3,544 research outputs found
Dissecting lipid metabolism alterations in SARS-CoV-2
No full textSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the COVID-19 pandemic that has infected over a hundred million people globally. There have been more than two million deaths recorded worldwide, with no end in sight until a widespread vaccination will be achieved. Current research has centred on different aspects of the virus interaction with cell surface receptors, but more needs to be done to further understand its mechanism of action in order to develop a targeted therapy and a method to control the spread of the virus. Lipids play a crucial role throughout the viral life cycle, and viruses are known to exploit lipid signalling and synthesis to affect host cell lipidome. Emerging studies using untargeted metabolomic and lipidomic approaches are providing new insight into the host response to COVID-19 infection. Indeed, metabolomic and lipidomic approaches have identified numerous circulating lipids that directly correlate to the severity of the disease, making lipid metabolism a potential therapeutic target. Circulating lipids play a key function in the pathogenesis of the virus and exert an inflammatory response. A better knowledge of lipid metabolism in the host-pathogen interaction will provide valuable insights into viral pathogenesis and to the development of novel therapeutic targets
Letter from Pat [Cummings] to Michi Weglyn, January 22, 1993
No full textA letter from Pat Cummings to Michi Weglyn about a story of Frank Chin's that they both think should be published. The author of the letter is probably children's book author and illustrator Pat Cummings.These materials are from box 73 and 74 of the Frank Chin Papers. The Frank Chin Papers contain personal and professional correspondence between Frank Chin and Michi Weglyn relating to particular projects on which either author was working as well as files related to the Day of Remembrance Tribute to Michi Weglyn
Letter from Pat Cummings to Eleanor Tellemac, April 6, 1992
No full textA letter from Pat Cummings to Eleanor Tellemac about plans to create a Multicultural Resource Center at HarperCollins publishing company.These materials are from box 73 and 74 of the Frank Chin Papers. The Frank Chin Papers contain personal and professional correspondence between Frank Chin and Michi Weglyn relating to particular projects on which either author was working as well as files related to the Day of Remembrance Tribute to Michi Weglyn
The History of Armand Trousseau and Cancer-Associated Thrombosis
No full text“Je suis perdu; une phlegmatia qui vient de se déclarer cette nuit, ne me laisse aucun doute sur nature de mon mal.”
—Armand Trousseau
“I am lost; a phlebitis which has declared itself this night leaves me no doubt about the nature of my illness.
Role of focal adhesion tyrosine kinases in GPVI-dependent platelet activation and reactive oxygen species formation.
No full textWe have previously shown the presence of a TRAF4/p47phox/Hic5/Pyk2 complex associated with the platelet collagen receptor, GPVI, consistent with a potential role of this complex in GPVI-dependent ROS formation. In other cell systems, NOX-dependent ROS formation is facilitated by Pyk2, which along with its closely related homologue FAK are known to be activated and phosphorylated downstream of ligand binding to GPVI.To evaluate the relative roles of Pyk2 and FAK in GPVI-dependent ROS formation and to determine their location within the GPVI signaling pathway.Human and mouse washed platelets (from WT or Pyk2 KO mice) were pre-treated with pharmacological inhibitors targeting FAK or Pyk2 (PF-228 and Tyrphostin A9, respectively) and stimulated with the GPVI-specific agonist, CRP. FAK, but not Pyk2, was found to be essential for GPVI-dependent ROS production and aggregation. Subsequent human platelet studies with PF-228 confirmed FAK is essential for GPVI-mediated phosphatidylserine exposure, α-granule secretion (P-selectin (CD62P) surface expression) and integrin αIIbβ3 activation. To determine the precise location of FAK within the GPVI pathway, we analyzed the effect of PF-228 inhibition in CRP-stimulated platelets in conjunction with immunoprecipitation and pulldown analysis to show that FAK is downstream of Lyn, Spleen tyrosine kinase (Syk), PI3-K and Bruton's tyrosine kinase (Btk) and upstream of Rac1, PLCγ2, Ca2+ release, PKC, Hic-5, NOX1 and αIIbβ3 activation.Overall, these data suggest a novel role for FAK in GPVI-dependent ROS formation and platelet activation and elucidate a proximal signaling role for FAK within the GPVI pathway
Pat\u27s Leather Breeches
No full textMob demands Pat feed them and he cooks them his prized leather pantshttps://egrove.olemiss.edu/kgbsides_ire/1043/thumbnail.jp
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