Routine Outcomes Monitoring to Support Improving Care for Schizophrenia: Report from the VA Mental Health QUERI

In schizophrenia, treatments that improve outcomes have not been reliably disseminated. A major barrier to improving care has been a lack of routinely collected outcomes data that identify patients who are failing to improve or not receiving effective treatments. To support high quality care, the VA Mental Health QUERI used literature review, expert interviews, and a national panel process to increase consensus regarding outcomes monitoring instruments and strategies that support quality improvement. There was very good consensus in the domains of psychotic symptoms, side-effects, drugs and alcohol, depression, caregivers, vocational functioning, and community tenure. There are validated instruments and assessment strategies that are feasible for quality improvement in routine practice

Competition and Combative Advertising: An Historical Analysis

Fred K. Beard (PhD, University of Oklahoma) is a professor of advertising in the Gaylord College of Journalism and Mass Communication, University of Oklahoma. His research interests include comparative advertising, advertising humor, and advertising history. His work has appeared in the Journal of Advertising, the Journal of Advertising Research, the Journal of Business Ethics, the Journal of Business Research, Journalism History, the Journal of Historical Research in Marketing, the Journal of Macromarketing, and the Journal of Marketing Communications, among others.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

Role of pulmonary edema in phasic changes of cerebral oxygenation during serial seizures

To examine whether pulmonary dysfunction leads to episodes of cerebral hypoxia during recurrent seizures, measurements were made of arterial blood pressure, blood-gases, cerebral pO 2, and relative changes in cytochrome a, a 3 redox levels in anesthetized, paralyzed rats. Seizures were induced serially with bicuculline (BIC) or pentylenetetrazol (PTZ). During early seizures, cerebral oxygenation increased phasically. As seizures continued, a transition often occurred following which seizures were accompanied by phasic decreases in cerebral oxygenation. In addition, pulmonary edema often occurred at an unpredictable point during a series of seizures. Seizure-associated pulmonary edema was less likely to occur with pentobarbital anesthesia and PTZ seizures, than with nitrous oxide anesthesia and BIC seizures. Pulmonary edema was always accompanied by prolonged increases in blood pressure and paroxysmal electrocortical activity, and by hypoxemia, acidemia, and decreased cerebral oxygen supply. Despite the severity of these physiological changes, the transition from phasic increases to decreases in cerebral oxygenation during serial seizures occurred with virtually the same frequency in rats with and without pulmonary edema. This indicates that this transition is independent of pulmonary edema

Insulin‐induced hypoglycaemia suppresses pulsatile luteinising hormone secretion and arcuate Kiss1 cell activation in female mice

Stress suppresses pulsatile luteinising hormone (LH) secretion in a variety of species, although the mechanism underlying this inhibition of reproductive function remains unclear. Metabolic stress, particularly hypoglycaemia, is a clinically-relevant stress type that is modelled with bolus insulin injection (insulin-induced hypoglycaemia). The present study utilised ovariectomised C57BL/6 mice to test the hypothesis that acute hypoglycaemia suppresses pulsatile LH secretion via central mechanisms. Pulsatile LH secretion was measured in 90-minute sampling periods immediately prior to and following i.p. injection of saline or insulin. The secretion of LH was not altered over time in fed animals or acutely fasted (5 hours) animals following an i.p. saline injection. By contrast, insulin elicited a robust suppression of pulsatile LH secretion in fasted animals, preventing LH pulses in five of six mice. To identify the neuroendocrine site of impairment, a kisspeptin challenge was performed in saline or insulin pre-treated animals in a cross-over design. LH secretion in response to exogenous kisspeptin was not different between animals pre-treated with saline or insulin, indicating normal gonadotrophin-releasing hormone cell and pituitary responses during acute hypoglycaemia. Based on this finding, the effect of insulin-induced hypoglycaemia on arcuate kisspeptin (Kiss1) cell function was determined using c-Fos as a marker of neuronal activation. Insulin caused a significant suppression in the percentage of Kiss1 cells in the arcuate nucleus that contained c-Fos compared to saline-injected controls. Taken together, these data support the hypothesis that insulin-induced hypoglycaemia suppresses pulsatile LH secretion in the female mouse via predominantly central mechanisms, which culminates in the suppression of the arcuate Kiss1 population