GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Wiley  (4)
  • 1
    Online Resource
    Online Resource
    Wiley ; 2017
    In:  Basic & Clinical Pharmacology & Toxicology Vol. 120, No. 1 ( 2017-01), p. 86-96
    In: Basic & Clinical Pharmacology & Toxicology, Wiley, Vol. 120, No. 1 ( 2017-01), p. 86-96
    Abstract: The early identification of toxic paraquat ( PQ ) poisoning in patients is critical to ensure timely and accurate prognosis. Although plasma PQ concentration has been reported as a clinical indicator of PQ poisoning, it is not commonly applied in practice due to the inconvenient necessary instruments and operation. In this study, we explored the use of blood routine indexes to identify the degree of PQ toxicity and/or diagnose PQ poisoning in patients via machine learning approach. Specifically, we developed a method based on support vector machine combined with the feature selection technique to accurately predict PQ poisoning risk status, then tested the method on 79 (42 male and 37 female; 41 living and 38 deceased) patients. The detection method was rigorously evaluated against a real‐world data set to determine its accuracy, sensitivity and specificity. Feature selection was also applied to identify the factors correlated with risk status, and the results showed that there are significant differences in blood routine indexes between dead and living PQ ‐poisoned individuals ( p ‐value 〈 0.01). Feature selection also showed that the most important correlated indexes are white blood cell and neutrophils. In conclusion, the toxicity or prognosis of PQ poisoning can be preliminarily ascertained by blood routine testing without PQ concentration data, representing an additional tool and innovative approach to assess the prognosis of PQ poisoning.
    Type of Medium: Online Resource
    ISSN: 1742-7835 , 1742-7843
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2151592-X
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    In: Advanced Science, Wiley, Vol. 9, No. 23 ( 2022-08)
    Abstract: MicroRNAs (miRNAs) are involved in the regulation of gene expression via incomplete base pairing to sequence motifs at the three prime untranslated regions (3′‐UTRs) of mRNAs and play critical roles in the etiology of cancers. Single nucleotide polymorphisms (SNPs) in the 3′‐UTR miRNA‐binding regions may influence the miRNA affinity. However, this biological mechanism in prostate cancer (PCa) remains unclear. Here, a three‐stage genome‐wide association study of 3′‐UTR SNPs ( n =33 117) is performed in 5515 Chinese men. Three genome‐wide significant variants are discovered at 8p21.2 (rs1567669, rs4872176, and rs4872177), which are all located in a linkage disequilibrium region of the NKX3‐1 gene. Phenome‐wide association analysis using the FinnGen data reveals a specific association of rs1567669 with PCa over 2,264 disease endpoints. Expression quantitative trait locus analyses based on both Chinese PCa cohort and the GTEx database show that risk alleles of these SNPs are significantly associated with low expression of NKX3‐1 . Based on the MirSNP database, dual‐luciferase reporter assays show that risk alleles of these SNPs downregulate the expression of NKX3‐1 via increased miRNA binding. These results indicate that the SNPs at the 3′‐UTR of NKX3‐1 significantly downregulate NKX3‐1 expression by influencing the affinity of miRNA and increase the PCa risk.
    Type of Medium: Online Resource
    ISSN: 2198-3844 , 2198-3844
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2808093-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    Online Resource
    Online Resource
    Wiley ; 2021
    In:  Phytotherapy Research Vol. 35, No. 9 ( 2021-09), p. 5203-5213
    In: Phytotherapy Research, Wiley, Vol. 35, No. 9 ( 2021-09), p. 5203-5213
    Abstract: Myocardial injury and cardiovascular dysfunction are serious consequences of sepsis and contribute to high mortality. Currently, the pathogenesis of myocardial injury in sepsis is still unclear, and therapeutic approaches are limited. In this study, we investigated the protective effect of emodin on septic myocardial injury and the underlying mechanism. Lipopolysaccharide (LPS)‐induced C57BL/6 mice and cardiomyocytes were used as models of sepsis in vivo and in vitro, respectively. The results showed that emodin alleviated cardiac dysfunction, myocardial injury and improved survival rate in LPS‐induced septic mice. Emodin attenuated the levels of inflammatory cytokines and cardiac inflammation induced by LPS. Emodin reduced NOD‐like receptor protein 3 (NLRP3) and Gasdermin D (GSDMD) expression in the heart tissue of LPS‐induced septic mice. In vitro, emodin alleviated LPS‐induced cell injury and inflammation in cardiomyocytes by inhibiting NLRP3 inflammasome activation. In addition, an NLRP3 inhibitor was used to further confirm the function of the NLRP3 inflammasome in LPS‐induced myocardial injury. Taken together, our findings suggest that emodin improves LPS‐induced myocardial injury and cardiac dysfunction by alleviating the inflammatory response and cardiomyocyte pyroptosis by inhibiting NLRP3 inflammasome activation, which provides a feasible strategy for preventing and treating myocardial injury in sepsis.
    Type of Medium: Online Resource
    ISSN: 0951-418X , 1099-1573
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1493490-5
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    In: FEBS Letters, Wiley, Vol. 593, No. 9 ( 2019-05), p. 952-961
    Abstract: Interleukin (IL)‐17 plays a critical role in the pathogenesis of inflammation and autoimmune diseases. The aryl hydrocarbon receptor (AHR) is a transcription factor responsible for the elimination of xenobiotic chemicals. However, it remains unknown whether AHR is involved in IL‐17 signaling. Here, we demonstrate that knockdown of AHR significantly enhances, while overexpression or activation of AHR inhibits IL‐17‐induced inflammation in Hela cells. AHR specifically suppresses IL‐17‐induced p38 activation, and inhibition of p38 activity markedly reverses the effect of AHR knockdown on IL‐17‐induced inflammation. Mechanistically, AHR physically interacts with TAK1 and mitogen‐activated protein kinase kinase 3/6 (MKK3/6) and disrupts TAK1‐MKK3/6 interaction, leading to impaired IL‐17 signaling. Thus, our study indicates that AHR negatively regulates IL‐17‐mediated signaling and inflammation at least partially through interfering with the interaction between TAK1 and MKK3/6.
    Type of Medium: Online Resource
    ISSN: 0014-5793 , 1873-3468
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 1460391-3
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...