Loss of expression of <i>dbt</i> in <i>tim-</i>GAL4-expressing neurons can lead to a sleep decrease during the nighttime, while loss of expression of <i>dbt</i> with <i>per-</i>GAL... by Jialin Wang (490082)

Image 5_Quality of life in patients with pan-cancer undergoing concurrent chemoradiotherapy: a bibliometric analysis (1995-2024).tif by Ao Shen (127290)

“…R-bibliometrix, VOSviewer, and CiteSpace were employed to conduct quantitative analysis and visualize research trends and factors influencing QOL. Complementarily, a cross-sectional study of 117 cervical cancer patients assessed symptom prevalence via CTCAE v5.0, with symptom clusters identified.…”

Table 5_Quality of life in patients with pan-cancer undergoing concurrent chemoradiotherapy: a bibliometric analysis (1995-2024).docx by Ao Shen (127290)

“…R-bibliometrix, VOSviewer, and CiteSpace were employed to conduct quantitative analysis and visualize research trends and factors influencing QOL. Complementarily, a cross-sectional study of 117 cervical cancer patients assessed symptom prevalence via CTCAE v5.0, with symptom clusters identified.…”

Representative images of the right eye of a 51-year-old woman with active central serous chorioretinopathy. by Dae Joong Ma (5687885)

Table_5_The Advantage of Supine and Standing Heart Rate Variability Analysis to Assess Training Status and Performance in a Walking Ultramarathon.DOCX by Martina Anna Maggioni (8568585)

“…Highly trained athletes accounted for higher HF_nu during standing compared to poorly trained competitors (+11.5, p = 0.01). Similarly, greater training volume (total km/week) would predict higher HF_nu during standing (r = 0.5, p = 0.01). …”

Image_5_ZPD-2, a Small Compound That Inhibits α-Synuclein Amyloid Aggregation and Its Seeded Polymerization.JPEG by Samuel Peña-Díaz (8131068)

“…ZPD-2 inhibits the aggregation of wild-type α-Syn and the A30P and H50Q familial variants in vitro at substoichiometric compound:protein ratios. …”

Stress responses after knockdown of octopamine receptor OAMB and serotonin receptor 5-HT_1A in IPCs. by Jiangnan Luo (218899)

“…In an earlier study it was shown that 5-HT_1A knockdown decreased starvation resistance <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0099732#pone.0099732-Luo1" target="_blank">[22]</a>. …”

Effects of 50 µM stearic acid, oleic acid and linoleic acid on cell death and apoptosis of 3T3L1 preadipocytes. by Ming-Che Shen (629982)

Loss of exostosin-1 (EXT1), specific reduction of heparan sulfate (HS) in fibroblasts, and decreased acidic mucosubstances in the stroma of <i>S100a4-Cre; Ext1</i><sup><i>f/f</i></... by Ayumi Niwa (6256790)

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

“…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. …”

presentation1_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.pptx by Xin Zhi (1829224)

“…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. …”

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

“…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. …”

presentation1_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.pptx by Xin Zhi (1829224)

“…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. …”

presentation1_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.pptx by Xin Zhi (1829224)

“…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. …”

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

“…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. …”

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

“…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. …”

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

“…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. …”

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

“…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. …”

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

“…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. …”

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

“…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. …”