East central European urbanization: a political economy of the world-system perspective

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73059/1/j.1468-2427.1989.tb00138.x.pd

Alcohol, Cannabis, and Opioid Use Disorders, and Disease Burden in an Integrated Health Care System.

ObjectivesWe examined prevalence of major medical conditions and extent of disease burden among patients with and without substance use disorders (SUDs) in an integrated health care system serving 3.8 million members.MethodsMedical conditions and SUDs were extracted from electronic health records in 2010. Patients with SUDs (n = 45,461; alcohol, amphetamine, barbiturate, cocaine, hallucinogen, and opioid) and demographically matched patients without SUDs (n = 45,461) were compared on the prevalence of 19 major medical conditions. Disease burden was measured as a function of 10-year mortality risk using the Charlson Comorbidity Index. P-values were adjusted using Hochberg's correction for multiple-inference testing within each medical condition category.ResultsThe most frequently diagnosed SUDs in 2010 were alcohol (57.6%), cannabis (14.9%), and opioid (12.9%). Patients with these SUDs had higher prevalence of major medical conditions than non-SUD patients (alcohol use disorders, 85.3% vs 55.3%; cannabis use disorders, 41.9% vs 23.0%; and opioid use disorders, 44.9% vs 26.1%; all P < 0.001). Patients with these SUDs also had higher disease burden than non-SUD patients; patients with opioid use disorders (M = 0.48; SE = 1.46) had particularly high disease burden (M = 0.23; SE = 0.09; P < 0.001).ConclusionsCommon SUDs, particularly opioid use disorders, are associated with substantial disease burden for privately insured individuals without significant impediments to care. This signals the need to explore the full impact SUDs have on the course and outcome of prevalent conditions and initiate enhanced service engagement strategies to improve disease burden

Glucagon activates Ca(2+) and Cl(−) channels in rat hepatocytes

Glucagon is one of the major hormonal regulators of glucose metabolism, counteracting the hepatic effects of insulin when the concentration of glucose in the bloodstream falls below a certain level. Glucagon also regulates bile flow, hepatocellular volume and membrane potential of hepatocytes. It is clear that changes in cell volume and membrane potential cannot occur without significant ion fluxes across the plasma membrane. The effects of glucagon on membrane currents in hepatocytes, however, are not well understood. Here we show, by patch-clamping of rat hepatocytes, that glucagon activates two types of currents: a small inwardly rectifying Ca(2+) current with characteristics similar to those of the store-operated Ca(2+) current and a larger outwardly rectifying Cl(−) current similar to that activated by cell swelling. We show that the mechanism of glucagon action on membrane conductance involves phospholipase C and adenylyl cyclase. Contribution of the adenylyl cyclase-dependent pathway to activation of the currents depended on Epac (exchange protein directly activated by cAMP), but not on protein kinase A. The activation of Ca(2+) and Cl(−) channels is likely to play a key role in the mechanisms by which glucagon regulates hepatocyte metabolism and volume