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br Conclusions br Acknowledgments The authors
2024-01-11
Conclusions Acknowledgments The authors are thankful to Hugo Santos, Olga Martinez and Ricardo Lacerda for the technical assistance provided in the maintenance of the aquaria. This work was supported by national funds, through FCT and co-funded by the European Regional Development Fund (ERDF)
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br Author contributions br Acknowledgements We thank Dr
2024-01-11
Author contributions Acknowledgements We thank Dr. Bob Hammer and the Transgenic Core Facility at UTSW for the generation of the transgenic lines, John Shelton and the Histology Core for assistance with histology and the UTSW Metabolic Core Unit for help in phenotyping. We acknowledge support
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As we previously observed in the NSFT
2024-01-10
As we previously observed in the NSFT (Fukumoto et al., 2014), the effect of LY341495 in the FST was also inhibited by a 5-HT1A receptor antagonist, indicating the role of the 5-HT1A receptor in the actions of LY341495. Among the 5-HT1A receptors, which exist both presynaptically and postsynapticall
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br Materials and Methods br Author Contributions br Conflict
2024-01-10
Materials and Methods Author Contributions Conflicts of Interest Acknowledgments This study was funded by the NIH Common Fund (UH2TR000943) through the Office of Strategic Coordination/Office of the NIH Director, an NCI/NIH grant (1R21CA199050), the MD Anderson Cancer Center support gran
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cyproheptadine hcl br Experimental Procedures Additional inf
2024-01-10
Experimental Procedures Additional information can be found in Supplemental Experimental Procedures. Author Contributions Acknowledgments We thank all members of Lab of Health Chemistry for helpful discussions. This work was supported by Grant-in-Aid for Scientific Research (KAKENHI) from
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br Materials and methods br Results
2024-01-10
Materials and methods Results Discussion In this study, we administrated BDE-153 to newborn rat pups at PND 10 and cultured primary neurons, measured neuronal apoptosis and LDH activity in vivo and in vitro, then explored the possible predominant pathway underlying the neuronal apoptosis by
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It has been demonstrated that
2024-01-10
It has been demonstrated that the hallmarks of pulmonary fibrosis are a loss of endothelial function and subsequent activation of the immune system, which is considered as a direct outcome affected by intracellular pro-inflammatory responses [26]. Thus, inhibition of early inflammation could be an i
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Recent work has detailed the impact of
2024-01-10
Recent work has detailed the impact of genetic CVT 10216 of AMPK in the liver, revealing only minor phenotypes upon removal in mice (Boudaba et al., 2018). However, these studies very elegantly showed the potential for small molecule-mediated activation of AMPK to elicit large changes in lipid metab
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br Conclusions Extract of non germinated winter
2024-01-10
Conclusions Extract of non-germinated winter rape seeds cv. Bellevue was screened for the aminopeptidase activity. It revealed broad substrate specificity, with the highest activity toward Phe-pNA. Also in the partially purified sample, phenylalanine was preferentially hydrolysed. PMSF, known ser
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First investigation of numerous membered
2024-01-10
First, investigation of numerous 12-14-membered ether-linked macrocycles revealed that smaller motifs were most lipophilic efficient. Compound (3) (12-membered macrocycle) exhibited good cellular potencies (ALK IC50 = 1.0 nM; ALK-L1196 M IC50 = 20 nM) and the highest LipE (4.4) with picomolar bindin
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br Development of lorlatinib from
2024-01-10
Development of lorlatinib from crizotinib (1) to a clinical candidate (6) Xalkori (1, PF-02341066, crizotinib), was the first-in-class ALK inhibitor approved by the Unites States Food and Drug Administration (FDA) in 2011 as a first-line treatment for ALK+- NSCLC patients. This section describes
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Acknowledgments br P c is expressed
2024-01-09
Acknowledgments P450c17 is expressed in several steroidogenic tissues, including the adrenal cortex, the ovary, and the testes (). Thus, 17α-hydroxylase/17,20-lyase is a key enzyme required for the production of both cortisol and sex steroids. This enzyme defect blocks the synthesis of cortisol,
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taselisib For the NSCLC patients with EGFR activating mutati
2024-01-09
For the NSCLC patients with EGFR-activating mutations, EGFR-TKIs (gefitinib and erlotinib) are effective clinical therapies [21], [22]. However, approximately 10% of patients harboring EGFR-sensitizing mutations exhibit intrinsic resistance, and up to 40% do not attain a major response to treatment
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Further analysis sought to understand
2024-01-09
Further analysis sought to understand the mechanism associated with the autotaxin-mediated increase of miR-489-3p in circulation. Based upon sequence complementarity, DIANA TarBase predicted miR-489-3p targets MAPK2K1, or MEK1, an oncogene widely dysregulated in cancer (Fig. 4A). To test this relati
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SB-334867 free base br Leptin Adiponectin a permissive imbal
2024-01-09
Leptin/Adiponectin: a permissive imbalance Leptin, a satiety hormone, is encoded by the obesity (ob) gene. It essentially functions as an energy sensor which is involved in the regulation of body weight by sending signals to the SB-334867 free base to reduce appetite (Woods and D'Alessio, 2008).
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