Secretary of State John Kerry and United Nations Secretary-General Ban Ki-Moon jointly announced late Thursday that an unconditional ceasefire between Israel and Palestinian groups fighting in the Gaza Strip had been agreed to, and that "this humanitarian ceasefire will commence at 8am local time on Friday, August 1." The announcement came after the United Nations Security Council had again called for an immediate halt to the fighting, and two days after top Hamas figure Mohammed Deif had committed Hamas to continued fighting in the absence of concessions from Israel, Egypt, and the Palestinian Authority. A tweet from Ali Weinberg, an ABC News journalist stationed at the State Department, clarified that that the Friday truce was set to initially last 72 hours and that IDF forces would remain in the Hamas-controlled territory throughout its duration. Associated Press veteran diplomatic correspondent Matt Lee further reported that Israeli and Palestinian delegations would travel to Cairo for negotiations "aimed at reaching a durable ceasefire." The developments came amid deepening focus on strategic threats posed by Hamas's rocket arsenal and its offensive tunnel infrastructure. Nine Israeli civilians had been wounded earlier that day by a series of mortar attacks that scored direct and indirect hits. Multiple rocket barrages had per Yediot Aharonot "rained on Israel's south." Meanwhile Israeli Finance Minister Yair Lapid had separately emphasized on Thursday that the ongoing risk of mass casualty infiltrations from Hamas's attack tunnels would keep Israeli forces in the Gaza Strip until those tunnels were eliminated. Roughly 30 tunnels, accessible through dozens of entrances across the Gaza Strip, have been uncovered since the ground phase of Operation Protective Edge began. There have been reports of heavy firefights around many of the access shafts.
An Israeli research team has announced new findings that link Alzheimer’s disease to brain hyperactivity and says its research helps explain why so many patients of this debilitating disease run a high risk of seizures. While the amyloid-beta protein involved in the development and progression of Alzheimer’s seems the most likely cause for this neuronal hyperactivity, how and why the elevated activity takes place hasn’t been explained until now. “These are truly exciting results,” said Dr. Inna Slutsky, who led the Tel Aviv University research team. The study, recently published in Cell Reports, shows that the guilty party in enhancing neuronal activity in Alzheimer’s patients is a molecular mechanism involving the amyloid precursor protein (APP). APP is well-known for its role in producing amyloid-beta. But it also acts as a receptor for amyloid-beta. Elevated activity in the hippocampus — the area of the brain that controls learning and memory — has been observed in patients with mild cognitive impairment and early stages of Alzheimer’s disease. Hyperactive hippocampal neurons, which precede amyloid plaque formation, have also been observed in mouse models with early-onset Alzheimer’s disease. Now, the Israeli researchers found that the binding of amyloid-beta to pairs of APP molecules triggers a change and causes elevated brain hyperactivity. “Our work suggests that APP molecules, like many other known cell surface receptors, may modulate the transfer of information between neurons,” said neuroscientist Slutsky, who last year reported that bursts of gentle electricity can slow the progression of Alzheimer’s. With this added piece of the puzzle, the potential for restoring memory and protecting the brain is greatly increased. (via Israel21c)
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