A. Western blot showing accumulation of FoxD3 in CR+DBZ-treated crypt extracts from the colons of Dclk1^ΔIEC mice. by Kafayat Yusuf (22104155)

Hazard ratios for Sex across age based on unadjusted (A) and adjusted (B) Cox model. Note: shaded areas representing the 95% confidence intervals; green bars indicating the distrib... by Hui Ouyang (245739)

Structural clashes in TP53 mutants: (A) G266E mutation causes steric clashes with PHE109 and LEU257, destabilizing the structure. by Ashraf Attia Mahmoud (21262201)

FGF18 injections increase chondroprogenitors and extracellular matrix and reduce chondrocyte hypertrophy after TMJ experimental degeneration. by Flavia Gomes Velasque Gama (21175112)

Data Sheet 1_Knockdown of annexin A2 enhances the host cell apoptosis induced by Eimeria tenella.zip by Jixia Wang (1685902)

“…Following ANXA2 knockdown, the cell apoptosis rate, caspase-3 activity, and Bax expression levels were significantly increased (P < 0.01), whereas the infection rate and Bcl-2 expression levels were significantly decreased (P < 0.01) compared to the group infected with E. tenella alone. …”

FGF18 injections increase cartilage thickness, chondrocyte proliferation and induce healing after TMJ experimental degeneration. by Flavia Gomes Velasque Gama (21175112)

Data Sheet 6_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Data Sheet 1_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.docx by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Data Sheet 7_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Data Sheet 3_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Table 1_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.xlsx by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Data Sheet 2_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Image 1_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.tif by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Data Sheet 4_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Data Sheet 5_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Table 2_Clinical features and genetic analysis of acrodermatitis enteropathica in an ethnic minority infant from Western China: a case report and literature review.xlsx by Tuerhongjiang Axirejiang (22346272)

“…Her serum zinc level significantly decreased (0.19 mg/L). Whole-exome sequencing revealed a homozygous c.197G > T(p. …”

Table 1_Clinical features and genetic analysis of acrodermatitis enteropathica in an ethnic minority infant from Western China: a case report and literature review.xlsx by Tuerhongjiang Axirejiang (22346272)

“…Her serum zinc level significantly decreased (0.19 mg/L). Whole-exome sequencing revealed a homozygous c.197G > T(p. …”

Data Sheet 1_Regulation of SLC7A11 by LncRNA GPRC5D-AS1 mediates ferroptosis in skeletal muscle: Mechanistic exploration of sarcopenia.pdf by Wei Gong (112494)

“…In the sarcopenia group, both GPRC5D-AS1 and SLC7A11 expression levels decreased significantly, along with SLC7A11 protein translation. …”

Supplementary file 1_Regulation of SLC7A11 by LncRNA GPRC5D-AS1 mediates ferroptosis in skeletal muscle: Mechanistic exploration of sarcopenia.pdf by Wei Gong (112494)

“…In the sarcopenia group, both GPRC5D-AS1 and SLC7A11 expression levels decreased significantly, along with SLC7A11 protein translation. …”

Flowchart of the study population. by Gábor Szaló (22615130)

“…Among those 803 individuals who did not take antihypertensive medication, there was a significant association in linear regression between increase in PSS-10 and decrease in C2 (B: −0.2, 95% CI: −0.4- −0.02; p = 0.03) that was lost after adjustment for physical activity (B: −0.16, 95% CI: −0.35–0.03; p = 0.1). …”