International guidelines define relapse prevention for schizophrenia patients as a key therapeutic aim. However, approximately 80% to 90% of schizophrenia patients experience further symptom exacerbation after the first episode. The purpose of this study was to investigate whether group integrated neurocognitive therapy (INT), a cognitive remediation approach, reduces relapse rates in schizophrenia outpatients. INT was compared with treatment as usual (TAU) in a randomized controlled trial. Fifty-eight stabilized outpatients participated in the study with 32 allocated to the INT group and 26 to the TAU group. A test battery was used at baseline, posttreatment at 15 weeks, and a 1-year follow-up. Relapse rates were significantly lower in the INT condition compared with TAU during therapy as well as at follow-up. The relapse rate after therapy was associated with significant reductions in negative and general symptoms, improvements in functional outcome, and overall cognition. Out of these variables, negative symptoms were identified to show the strongest association with relapses after therapy. The primary outcome of this study suggests that INT can prevent relapses in schizophrenia outpatients.Aberrant threat reactivity has been implicated in the pathophysiology of posttraumatic stress disorder (PTSD); however, the literature on this association is mixed. One factor that may contribute to this inconsistent association is differences in severity of posttraumatic stress symptoms (PTSSs) across studies, but no studies have tested this hypothesis. The relation between PTSD and threat reactivity may also differ between unpredictable threats (U-threats) and predictable threats (P-threats), given burgeoning evidence to support a particular role for aberrant responding to U-threat in PTSD. The present study examined how PTSS severity relates to startle potentiation to U-threat and P-threat in a trauma-exposed community sample (N = 258). There was a negative linear, but not quadratic, relation between PTSS severity and startle potentiation to U-threat, but not P-threat. Blunted defensive responding to U-threat may therefore contribute to higher levels of PTSSs and may represent a novel treatment target for higher levels of PTSSs.BACKGROUND Intravenous vancomycin is used to treat ventilator-associated pneumonia caused by methicillin-resistant Staphylococcus aureus, but achieves high rates of failure. Vancomycin nebulization may be efficient to provide high vancomycin lung tissue concentrations. The aim of this study was to compare lung tissue and serum concentrations of vancomycin administered intravenously and by aerosol in mechanically ventilated and anesthetized healthy piglets. METHODS Twelve female piglets received a single intravenous dose of vancomycin (15 mg/kg) and were killed 1 (n = 6) or 12 h (n = 6) after the end of administration. Twelve piglets received a single nebulized dose of vancomycin (37.5 mg/kg) and were killed 1 (n = 6) or 12 h (n = 6) after the end of the aerosol administration. In each group, vancomycin lung tissue concentrations were assessed on postmortem lung specimens using high-performance liquid chromatography. Blood samples were collected for serum vancomycin concentration measurement 30 min and 1, 2, 4 85%) and absorption rate was slow (absorption half life = 0.3 h). CONCLUSIONS Administration of vancomycin by nebulization resulted in higher lung tissue concentrations than the intravenous route.BACKGROUND Although clinical factors related to intraoperative opioid administration have been described, there is little research evaluating whether administration is influenced by drug formulation and, specifically, the unit dose of the drug. The authors hypothesized that the unit dose of hydromorphone is an independent determinant of the quantity of hydromorphone administered to patients intraoperatively. METHODS This observational cohort study included 15,010 patients who received intraoperative hydromorphone as part of an anesthetic at the University of California, Los Angeles hospitals from February 2016 to March 2018. Before July 2017, hydromorphone was available as a 2-mg unit dose. From July 1, 2017 to November 20, 2017, hydromorphone was only available in a 1-mg unit dose. On November 21, 2017, hydromorphone was reintroduced in the 2-mg unit dose. An interrupted time series analysis was performed using segmented Poisson regression with two change-points, the first representing the switch from a 2-mg to 1-mg unit dose, and the second representing the reintroduction of the 2-mg dose. RESULTS The 2-mg to 1-mg unit dose change was associated with a 49% relative decrease in the probability of receiving a hydromorphone dose greater than 1 mg (risk ratio, 0.51; 95% CI, 0.40-0.66; P less then 0.0001). The reintroduction of a 2-mg unit dose was associated with a 48% relative increase in the probability of administering a dose greater than 1 mg (risk ratio, 1.48; 95% CI, 1.11-1.98; P = 0.008). CONCLUSIONS This observational study using an interrupted time series analysis demonstrates that unit dose of hydromorphone (2 mg vs. 1 mg) is an independent determinant of the quantity of hydromorphone administered to patients in the intraoperative period.BACKGROUND Ketamine is a noncompetitive N-methyl-D-aspartate antagonist and is known for unique electrophysiologic profiles in electroencephalography. However, the mechanisms of ketamine-induced unconsciousness are not clearly understood. The authors have investigated neuronal dynamics of ketamine-induced loss and return of consciousness and how multisensory processing is modified in the primate neocortex. METHODS The authors performed intracortical recordings of local field potentials and single unit activity during ketamine-induced altered states of consciousness in a somatosensory and ventral premotor network. The animals were trained to perform a button holding task to indicate alertness.  https://www.selleckchem.com/PI3K.html  Air puff to face or sound was randomly delivered in each trial regardless of their behavioral response. Ketamine was infused for 60 min. RESULTS Ketamine-induced loss of consciousness was identified during a gradual evolution of the high beta-gamma oscillations. The slow oscillations appeared to develop at a later stage of ketamine anesthesia.