Data Sheet 1_5-deoxy-rutaecarpine protects against LPS-induced acute lung injury via inhibiting NLRP3 inflammasome-related inflammation.pdf by Jinque Luo (9645983)

“…Introduction<p>Acute lung injury (ALI) induced by lipopolysaccharide (LPS) is a significant medical condition characterized by severe pulmonary inflammation and tissue damage. …”

Table 1_5-deoxy-rutaecarpine protects against LPS-induced acute lung injury via inhibiting NLRP3 inflammasome-related inflammation.docx by Jinque Luo (9645983)

“…Introduction<p>Acute lung injury (ALI) induced by lipopolysaccharide (LPS) is a significant medical condition characterized by severe pulmonary inflammation and tissue damage. …”

ABR wave I and IV parameters in response to clicks. by Carolin Jüchter (17384611)

“…The P1-N1 amplitude at 90 dB SPL (<b>A</b>) was significantly reduced two days post-trauma compared to pre-trauma and stayed decreased three weeks post-trauma. …”

Data Sheet 1_hERG activators exhibit antitumor effects in breast cancer through calcineurin and β-catenin-mediated signaling pathways.doc by Yan Yu (56143)

“…Background<p>Breast cancer remains a leading cause of mortality among women worldwide, with existing therapeutic options often accompanied by significant side effects and a persistent risk of disease recurrence. …”

CRISPR/Cas9-mediated editing of barley lipoxygenase genes promotes grain fatty acid accumulation and storability by Zhanghui Zeng (3571331)

“…Compared to the wild-type, all mutants displayed normal plant height, tiller number, and grain size, although the <i>loxC1</i> and <i>loxAloxC1</i> mutants exhibited significantly lower thousand grain weights. Notably, the total LOX activity in mature grains decreased by 36–42% in <i>loxC1</i> mutants and by 94% in <i>loxAloxC1</i> mutants, with no significant change observed in <i>loxB</i> mutants. …”

Image 2_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.tif by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Image 6_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.tif by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Image 5_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.tif by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Image 4_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.tif by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Image 1_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.tif by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Image 7_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.tif by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Table 1_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.docx by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Image 11_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.tif by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Presentation 1_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.pptx by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Table 2_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.docx by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Image 9_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.tif by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Image 3_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.tif by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Image 10_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.tif by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Image 8_Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.tif by Helena Hernández-Cuervo (9956465)

“…</p>Results<p>Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.</p>Discussion<p>Bmi1^−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. …”

Effect of overexpressing <i>CEBPB</i> and <i>GFI-1</i> on <i>SOST</i> expression. by Avneesh Chopra (20927514)

“…Increased LAP2 expression correlated with weakly reduced <i>SOST</i> expression (1.89-fold reduction, P <  0.01), and an increase in LIP expression showed a very slightly decreased <i>SOST</i> expression level (1.2-fold reduction, P <  0.05) (<b>right panel</b>). …”