Showing 641 - 660 results of 16,867 for search '(( 50 ((nn decrease) OR (a decrease)) ) OR ( 50 ((mean decrease) OR (we decrease)) ))', query time: 0.69s Refine Results
  1. 641

    image1_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

    Published 2020
    “…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”
  2. 642

    image1_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

    Published 2021
    “…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”
  3. 643

    image3_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

    Published 2020
    “…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”
  4. 644

    image1_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

    Published 2020
    “…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”
  5. 645

    image3_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

    Published 2021
    “…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”
  6. 646

    image2_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

    Published 2021
    “…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”
  7. 647

    image2_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

    Published 2020
    “…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”
  8. 648

    Flow diagram of the study population. by Dina Evyana (18462048)

    Published 2024
    “…MetS was found in 64.3% of patients. Patients with a PASI score>10 had a significantly higher risk of metabolic syndrome compared to those with a score ≤ 10 (78.6% vs 50%, OR 3.667; 95% CI 1.413–9.514; <i>p</i> = 0.006). …”
  9. 649

    Identification, Synthesis, and Biological Evaluations of Potent Inhibitors Targeting Type I Protein Arginine Methyltransferases by Xiao Li (107004)

    Published 2022
    “…In this study, we first identified several hit compounds against CARM1 by structure-based virtual screening (IC<sub>50</sub> = 35.51 ± 6.68 to 68.70 ± 8.12 μM) and then carried out chemical structural optimizations, leading to six compounds with significantly improved activities targeting CARM1 (IC<sub>50</sub> = 18 ± 2 to 107 ± 6 nM). …”
  10. 650

    Variable included in analysis. by Molebatsi Moholola (20513371)

    Published 2025
    “…</p><p>Conclusion</p><p>Close to half of the clients had a VL below 50 copies/ml after case management. …”
  11. 651

    Full dataset of the study. by Molebatsi Moholola (20513371)

    Published 2025
    “…</p><p>Conclusion</p><p>Close to half of the clients had a VL below 50 copies/ml after case management. …”
  12. 652

    Discovery of Betulinic Acid Derivatives as Potent Intestinal Farnesoid X Receptor Antagonists to Ameliorate Nonalcoholic Steatohepatitis by Chenlu Zhang (508309)

    Published 2022
    “…Evidence showed that intestinal FXR antagonism exhibited remarkable metabolic improvements in mice. Herein, we developed a series of betulinic acid derivatives as potent intestinal FXR antagonists, and <b>F6</b> was identified as the most potent one with an IC<sub>50</sub> at 2.1 μM. …”
  13. 653

    Discovery of Betulinic Acid Derivatives as Potent Intestinal Farnesoid X Receptor Antagonists to Ameliorate Nonalcoholic Steatohepatitis by Chenlu Zhang (508309)

    Published 2022
    “…Evidence showed that intestinal FXR antagonism exhibited remarkable metabolic improvements in mice. Herein, we developed a series of betulinic acid derivatives as potent intestinal FXR antagonists, and <b>F6</b> was identified as the most potent one with an IC<sub>50</sub> at 2.1 μM. …”
  14. 654

    Combination of DNA Damage, Autophagy, and ERK Inhibition: Novel Evodiamine-Inspired Multi-Action Pt(IV) Prodrugs with High-Efficiency and Low-Toxicity Antitumor Activity by Xiao-Meng Liu (778197)

    Published 2023
    “…Among them, compound <b>10</b> exhibited a 118-fold enhancement in the IC<sub>50</sub> value compared to cisplatin and low toxicity to normal cells. …”
  15. 655

    Combination of DNA Damage, Autophagy, and ERK Inhibition: Novel Evodiamine-Inspired Multi-Action Pt(IV) Prodrugs with High-Efficiency and Low-Toxicity Antitumor Activity by Xiao-Meng Liu (778197)

    Published 2023
    “…Among them, compound <b>10</b> exhibited a 118-fold enhancement in the IC<sub>50</sub> value compared to cisplatin and low toxicity to normal cells. …”
  16. 656

    Combination of DNA Damage, Autophagy, and ERK Inhibition: Novel Evodiamine-Inspired Multi-Action Pt(IV) Prodrugs with High-Efficiency and Low-Toxicity Antitumor Activity by Xiao-Meng Liu (778197)

    Published 2023
    “…Among them, compound <b>10</b> exhibited a 118-fold enhancement in the IC<sub>50</sub> value compared to cisplatin and low toxicity to normal cells. …”
  17. 657

    Combination of DNA Damage, Autophagy, and ERK Inhibition: Novel Evodiamine-Inspired Multi-Action Pt(IV) Prodrugs with High-Efficiency and Low-Toxicity Antitumor Activity by Xiao-Meng Liu (778197)

    Published 2023
    “…Among them, compound <b>10</b> exhibited a 118-fold enhancement in the IC<sub>50</sub> value compared to cisplatin and low toxicity to normal cells. …”
  18. 658

    Combination of DNA Damage, Autophagy, and ERK Inhibition: Novel Evodiamine-Inspired Multi-Action Pt(IV) Prodrugs with High-Efficiency and Low-Toxicity Antitumor Activity by Xiao-Meng Liu (778197)

    Published 2023
    “…Among them, compound <b>10</b> exhibited a 118-fold enhancement in the IC<sub>50</sub> value compared to cisplatin and low toxicity to normal cells. …”
  19. 659
  20. 660