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The move came after two years of Thea having a reduced role, which was sometimes controversial with fans and had been a topic of conversation for quite some time. Producers explained in season five that the reduced role was Holland's choice -- as was leaving the show entirely with last night's "The Thanatos Guild."

"Season six is the end of her contract, and going into season six, with all of us knowing it was the end of her contract, Willa expressed the desire to move on, not re-up," executive producer Marc Guggenheim told nike free run 3 trainer v3 lite
. "She expressed a desire to be written out at a certain time in the season, which is around episode 16, so we accommodated her on that front as well."

Thea left the series as most fans expected her to -- with Roy Harper (Colton Haynes), her longtime onscreen love interest, who had come to Star City for a two-episode arc that centered on Thea. Elements of her family's past, including Malcolm's time as the head of the League of Assassins, played in as well.

"We love Willa, we love Thea the character and we particularly love Thea's relationship with Oliver," Guggenheim told ComicBook.com in October . "That said, Willa came to us at the end of season four and she, very honestly, expressed a desire to cut back how many episodes a season she was doing. She's a member of our family, and we wanted to honor that request. That's what happens when you have a show that goes over a hundred episodes, people start to say, 'hey, I would like to pull back,' some people don't want to renew their contract. There's a whole host of different things that start to come into play and you work that into the storytelling."

This week, he reiterated many of those remarks, providing a little more detail.

"That relationship is one of the things that we deviated from the comic book early on. It was one of the very first major creative decisions we made in terms of adapting the Green Arrow comic for live action television. So it’s always been an incredibly important, critical part of the show for us," Guggenheim admitted in the EW interview. "We never want to stand in the way of someone wanting to express themselves creatively in a different way, on a different show, or through a different medium. So we took Willa’s request and took it seriously, and decided 'Okay, well, if this is the hand we’re dealt, how do we play it as best we can and write off Thea in the most emotional and interesting way possible?'"

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In late 2015, the first example of a transferrable polymyxin resistance mechanism in Gram-negative pathogens, MCR-1, was reported. Since that report, MCR-1 has been described to occur in many Gram-negative pathogens, and the mechanism of MCR-1-mediated resistance was rapidly determined: an ethanolamine is attached to lipid A phosphate groups, rendering the membrane more electropositive and repelling positively charged polymyxins. Acquisition of MCR-1 is clinically significant because polymyxins are frequently last-line antibiotics used to treat extensively resistant organisms, so acquisition of this mechanism might lead to pan-resistant strains. Therefore, the ability to inhibit MCR-1 and restore polymyxin sensitivity would be an important scientific advancement. Peptide-conjugated phosphorodiamidate morpholino oligomers (PPMOs) are antisense molecules that were designed to target mRNA, preventing translation. Peptide conjugation enhances cellular entry, but they are positively charged, so we tested our lead antibacterial PPMOs by targeting an essential Escherichia coli gene, acpP , and demonstrated that they were still effective in mcr - 1 -positive E.coli strains. We then designed and synthesized two PPMOs targeted to mcr-1 mRNA. Five clinical mcr-1 -positive E.coli strains were resensitized to polymyxins by MCR-1 inhibition, reducing MICs 2- to 16-fold. Finally, therapeutic dosing of BALB/c mice with MCR-1 PPMO combined with colistin in a sepsis model reduced morbidity and bacterial burden in the spleen at 24h and offered a survival advantage out to 5days. This is the first example of a way to modulate colistin resistance with an antisense approach and may be a viable strategy to combat this globally emerging antibiotic resistance threat.

IMPORTANCE Polymyxin use has been increasing as a last line of defense against Gram-negative pathogens with high-level resistance mechanisms, such as carbapenemases. The recently described MCR-1 is a plasmid-mediated mechanism of resistance to polymyxins. MCR-1 is currently found in Gram-negative organisms already possessing high-level resistance mechanisms, leaving clinicians few or no antibacterial options for infections caused by these strains. This study utilizes antisense molecules that target mRNA, preventing protein translation. Herein we describe antisense molecules that can be directly antibacterial because they target genes essential to bacterial growth or blockade of MCR-1, restoring polymyxin sensitivity. We also demonstrate that MCR-1 antisense molecules restore the efficacies of polymyxins in mouse models of E.coli septicemia. Considering all things together, we demonstrate that antisense molecules may be effective therapeutics either alone when they target an essential gene or combined with antibiotics when they target specific resistance mechanisms, such as those seen with MCR-1.

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