax, and epidermis compared with its levels in other tissues. In addition, the expression of AccGalectin1 was induced by several adverse stresses, including both abiotic and biotic stresses. A disk diffusion assay of recombinant AccGalectin1 protein revealed possible roles in protecting cells from oxidative stress. Furthermore, the expression levels of multiple oxidative genes (AccCAT, AccTpx1, AccTrx2, etc) were increased after AccGalectin1 was knocked down in Apis cerana cerana using RNA interference. We also observed that the malondialdehyde content in the AccGalectin1‐silenced bees was higher than that in the control bees, while the antioxidant enzymatic activities of superoxide dismutase and peroxidase were lower. Considering these results, we suggest that AccGalectin1 may be indispensable for protecting honeybees from biotic and abiotic damage by participating in the oxidative resistance response and the immune response. These results may provide insight into the precise functions of galectins in mammals and other insects.
Neutrophil‐to‐C3 ratio and neutrophil‐to‐lymphocyte ratio were associated with disease activity in patients with systemic lupus erythematosus
Authors: Yu Jianlin , Zeng Tingting , Wu Yang , Tian Yongjian , Tan Liming , Duan Xinwang , Wu Qiong , Li Hua , Yu Le 
Published: August 2018

BackgroundSystemic lupus erythematosus is prone to recurrent attacks, and its treatment is related to disease activities. It is important to accurately assess the patient's disease activity. So, the purpose of this study was to investigate the relation between neutrophil‐to‐C3 ratio (NC3R), neutrophil‐to‐lymphocyte ratio (NLR), and disease activity in patients with Systemic lupus erythematosus (SLE).MethodsThis was a retrospective study. One hundred and ninety‐four patients with SLE and 71 healthy controls were included in this study. We divided the patients into two groups according to the SLE disease activity (SLEDAI). Group 1 included patients with a score of >9 (patients with severe disease activity), and Group 2 included patients with a score of 9 and lower (patients with mild disease activity). Correlations between NC3R, NLR, and disease activity were analyzed.ResultsNC3R and NLR in patients with SLE were obviously higher compared to healthy controls (P < 0.05). There was an obviously significant difference in NC3R and NLR between Group 1 and Group 2 (P < 0.05). SLEDAI scores were positively correlated with NC3R (r = 0.353, P < 0.01) and NLR (r = 0.237, P = 0.01). Receiver operating characteristic (ROC) curve analysis showed that the cutoff value of NC3R to identify SLE with high disease activity was 5.935, with sensitivity and specificity being 75.9% and 67.0%, while that of NLR was 2.293, with sensitivity being 68.9% and specificity being 82.8%.ConclusionNC3R and NLR are two useful inflammatory markers for evaluating disease activity in patients with SLE.