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  • Oxford University Press (OUP)  (15)
  • 2015-2019  (15)
  • 2019  (15)
  • 1
    In: Database, Oxford University Press (OUP), Vol. 2019 ( 2019-01-01)
    Abstract: Document recommendation systems for locating relevant literature have mostly relied on methods developed a decade ago. This is largely due to the lack of a large offline gold-standard benchmark of relevant documents that cover a variety of research fields such that newly developed literature search techniques can be compared, improved and translated into practice. To overcome this bottleneck, we have established the RElevant LIterature SearcH consortium consisting of more than 1500 scientists from 84 countries, who have collectively annotated the relevance of over 180 000 PubMed-listed articles with regard to their respective seed (input) article/s. The majority of annotations were contributed by highly experienced, original authors of the seed articles. The collected data cover 76% of all unique PubMed Medical Subject Headings descriptors. No systematic biases were observed across different experience levels, research fields or time spent on annotations. More importantly, annotations of the same document pairs contributed by different scientists were highly concordant. We further show that the three representative baseline methods used to generate recommended articles for evaluation (Okapi Best Matching 25, Term Frequency–Inverse Document Frequency and PubMed Related Articles) had similar overall performances. Additionally, we found that these methods each tend to produce distinct collections of recommended articles, suggesting that a hybrid method may be required to completely capture all relevant articles. The established database server located at https://relishdb.ict.griffith.edu.au is freely available for the downloading of annotation data and the blind testing of new methods. We expect that this benchmark will be useful for stimulating the development of new powerful techniques for title and title/abstract-based search engines for relevant articles in biomedical research.
    Type of Medium: Online Resource
    ISSN: 1758-0463
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2496706-3
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  • 2
    In: Journal of Experimental Botany, Oxford University Press (OUP), ( 2019-10-23)
    Abstract: Here, cytosine methylation at single-base resolution across the whole genome of cotton (Gossypium hirsutum L.) anthers was mapped using the whole-genome bisulfite sequencing technique, and the methylome changes associated with high-temperature (HT) stress were analysed in two cotton lines of the CMS system with contrasting HT stress tolerance. The cotton anther genome was found to display approximately 31.6%, 68.7%, 61.8%, and 21.8% methylation across all sequenced C sites and in the CG, CHG and CHH sequence contexts, respectively. In an integrated global methylome and transcriptome analysis, only promoter-unmethylated genes showed higher expression levels than promoter-methylated genes, whereas gene body methylation presented an obvious positive correlation with gene expression. The methylation profiles of transposable elements in cotton anthers were characterized, and more differentially methylated transposable elements were demethylated under HT stress. HT-induced promoter methylation changes caused upregulated expression of the mitochondrial respiratory chain enzyme-associated genes GhNDUS7, GhCOX6A, GhCX5B2, and GhATPBM, ultimately promoting a series of redox processes to form ATP for normal anther development under HT stress. In vitro application of the common DNA methylation inhibitor 5-azacytidine and accelerator methyl trifluoromethanesulfonate demonstrated that DNA demethylation promoted anther development, while increased methylation only partially inhibited anther development under HT stress.
    Type of Medium: Online Resource
    ISSN: 0022-0957 , 1460-2431
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 1466717-4
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2019
    In:  Epidemiologic Reviews Vol. 41, No. 1 ( 2019-01-31), p. 97-108
    In: Epidemiologic Reviews, Oxford University Press (OUP), Vol. 41, No. 1 ( 2019-01-31), p. 97-108
    Abstract: Eradication of Helicobacter pylori colonization has been reported to affect the progression of gastric cancer. A comprehensive literature search was performed from 1997 to 2017 using electronic databases. All randomized controlled trials (RCTs) and nonrandomized controlled trials (non-RCT) evaluated the effect of H. pylori eradication on development of gastric cancer. Four RCTs and 9 non-RCTs were included (n = 40,740 participants; 321,269 person-years). Overall, H. pylori eradication therapy was associated with a significantly reduced risk of gastric cancer (incidence rate ratio (IRR) = 0.52, 95% confidence interval (CI): 0.41, 0.65). Results of mixed-effect Poisson regression meta-analysis were similar to those of traditional meta-analyses. In stratified analyses, the IRRs were 0.59 (95% CI: 0.41, 0.86) in RCTs and 0.48 (95% CI: 0.36, 0.64) in non-RCTs. The IRRs were 0.45 (95% CI: 0.34, 0.61) in patients and 0.63 (95% CI: 0.44, 0.90) in the general population. Moreover, the relative risk reduction was approximately 77% on the development of noncardiac gastric cancer with H. pylori eradication therapy in China. Attributable risk percentage and population attributable risk percentage for Chinese patients were 77.08% and 75.33%, respectively, and for Japanese patients were 57.80% and 45.99%, respectively. H. pylori eradication therapy reduces the risk of noncardiac gastric cancer development. The findings indicate the importance of early intervention with H. pylori eradication therapy from the perspective of epidemiology.
