Acute systemic administration of morphine selectively increases mu opioid receptor binding in the rat brain

Opioid receptor binding, including the mu, delta, and kappa receptor subtypes, was compared in morphine-injected and control rats. Brain tissues were homogenized and centrifuged either one or two times prior to receptor binding assay. In brain membranes from morphine-injected rats centrifuged once, there was a decrease in mu, but not delta or kappa, binding compared to controls, perhaps indicating occupation of these sites by morphine. By contrast, homogenates from morphine-injected rats centrifuged twice manifested an increase inmu, but not delta or kappa, binding sites. These results suggest that pharmacological stimulation of central opioid receptors with morphine causes a rapid, selective increase in the number of available mu binding sites.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24608/1/0000018.pd

The diagnosis and management of idiosyncratic drug‐induced liver injury

Drug‐induced liver injury (DILI) is an uncommon but important cause of liver disease that can arise after exposure to a multitude of drugs and herbal and dietary supplements. The severity of idiosyncratic DILI varies from mild serum aminotransferase elevations to the development of severe liver injury that can progress to acute liver failure resulting in death or liver transplantation within days of DILI onset. Chronic liver injury that persists for more than 6 months after DILI onset is also becoming increasingly recognized in up to 20% of DILI patients. Host demographic (age, gender, race), clinical and laboratory features at DILI onset have been associated with the severity and outcome of liver injury in DILI patients. In addition to cessation of the suspect drug, other medical interventions including the use of N‐acetylcysteine and corticosteroids in selected patients have shown some clinical benefit, but additional prospective studies are needed. A number of promising diagnostic, prognostic and mechanistic serum and genetic biomarkers may help improve our understanding of the pathogenesis and treatment of idiosyncratic DILI.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/147192/1/liv13931.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/147192/2/liv13931_am.pd