These other definitions are perfectly valid, but they are far less common. You might see this used on Twitch.Īccording to The Free Dictionary, the acronym GLHF can stand for much more than just good luck have fun. While the phrase would have a comma, it is not used in the acronym. These competitive games can get feisty, so it is good to keep your sportsmanship. This salutation is a sign of good will used at the beginning of a game played online as a way for gamers to show sportsmanship at the start of the game in eSports. Collectively, the neuroprotection of exogenous H 2S against ischemia/hypoxia and reperfusion/reoxygenation injury is mediated by the enhancement of autophagic degradation.Īutophagic flux Cerebral ischemia/reperfusion Hydrogen sulfide Neuroprotection ULK1.What does the abbreviation GLHF stand for?Īccording to Slang It, the abbreviation GLHF means good luck, have fun. Moreover, BafA1 treatment abolished the protection of H 2S on the cerebral infarction. This H 2S-induced decline of LC3-II in ischemic brain was reversed by BafA1. Cerebral I/R injury caused an increase in LC3-II, a decrease in p62 and the accumulation of autophagosomes in the cortex and the hippocampus, which were inhibited by NaHS treatment. However, H 2S did not affect the OGD/R-induced increase of the ULK1 self-association and decrease of the ATG13 phosphorylation, which are the critical steps for the initiation of autophagosome formation. NaHS treatment reduced the OGD/R-induced elevation in LC3-II (an autophagic marker), which was completely reversed by co-treatment with an autophagic flux inhibitor bafilomycin A 1 (BafA1). NaHS (a donor of H 2S) treatment significantly increased cell viability and reduced cerebral infarct volume.
To further investigate whether this H 2S-induced reduction of autophagic vacuoles is caused by the decreased autophagosome synthesis and/or the increased autophagic degradation inautophagic flux, we performed in vitro and in vivo studies using SH-SY5Y cells for the oxygen and glucose deprivation/reoxygenation (OGD/R) and mice for the cerebral I/R, respectively.
We have recently reported that exogenous H 2S decreases the accumulation of autophagic vacuoles in mouse brain with ischemia/reperfusion (I/R) injury. However, its underlying mechanism is not fully understood. Hydrogen sulfide (H 2S), an endogenous gaseous signal molecule, exhibits protective effect against ischemic injury.
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