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To test this, we pretreated islets with PTX [31]

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These agents are known to delay gastric emptying, enhance pyloric contraction, and alter small-bowel motility, which can contribute to fecal stasis, increased intraluminal pressure, bacterial overgrowth, and, ultimately, mechanical obstruction

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Collectively, inflammatory signaling, mitochondrial dysfunction, aberrant neurovascular invasion, and cartilage destruction act in concert to propel OA progression