the leader of hezbollah hassan nazrallah spoke yesterday, he said that this would not go unpunished but he seemed ambiguous as to exactly what a response could be. what do you think hezbollah might do, if anything? hassan nasrallah did not give it away yesterday, he will talk to maurice arutyunyan and perhaps reveal some. it s important to point out the current status quo that prevailed over the past 2.5 months since the conflict in gaza started suits hezbollah very well. hezbollah and the israeli and responses before agrees and warfare, taking the fight israel any form of cross border skirmishes and harassment, forcing it to divert resources and soldiers up divert resources and soldiers up to the northern border away from gaza, however show support to palestinians and microtubules stopping short of war. all out war is not necessarily hezbollah plasma interests are if we were to reduce conclusions from yesterday, it seems indicate
Hereditary sensory neuropathy type 1A (HSN1A) is an autosomal, dominantly inherited peripheral neuropathy caused by mutations in serine palmitoyl transferase long chain 1 (SPTLC1), involved in the de novo synthesis of sphingolipids. We have previously reported calcium imbalance, as well as mitochondrial and ER stress in both HSN1 patient lymphoblasts and a transiently transfected cell model. In this study, we investigated the role of the Ca2+-activated protease calpain in destabilizing the cell cytoskeleton, by examining calpain activity in SH-SY5Y cells overexpressing the V144D mutant and changes in microtubule-associated proteins (MAP). Intramitochondrial Ca2+ was found to be significantly depleted and cytoplasmic Ca2+ increased in the V144D mutant. Subsequently, calpain and proteasome activity were increased and calpain substrates, microtubule associated proteins MAP2, and tau were significantly reduced in the microtubule fraction of the mutant. Significant changes were also found i
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from the microtubules they stick together and form thread and then tangles inside the neurons and eventually destroy them. in the battle against better amyloid plaques researchers have identified a possible ally. christine hans from the jim incentive for nero to generative diseases is a biochemist he s been researching all scientists for decades one focus of his what is the role of amyloid protein aggregates and how they develop into plaques in the brain. as a feeder forces like it was a thought in my many studies indicate that we re all as extremely high risk of developing alzheimer s. the time the risk rises dramatically with age. the tomato that me answer since society as a whole is aging we have to reckon with rising numbers of patients and that s exactly what we re seeing little. so what if the brain could be cleared of plaque