Image_15_Topoisomerase 2B Decrease Results in Diastolic Dysfunction via p53 and Akt: A Novel Pathway.TIFF by Rohit Moudgil (540119)

Image_1_Topoisomerase 2B Decrease Results in Diastolic Dysfunction via p53 and Akt: A Novel Pathway.TIFF by Rohit Moudgil (540119)

Image_9_Topoisomerase 2B Decrease Results in Diastolic Dysfunction via p53 and Akt: A Novel Pathway.TIF by Rohit Moudgil (540119)

Image_14_Topoisomerase 2B Decrease Results in Diastolic Dysfunction via p53 and Akt: A Novel Pathway.TIFF by Rohit Moudgil (540119)

Image_5_Topoisomerase 2B Decrease Results in Diastolic Dysfunction via p53 and Akt: A Novel Pathway.TIF by Rohit Moudgil (540119)

Image_2_Topoisomerase 2B Decrease Results in Diastolic Dysfunction via p53 and Akt: A Novel Pathway.TIFF by Rohit Moudgil (540119)

Image 1_Using sodium glycodeoxycholate to develop a temporary infant-like gut barrier model, in vitro.pdf by Francesca Bietto (21511316)

“…The treatment also reduced the key tight junction protein, occludin, at the cell membrane, and increased acidic mucins and extracellular alkaline phosphatase activity. Additionally, GDC decreased cAMP, suggesting its mechanism of action was via activation of a G-protein coupled receptor. …”

Table 1_Using sodium glycodeoxycholate to develop a temporary infant-like gut barrier model, in vitro.docx by Francesca Bietto (21511316)

“…The treatment also reduced the key tight junction protein, occludin, at the cell membrane, and increased acidic mucins and extracellular alkaline phosphatase activity. Additionally, GDC decreased cAMP, suggesting its mechanism of action was via activation of a G-protein coupled receptor. …”

Image 5_Using sodium glycodeoxycholate to develop a temporary infant-like gut barrier model, in vitro.pdf by Francesca Bietto (21511316)

“…The treatment also reduced the key tight junction protein, occludin, at the cell membrane, and increased acidic mucins and extracellular alkaline phosphatase activity. Additionally, GDC decreased cAMP, suggesting its mechanism of action was via activation of a G-protein coupled receptor. …”

Image 4_Using sodium glycodeoxycholate to develop a temporary infant-like gut barrier model, in vitro.pdf by Francesca Bietto (21511316)

“…The treatment also reduced the key tight junction protein, occludin, at the cell membrane, and increased acidic mucins and extracellular alkaline phosphatase activity. Additionally, GDC decreased cAMP, suggesting its mechanism of action was via activation of a G-protein coupled receptor. …”

Image 2_Using sodium glycodeoxycholate to develop a temporary infant-like gut barrier model, in vitro.pdf by Francesca Bietto (21511316)

“…The treatment also reduced the key tight junction protein, occludin, at the cell membrane, and increased acidic mucins and extracellular alkaline phosphatase activity. Additionally, GDC decreased cAMP, suggesting its mechanism of action was via activation of a G-protein coupled receptor. …”

Image 3_Using sodium glycodeoxycholate to develop a temporary infant-like gut barrier model, in vitro.pdf by Francesca Bietto (21511316)

“…The treatment also reduced the key tight junction protein, occludin, at the cell membrane, and increased acidic mucins and extracellular alkaline phosphatase activity. Additionally, GDC decreased cAMP, suggesting its mechanism of action was via activation of a G-protein coupled receptor. …”

Sevoflurane induces cognitive impairment in young mice via autophagy by Xiaoning Wang (16150)

“…We used different groups of mice for behavioral testing via the Morris Water Maze from P31 to P37.</p><p>Results</p><p>The anesthetic sevoflurane increased the level of LC3-II and ratio of LC3-II/LC3-I, decreased the p62 level in the hippocampus of the young mice, and induced cognitive impairment in the mice. 3-Methyladenine, the inhibitor of autophagy, attenuated the activation of autophagy and ameliorated the cognitive impairment induced by sevoflurane in the young mice.…”

AMPK regulates Fet-A expression by proteosomal degradation and decreased C/EBP beta expression. by Vishal Kothari (12511601)

Novel Equivalent Carbon Number Strategy for Large-Scale Lipidomics Data Analysis via Ultrahigh–Performance Liquid Chromatography–Orbitrap Astral Mass Spectrometry by Yao Chen (149006)

Novel Equivalent Carbon Number Strategy for Large-Scale Lipidomics Data Analysis via Ultrahigh–Performance Liquid Chromatography–Orbitrap Astral Mass Spectrometry by Yao Chen (149006)

Novel Equivalent Carbon Number Strategy for Large-Scale Lipidomics Data Analysis via Ultrahigh–Performance Liquid Chromatography–Orbitrap Astral Mass Spectrometry by Yao Chen (149006)

Novel Equivalent Carbon Number Strategy for Large-Scale Lipidomics Data Analysis via Ultrahigh–Performance Liquid Chromatography–Orbitrap Astral Mass Spectrometry by Yao Chen (149006)

Novel Equivalent Carbon Number Strategy for Large-Scale Lipidomics Data Analysis via Ultrahigh–Performance Liquid Chromatography–Orbitrap Astral Mass Spectrometry by Yao Chen (149006)

Novel Equivalent Carbon Number Strategy for Large-Scale Lipidomics Data Analysis via Ultrahigh–Performance Liquid Chromatography–Orbitrap Astral Mass Spectrometry by Yao Chen (149006)