    Type of Medium: Online Resource
    ISSN: 1478-6729
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2097603-3
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  • 4
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2019
    In:  Molecular Human Reproduction Vol. 25, No. 9 ( 2019-09-01), p. 550-561
    In: Molecular Human Reproduction, Oxford University Press (OUP), Vol. 25, No. 9 ( 2019-09-01), p. 550-561
    Abstract: Fibrotic tissue may contribute to the origin of some endometriosis-related symptoms, such as chronic pelvic pain and infertility. Alterations in the H19/miR-216a-5p/ACTA2 pathway may mediate the regulation of eutopic endometrial stromal cell (euESC) invasion and migration and may represent a potential mechanism underlying fibrous tissue formation or fibrosis in women with endometriosis. In this study, we aimed to determine the expression of H19 and ACTA2 in endometrial tissues of women with endometriosis. Two groups of 23 infertile women with endometriosis and 23 matched infertile women without endometriosis were investigated. Primary cultured cells of endometrial tissues were analyzed using RT-PCR and western blotting (WB) to determine expression of H19 and ACTA2. 5-Ethyl-2′-deoxyuridine, CCK8 and Transwell assays were used to study the functions of H19 and ACTA2. Human embryonic kidney 293 cells were used for luciferase assays to study miR-216a-5p binding sites with H19 and ACTA2. We found that H19 and ACTA2 levels were significantly higher in endometriosis euESCs than in control euESCs (P  〈  0.05) and were positively correlated in endometriosis euESCs. Luciferase assays indicated that H19 regulates ACTA2 expression via competition for inhibitory miR-216a-5p binding sites. Our results indicate that alterations in the estrogen/H19/miR-216a-5p/ACTA2 pathway regulated endometriosis euESC invasion and migration. Downregulation of H19 or ACTA2 inhibited endometriosis euESC invasion and migration; however, estrogen promoted endometriosis euESC invasion and migration via H19. The main limitation of our study was that experiments were conducted in vitro and further in vivo studies are required in the future. However, our study showed that primary cultured cells represented endometriosis cells more clearly than cell lines.
    Type of Medium: Online Resource
    ISSN: 1460-2407
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 1497467-8
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  • 5
    In: Journal of Pharmacy and Pharmacology, Oxford University Press (OUP), Vol. 72, No. 1 ( 2019-12-10), p. 29-43
    Abstract: Arctigenin (ARG) has been proved to inhibit the viability of hepatocellular carcinoma (HCC) via inducing apoptosis. However, the precise mechanism remains unknown. The present study was aimed to further investigate the mechanism of ARG against HCC in vitro and in vivo. Methods Arctigenin was applied in vitro and in vivo. Western blotting, immunohistochemistry, etc., were used to investigate the mechanisms. Key findings The time-dependent enhancement of Bax/Bcl-2 ratio, cytochrome c release, Fas and FasL levels, caspase cascade activation and the loss in the mitochondrial out membrane potential indicated that both intrinsic and extrinsic apoptotic pathways were triggered by ARG. Moreover, Jun NH2-terminal kinase (JNK) and p38 phosphorylated time-dependently. And inhibition of the phosphorylation of either p38 or JNK led to a significant reduction in HepG2 apoptosis, owing to the crucial roles of p38 and JNK played in regulating the apoptosis pathways. In addition, ARG increased the generation of reactive oxygen species (ROS) in HepG2 cells, while the antioxidant N-acetyl cysteine almost reversed ARG-induced JNK and p38 activation, and dramatically decreased cell apoptosis. In vivo, ARG increased the cell apoptosis in tumour tissues, and p-p38, p-JNK and Bax were significantly upregulated. Conclusions Our findings demonstrated that ARG induced apoptosis in HCC via ROS-mediated mitogen-activated protein kinases apoptosis pathway.
    Type of Medium: Online Resource
    ISSN: 0022-3573 , 2042-7158
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2041988-0
    detail.hit.zdb_id: 2050532-2
    SSG: 15,3
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  • 6
    In: Horticulture Research, Oxford University Press (OUP), Vol. 6, No. 1 ( 2019-12)
    Abstract: The dwarf architecture is an important and valuable agronomic trait in watermelon breeding and has the potential to increase fruit yield and reduce labor cost in crop cultivation. However, the molecular basis for dwarfism in watermelon remains largely unknown. In this study, a recessive dwarf allele (designated as Cldf ( Citrullus lanatus dwarfism )) was fine mapped in a 32.88 kb region on chromosome 09 using F 2 segregation populations derived from reciprocal crossing of a normal line M08 and a dwarf line N21. Gene annotation of the corresponding region revealed that the Cla015407 gene encoding a gibberellin 3β-hydroxylase functions as the best possible candidate gene for Cldf . Sequence analysis showed that the fourth polymorphism site (a G to A point mutation) at the 3′ AG splice receptor site of the intron leads to a 13 bp deletion in the coding sequence of Cldf in dwarf line N21 and thus results in a truncated protein lacking the conserved domain for binding 2-oxoglutarate. In addition, the dwarf phenotype of Cldf could be rescued by exogenous GA 3 application. Phylogenetic analysis suggested that the small multigene family GA3ox (GA3 oxidase) in cucurbit species may originate from three ancient lineages in Cucurbitaceae. All these data support the conclusion that Cldf is a GA-deficient mutant, which together with the cosegregated marker can be used for breeding new dwarf cultivars.
