ABSTRACT
Antipsychotic medications carry an established lifetime risk of metabolic syndrome. This retrospective chart review evaluated feasibility of a metabolic monitoring clinical decision support tool (CDST) for weight, lipid, blood glucose, and blood pressure management of 163 clients in an early psychosis outpatient clinic over 2 years. Each parameter had at least 98 (60.1%) clients with a recorded value, the most being documented for weight with 112 (68.7%) clients. CDST adherence ranged from at least 54.3-100% for non-pharmacologic interventions (e.g. clinic counseling, referral to health program or primary care) and at least 33.3-100% for pharmacologic interventions (e.g. metformin). Though no baseline cardiometabolic abnormalities were identified, dyslipidemia and obesity were later found in 37 (22.7%) and 35 (21.5%) clients, respectively. Only 14 (8.6%) clients were prescribed medications for cardiometabolic abnormalities by psychiatrists in the clinic. Increasing focus on physical health is needed to better this population's long-term prognosis.
Subject(s)
Antipsychotic Agents/adverse effects , Dyslipidemias/chemically induced , Obesity/chemically induced , Psychotic Disorders/drug therapy , Psychotic Disorders/psychology , Schizophrenia/drug therapy , Adolescent , Adult , Community Mental Health Centers , Decision Support Systems, Clinical , Dyslipidemias/epidemiology , Female , Health Behavior , Humans , Indiana/epidemiology , Male , Metabolic Syndrome/chemically induced , Middle Aged , Obesity/epidemiology , Psychotic Disorders/epidemiology , Retrospective Studies , Risk Factors , Schizophrenia/epidemiology , Schizophrenic Psychology , Young AdultABSTRACT
Bioluminescence generated by the Vibrio fischeri Lux system consumes oxygen and reducing power, and it has been proposed that cells use this to counteract either oxidative stress or the accumulation of excess reductant. These models predict that lux expression should respond to redox conditions; yet no redox-responsive regulator of lux is known. We found that the luxICDABEG operon responsible for bioluminescence is repressed by the ArcAB system, which is activated under reducing conditions. Consistent with a role for ArcAB in connecting redox monitoring to lux regulation, adding reductant decreased luminescence in an arc-dependent manner. ArcA binds to and regulates transcription from the luxICDABEG promoter, and it represses luminescence both in the bright strain MJ1 and in ES114, an isolate from the squid Euprymna scolopes that is not visibly luminescent in culture. In ES114, deleting arcA increased luminescence in culture approximately 500-fold to visible levels comparable to that of symbiotic cells. ArcA did not repress symbiotic luminescence, but by 48 h after inoculation, ArcA did contribute to colonization competitiveness. We hypothesize that inactivation of ArcA in response to oxidative stress during initial colonization derepresses luxICDABEG, but that ArcAB actively regulates other metabolic pathways in the more reduced environment of an established infection.
