Gender-specific incidence trends of HFMD in Guangzhou from 2013 to 2023. by Haipeng Luo (5322419)

Effect of alexidine, amorolfine and olorofim on preformed biofilms of <i>Scedosporium</i> and <i>Lomentospora</i> species. by Rodrigo Rollin-Pinheiro (239450)

Effect of alexidine, amorolfine and olorofim on biofilm formation of <i>Scedosporium</i> and <i>Lomentospora</i> species. by Rodrigo Rollin-Pinheiro (239450)

The effects of GRK2, GRK2-K220R and β-arrestin 2 on GPR3 WT and ST/A activity and surface localization. by Katie M. Lowther (427408)

“…<p>GPR3-HA WT (<b>A</b>) and ST/A (<b>B</b>) were co-transfected with pcDNA, or GRK2, or GRK2 and β-arrestin-2, or GRK2-K220R, or GRK2-K220R and β-arr-2. …”

Immunofluorescence of select extracellular matrix (ECM) components. by Melissa A. MacIver (12850566)

“…<p>Matched sections from traditional histology (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0269571#pone.0269571.g008" target="_blank">Fig 8</a>) were assessed via immunofluorescence for aggrecan, Collagen Type II, and Collagen Type X. …”

SEM examination on corneal epithelial cells at different time points after exposure (A) At post-exposure 1 hour, no obvious superficial epithelial sloughing, or increased intercell... by Chun-Ting Lai (791855)

Cellular senescence was not detected in <i>Rap1</i> knockin mice. by Amanda J. Stock (3139719)

Effect of CPAF treatment on ear thickness changes over an 18 day course of thrice weekly PMA applications in WT and <i>Ptafr</i>-/- mice. by Ravi P. Sahu (342322)

“…For the sake of comparison, the data for the PMA + CPAF treatment in WT mice is included. (mean and SEM; n = 4–5 mice per group). …”

Intracellular Delivery of Bioactive Molecules using Light-Addressable Nanocapsules by Kimberly A. D. Gregersen (2241349)

“…We demonstrate this method with the intracellular release of the second messenger IP₃ in CHO-M1 cells and report that calcium responses from the cells changed from a sustained increase to a transient spike when the average number of IP₃ released is decreased below 50 molecules per nanocapsule. …”

Changes in PE acyl chain composition in cellular membranes of DD13 expressing LH2 WT and LH2 αAL/βAL by Lee Gyan Kwa (40157)

Period of influence of each daily variable on the pod status change, from healthy to diseased with no signs of sporulation, 40 to 50 days after tagging. by Mariela E. Leandro-Muñoz (4487608)

Exposure to a stressor activates the hypothalamic-pituitary-adrenal axis and sympathetic nervous system resulting in changes to the commensal flora (including a decrease in prevote... by Thomas Maslanik (295204)

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. …”