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largest decrease » largest decreases (Expand Search), marked decrease (Expand Search)
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a decrease » _ decrease (Expand Search), _ decreased (Expand Search), _ decreases (Expand Search)
largest decrease » largest decreases (Expand Search), marked decrease (Expand Search)
linear decrease » linear increase (Expand Search)
larger decrease » marked decrease (Expand Search)
a decrease » _ decrease (Expand Search), _ decreased (Expand Search), _ decreases (Expand Search)
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8321
Ecosim flow diagram for Scenario 3.
Published 2024“…We further show that increasing capelin with a simultaneous decrease in Arctic cod biomass causes large decreases in the biomass of marine mammals such as polar bear, beluga and ringed seal. …”
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8322
Ecosim flow diagram for Scenario 2.2.
Published 2024“…We further show that increasing capelin with a simultaneous decrease in Arctic cod biomass causes large decreases in the biomass of marine mammals such as polar bear, beluga and ringed seal. …”
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8323
Ecosim flow diagram for Scenario 1.2.
Published 2024“…We further show that increasing capelin with a simultaneous decrease in Arctic cod biomass causes large decreases in the biomass of marine mammals such as polar bear, beluga and ringed seal. …”
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8324
Data_Sheet_2_MEF2A Is the Trigger of Resveratrol Exerting Protection on Vascular Endothelial Cell.PDF
Published 2022“…In conclusion, resveratrol enhances MEF2A expression, and the upregulation of MEF2A is required for the endothelial protective benefits of resveratrol in vitro via activating SIRT1. …”
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8325
Data_Sheet_1_MEF2A Is the Trigger of Resveratrol Exerting Protection on Vascular Endothelial Cell.PDF
Published 2022“…In conclusion, resveratrol enhances MEF2A expression, and the upregulation of MEF2A is required for the endothelial protective benefits of resveratrol in vitro via activating SIRT1. …”
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8326
Data_Sheet_3_MEF2A Is the Trigger of Resveratrol Exerting Protection on Vascular Endothelial Cell.PDF
Published 2022“…In conclusion, resveratrol enhances MEF2A expression, and the upregulation of MEF2A is required for the endothelial protective benefits of resveratrol in vitro via activating SIRT1. …”
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8327
Control of On–Off or Off–On Fluorescent and Optical [Cu<sup>2+</sup>] and [Hg<sup>2+</sup>] Responses via Formal Me/H Substitution in Fully Characterized Thienyl “Scorpionate”-like...
Published 2011“…Importantly, differences in their solution (MeCN) optical Cu<sup>2+</sup> and Hg<sup>2+</sup> probing capacity via <i>SSS</i>-chelation were investigated. Compounds <b>2a</b>–<b>3a</b> were prepared from the requisite 8-substituted BODIPY complexes. …”
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8328
Control of On–Off or Off–On Fluorescent and Optical [Cu<sup>2+</sup>] and [Hg<sup>2+</sup>] Responses via Formal Me/H Substitution in Fully Characterized Thienyl “Scorpionate”-like...
Published 2011“…Importantly, differences in their solution (MeCN) optical Cu<sup>2+</sup> and Hg<sup>2+</sup> probing capacity via <i>SSS</i>-chelation were investigated. Compounds <b>2a</b>–<b>3a</b> were prepared from the requisite 8-substituted BODIPY complexes. …”
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8329
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8330
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8331
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8332
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8333
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8334
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8335
Data Sheet 1_Jing-Yin-Gu-Biao formula protects mice from postinfluenza Staphylococcus aureus infection by ameliorating acute lung injury and improving hypercoagulable state via inh...
Published 2025“…JYGBF inhibited ERK1/2 phosphorylation in neutrophils and in lungs of infected mice. Acacetin, a critical compound from JYGBF, inhibited NET formation via downregulating ERK/ROS axis.…”
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8336
Image_1_Mitophagy-Mediated mtDNA Release Aggravates Stretching-Induced Inflammation and Lung Epithelial Cell Injury via the TLR9/MyD88/NF-κB Pathway.TIF
Published 2020“…Down-regulating MyD88 protected lung epithelial cells from stretching injury and decreased NF-κB/p65 expression.</p>Conclusion<p>These findings suggest that PINK1-dependent mitophagy and associated TLR9 activation is indeed a major factor in stretch-induced cell injury via a mechanism in which released mtDNA activates TLR9 and thereby the MyD88/NF-κB pathway. …”
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8337
Image_4_Mitophagy-Mediated mtDNA Release Aggravates Stretching-Induced Inflammation and Lung Epithelial Cell Injury via the TLR9/MyD88/NF-κB Pathway.TIF
Published 2020“…Down-regulating MyD88 protected lung epithelial cells from stretching injury and decreased NF-κB/p65 expression.</p>Conclusion<p>These findings suggest that PINK1-dependent mitophagy and associated TLR9 activation is indeed a major factor in stretch-induced cell injury via a mechanism in which released mtDNA activates TLR9 and thereby the MyD88/NF-κB pathway. …”
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8338
Image_3_Mitophagy-Mediated mtDNA Release Aggravates Stretching-Induced Inflammation and Lung Epithelial Cell Injury via the TLR9/MyD88/NF-κB Pathway.TIF
Published 2020“…Down-regulating MyD88 protected lung epithelial cells from stretching injury and decreased NF-κB/p65 expression.</p>Conclusion<p>These findings suggest that PINK1-dependent mitophagy and associated TLR9 activation is indeed a major factor in stretch-induced cell injury via a mechanism in which released mtDNA activates TLR9 and thereby the MyD88/NF-κB pathway. …”
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8339
Image_2_Mitophagy-Mediated mtDNA Release Aggravates Stretching-Induced Inflammation and Lung Epithelial Cell Injury via the TLR9/MyD88/NF-κB Pathway.TIF
Published 2020“…Down-regulating MyD88 protected lung epithelial cells from stretching injury and decreased NF-κB/p65 expression.</p>Conclusion<p>These findings suggest that PINK1-dependent mitophagy and associated TLR9 activation is indeed a major factor in stretch-induced cell injury via a mechanism in which released mtDNA activates TLR9 and thereby the MyD88/NF-κB pathway. …”
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8340
Image_3_Mitophagy-Mediated mtDNA Release Aggravates Stretching-Induced Inflammation and Lung Epithelial Cell Injury via the TLR9/MyD88/NF-κB Pathway.TIF
Published 2020“…Down-regulating MyD88 protected lung epithelial cells from stretching injury and decreased NF-κB/p65 expression.</p>Conclusion<p>These findings suggest that PINK1-dependent mitophagy and associated TLR9 activation is indeed a major factor in stretch-induced cell injury via a mechanism in which released mtDNA activates TLR9 and thereby the MyD88/NF-κB pathway. …”