he years were slipping by for her, one by one, and but for that one shortcoming she knew she need fear no competition and that was an accident coming down Dalkey hill and she always tried to conceal it.
Was it her disability that "she always tried to conceal"?
when Edy asked her was she heartbroken about her best boy throwing her over. Gerty winced sharply. A brief cold blaze shone from her eyes that spoke volumes of scorn immeasurable. It hurt. O yes, it cut deep because Edy had her own quiet way of saying things like that she knew would wound like the confounded little cat she was. Gerty's lips parted swiftly to frame the word but she fought back the sob that rose to her throat, so slim, so flawless, so beautifully moulded it seemed one an artist might have dreamed of. She had loved him better than he knew.
Gerty's pride was wounded.
The EWN embraces argument and reframes it as a human endeavor. It asks students to think critically about howbeliefs are formed and to write clearly about that formation. But this is a different type of argumentation than we traditionally assign. As Blankenship reminds us, “the goal of rhetoric . . . established in Aristotle is to defeat an opponent through persuading him . . . that your position, and by extension you, are superior” (21–22).
distinguishes empathetic (aka Rogerian argument) from agonistic argument
Overall, the dosage level of Aducanumab was found to be important for its efficacy towards reducing clinical decline in AD.
Was it effective in reducing cognitive decline as well as "clinical decline"?
40% of Emerge patients had discontinued the trial
Why?
For high-dose Engage, the results still did not demonstrate a reduction in clinical decline; a 6% worsening in performance on the CDR-SB scale was measured (p = 0.627) [32].
Was there a comparable decline in the placebo group?
Consequently, the CNS Aβ level becomes reduced. Likewise, CSF Aβ assessments revealed a reduction in the concentration of free Aβ40, an increase in total Aβ40, and an increase in total Aβ42 had occurred (between-group difference: p = 0.01, p = 0.002, and p < 0.001) [19].
So, do the higher plasma levels and lower CNS level suggest that the Aβ40 and Aβ42 are released into the bloodstream, where they can be cleared? Does the decrease in free Aβ40 in CSF and increase in total Aβ40 and Aβ42 mean that the Aβ peptides are bound with Solanezumab and therefore not accumulating in Aβ plaques?
Aβ40 and Aβ42 both increased
increased???
phase 3 trials of DMTs Solanezumab, Aducanumab, Crenezumab, and Gantenerumab.
What about lecanemab, which is also a DMT (Disease Modifying Therapy) in phase 3 trials (AHEAD 3-45)?
targets Aβ fibrils
I believe that lecanemab also targets Aβ fibrils (or protofibrils?):
"Lecanemab selectively binds to neutralize and eliminate soluble, toxic amyloid-beta (Aβ) aggregates (protofibrils) that are thought to contribute to the neurodegenerative process in AD." (Source Biogen)