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GLOSSIP v. GROSS SOTOMAYOR, J., dissenting

anybody,” he noted that deaths had occurred in doses as low as 0.04 to 0.07 milligrams per kilogram (2.8 to 4.9 milligrams for a 70-kilogram adult), and contended that a 500-milligram dose would itself cause death within less than an hour—a conclusion he characterized as “essentially an extrapolation from a toxic effect.” Id., at 327; see id., at 308. Second, in explaining how he reconciled his opinion with the evidence of midazolam’s ceiling effect, Dr. Evans testi­ fied that while “GABA receptors are found across the entire body,” midazolam’s ceiling effect is limited to the “spinal cord” and there is “no ceiling effect” at the “higher level of [the] brain.” Id., at 311–312. Consequently, in his view, “as you increase the dose of midazolam, it’s a linear effect, so you’re going to continue to get an impact from higher doses of the drug,” id., at 332, until eventually “you’re paralyzing the brain,” id., at 314. Dr. Evans also understood the chemical source of midazolam’s ceiling effect somewhat differently from petitioners’ experts. Although he agreed that midazolam produces its effect by “binding to [GABA] receptors,” id., at 293, he appeared to believe that midazolam produced sedation by “inhibiting GABA” from attaching to GABA receptors, not by promot­ ing GABA’s sedative effects, id., at 312. Thus, when asked about Dr. Lubarsky’s description of the ceiling effect, Dr. Evans characterized the phenomenon as stemming from “the competitive nature of substances trying to attach to GABA receptors.” Id., at 313. Dr. Evans cited no scholarly research in support of his opinions. Instead, he appeared to rely primarily on two sources: the Web site www.drugs.com, and a “Material Safety Data Sheet” produced by a midazolam manufacturer. See id., at 303. Both simply contained general infor­ mation that covered the experts’ areas of agreement.