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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
There continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes, so it is important to update guidelines for monitoring autophagic activity in different organisms.
Streptococcal Toxic Shock Syndrome Caused by Streptococcus suis Serotype 2
Clinical and pathological characterization of the human patients revealed the hallmarks of typical STSS, which to date had only been associated with GAS infection, and multiple lines of evidence confirmed that highly virulent strains of SS2 were the causative agents of both outbreaks.
Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion
It is documents that type I, but not type II, IFN pathway is required for IR‐triggered liver inflammation/damage and type I IFN mediates potential synergy between nonparenchyma and parenchyma cells in response to TLR4 activation.
Hypoxic postconditioning enhances the survival and inhibits apoptosis of cardiomyocytes following reoxygenation: role of peroxynitrite formation
Testing the hypothesis that enhancement of survival and prevention of apoptosis in hypoxic/reoxygenated cardiomyocytes by hypoxic postconditioning are associated with the reduction in peroxynitrite (ONOO−) formation induced by hypoxia/re Oxygenation (H/R) demonstrates that hypoxicPostconditioning protects myocytes against apoptosis following reoxygenation and enhances myocytes survival.
Inhibition of glycogen synthase kinase 3 beta ameliorates liver ischemia reperfusion injury by way of an interleukin‐10‐mediated immune regulatory mechanism
The novel findings document the key immune regulatory function of Gsk3β signaling in the pathophysiology of liver IRI, and provide a rationale to target GSk3β as a refined therapeutic strategy to ameliorate liver I RI.
CD4 T cells promote tissue inflammation via CD40 signaling without de novo activation in a murine model of liver ischemia/reperfusion injury
Evidence is provided that CD4 T cells function in liver IRI via CD154 without de novo Ag‐specific activation, and innate immunity–induced CD40 up‐regulation may trigger the engagement of CD154‐CD40 to facilitate tissue inflammation and injury.
Developmental and seed aging mediated regulation of antioxidative genes and differential expression of proteins during pre- and post-germinative phases in pea.
- Z. Yao, Lingwei Liu, +4 authors Belay T. Ayele
- Biology, MedicineJournal of plant physiology
- 15 October 2012
Proteomic analysis indicated the association of seed aging with changes in the abundance of specific proteins, revealing additional mechanisms underlying seed aging in pea.
Structural and Functional Analysis of Laninamivir and its Octanoate Prodrug Reveals Group Specific Mechanisms for Influenza NA Inhibition
It is found that laninamivir and its octanoate prodrug display group specific preferences to different influenza NAs and provide the structural basis of their specific action based upon their novel complex crystal structures.
Mitochondrial JNK activation triggers autophagy and apoptosis and aggravates myocardial injury following ischemia/reperfusion.
- Jie Xu, Xinghua Qin, +8 authors F. Gao
- Chemistry, MedicineBiochimica et biophysica acta
- 1 February 2015
It is demonstrated for the first time that activation of mitochondrial JNK, rather than JNK localization on mitochondria, induces autophagy and apoptosis and aggravates myocardial ischemia/reperfusion injury.
The Development of Myocardial Fibrosis in Transgenic Mice With Targeted Overexpression of Tumor Necrosis Factor Requires Mast Cell–Fibroblast Interactions
It is suggested that increased mast cell density with resultant mast cell–cardiac fibroblast cross-talk is required for the development of myocardial fibrosis in inflammatory cardiomyopathy.