Assessing cardiometabolic parameter monitoring in inpatients taking a second-generation antipsychotic : the CAMI-SGA study – a crosssectional study

Objectives This study aims to determine the proportion of initial cardiometabolic assessment and its predicting factors in adults with schizophrenia, bipolar disorder or other related diagnoses for whom a second-generation antipsychotic was prescribed in the hospital setting. Design Cross-sectional study. Setting The psychiatry unit of a Canadian tertiary care teaching hospital in Montreal, Canada. Participants 402 patients with aforementioned disorders who initiated, restarted or switched to one of the following antipsychotics: clozapine, olanzapine, risperidone, paliperidone or quetiapine, between 2013 and 2016. Primary outcome measures We assessed the proportion of cardiometabolic parameters monitored. Secondary outcome measures We identified predictors that influence the monitoring of cardiometabolic parameters and we assessed the proportion of adequate interventions following the screening of uncontrolled blood pressure and fasting glucose or glycated haemoglobin (HbA1c) results. Results Only 37.3% of patients received monitoring for at least three cardiometabolic parameters. Blood pressure was assessed in 99.8% of patients; lipid profile in 24.4%; fasting glucose or HbA1c in 33.3% and weight or body mass index in 97.8% of patients while waist circumference was assessed in 4.5% of patients. For patients with abnormal blood pressure and glycaemic values, 42.3% and 41.2% subsequent interventions were done, respectively. The study highlighted the psychiatric diagnosis (substance induced disorder OR 0.06 95% CI 0.00 to 0.44), the presence of a court-ordered treatment (OR 0.79 95% CI 0.35 to 1.79) and the treating psychiatrist (up to OR 34.0 95% CI 16.2 to 140.7) as predictors of cardiometabolic monitoring. Conclusions This study reports suboptimal baseline cardiometabolic monitoring of patients taking an antipsychotic in a Canadian hospital. Optimising collaboration within a multidisciplinary team may increase cardiometabolic monitoring

The Vehicle, Spring 1997

Vol. 38, No. 2 Table of Contents Poetry: Don QuixotePatrick Scanlanpage 1 Last SupperChristine Starrpage 1 Marriage VowsKristopher Clausingpage 2 The LibraryPatrick Lairpage 4 GuruJohn Dylan McNeilpage 5 Tripping in OzKim Evanspage 5 TranceStephanie Kavanaughpage 6 The CleftEmilie Roypage 7 FlannelAmanda Watsonpage 8 Strip PokerEbben Moorepage 8 IceJohn Dylan McNeilpage 9 ChloeMichael Kawapage 11 OrchardCarmella Cosenzapage 12 Jenn & Cookie MonsterJacob Tolbertpage 13 Barry ManilowKatie Wrightpage 14 GoodbyesShannon Goodallpage 15 Prose: Alice (A Short, Short Story)Carmella Cosenzapage 17 UntitledJoe Robesonpage 17 A New World AloneKendall W. Baumanpage 22 Biographiespage 35https://thekeep.eiu.edu/vehicle/1069/thumbnail.jp

Acrolein Induces Endoplasmic Reticulum Stress and Causes Airspace Enlargement

BACKGROUND: Given the relative abundance and toxic potential of acrolein in inhaled cigarette smoke, it is surprising how little is known about the pulmonary and systemic effects of acrolein. Here we test the hypothesis whether systemic administration of acrolein could cause endoplasmic reticulum (ER) stress, and lung cell apoptosis, leading to the enlargement of the alveolar air spaces in rats. METHODS: Acute and chronic effects of intraperitoneally administered acrolein were tested. Mean alveolar airspace area was measured by using light microscopy and imaging system software. TUNEL staining and immunohistochemistry (IHC) for active caspase 3 and Western blot analysis for active caspase 3, and caspase 12 were performed to detect apoptosis. The ER-stress related gene expression in the lungs was determined by Quantitative real-time PCR analysis. Acrolein-protein adducts in the lung tissue were detected by IHC. RESULTS: Acute administration of acrolein caused a significant elevation of activated caspase 3, upregulation of VEGF expression and induced ER stress proteins in the lung tissue. The chronic administration of acrolein in rats led to emphysematous lung tissue remodeling. TUNEL staining and IHC for cleaved caspase 3 showed a large number of apoptotic septal cells in the acrolein-treated rat lungs. Chronic acrolein administration cause the endoplasmic reticulum stress response manifested by significant upregulation of ATF4, CHOP and GADd34 expression. In smokers with COPD there was a considerable accumulation of acrolein-protein adducts in the inflammatory, airway and vascular cells. CONCLUSIONS: Systemic administration of acrolein causes endoplasmic reticulum stress response, lung cell apoptosis, and chronic administration leads to the enlargement of the alveolar air spaces and emphysema in rats. The substantial accumulation of acrolein-protein adducts in the lungs of COPD patients suggest a role of acrolein in the pathogenesis of emphysema