    Type of Medium: Online Resource
    ISSN: 2662-6810 , 2052-7276
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2781828-7
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  • 7
    In: Plant and Cell Physiology, Oxford University Press (OUP), Vol. 60, No. 3 ( 2019-03-01), p. 587-598
    Type of Medium: Online Resource
    ISSN: 0032-0781 , 1471-9053
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2020758-X
    SSG: 12
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  • 8
    In: Toxicological Sciences, Oxford University Press (OUP), Vol. 171, No. 1 ( 2019-09-01), p. 193-210
    Abstract: Dexmedetomidine has been reported to ameliorate propofol-induced neurotoxicity in neonatal animals. However, the underlying mechanism is still undetermined. Glycogen synthase kinase-3β (GSK-3β), cycline-dependent kinase-5 (CDK5), and Rho-kinase (RhoA) pathways play critical roles in neuronal development. The present study is to investigate whether GSK-3β, CDK5, and RhoA pathways are involved in the neuroprotection of dexmedetomidine. Seven-day-old (P7) Sprague Dawley rats were anesthetized with propofol for 6 h. Dexmedetomidine at various concentrations were administered before propofol exposure. Neuroapoptosis, the neuronal proliferation, and the level of neurotransmitter in the hippocampus were evaluated. The effects of GSK-3β inhibitor SB415286, CDK5 inhibitor roscovitine, or RhoA inhibitor Y276321 on propofol-induced neurotoxicity were assessed. Propofol-induced apoptosis in the hippocampal neurons and astrocytes, inhibited neuronal proliferation in the dentate gyrus region, down-regulated the level of γ-aminobutyric acid and glutamate in the hippocampus, and impaired long-term cognitive function. These harmful effects were reduced by pretreatment with 50 μg·kg−1 dexmedetomidine. Moreover, propofol-activated GSK-3β and CDK5 pathways, but not RhoA pathway, by reducing the phosphorylation of GSK-3β (ser 9), increasing the expression of CDK5 activator P25 and increasing the phosphorylation of their target sites on collapsin response mediator protein 2 (CRMP2) shortly after exposure. These effects were reversed by pretreatment with 50 μg·kg−1 dexmedetomidine. Furthermore, SB415286 and roscovitine, not Y276321, attenuated the propofol-induced neuroapoptosis, brain cell proliferation inhibition, γ-aminobutyric acid and glutamate downregulation, and learning and memory dysfunction. Our results indicate that dexmedetomidine reduces propofol-induced neurotoxicity and neurocognitive impairment via inhibiting activation of GSK-3β/CRMP2 and CDK5/CRMP2 pathways in the hippocampus of neonatal rats.
    Type of Medium: Online Resource
    ISSN: 1096-6080 , 1096-0929
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 1471974-5
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  • 9
    In: The Oncologist, Oxford University Press (OUP), Vol. 24, No. 4 ( 2019-04-01), p. 449-454
    Abstract: With the advent of next-generation sequencing (NGS) and precision medicine, investigators have determined that tumors from different tissue sources that have the same types of genetic mutations will have a positive response to the same targeted therapy. This finding has prompted us to seek potential therapeutic targets for patients with carcinoma of unknown primary (CUP) using NGS technology. Here, we reported a case of a woman with CUP resistance to chemotherapy. We detected 450 cancer-related gene alterations using three metastatic tumor specimens and found the presence of EML4 exon13 and ALK exon20 fusion. The tumor did respond to crizotinib, a first-generation ALK inhibitor. When her tumor progressed, circulating tumor DNA detection revealed ALK L1196 M and G1269A mutation resistance to crizotinib, but she had a response to brigatinib. This case revealed that NGS technology used to detect the genetic alterations in patients with CUP might be a reliable method to find potential therapeutic targets, although the primary lesion could not always be confirmed. Key Points This case exemplifies responsiveness to ALK inhibitor in carcinoma of unknown primary (CUP) with EML4-ALK fusion. Next-generation sequencing is an important diagnostic tool to find potential therapeutic targets in CUP. Liquid biopsy may be useful to provide critical information about resistance mechanisms in CUP to guide sequential treatment decision with targeted therapy.
    Type of Medium: Online Resource
    ISSN: 1083-7159 , 1549-490X
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2023829-0
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  • 10
    In: The Plant Cell, Oxford University Press (OUP), Vol. 31, No. 2 ( 2019-02), p. 486-501
    Type of Medium: Online Resource
    ISSN: 1040-4651 , 1532-298X
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 623171-8
    detail.hit.zdb_id: 2004373-9
    SSG: 12
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