It's been 24 years since Microsoft released the SideWinder Dual Strike, a controller that looked like two joysticks mating.
This article first appeared in PC Gamer magazine issue 378 in December 2022, as part of our Tech Tales series. Every month we talk about the ups and downs of PC hardware, with a look back on our own history with the hobby.
Without the innovations of PC gaming's hardware manufacturers, we wouldn't have arrived at such a high standard for input devices. Mice that NASA could probably trust to control a rocket launch and calculate a trip to Saturn. Keyboards that will still be registering inputs correctly when we're just biomass in the ground. And the greatest innovation in PC gaming history: RGB lighting.
This striking gamepad retailed for one hundred English pounds . That'd buy you three full-price PC games and a re-release in 1999, or a semi-detached in Lowestoft. It didn't look anything like console controllers, this thing was more like two joysticks mating. On the left-hand side, a D-pad and three buttons. On the right, four buttons were arranged on the front of a flightstick, attached to the left-hand piece by a giant ball.
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Dual mTORC1/2 inhibition synergistically enhances AML cell death in combination with the BCL2 antagonist venetoclaxAbstract. Purpose: Acute myeloid leukemia (AML) is an aggressive disease with a poor outcome. We investigated mechanisms by which the anti-AML activity of ABT-199 (venetoclax) could be potentiated by dual mTORC1/TORC2 inhibition. Methods: Venetoclax/INK128 synergism was assessed in various AML cell lines and primary patient AML samples in vitro. AML cells over-expressing MCL-1, constitutively active AKT, BAK and/or BAX knock-out, and acquired venetoclax resistance were investigated to define mechanisms underlying interactions. The antileukemic efficacy of this regimen was also examined in xenograft and patient-derived xenograft (PDX) models. Results: Combination treatment with venetoclax and INK128 (but not the mTORC1 inhibitor Rapamycin) dramatically enhanced cell death in AML cell lines. Synergism was associated with p-AKT and p-4EBP1 down-regulation and dependent upon MCL-1 downregulation and BAK/BAX up-regulation as MCL-1 overexpression and BAX/BAK knock out abrogated cell death. Constitutive AKT activation opposed synergism between venetoclax and PI3K or AKT inhibitors, but not INK128. Combination treatment also synergistically induced cell death in venetoclax- resistant AML cells. Similar events occurred in primary patient-derived leukemia samples but not normal CD34+ cells. Finally, venetoclax and INK128 co-treatment displayed increased anti-leukemia effects in in vivo xenograft and PDX models. Conclusions: The venetoclax/INK128 regimen exerts significant anti-leukemic activity in various preclinical models through mechanisms involving MCL-1 down-regulation and BAK/BAX activation, and offers potential advantages over PI3K or AKT inhibitors in cells with constitutive AKT activation. This regimen is active against primary and venetoclax resistant AML cells, and in in vivoAML models. Further investigation of this strategy appears warranted.
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