Changes in defensive functioning in completed psychoanalyses : the penn psychoanalytic treatment collection

Objective. The aim of this naturalistic study is to examine whether a sample of subjects showed improvements in their defensive functioning after undergoing psychoanalysis.Methods. Seventeen subjects from the Penn Psychoanalytic Treatment Collection with completed, tape-recorded psychoanalyses had their defense mechanisms rated both for early and late sessions.Results. The pre-post effect size for the change in overall defensive functioning (ODF) of the sample was large (0.76) and statistically significant. The percentage of subjects who improved (71%) in their ODF was similar to that found by others who studied the same sample using general functioning measures.Conclusions. These findings provide the first empirical evidence to support a sustained trait-like change in dynamic personality functioning in patients who have undergone psychoanalysis. Future randomized and controlled studies with homogeneous samples are needed to further confirm these findings

The Vehicle, Spring 1997

Vol. 38, No. 2 Table of Contents Poetry: Don QuixotePatrick Scanlanpage 1 Last SupperChristine Starrpage 1 Marriage VowsKristopher Clausingpage 2 The LibraryPatrick Lairpage 4 GuruJohn Dylan McNeilpage 5 Tripping in OzKim Evanspage 5 TranceStephanie Kavanaughpage 6 The CleftEmilie Roypage 7 FlannelAmanda Watsonpage 8 Strip PokerEbben Moorepage 8 IceJohn Dylan McNeilpage 9 ChloeMichael Kawapage 11 OrchardCarmella Cosenzapage 12 Jenn & Cookie MonsterJacob Tolbertpage 13 Barry ManilowKatie Wrightpage 14 GoodbyesShannon Goodallpage 15 Prose: Alice (A Short, Short Story)Carmella Cosenzapage 17 UntitledJoe Robesonpage 17 A New World AloneKendall W. Baumanpage 22 Biographiespage 35https://thekeep.eiu.edu/vehicle/1069/thumbnail.jp

Effect of Verapamil on Pancreatic Beta Cell Function in Newly Diagnosed Pediatric Type 1 Diabetes: A Randomized Clinical Trial

Importance: In preclinical studies, thioredoxin-interacting protein overexpression induces pancreatic beta cell apoptosis and is involved in glucotoxicity-induced beta cell death. Calcium channel blockers reduce these effects and may be beneficial to beta cell preservation in type 1 diabetes. Objective: To determine the effect of verapamil on pancreatic beta cell function in children and adolescents with newly diagnosed type 1 diabetes. Design, setting, and participants: This double-blind, randomized clinical trial including children and adolescents aged 7 to 17 years with newly diagnosed type 1 diabetes who weighed 30 kg or greater was conducted at 6 centers in the US (randomized participants between July 20, 2020, and October 13, 2021) and follow-up was completed on September 15, 2022. Interventions: Participants were randomly assigned 1:1 to once-daily oral verapamil (n = 47) or placebo (n = 41) as part of a factorial design in which participants also were assigned to receive either intensive diabetes management or standard diabetes care. Main outcomes and measures: The primary outcome was area under the curve values for C-peptide level (a measure of pancreatic beta cell function) stimulated by a mixed-meal tolerance test at 52 weeks from diagnosis of type 1 diabetes. Results: Among 88 participants (mean age, 12.7 [SD, 2.4] years; 36 were female [41%]; and the mean time from diagnosis to randomization was 24 [SD, 4] days), 83 (94%) completed the trial. In the verapamil group, the mean C-peptide area under the curve was 0.66 pmol/mL at baseline and 0.65 pmol/mL at 52 weeks compared with 0.60 pmol/mL at baseline and 0.44 pmol/mL at 52 weeks in the placebo group (adjusted between-group difference, 0.14 pmol/mL [95% CI, 0.01 to 0.27 pmol/mL]; P = .04). This equates to a 30% higher C-peptide level at 52 weeks with verapamil. The percentage of participants with a 52-week peak C-peptide level of 0.2 pmol/mL or greater was 95% (41 of 43 participants) in the verapamil group vs 71% (27 of 38 participants) in the placebo group. At 52 weeks, hemoglobin A1c was 6.6% in the verapamil group vs 6.9% in the placebo group (adjusted between-group difference, -0.3% [95% CI, -1.0% to 0.4%]). Eight participants (17%) in the verapamil group and 8 participants (20%) in the placebo group had a nonserious adverse event considered to be related to treatment. Conclusions and relevance: In children and adolescents with newly diagnosed type 1 diabetes, verapamil partially preserved stimulated C-peptide secretion at 52 weeks from diagnosis compared with placebo. Further studies are needed to determine the longitudinal durability of C-peptide improvement and the optimal length of therapy