Supporting Physicians and Practice Teams in Efforts to Address the Opioid Epidemic.

Primary care physicians and practice teams increasingly recognize the need to take a role in addressing the growing epidemic of opioid use disorder (OUD) and opioid-related drug overdose deaths, but face considerable challenges in doing so. Through its work supporting practice transformation efforts, sharing innovations, and connecting key sectors within communities, the Network for Regional Healthcare Improvement and several of its member regional health improvement collaboratives have identified innovative ways to support physicians and practice teams in transforming practice in ways that address a spectrum of issues related to opioid use. These strategies include efforts to prevent, identify, and treat opioid addiction, including reducing inappropriate prescribing; improving opioid prescribing safety; compassionately tapering chronic and/or high-dose opioid regimens; appropriately screening for and identifying OUD; initiating treatment with evidence-based medications for OUD within practice settings; and prescribing life-saving naloxone to reverse opioid overdose.

Cleveland Clinic Health System: A comprehensive framework for a health system patient safety initiative.

The Cleveland Clinic Health System (CCHS) is committed to the enhancement of patient safety throughout the CCHS. This article describes the CCHS patient safety initiative, the development, objectives, strategies, goals, and activities.

Phosphorylation of v-mos Ser 47 by the mitotic form of p34cdc2.

P85gag-mos is hyperphosphorylated during mitosis in normal rat kidney (NRK) cells transformed by Moloney murine sarcoma virus ts110. We now report that P85gag-mos is phosphorylated in vitro by the mitotic form of the cdc2 kinase (p34cdc2, known as M-phase kinase) derived from virus-transformed cells. The major site of P85gag-mos phosphorylation by the M-phase kinase in vitro lies within the amino-terminal portion of the viral mos protein sequence spanning residues 45-53, as determined by tryptic peptide mapping.

Ontogeny of adenosine 3',5'-monophosphate metabolism in rabbit cerebral cortex. Development of responses to histamine, norepinephrine, adenosine, and glutamate.

The effects of norepinephrine (NE), histamine (HIST), glutamate, and adenosine, singly and in combinations, on the accumulation of adenosine 3',5'-monophosphate (cyclic AMP) in slices of rabbit cerebral cortex were examined using tissue from animals 4 days before to 38 days after birth. A response to NE became visible 2 days before birth and increased to a maximum at 7 days after birth before declining toward the small adult value during the second post-natal week. During this period NE was at least twice as efficacious as isoproterenol, and both alpha- and beta-adrenergic antagonists had prominent inhibitory effects.

Ontogeny of adenosine 3',5'-monophosphate metabolism in guinea pig cerebral cortex. I. Development of responses to histamine, norepinephrine and adenosine.

The effects of norepinephrine, histamine and adenosine, singly or in combinations, on the accumulation of adenosine 3',5'-monophosphate were examined in slices of cerebral cortex from strain 2 guinea pigs at 40 to 68 days of gestation. The response to histamine was 2-fold at 40 days, increased to 19-fold at 55 days and declined there after toward the adult value of 4-fold. The response to adenosine was first apparent at 44 days and developed rapidly to a maximum of about 40-fold at 55 days.